Perspectives

Cutaneous melanoma is a type of skin cancer typically associated with significant ultraviolet radiation exposure. Melanoma arises from melanocytes, cells found within the lower portion of the epidermis that make the pigment melanin.

While much less common than squamous cell carcinoma or basal cell carcinoma, melanoma is responsible for most deaths from skin cancer. In 2024, there will be more than 100,000 new cases of melanoma and over 8,000 melanoma-related deaths.¹ If localized at the time of diagnosis, survival rates are excellent. Cutaneous melanomas are more common in those with fair complexions or who have had long periods of exposure to natural or artificial sunlight.

Melanoma can also occur in mucous membranes. Mucosal melanoma is much less common than cutaneous melanoma and accounts for only a very small percentage of all new melanoma diagnoses. Unlike their cutaneous counterparts, risk factors for mucosal melanomas have yet to be identified. Although there is some disagreement on whether vulvar melanomas represent cutaneous or mucous melanomas, vulvovaginal melanomas have historically been considered to be mucosal melanomas.

Vulvovaginal melanomas are characterized by a high mortality rate, diagnostic challenges, and lack of awareness, making early detection and intervention crucial to improving patient outcomes. The 5-year overall survival rate for vulvar melanoma is 36% and for vaginal melanoma ranges between 5% and 25%.² Survival rates for vulvovaginal melanomas are lower than for other types of vulvar cancers (72%) or for cutaneous melanomas (72%-81%).²

Racial disparities in survival rates for mucosal and cutaneous melanomas were highlighted in a retrospective study using the Surveillance Epidemiology and End Results (SEER) database. Although the number of Black patients included was small, the median overall survival in that population was less than that in non-Black patients with vulvovaginal melanoma (16 vs. 39 months). Similar findings were noted in Black patients with cutaneous melanoma, compared with non-Black patients (median overall survival, 124 vs 319 months).³

One of the most significant obstacles in the diagnosis of vulvar and vaginal melanoma is its rarity. Both patients and clinicians alike may fail to recognize early warning signs. In a world where skin cancer is heavily publicized, melanoma in the genital area is not as frequently discussed or understood. Postmenopausal patients may have less regular gynecologic care, and unless they present with specific symptoms prompting an exam, melanomas can grow undetected, progressing to more advanced stages before they are discovered.

The median age of patients diagnosed with vulvar and vaginal melanomas is 67-68.^4,5 Symptoms can be subtle and nonspecific. Women with vulvar melanoma may experience symptoms that are similar to other vulvar cancers including pruritus, irritation, pain, bleeding, or a new or growing mass. While vaginal melanoma can be asymptomatic, patients frequently present with vaginal bleeding, discharge, and/or pain (including dyspareunia).

Vulvovaginal melanomas may present differently than cutaneous melanomas. Vulvar melanomas are often pigmented and frequently present as ulcerated lesions. In some cases, though, they appear amelanotic (lacking pigment), making them even harder to identify. The ABCDEs of skin cancer (asymmetry, border, color, diameter, evolving) should be applied to these lesions. Change in the size, shape, or pigment of preexisting melanosis (areas of hyperpigmentation caused by increased melanin), should raise concern for possible malignant transformation. 

Most vaginal melanomas occur within the distal third of the vagina, frequently along the anterior vaginal wall.⁶ They can be polypoid or nodular in appearance and may be ulcerated. While biopsy of any suspicious, enlarging/changing, or symptomatic lesion should be performed, it may be prudent to pause prior to biopsy of a vaginal lesion depending on its appearance. Although rare, gestational trophoblastic neoplasia (GTN) can present with vaginal metastases, and these lesions are frequently very vascular and pose a high bleeding risk if biopsied. They may look dark blue or black. If there is any concern for metastatic GTN on vaginal exam, a beta-hCG level should be obtained prior to biopsy.

Treatment of vulvovaginal melanoma may include surgical excision, systemic therapy, radiation therapy, or a combination of treatments. There is growing use of immunotherapy that mirrors cutaneous melanoma therapy.

Vulvar and vaginal melanoma represent a rare yet serious health issue for women and their impact on public health should not be underestimated. Vulvovaginal melanoma often goes unrecognized until it has reached an advanced stage. Increased awareness about these rare forms of melanoma among both patients and healthcare professionals is vital to improve early detection and treatment outcomes. With greater attention to this disease, we can strive for better diagnostic methods, more effective treatments, and ultimately, a reduction in mortality rates associated with vulvar and vaginal melanoma.

Dr. Tucker is assistant professor of gynecologic oncology at the University of North Carolina at Chapel Hill. She has no conflicts of interest.

References

1. National Cancer Institute. Cancer Stat Facts: Melanoma of the skin. 2024 Dec 2. Available from: https://seer.cancer.gov/statfacts/html/melan.html.

2. Piura B. Lancet Oncol. 2008 Oct;9(10):973-81. .

3. Mert I et al. Int J Gynecol Cancer. 2013;23(6):1118-25.

4. Wang D et al. Am J Cancer Res. 2020 Dec 1;10(12):4017-37.

5. Albert A et al. J Gynecol Oncol. 2020 Sep;31(5):e66.

Cutaneous melanoma is a type of skin cancer typically associated with significant ultraviolet radiation exposure. Melanoma arises from melanocytes, cells found within the lower portion of the epidermis that make the pigment melanin.

While much less common than squamous cell carcinoma or basal cell carcinoma, melanoma is responsible for most deaths from skin cancer. In 2024, there will be more than 100,000 new cases of melanoma and over 8,000 melanoma-related deaths.¹ If localized at the time of diagnosis, survival rates are excellent. Cutaneous melanomas are more common in those with fair complexions or who have had long periods of exposure to natural or artificial sunlight.

Melanoma can also occur in mucous membranes. Mucosal melanoma is much less common than cutaneous melanoma and accounts for only a very small percentage of all new melanoma diagnoses. Unlike their cutaneous counterparts, risk factors for mucosal melanomas have yet to be identified. Although there is some disagreement on whether vulvar melanomas represent cutaneous or mucous melanomas, vulvovaginal melanomas have historically been considered to be mucosal melanomas.

Vulvovaginal melanomas are characterized by a high mortality rate, diagnostic challenges, and lack of awareness, making early detection and intervention crucial to improving patient outcomes. The 5-year overall survival rate for vulvar melanoma is 36% and for vaginal melanoma ranges between 5% and 25%.² Survival rates for vulvovaginal melanomas are lower than for other types of vulvar cancers (72%) or for cutaneous melanomas (72%-81%).²

Racial disparities in survival rates for mucosal and cutaneous melanomas were highlighted in a retrospective study using the Surveillance Epidemiology and End Results (SEER) database. Although the number of Black patients included was small, the median overall survival in that population was less than that in non-Black patients with vulvovaginal melanoma (16 vs. 39 months). Similar findings were noted in Black patients with cutaneous melanoma, compared with non-Black patients (median overall survival, 124 vs 319 months).³

One of the most significant obstacles in the diagnosis of vulvar and vaginal melanoma is its rarity. Both patients and clinicians alike may fail to recognize early warning signs. In a world where skin cancer is heavily publicized, melanoma in the genital area is not as frequently discussed or understood. Postmenopausal patients may have less regular gynecologic care, and unless they present with specific symptoms prompting an exam, melanomas can grow undetected, progressing to more advanced stages before they are discovered.

The median age of patients diagnosed with vulvar and vaginal melanomas is 67-68.^4,5 Symptoms can be subtle and nonspecific. Women with vulvar melanoma may experience symptoms that are similar to other vulvar cancers including pruritus, irritation, pain, bleeding, or a new or growing mass. While vaginal melanoma can be asymptomatic, patients frequently present with vaginal bleeding, discharge, and/or pain (including dyspareunia).

Vulvovaginal melanomas may present differently than cutaneous melanomas. Vulvar melanomas are often pigmented and frequently present as ulcerated lesions. In some cases, though, they appear amelanotic (lacking pigment), making them even harder to identify. The ABCDEs of skin cancer (asymmetry, border, color, diameter, evolving) should be applied to these lesions. Change in the size, shape, or pigment of preexisting melanosis (areas of hyperpigmentation caused by increased melanin), should raise concern for possible malignant transformation. 

Most vaginal melanomas occur within the distal third of the vagina, frequently along the anterior vaginal wall.⁶ They can be polypoid or nodular in appearance and may be ulcerated. While biopsy of any suspicious, enlarging/changing, or symptomatic lesion should be performed, it may be prudent to pause prior to biopsy of a vaginal lesion depending on its appearance. Although rare, gestational trophoblastic neoplasia (GTN) can present with vaginal metastases, and these lesions are frequently very vascular and pose a high bleeding risk if biopsied. They may look dark blue or black. If there is any concern for metastatic GTN on vaginal exam, a beta-hCG level should be obtained prior to biopsy.

Treatment of vulvovaginal melanoma may include surgical excision, systemic therapy, radiation therapy, or a combination of treatments. There is growing use of immunotherapy that mirrors cutaneous melanoma therapy.

Vulvar and vaginal melanoma represent a rare yet serious health issue for women and their impact on public health should not be underestimated. Vulvovaginal melanoma often goes unrecognized until it has reached an advanced stage. Increased awareness about these rare forms of melanoma among both patients and healthcare professionals is vital to improve early detection and treatment outcomes. With greater attention to this disease, we can strive for better diagnostic methods, more effective treatments, and ultimately, a reduction in mortality rates associated with vulvar and vaginal melanoma.

Dr. Tucker is assistant professor of gynecologic oncology at the University of North Carolina at Chapel Hill. She has no conflicts of interest.

References

1. National Cancer Institute. Cancer Stat Facts: Melanoma of the skin. 2024 Dec 2. Available from: https://seer.cancer.gov/statfacts/html/melan.html.

2. Piura B. Lancet Oncol. 2008 Oct;9(10):973-81. .

3. Mert I et al. Int J Gynecol Cancer. 2013;23(6):1118-25.

4. Wang D et al. Am J Cancer Res. 2020 Dec 1;10(12):4017-37.

5. Albert A et al. J Gynecol Oncol. 2020 Sep;31(5):e66.

Cutaneous melanoma is a type of skin cancer typically associated with significant ultraviolet radiation exposure. Melanoma arises from melanocytes, cells found within the lower portion of the epidermis that make the pigment melanin.

While much less common than squamous cell carcinoma or basal cell carcinoma, melanoma is responsible for most deaths from skin cancer. In 2024, there will be more than 100,000 new cases of melanoma and over 8,000 melanoma-related deaths.¹ If localized at the time of diagnosis, survival rates are excellent. Cutaneous melanomas are more common in those with fair complexions or who have had long periods of exposure to natural or artificial sunlight.

Melanoma can also occur in mucous membranes. Mucosal melanoma is much less common than cutaneous melanoma and accounts for only a very small percentage of all new melanoma diagnoses. Unlike their cutaneous counterparts, risk factors for mucosal melanomas have yet to be identified. Although there is some disagreement on whether vulvar melanomas represent cutaneous or mucous melanomas, vulvovaginal melanomas have historically been considered to be mucosal melanomas.

Vulvovaginal melanomas are characterized by a high mortality rate, diagnostic challenges, and lack of awareness, making early detection and intervention crucial to improving patient outcomes. The 5-year overall survival rate for vulvar melanoma is 36% and for vaginal melanoma ranges between 5% and 25%.² Survival rates for vulvovaginal melanomas are lower than for other types of vulvar cancers (72%) or for cutaneous melanomas (72%-81%).²

Racial disparities in survival rates for mucosal and cutaneous melanomas were highlighted in a retrospective study using the Surveillance Epidemiology and End Results (SEER) database. Although the number of Black patients included was small, the median overall survival in that population was less than that in non-Black patients with vulvovaginal melanoma (16 vs. 39 months). Similar findings were noted in Black patients with cutaneous melanoma, compared with non-Black patients (median overall survival, 124 vs 319 months).³

One of the most significant obstacles in the diagnosis of vulvar and vaginal melanoma is its rarity. Both patients and clinicians alike may fail to recognize early warning signs. In a world where skin cancer is heavily publicized, melanoma in the genital area is not as frequently discussed or understood. Postmenopausal patients may have less regular gynecologic care, and unless they present with specific symptoms prompting an exam, melanomas can grow undetected, progressing to more advanced stages before they are discovered.

The median age of patients diagnosed with vulvar and vaginal melanomas is 67-68.^4,5 Symptoms can be subtle and nonspecific. Women with vulvar melanoma may experience symptoms that are similar to other vulvar cancers including pruritus, irritation, pain, bleeding, or a new or growing mass. While vaginal melanoma can be asymptomatic, patients frequently present with vaginal bleeding, discharge, and/or pain (including dyspareunia).

Vulvovaginal melanomas may present differently than cutaneous melanomas. Vulvar melanomas are often pigmented and frequently present as ulcerated lesions. In some cases, though, they appear amelanotic (lacking pigment), making them even harder to identify. The ABCDEs of skin cancer (asymmetry, border, color, diameter, evolving) should be applied to these lesions. Change in the size, shape, or pigment of preexisting melanosis (areas of hyperpigmentation caused by increased melanin), should raise concern for possible malignant transformation. 

Most vaginal melanomas occur within the distal third of the vagina, frequently along the anterior vaginal wall.⁶ They can be polypoid or nodular in appearance and may be ulcerated. While biopsy of any suspicious, enlarging/changing, or symptomatic lesion should be performed, it may be prudent to pause prior to biopsy of a vaginal lesion depending on its appearance. Although rare, gestational trophoblastic neoplasia (GTN) can present with vaginal metastases, and these lesions are frequently very vascular and pose a high bleeding risk if biopsied. They may look dark blue or black. If there is any concern for metastatic GTN on vaginal exam, a beta-hCG level should be obtained prior to biopsy.

Treatment of vulvovaginal melanoma may include surgical excision, systemic therapy, radiation therapy, or a combination of treatments. There is growing use of immunotherapy that mirrors cutaneous melanoma therapy.

Vulvar and vaginal melanoma represent a rare yet serious health issue for women and their impact on public health should not be underestimated. Vulvovaginal melanoma often goes unrecognized until it has reached an advanced stage. Increased awareness about these rare forms of melanoma among both patients and healthcare professionals is vital to improve early detection and treatment outcomes. With greater attention to this disease, we can strive for better diagnostic methods, more effective treatments, and ultimately, a reduction in mortality rates associated with vulvar and vaginal melanoma.

Dr. Tucker is assistant professor of gynecologic oncology at the University of North Carolina at Chapel Hill. She has no conflicts of interest.

References

1. National Cancer Institute. Cancer Stat Facts: Melanoma of the skin. 2024 Dec 2. Available from: https://seer.cancer.gov/statfacts/html/melan.html.

2. Piura B. Lancet Oncol. 2008 Oct;9(10):973-81. .

3. Mert I et al. Int J Gynecol Cancer. 2013;23(6):1118-25.

4. Wang D et al. Am J Cancer Res. 2020 Dec 1;10(12):4017-37.

5. Albert A et al. J Gynecol Oncol. 2020 Sep;31(5):e66.

This transcript has been edited for clarity. 

Oh, insurance claim denials. When patient care or treatment is warranted by a specific diagnosis, I wish insurers would just reimburse it without any hassle. That’s not reality. Let’s talk about insurance claim denials, how they’re rising and harming patient care, and what we can do about it. That’s kind of complicated.

Rising Trend in Claim Denials and Financial Impact

First, denials are increasing. Experian Health surveyed provider revenue cycle leaders— that’s a fancy term for people who manage billing and insurance claims — and 75% said that denials are increasing. This is up from 42% a few years ago. Those surveyed also said that reimbursement times and errors in claims are also increasing, and changes in policy are happening more frequently. This all adds to the problem. 

Aside from being time-consuming and annoying, claim denials take a toll on hospitals and patients. One analysis, which made headlines everywhere, showed that hospitals and health systems spent nearly $20 billion in 2022 trying to repeal overturned claims. This analysis was done by Premier, a health insurance performance company.

 

Breakdown of Denial Rates and Costs

Let’s do some quick whiteboard math. Health insurance companies get about 3 billion claims per year. According to surveys, about 15% of those claims are denied, so that leaves us with 450 million denied claims. Hospitals spend, on average, $43.84 per denied claim in administrative fees trying to get them overturned.

That’s about $19.7 billion spent on claim denials. Here’s the gut punch: Around 54% of those claims are ultimately paid, so that leaves us with $10.7 billion that we definitely should have saved. 

 

Common Reasons for Denials

Let’s take a look at major causes and what’s going on. 

Insurance denial rates are all over the place. It depends on state and plan. According to one analysis, the average for in-network claim denials across some states was 4% to 5%. It was 40% in Mississippi. According to HealthCare.gov, in 2021, around 17% of in-network claims were denied. 

The most common reasons were excluded services, a lack of referral or preauthorization, or a medical treatment not being deemed necessary. Then there’s the black box of “other,” just some arbitrary reason to make a claim denial. 

Many times, these denials are done by an algorithm, not by individual people. 

What’s more, a Kaiser Family Foundation analysis found that private insurers, including Medicare Advantage plans, were more likely to deny claims than public options. 

When broken down, the problem was higher among employer-sponsored and marketplace insurance, and less so with Medicare and Medicaid. 

 

Impact on Patient Care

Many consumers don’t truly understand what their health insurance covers and what’s going to be out of pocket, and many people don’t know that they have appeal rights. They don’t know who to call for help either. 

The ACA set up Consumer Assistance Programs (CAPs), which are designed to help people navigate health insurance problems. By law, private insurers have to share data with CAPs. Yet, only 3% of people who had trouble with health insurance claims called a CAP for help.

We all know some of the downstream effects of this problem. Patients may skip or delay treatments if they can’t get insurance to cover it or it’s too expensive. When post-acute care, such as transfer to a skilled nursing facility or rehab center, isn’t covered and we’re trying to discharge patients from the hospital, hospital stays become lengthened, which means they’re more expensive, and this comes with its own set of complications.

 

How Can We Address This?

I’m genuinely curious about what you all have done to efficiently address this problem. I’m looking at this publication from the American Health Information Management Association about major reasons for denial. We’ve already talked about a lack of preauthorization or procedures not being covered, but there are also reasons such as missing or incorrect information, duplicate claims, and not filing within the appropriate time.

Also, if treatments or procedures are bundled, they can’t be filed separately. 

Preventing all of this would take a large effort. Healthcare systems would have to have a dedicated team, who would understand all the major reasons for denials, identify common patterns, and then fill everything out with accurate information, with referrals, with preauthorizations, high-specificity codes, and the correct modifiers — and do all of this within the filing deadline every time. 

You would need physicians on board, but also people from IT, finance, compliance, case management, registration, and probably a bunch of other people who are already stretched too thin. 

Perhaps our government can do more to hold insurers accountable and make sure plans, such as Medicare Advantage, are holding up their end of the public health bargain.

It’s an uphill $20 billion battle, but I’m optimistic. What about you? What’s your unfiltered take on claim denials? What more can we be doing?

Dr. Patel is a clinical instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons; pediatric hospitalist, Morgan Stanley Children’s Hospital of NewYork-Presbyterian, New York City, and Benioff Children’s Hospital, University of California, San Francisco. He reported a conflict of interest with Medumo.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity. 

Oh, insurance claim denials. When patient care or treatment is warranted by a specific diagnosis, I wish insurers would just reimburse it without any hassle. That’s not reality. Let’s talk about insurance claim denials, how they’re rising and harming patient care, and what we can do about it. That’s kind of complicated.

Rising Trend in Claim Denials and Financial Impact

First, denials are increasing. Experian Health surveyed provider revenue cycle leaders— that’s a fancy term for people who manage billing and insurance claims — and 75% said that denials are increasing. This is up from 42% a few years ago. Those surveyed also said that reimbursement times and errors in claims are also increasing, and changes in policy are happening more frequently. This all adds to the problem. 

Aside from being time-consuming and annoying, claim denials take a toll on hospitals and patients. One analysis, which made headlines everywhere, showed that hospitals and health systems spent nearly $20 billion in 2022 trying to repeal overturned claims. This analysis was done by Premier, a health insurance performance company.

 

Breakdown of Denial Rates and Costs

Let’s do some quick whiteboard math. Health insurance companies get about 3 billion claims per year. According to surveys, about 15% of those claims are denied, so that leaves us with 450 million denied claims. Hospitals spend, on average, $43.84 per denied claim in administrative fees trying to get them overturned.

That’s about $19.7 billion spent on claim denials. Here’s the gut punch: Around 54% of those claims are ultimately paid, so that leaves us with $10.7 billion that we definitely should have saved. 

 

Common Reasons for Denials

Let’s take a look at major causes and what’s going on. 

Insurance denial rates are all over the place. It depends on state and plan. According to one analysis, the average for in-network claim denials across some states was 4% to 5%. It was 40% in Mississippi. According to HealthCare.gov, in 2021, around 17% of in-network claims were denied. 

The most common reasons were excluded services, a lack of referral or preauthorization, or a medical treatment not being deemed necessary. Then there’s the black box of “other,” just some arbitrary reason to make a claim denial. 

Many times, these denials are done by an algorithm, not by individual people. 

What’s more, a Kaiser Family Foundation analysis found that private insurers, including Medicare Advantage plans, were more likely to deny claims than public options. 

When broken down, the problem was higher among employer-sponsored and marketplace insurance, and less so with Medicare and Medicaid. 

 

Impact on Patient Care

Many consumers don’t truly understand what their health insurance covers and what’s going to be out of pocket, and many people don’t know that they have appeal rights. They don’t know who to call for help either. 

The ACA set up Consumer Assistance Programs (CAPs), which are designed to help people navigate health insurance problems. By law, private insurers have to share data with CAPs. Yet, only 3% of people who had trouble with health insurance claims called a CAP for help.

We all know some of the downstream effects of this problem. Patients may skip or delay treatments if they can’t get insurance to cover it or it’s too expensive. When post-acute care, such as transfer to a skilled nursing facility or rehab center, isn’t covered and we’re trying to discharge patients from the hospital, hospital stays become lengthened, which means they’re more expensive, and this comes with its own set of complications.

 

How Can We Address This?

I’m genuinely curious about what you all have done to efficiently address this problem. I’m looking at this publication from the American Health Information Management Association about major reasons for denial. We’ve already talked about a lack of preauthorization or procedures not being covered, but there are also reasons such as missing or incorrect information, duplicate claims, and not filing within the appropriate time.

Also, if treatments or procedures are bundled, they can’t be filed separately. 

Preventing all of this would take a large effort. Healthcare systems would have to have a dedicated team, who would understand all the major reasons for denials, identify common patterns, and then fill everything out with accurate information, with referrals, with preauthorizations, high-specificity codes, and the correct modifiers — and do all of this within the filing deadline every time. 

You would need physicians on board, but also people from IT, finance, compliance, case management, registration, and probably a bunch of other people who are already stretched too thin. 

Perhaps our government can do more to hold insurers accountable and make sure plans, such as Medicare Advantage, are holding up their end of the public health bargain.

It’s an uphill $20 billion battle, but I’m optimistic. What about you? What’s your unfiltered take on claim denials? What more can we be doing?

Dr. Patel is a clinical instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons; pediatric hospitalist, Morgan Stanley Children’s Hospital of NewYork-Presbyterian, New York City, and Benioff Children’s Hospital, University of California, San Francisco. He reported a conflict of interest with Medumo.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity. 

Oh, insurance claim denials. When patient care or treatment is warranted by a specific diagnosis, I wish insurers would just reimburse it without any hassle. That’s not reality. Let’s talk about insurance claim denials, how they’re rising and harming patient care, and what we can do about it. That’s kind of complicated.

Rising Trend in Claim Denials and Financial Impact

First, denials are increasing. Experian Health surveyed provider revenue cycle leaders— that’s a fancy term for people who manage billing and insurance claims — and 75% said that denials are increasing. This is up from 42% a few years ago. Those surveyed also said that reimbursement times and errors in claims are also increasing, and changes in policy are happening more frequently. This all adds to the problem. 

Aside from being time-consuming and annoying, claim denials take a toll on hospitals and patients. One analysis, which made headlines everywhere, showed that hospitals and health systems spent nearly $20 billion in 2022 trying to repeal overturned claims. This analysis was done by Premier, a health insurance performance company.

 

Breakdown of Denial Rates and Costs

Let’s do some quick whiteboard math. Health insurance companies get about 3 billion claims per year. According to surveys, about 15% of those claims are denied, so that leaves us with 450 million denied claims. Hospitals spend, on average, $43.84 per denied claim in administrative fees trying to get them overturned.

That’s about $19.7 billion spent on claim denials. Here’s the gut punch: Around 54% of those claims are ultimately paid, so that leaves us with $10.7 billion that we definitely should have saved. 

 

Common Reasons for Denials

Let’s take a look at major causes and what’s going on. 

Insurance denial rates are all over the place. It depends on state and plan. According to one analysis, the average for in-network claim denials across some states was 4% to 5%. It was 40% in Mississippi. According to HealthCare.gov, in 2021, around 17% of in-network claims were denied. 

The most common reasons were excluded services, a lack of referral or preauthorization, or a medical treatment not being deemed necessary. Then there’s the black box of “other,” just some arbitrary reason to make a claim denial. 

Many times, these denials are done by an algorithm, not by individual people. 

What’s more, a Kaiser Family Foundation analysis found that private insurers, including Medicare Advantage plans, were more likely to deny claims than public options. 

When broken down, the problem was higher among employer-sponsored and marketplace insurance, and less so with Medicare and Medicaid. 

 

Impact on Patient Care

Many consumers don’t truly understand what their health insurance covers and what’s going to be out of pocket, and many people don’t know that they have appeal rights. They don’t know who to call for help either. 

The ACA set up Consumer Assistance Programs (CAPs), which are designed to help people navigate health insurance problems. By law, private insurers have to share data with CAPs. Yet, only 3% of people who had trouble with health insurance claims called a CAP for help.

We all know some of the downstream effects of this problem. Patients may skip or delay treatments if they can’t get insurance to cover it or it’s too expensive. When post-acute care, such as transfer to a skilled nursing facility or rehab center, isn’t covered and we’re trying to discharge patients from the hospital, hospital stays become lengthened, which means they’re more expensive, and this comes with its own set of complications.

 

How Can We Address This?

I’m genuinely curious about what you all have done to efficiently address this problem. I’m looking at this publication from the American Health Information Management Association about major reasons for denial. We’ve already talked about a lack of preauthorization or procedures not being covered, but there are also reasons such as missing or incorrect information, duplicate claims, and not filing within the appropriate time.

Also, if treatments or procedures are bundled, they can’t be filed separately. 

Preventing all of this would take a large effort. Healthcare systems would have to have a dedicated team, who would understand all the major reasons for denials, identify common patterns, and then fill everything out with accurate information, with referrals, with preauthorizations, high-specificity codes, and the correct modifiers — and do all of this within the filing deadline every time. 

You would need physicians on board, but also people from IT, finance, compliance, case management, registration, and probably a bunch of other people who are already stretched too thin. 

Perhaps our government can do more to hold insurers accountable and make sure plans, such as Medicare Advantage, are holding up their end of the public health bargain.

It’s an uphill $20 billion battle, but I’m optimistic. What about you? What’s your unfiltered take on claim denials? What more can we be doing?

Dr. Patel is a clinical instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons; pediatric hospitalist, Morgan Stanley Children’s Hospital of NewYork-Presbyterian, New York City, and Benioff Children’s Hospital, University of California, San Francisco. He reported a conflict of interest with Medumo.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. 

We had a great discussion with Kidney Boy, Dr Joel Topf, everyone’s favorite nephrologist, and he taught us how to manage blood pressure in chronic kidney disease (CKD).

When should I start freaking out about a patient’s kidney function? 

Paul N. Williams, MD: Dr Topf focuses more on albuminuria than we are used to doing. It’s probably one of the most important prognostic indicators of how a patient is going to do from a renal standpoint.

Historically, I’ve tended to focus on the estimated glomerular filtration rate (eGFR), and the lower that number gets, the more I sweat, but albuminuria is probably equally, if not more, important as a way of prognosticating whether a patient is going to progress to dialysis or transplant. He directed us towards this nifty little calculator, kidneyfailurerisk.com, where you plug in the patient’s age, eGFR, and degree of albuminuria, and it spits out their risk of progressing to hemodialysis or renal transplantation over the next 5 years. It’s a nice way to concretely explain to patients their risk for progression.

Instead of telling the patient, “You are high risk,” Dr Topf will say, “Your risk is 6% of needing dialysis in the next 5 years.” You can even use these thresholds to gauge when to refer a patient. If someone has a 5-year risk between 3% and 5% or higher, that patient should probably be seeing a nephrologist.

If their 2-year risk is greater than 20%, that patient probably should be evaluated for transplantation. This gives us have more concrete numbers to work with rather than just saying, “Your kidneys aren’t working as well as we would like and you should see a kidney doctor.” Patients have a better sense of how serious things might be. 

Watto: It’s just easier for them to understand. Dr Topf made the point that we used to have a heat map based on the stage of CKD that would tell you how high a patient’s risk was compared with other people. But patients don’t really understand relative risk, so Dr Topf tells them their absolute risk for ending up on dialysis over the next 2-5 years. 

Patients come in and they are worried because they looked at their lab results and see that their creatinine level is red, or their eGFR is low. They think, It says I have stage 3a CKD. 

We should probably have the stages of CKD start at stage 3, which should be called stage 1 so it doesn’t sound as bad. Patients think they are halfway to dialysis; they are already at stage 3 and didn’t even know their kidneys were a problem. 

Dr Topf said that cystatin C (something I only recently started ordering) can be obtained, and sometimes you can recategorize the patient, especially those with an eGFR between 45 and 60. The cystatin C can predict their renal function better than the creatinine-based equations. If you are using the creatinine equation, he recommends using the 2021 equations.

Another nice thing about cystatin C is that it isn’t tripped up in younger patients with a lot of muscle mass. You just have to watch out for inflammation, which can throw the test off. For example, when a patient is in the intensive care unit, it’s probably not that helpful, but for your outpatients, cystatin C works well. 

Williams: I’ve been using it a fair amount in my patients with more muscle mass. And some patients have been taking creatine as a supplement, and that can alter the numbers as well. This is a nice way to get them out of CKD stage 2 or 3 and back where they belong, with normal healthy functioning kidneys.

Watto: Now, Paul, if we find a patient with more advanced CKD — let’s say stage 4, whether by cystatin C or serum creatinine, and their eGFR is less than 30 — should we start peeling off the angiotensin-converting enzyme ACE inhibitor or the angiotensin receptor blocker (ARB)? Those drugs can raise potassium. What should we do here? 

Williams: That’s the temptation, Matt, and I feel like that was the old orthodoxy, back in residency. It didn’t take much for us to start taking off ACE inhibitors or ARBs once the kidney function started to drop, but it turns out you may be doing more harm than good.

Some data have shown that if you peel off those medications, you actually increase mortality and cardiovascular risk. So, in general, if you can keep them going, the patient will be better off. Hang onto the ACE inhibitors or ARBs as long as you are able to, because they confer a fair amount of benefit.

Watto: As long as the potassium isn’t in red on your lab’s range. It might go up to 5.2 or 5.4, but as long as it’s stable, that should be OK. You probably wouldn’t initiate an ACE inhibitor or ARB or spironolactone with a potassium level above 5, but if it’s below 5 when you start and it goes up slightly after you start the drug, that could be acceptable. 

Another thing we talked about was when a patient progresses to CKD and ends up on dialysis, how helpful are those intradialysis blood pressures in predicting cardiovascular outcomes? 

Williams: For someone who’s performing the dialysis, probably really helpful. In the outpatient setting to predict cardiovascular risk, probably less so. Dr Topf makes the point that the readings are done either shortly after or right when the patient is about to have a large-bore catheter inserted into their arm. And then they have liters of fluid drained out of them. So those numbers are going to have huge amounts of variability. You would not base the patient’s blood pressure treatment solely on those numbers. But regardless of what the numbers are, or even regardless of your office numbers, hopefully you’re working with a nephrologist to make sure that you’re actually in concert and not fighting each other with the blood pressure medications.

Watto: Dr Topf said that a lot of the hypertension in dialysis is because of too much volume. If you can get the volume down, you might be able to peel off blood pressure medications instead of adding more. But some patients have issues with cramping; it’s uncomfortable and not everyone tolerates it. 

I was really surprised to learn that beta blockers, specifically atenolol, have some evidence of improving cardiovascular outcomes in patients on dialysis. Dr Topf speculated that this was because they are largely dying of cardiovascular disease, so maybe that’s why, but that’s one of the places, the only places I can think of aside from thyroid disease, where atenolol really shines. 

If you want to hear this fantastic episode and all the great pearls, then click on this link. 

Matthew F. Watto, MD, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, disclosed no relevant financial relationships. Paul N. Williams, MD, has disclosed ties with The Curbsiders.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. 

We had a great discussion with Kidney Boy, Dr Joel Topf, everyone’s favorite nephrologist, and he taught us how to manage blood pressure in chronic kidney disease (CKD).

When should I start freaking out about a patient’s kidney function? 

Paul N. Williams, MD: Dr Topf focuses more on albuminuria than we are used to doing. It’s probably one of the most important prognostic indicators of how a patient is going to do from a renal standpoint.

Historically, I’ve tended to focus on the estimated glomerular filtration rate (eGFR), and the lower that number gets, the more I sweat, but albuminuria is probably equally, if not more, important as a way of prognosticating whether a patient is going to progress to dialysis or transplant. He directed us towards this nifty little calculator, kidneyfailurerisk.com, where you plug in the patient’s age, eGFR, and degree of albuminuria, and it spits out their risk of progressing to hemodialysis or renal transplantation over the next 5 years. It’s a nice way to concretely explain to patients their risk for progression.

Instead of telling the patient, “You are high risk,” Dr Topf will say, “Your risk is 6% of needing dialysis in the next 5 years.” You can even use these thresholds to gauge when to refer a patient. If someone has a 5-year risk between 3% and 5% or higher, that patient should probably be seeing a nephrologist.

If their 2-year risk is greater than 20%, that patient probably should be evaluated for transplantation. This gives us have more concrete numbers to work with rather than just saying, “Your kidneys aren’t working as well as we would like and you should see a kidney doctor.” Patients have a better sense of how serious things might be. 

Watto: It’s just easier for them to understand. Dr Topf made the point that we used to have a heat map based on the stage of CKD that would tell you how high a patient’s risk was compared with other people. But patients don’t really understand relative risk, so Dr Topf tells them their absolute risk for ending up on dialysis over the next 2-5 years. 

Patients come in and they are worried because they looked at their lab results and see that their creatinine level is red, or their eGFR is low. They think, It says I have stage 3a CKD. 

We should probably have the stages of CKD start at stage 3, which should be called stage 1 so it doesn’t sound as bad. Patients think they are halfway to dialysis; they are already at stage 3 and didn’t even know their kidneys were a problem. 

Dr Topf said that cystatin C (something I only recently started ordering) can be obtained, and sometimes you can recategorize the patient, especially those with an eGFR between 45 and 60. The cystatin C can predict their renal function better than the creatinine-based equations. If you are using the creatinine equation, he recommends using the 2021 equations.

Another nice thing about cystatin C is that it isn’t tripped up in younger patients with a lot of muscle mass. You just have to watch out for inflammation, which can throw the test off. For example, when a patient is in the intensive care unit, it’s probably not that helpful, but for your outpatients, cystatin C works well. 

Williams: I’ve been using it a fair amount in my patients with more muscle mass. And some patients have been taking creatine as a supplement, and that can alter the numbers as well. This is a nice way to get them out of CKD stage 2 or 3 and back where they belong, with normal healthy functioning kidneys.

Watto: Now, Paul, if we find a patient with more advanced CKD — let’s say stage 4, whether by cystatin C or serum creatinine, and their eGFR is less than 30 — should we start peeling off the angiotensin-converting enzyme ACE inhibitor or the angiotensin receptor blocker (ARB)? Those drugs can raise potassium. What should we do here? 

Williams: That’s the temptation, Matt, and I feel like that was the old orthodoxy, back in residency. It didn’t take much for us to start taking off ACE inhibitors or ARBs once the kidney function started to drop, but it turns out you may be doing more harm than good.

Some data have shown that if you peel off those medications, you actually increase mortality and cardiovascular risk. So, in general, if you can keep them going, the patient will be better off. Hang onto the ACE inhibitors or ARBs as long as you are able to, because they confer a fair amount of benefit.

Watto: As long as the potassium isn’t in red on your lab’s range. It might go up to 5.2 or 5.4, but as long as it’s stable, that should be OK. You probably wouldn’t initiate an ACE inhibitor or ARB or spironolactone with a potassium level above 5, but if it’s below 5 when you start and it goes up slightly after you start the drug, that could be acceptable. 

Another thing we talked about was when a patient progresses to CKD and ends up on dialysis, how helpful are those intradialysis blood pressures in predicting cardiovascular outcomes? 

Williams: For someone who’s performing the dialysis, probably really helpful. In the outpatient setting to predict cardiovascular risk, probably less so. Dr Topf makes the point that the readings are done either shortly after or right when the patient is about to have a large-bore catheter inserted into their arm. And then they have liters of fluid drained out of them. So those numbers are going to have huge amounts of variability. You would not base the patient’s blood pressure treatment solely on those numbers. But regardless of what the numbers are, or even regardless of your office numbers, hopefully you’re working with a nephrologist to make sure that you’re actually in concert and not fighting each other with the blood pressure medications.

Watto: Dr Topf said that a lot of the hypertension in dialysis is because of too much volume. If you can get the volume down, you might be able to peel off blood pressure medications instead of adding more. But some patients have issues with cramping; it’s uncomfortable and not everyone tolerates it. 

I was really surprised to learn that beta blockers, specifically atenolol, have some evidence of improving cardiovascular outcomes in patients on dialysis. Dr Topf speculated that this was because they are largely dying of cardiovascular disease, so maybe that’s why, but that’s one of the places, the only places I can think of aside from thyroid disease, where atenolol really shines. 

If you want to hear this fantastic episode and all the great pearls, then click on this link. 

Matthew F. Watto, MD, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, disclosed no relevant financial relationships. Paul N. Williams, MD, has disclosed ties with The Curbsiders.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. 

We had a great discussion with Kidney Boy, Dr Joel Topf, everyone’s favorite nephrologist, and he taught us how to manage blood pressure in chronic kidney disease (CKD).

When should I start freaking out about a patient’s kidney function? 

Paul N. Williams, MD: Dr Topf focuses more on albuminuria than we are used to doing. It’s probably one of the most important prognostic indicators of how a patient is going to do from a renal standpoint.

Historically, I’ve tended to focus on the estimated glomerular filtration rate (eGFR), and the lower that number gets, the more I sweat, but albuminuria is probably equally, if not more, important as a way of prognosticating whether a patient is going to progress to dialysis or transplant. He directed us towards this nifty little calculator, kidneyfailurerisk.com, where you plug in the patient’s age, eGFR, and degree of albuminuria, and it spits out their risk of progressing to hemodialysis or renal transplantation over the next 5 years. It’s a nice way to concretely explain to patients their risk for progression.

Instead of telling the patient, “You are high risk,” Dr Topf will say, “Your risk is 6% of needing dialysis in the next 5 years.” You can even use these thresholds to gauge when to refer a patient. If someone has a 5-year risk between 3% and 5% or higher, that patient should probably be seeing a nephrologist.

If their 2-year risk is greater than 20%, that patient probably should be evaluated for transplantation. This gives us have more concrete numbers to work with rather than just saying, “Your kidneys aren’t working as well as we would like and you should see a kidney doctor.” Patients have a better sense of how serious things might be. 

Watto: It’s just easier for them to understand. Dr Topf made the point that we used to have a heat map based on the stage of CKD that would tell you how high a patient’s risk was compared with other people. But patients don’t really understand relative risk, so Dr Topf tells them their absolute risk for ending up on dialysis over the next 2-5 years. 

Patients come in and they are worried because they looked at their lab results and see that their creatinine level is red, or their eGFR is low. They think, It says I have stage 3a CKD. 

We should probably have the stages of CKD start at stage 3, which should be called stage 1 so it doesn’t sound as bad. Patients think they are halfway to dialysis; they are already at stage 3 and didn’t even know their kidneys were a problem. 

Dr Topf said that cystatin C (something I only recently started ordering) can be obtained, and sometimes you can recategorize the patient, especially those with an eGFR between 45 and 60. The cystatin C can predict their renal function better than the creatinine-based equations. If you are using the creatinine equation, he recommends using the 2021 equations.

Another nice thing about cystatin C is that it isn’t tripped up in younger patients with a lot of muscle mass. You just have to watch out for inflammation, which can throw the test off. For example, when a patient is in the intensive care unit, it’s probably not that helpful, but for your outpatients, cystatin C works well. 

Williams: I’ve been using it a fair amount in my patients with more muscle mass. And some patients have been taking creatine as a supplement, and that can alter the numbers as well. This is a nice way to get them out of CKD stage 2 or 3 and back where they belong, with normal healthy functioning kidneys.

Watto: Now, Paul, if we find a patient with more advanced CKD — let’s say stage 4, whether by cystatin C or serum creatinine, and their eGFR is less than 30 — should we start peeling off the angiotensin-converting enzyme ACE inhibitor or the angiotensin receptor blocker (ARB)? Those drugs can raise potassium. What should we do here? 

Williams: That’s the temptation, Matt, and I feel like that was the old orthodoxy, back in residency. It didn’t take much for us to start taking off ACE inhibitors or ARBs once the kidney function started to drop, but it turns out you may be doing more harm than good.

Some data have shown that if you peel off those medications, you actually increase mortality and cardiovascular risk. So, in general, if you can keep them going, the patient will be better off. Hang onto the ACE inhibitors or ARBs as long as you are able to, because they confer a fair amount of benefit.

Watto: As long as the potassium isn’t in red on your lab’s range. It might go up to 5.2 or 5.4, but as long as it’s stable, that should be OK. You probably wouldn’t initiate an ACE inhibitor or ARB or spironolactone with a potassium level above 5, but if it’s below 5 when you start and it goes up slightly after you start the drug, that could be acceptable. 

Another thing we talked about was when a patient progresses to CKD and ends up on dialysis, how helpful are those intradialysis blood pressures in predicting cardiovascular outcomes? 

Williams: For someone who’s performing the dialysis, probably really helpful. In the outpatient setting to predict cardiovascular risk, probably less so. Dr Topf makes the point that the readings are done either shortly after or right when the patient is about to have a large-bore catheter inserted into their arm. And then they have liters of fluid drained out of them. So those numbers are going to have huge amounts of variability. You would not base the patient’s blood pressure treatment solely on those numbers. But regardless of what the numbers are, or even regardless of your office numbers, hopefully you’re working with a nephrologist to make sure that you’re actually in concert and not fighting each other with the blood pressure medications.

Watto: Dr Topf said that a lot of the hypertension in dialysis is because of too much volume. If you can get the volume down, you might be able to peel off blood pressure medications instead of adding more. But some patients have issues with cramping; it’s uncomfortable and not everyone tolerates it. 

I was really surprised to learn that beta blockers, specifically atenolol, have some evidence of improving cardiovascular outcomes in patients on dialysis. Dr Topf speculated that this was because they are largely dying of cardiovascular disease, so maybe that’s why, but that’s one of the places, the only places I can think of aside from thyroid disease, where atenolol really shines. 

If you want to hear this fantastic episode and all the great pearls, then click on this link. 

Matthew F. Watto, MD, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, disclosed no relevant financial relationships. Paul N. Williams, MD, has disclosed ties with The Curbsiders.

This transcript has been edited for clarity. 

Hello. I’m David Kerr, professor of cancer medicine at University of Oxford. As I become, sadly, older, I’ve become much more interested in the concept of cancer prevention than cancer treatment. Of course, I’m still a practicing cancer physician and researcher. That’s my daily bread and butter. But prevention is important. 

There’s a really interesting article in the Christmas edition of The BMJ. This is an opportunity for us to take good science, but lighthearted science, to titillate and amuse our Christmas readers. This is a nice article from the States led by Joshua Wallach. As I say, this brings together good science in a sometimes absurd setting. I’ll read its title: “Association of Health Benefits and Harms of Christmas Dessert Ingredients in Recipes From The Great British Bake Off: Umbrella Review of Umbrella Reviews of Meta-analyses of Observational Studies.”

It’s obviously a very strong statistical underpinning from this group from Yale, predominantly — a half-decent university, as those of us from Oxford would have to admit. They used The Great British Bake Off website, Embase, Medline, and Scopus. They looked at the whole host of umbrella reviews and so on. 

They were interested in looking at the relative balance of dangerous and protective ingredients that were recommended in Christmas desserts on this immensely popular television show called The Great British Bake Off. Some of you have watched it and have enjoyed watching the trials and tribulations of the various contestants. 

They looked at 48 recipes for Christmas desserts, including cakes, biscuits, pastries, puddings, and conventional desserts. Of all these, there were 178 unique ingredients. Literature research then parsed whether these ingredients were good for you or bad for you. 

It was very interesting that, when they put the summary together, the umbrella review of umbrella reviews of meta-analyses compressed together, it was good news for us all. Recipes for Christmas desserts, particularly from The Great British Bake Off — which should be enormously proud of this — tend to use ingredient groups that are associated with reductions rather than increases in the risk for disease. Hurrah!

This means that, clearly, Christmas is a time in which those of us who can, tend to overindulge in food. The granddad falling asleep with a full tummy, sitting with the family in front of a hot fire — all of us can remember and imagine all of that. 

Perhaps the most important takeaway point from this observationally, critically important study is that, yes — at Christmas time, enjoy the dessert. You can have your cake and eat it, too. You heard it here. It’s philosophically true and statistically proven: You can have your cake and eat it. 

Thanks for listening. I’d be very interested in your own recipes, and whether we think that the American Thanksgiving desserts correlate with British Christmas desserts in some way and are beneficial to your health. 

Have a look at this article that is cleverly, wittily written. As always, Medscapers, for the time being, thanks for listening. Over and out. 

 

Dr Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, has disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers (Board of Directors); Afrox (charity; Trustee); GlaxoSmithKline and Bayer HealthCare Pharmaceuticals (Consultant); Genomic Health; Merck Serono, Roche. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Hello. I’m David Kerr, professor of cancer medicine at University of Oxford. As I become, sadly, older, I’ve become much more interested in the concept of cancer prevention than cancer treatment. Of course, I’m still a practicing cancer physician and researcher. That’s my daily bread and butter. But prevention is important. 

There’s a really interesting article in the Christmas edition of The BMJ. This is an opportunity for us to take good science, but lighthearted science, to titillate and amuse our Christmas readers. This is a nice article from the States led by Joshua Wallach. As I say, this brings together good science in a sometimes absurd setting. I’ll read its title: “Association of Health Benefits and Harms of Christmas Dessert Ingredients in Recipes From The Great British Bake Off: Umbrella Review of Umbrella Reviews of Meta-analyses of Observational Studies.”

It’s obviously a very strong statistical underpinning from this group from Yale, predominantly — a half-decent university, as those of us from Oxford would have to admit. They used The Great British Bake Off website, Embase, Medline, and Scopus. They looked at the whole host of umbrella reviews and so on. 

They were interested in looking at the relative balance of dangerous and protective ingredients that were recommended in Christmas desserts on this immensely popular television show called The Great British Bake Off. Some of you have watched it and have enjoyed watching the trials and tribulations of the various contestants. 

They looked at 48 recipes for Christmas desserts, including cakes, biscuits, pastries, puddings, and conventional desserts. Of all these, there were 178 unique ingredients. Literature research then parsed whether these ingredients were good for you or bad for you. 

It was very interesting that, when they put the summary together, the umbrella review of umbrella reviews of meta-analyses compressed together, it was good news for us all. Recipes for Christmas desserts, particularly from The Great British Bake Off — which should be enormously proud of this — tend to use ingredient groups that are associated with reductions rather than increases in the risk for disease. Hurrah!

This means that, clearly, Christmas is a time in which those of us who can, tend to overindulge in food. The granddad falling asleep with a full tummy, sitting with the family in front of a hot fire — all of us can remember and imagine all of that. 

Perhaps the most important takeaway point from this observationally, critically important study is that, yes — at Christmas time, enjoy the dessert. You can have your cake and eat it, too. You heard it here. It’s philosophically true and statistically proven: You can have your cake and eat it. 

Thanks for listening. I’d be very interested in your own recipes, and whether we think that the American Thanksgiving desserts correlate with British Christmas desserts in some way and are beneficial to your health. 

Have a look at this article that is cleverly, wittily written. As always, Medscapers, for the time being, thanks for listening. Over and out. 

 

Dr Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, has disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers (Board of Directors); Afrox (charity; Trustee); GlaxoSmithKline and Bayer HealthCare Pharmaceuticals (Consultant); Genomic Health; Merck Serono, Roche. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Hello. I’m David Kerr, professor of cancer medicine at University of Oxford. As I become, sadly, older, I’ve become much more interested in the concept of cancer prevention than cancer treatment. Of course, I’m still a practicing cancer physician and researcher. That’s my daily bread and butter. But prevention is important. 

There’s a really interesting article in the Christmas edition of The BMJ. This is an opportunity for us to take good science, but lighthearted science, to titillate and amuse our Christmas readers. This is a nice article from the States led by Joshua Wallach. As I say, this brings together good science in a sometimes absurd setting. I’ll read its title: “Association of Health Benefits and Harms of Christmas Dessert Ingredients in Recipes From The Great British Bake Off: Umbrella Review of Umbrella Reviews of Meta-analyses of Observational Studies.”

It’s obviously a very strong statistical underpinning from this group from Yale, predominantly — a half-decent university, as those of us from Oxford would have to admit. They used The Great British Bake Off website, Embase, Medline, and Scopus. They looked at the whole host of umbrella reviews and so on. 

They were interested in looking at the relative balance of dangerous and protective ingredients that were recommended in Christmas desserts on this immensely popular television show called The Great British Bake Off. Some of you have watched it and have enjoyed watching the trials and tribulations of the various contestants. 

They looked at 48 recipes for Christmas desserts, including cakes, biscuits, pastries, puddings, and conventional desserts. Of all these, there were 178 unique ingredients. Literature research then parsed whether these ingredients were good for you or bad for you. 

It was very interesting that, when they put the summary together, the umbrella review of umbrella reviews of meta-analyses compressed together, it was good news for us all. Recipes for Christmas desserts, particularly from The Great British Bake Off — which should be enormously proud of this — tend to use ingredient groups that are associated with reductions rather than increases in the risk for disease. Hurrah!

This means that, clearly, Christmas is a time in which those of us who can, tend to overindulge in food. The granddad falling asleep with a full tummy, sitting with the family in front of a hot fire — all of us can remember and imagine all of that. 

Perhaps the most important takeaway point from this observationally, critically important study is that, yes — at Christmas time, enjoy the dessert. You can have your cake and eat it, too. You heard it here. It’s philosophically true and statistically proven: You can have your cake and eat it. 

Thanks for listening. I’d be very interested in your own recipes, and whether we think that the American Thanksgiving desserts correlate with British Christmas desserts in some way and are beneficial to your health. 

Have a look at this article that is cleverly, wittily written. As always, Medscapers, for the time being, thanks for listening. Over and out. 

 

Dr Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, has disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers (Board of Directors); Afrox (charity; Trustee); GlaxoSmithKline and Bayer HealthCare Pharmaceuticals (Consultant); Genomic Health; Merck Serono, Roche. 

A version of this article appeared on Medscape.com.

If you’ve ever taken a red-eye flight you have probably received a little packet of items the airline hopes will make your night flight more comfortable. If you had shelled out for “extra leg room” or “more comfort” seating, your little kit may have included some one-size-never-fits-all socks, a toothbrush large enough to brush one tooth at a time, and a miniature tube of toothpaste the GEICO gecko would laugh at. I have no personal knowledge what the folks in first class are getting, but I suspect it comes in a calf skin Gucci pouch. But, regardless of where you are sitting, at a minimum your night comfort kit will come with an eye mask and ear plugs. Unfortunately, these freebies are wasted on me because I already use a sleep mask every night and simply turn off my hearing aids to mute the noise. But I appreciate their effort.

Light and sound are well-known sleep disruptors. Temperature gets less attention, but is nonetheless a potent contributor to a poor night’s sleep in my experience. Just by chance while I was recovering from my most recent jet lag, I encountered two papers from investigators who were curious about the association between healthy sleep and ambient light and noise.

 

The first paper looked at the relationship between artificial light at night (ALAN) and the incidence of insomnia. Looking at more than 300 Chinese cities, the investigators measured ALAN using satellite images and correlated the data with insomnia-related posts on social media. The researchers found when ALAN increased insomnia, related posts also increased. Not surprisingly, this relationship was greater in less populated cities during extreme temperatures and when air quality was poor. 

The second paper came from University of Texas at Houston. Using Fitbit data from more than 3000 adolescents, the researchers looked for correlations between blood pressure, sleep health, and “median nighttime anthropogenic noise levels by ZIP code.” Turns out the Federal Highway Administration has a readily available map of these noise levels. 

What the investigators found was that adequate sleep significantly reduces the risk of hypertension in adolescents. Not an unexpected finding to an ex-pediatrician like myself who is obsessed with the importance of sleep deprivation. However, the investigators and I were surprised that they had found no association between neighborhood noise alone or in combination with sleep health. I still suspect there is an association lurking there in the weeds of their data, but obviously it is not robust enough to float to the surface. It may be that in an acute situation noise can contribute to hypertension, but over time individuals adjust to the new sound level and their blood pressure settles down. Sleep is such a critical factor that it is not something our cardiovascular system can adapt to so easily. For various reasons most of us may already be functioning at the margins of sleep deprivation.

How then do we respond to observations by these two research teams? Do we take an approach similar to that the airlines have taken and prescribe, hand out, or sell ear plugs and sleep masks to every patient, or at least those with hypertension? This is what we could call the put-the-onus-on-the-patient approach, which seems to be the default when we lack the political will to take a bolder step.

The other path we could call the socio-environmental approach. The airlines have made a passing attempt at this by turning the cabin lights down on red-eye flights. I recently wrote about the “exposome,” which some investigators define as the total non-genetic exposures an individual endures during a lifetime and which in many situations has a negative effect on the individual’s health. These two papers clearly demonstrate that noise and nighttime artificial light are potent features of an uncountable number of individuals’ exposomes.

Noise and artificial light are both things that as a society we have the power to control if we could only muster up the political will to do so. Unfortunately, it is going to require something far beyond these two relatively obscure studies to move the needle in the direction of a healthier population. It’s is not a stretch to put obesity and the attention deficit phenomenon under this same umbrella where our society needs to look at itself for the answers.

 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com. 

If you’ve ever taken a red-eye flight you have probably received a little packet of items the airline hopes will make your night flight more comfortable. If you had shelled out for “extra leg room” or “more comfort” seating, your little kit may have included some one-size-never-fits-all socks, a toothbrush large enough to brush one tooth at a time, and a miniature tube of toothpaste the GEICO gecko would laugh at. I have no personal knowledge what the folks in first class are getting, but I suspect it comes in a calf skin Gucci pouch. But, regardless of where you are sitting, at a minimum your night comfort kit will come with an eye mask and ear plugs. Unfortunately, these freebies are wasted on me because I already use a sleep mask every night and simply turn off my hearing aids to mute the noise. But I appreciate their effort.

Light and sound are well-known sleep disruptors. Temperature gets less attention, but is nonetheless a potent contributor to a poor night’s sleep in my experience. Just by chance while I was recovering from my most recent jet lag, I encountered two papers from investigators who were curious about the association between healthy sleep and ambient light and noise.

 

The first paper looked at the relationship between artificial light at night (ALAN) and the incidence of insomnia. Looking at more than 300 Chinese cities, the investigators measured ALAN using satellite images and correlated the data with insomnia-related posts on social media. The researchers found when ALAN increased insomnia, related posts also increased. Not surprisingly, this relationship was greater in less populated cities during extreme temperatures and when air quality was poor. 

The second paper came from University of Texas at Houston. Using Fitbit data from more than 3000 adolescents, the researchers looked for correlations between blood pressure, sleep health, and “median nighttime anthropogenic noise levels by ZIP code.” Turns out the Federal Highway Administration has a readily available map of these noise levels. 

What the investigators found was that adequate sleep significantly reduces the risk of hypertension in adolescents. Not an unexpected finding to an ex-pediatrician like myself who is obsessed with the importance of sleep deprivation. However, the investigators and I were surprised that they had found no association between neighborhood noise alone or in combination with sleep health. I still suspect there is an association lurking there in the weeds of their data, but obviously it is not robust enough to float to the surface. It may be that in an acute situation noise can contribute to hypertension, but over time individuals adjust to the new sound level and their blood pressure settles down. Sleep is such a critical factor that it is not something our cardiovascular system can adapt to so easily. For various reasons most of us may already be functioning at the margins of sleep deprivation.

How then do we respond to observations by these two research teams? Do we take an approach similar to that the airlines have taken and prescribe, hand out, or sell ear plugs and sleep masks to every patient, or at least those with hypertension? This is what we could call the put-the-onus-on-the-patient approach, which seems to be the default when we lack the political will to take a bolder step.

The other path we could call the socio-environmental approach. The airlines have made a passing attempt at this by turning the cabin lights down on red-eye flights. I recently wrote about the “exposome,” which some investigators define as the total non-genetic exposures an individual endures during a lifetime and which in many situations has a negative effect on the individual’s health. These two papers clearly demonstrate that noise and nighttime artificial light are potent features of an uncountable number of individuals’ exposomes.

Noise and artificial light are both things that as a society we have the power to control if we could only muster up the political will to do so. Unfortunately, it is going to require something far beyond these two relatively obscure studies to move the needle in the direction of a healthier population. It’s is not a stretch to put obesity and the attention deficit phenomenon under this same umbrella where our society needs to look at itself for the answers.

 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com. 

If you’ve ever taken a red-eye flight you have probably received a little packet of items the airline hopes will make your night flight more comfortable. If you had shelled out for “extra leg room” or “more comfort” seating, your little kit may have included some one-size-never-fits-all socks, a toothbrush large enough to brush one tooth at a time, and a miniature tube of toothpaste the GEICO gecko would laugh at. I have no personal knowledge what the folks in first class are getting, but I suspect it comes in a calf skin Gucci pouch. But, regardless of where you are sitting, at a minimum your night comfort kit will come with an eye mask and ear plugs. Unfortunately, these freebies are wasted on me because I already use a sleep mask every night and simply turn off my hearing aids to mute the noise. But I appreciate their effort.

Light and sound are well-known sleep disruptors. Temperature gets less attention, but is nonetheless a potent contributor to a poor night’s sleep in my experience. Just by chance while I was recovering from my most recent jet lag, I encountered two papers from investigators who were curious about the association between healthy sleep and ambient light and noise.

 

The first paper looked at the relationship between artificial light at night (ALAN) and the incidence of insomnia. Looking at more than 300 Chinese cities, the investigators measured ALAN using satellite images and correlated the data with insomnia-related posts on social media. The researchers found when ALAN increased insomnia, related posts also increased. Not surprisingly, this relationship was greater in less populated cities during extreme temperatures and when air quality was poor. 

The second paper came from University of Texas at Houston. Using Fitbit data from more than 3000 adolescents, the researchers looked for correlations between blood pressure, sleep health, and “median nighttime anthropogenic noise levels by ZIP code.” Turns out the Federal Highway Administration has a readily available map of these noise levels. 

What the investigators found was that adequate sleep significantly reduces the risk of hypertension in adolescents. Not an unexpected finding to an ex-pediatrician like myself who is obsessed with the importance of sleep deprivation. However, the investigators and I were surprised that they had found no association between neighborhood noise alone or in combination with sleep health. I still suspect there is an association lurking there in the weeds of their data, but obviously it is not robust enough to float to the surface. It may be that in an acute situation noise can contribute to hypertension, but over time individuals adjust to the new sound level and their blood pressure settles down. Sleep is such a critical factor that it is not something our cardiovascular system can adapt to so easily. For various reasons most of us may already be functioning at the margins of sleep deprivation.

How then do we respond to observations by these two research teams? Do we take an approach similar to that the airlines have taken and prescribe, hand out, or sell ear plugs and sleep masks to every patient, or at least those with hypertension? This is what we could call the put-the-onus-on-the-patient approach, which seems to be the default when we lack the political will to take a bolder step.

The other path we could call the socio-environmental approach. The airlines have made a passing attempt at this by turning the cabin lights down on red-eye flights. I recently wrote about the “exposome,” which some investigators define as the total non-genetic exposures an individual endures during a lifetime and which in many situations has a negative effect on the individual’s health. These two papers clearly demonstrate that noise and nighttime artificial light are potent features of an uncountable number of individuals’ exposomes.

Noise and artificial light are both things that as a society we have the power to control if we could only muster up the political will to do so. Unfortunately, it is going to require something far beyond these two relatively obscure studies to move the needle in the direction of a healthier population. It’s is not a stretch to put obesity and the attention deficit phenomenon under this same umbrella where our society needs to look at itself for the answers.

 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com. 

This transcript has been edited for clarity. 

I’d like to reflect a little on the ever-rising incidence of early-onset colorectal cancer. I saw two patients in the clinic on Friday, both in their early thirties, presenting with stage IV disease. Both had young families — a disaster.

This is an issue that we must address, I think, epidemiologically. We know that early-onset colorectal cancer is defined as a disease arising in those under the age of 50. There’s been a very sharp increase globally over the past 20-30 years, and currently, around 200,000 such cases are diagnosed every year, but it is said to increase unquestionably.

The epidemiologists, I think, correctly have identified that this sharp, rapid increase does imply that there is a new environmental change that is underpinning or underscoring this rise in early-onset disease. 

There’s a fantastic team that has been put together by Paul Brennan, Mike Stratton, and colleagues, a collaborative group of epidemiologists, geneticists, and bioinformaticians, who are looking at a global study to try to understand the basis of early-onset colorectal cancer. Their approach is to combine conventional epidemiology, genomics, and fantastic computational support to try to unpick the mutational signatures involved.

The dominant hypothesis is that, over the past 20-25 years or so, there has been a change in diet that has allowed an alteration in the gut microbiome such that we now harbor, in some cases, more bacteria capable of manufacturing, synthesizing, and releasing mutagenic chemicals. There’s a subtype of Escherichia coli which manufactures one such mutagen called colibactin.

Again, through some of the painstaking, extraordinary work that Mike Stratton and colleagues have done at the Sanger Institute, they have managed to, using a variety of different techniques — in vitro, observational, and so on — relate exposure to the mutagen colibactin to a particular mutational signature.

They plan to do a large global study — one of the strengths — involving many different countries around the globe, collect material from older colorectal cancer patients and early-onset colorectal cancer patients, and undertake a staggeringly large mutational study to see if the mutational signature associated with colibactin is more highly represented in these early-onset cases. The hypothesis is that, if you’re exposed to this mutagen in childhood, then it increases the tumor mutational burden and therefore the likelihood of developing cancer at an earlier age. 

All of us believe that converting a normal cell into a tumor cell usually requires five or six or seven separate mutational events occurring at random. The earlier these occur, the greater the tumor, the greater the normal single-cellular mutational burden, and the more likely it is to develop cancer sooner rather than later. 

This is a fantastically interesting study, and it’s the way ahead with modern genetic epidemiology, one would say. We wish them well. This will be a 3- to 5-year truly international effort, bringing together a genuinely internationally outstanding research team. We hope that they are able to shed more light on the epidemiology of this early-onset disease, because only by understanding can we deflect and deal with it. 

Knowledge is power, as I’ve said many times before. If we understand the underlying epidemiology, that will allow us to intervene, one would hope, and avoid the chaotic disaster of my clinic on Friday, with these two young patients with an extremely limited lifespan and large families who will be left bereft in having lost a parent.

More power to the team. We wish them well with the study, but again, this is a pointer to the future, one would hope, of modern genetic computational epidemiology. 

I’d be really interested in any ideas or comments that you might have. Are you in the field? Are you seeing more young patients? Do you have any ideas or hypotheses of your own around the microbiome and what bugs might be involved and so on?

Dr. Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford, England; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, has disclosed relevant financial relationships with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, Merck Serono, and Roche. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

I’d like to reflect a little on the ever-rising incidence of early-onset colorectal cancer. I saw two patients in the clinic on Friday, both in their early thirties, presenting with stage IV disease. Both had young families — a disaster.

This is an issue that we must address, I think, epidemiologically. We know that early-onset colorectal cancer is defined as a disease arising in those under the age of 50. There’s been a very sharp increase globally over the past 20-30 years, and currently, around 200,000 such cases are diagnosed every year, but it is said to increase unquestionably.

The epidemiologists, I think, correctly have identified that this sharp, rapid increase does imply that there is a new environmental change that is underpinning or underscoring this rise in early-onset disease. 

There’s a fantastic team that has been put together by Paul Brennan, Mike Stratton, and colleagues, a collaborative group of epidemiologists, geneticists, and bioinformaticians, who are looking at a global study to try to understand the basis of early-onset colorectal cancer. Their approach is to combine conventional epidemiology, genomics, and fantastic computational support to try to unpick the mutational signatures involved.

The dominant hypothesis is that, over the past 20-25 years or so, there has been a change in diet that has allowed an alteration in the gut microbiome such that we now harbor, in some cases, more bacteria capable of manufacturing, synthesizing, and releasing mutagenic chemicals. There’s a subtype of Escherichia coli which manufactures one such mutagen called colibactin.

Again, through some of the painstaking, extraordinary work that Mike Stratton and colleagues have done at the Sanger Institute, they have managed to, using a variety of different techniques — in vitro, observational, and so on — relate exposure to the mutagen colibactin to a particular mutational signature.

They plan to do a large global study — one of the strengths — involving many different countries around the globe, collect material from older colorectal cancer patients and early-onset colorectal cancer patients, and undertake a staggeringly large mutational study to see if the mutational signature associated with colibactin is more highly represented in these early-onset cases. The hypothesis is that, if you’re exposed to this mutagen in childhood, then it increases the tumor mutational burden and therefore the likelihood of developing cancer at an earlier age. 

All of us believe that converting a normal cell into a tumor cell usually requires five or six or seven separate mutational events occurring at random. The earlier these occur, the greater the tumor, the greater the normal single-cellular mutational burden, and the more likely it is to develop cancer sooner rather than later. 

This is a fantastically interesting study, and it’s the way ahead with modern genetic epidemiology, one would say. We wish them well. This will be a 3- to 5-year truly international effort, bringing together a genuinely internationally outstanding research team. We hope that they are able to shed more light on the epidemiology of this early-onset disease, because only by understanding can we deflect and deal with it. 

Knowledge is power, as I’ve said many times before. If we understand the underlying epidemiology, that will allow us to intervene, one would hope, and avoid the chaotic disaster of my clinic on Friday, with these two young patients with an extremely limited lifespan and large families who will be left bereft in having lost a parent.

More power to the team. We wish them well with the study, but again, this is a pointer to the future, one would hope, of modern genetic computational epidemiology. 

I’d be really interested in any ideas or comments that you might have. Are you in the field? Are you seeing more young patients? Do you have any ideas or hypotheses of your own around the microbiome and what bugs might be involved and so on?

Dr. Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford, England; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, has disclosed relevant financial relationships with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, Merck Serono, and Roche. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

I’d like to reflect a little on the ever-rising incidence of early-onset colorectal cancer. I saw two patients in the clinic on Friday, both in their early thirties, presenting with stage IV disease. Both had young families — a disaster.

This is an issue that we must address, I think, epidemiologically. We know that early-onset colorectal cancer is defined as a disease arising in those under the age of 50. There’s been a very sharp increase globally over the past 20-30 years, and currently, around 200,000 such cases are diagnosed every year, but it is said to increase unquestionably.

The epidemiologists, I think, correctly have identified that this sharp, rapid increase does imply that there is a new environmental change that is underpinning or underscoring this rise in early-onset disease. 

There’s a fantastic team that has been put together by Paul Brennan, Mike Stratton, and colleagues, a collaborative group of epidemiologists, geneticists, and bioinformaticians, who are looking at a global study to try to understand the basis of early-onset colorectal cancer. Their approach is to combine conventional epidemiology, genomics, and fantastic computational support to try to unpick the mutational signatures involved.

The dominant hypothesis is that, over the past 20-25 years or so, there has been a change in diet that has allowed an alteration in the gut microbiome such that we now harbor, in some cases, more bacteria capable of manufacturing, synthesizing, and releasing mutagenic chemicals. There’s a subtype of Escherichia coli which manufactures one such mutagen called colibactin.

Again, through some of the painstaking, extraordinary work that Mike Stratton and colleagues have done at the Sanger Institute, they have managed to, using a variety of different techniques — in vitro, observational, and so on — relate exposure to the mutagen colibactin to a particular mutational signature.

They plan to do a large global study — one of the strengths — involving many different countries around the globe, collect material from older colorectal cancer patients and early-onset colorectal cancer patients, and undertake a staggeringly large mutational study to see if the mutational signature associated with colibactin is more highly represented in these early-onset cases. The hypothesis is that, if you’re exposed to this mutagen in childhood, then it increases the tumor mutational burden and therefore the likelihood of developing cancer at an earlier age. 

All of us believe that converting a normal cell into a tumor cell usually requires five or six or seven separate mutational events occurring at random. The earlier these occur, the greater the tumor, the greater the normal single-cellular mutational burden, and the more likely it is to develop cancer sooner rather than later. 

This is a fantastically interesting study, and it’s the way ahead with modern genetic epidemiology, one would say. We wish them well. This will be a 3- to 5-year truly international effort, bringing together a genuinely internationally outstanding research team. We hope that they are able to shed more light on the epidemiology of this early-onset disease, because only by understanding can we deflect and deal with it. 

Knowledge is power, as I’ve said many times before. If we understand the underlying epidemiology, that will allow us to intervene, one would hope, and avoid the chaotic disaster of my clinic on Friday, with these two young patients with an extremely limited lifespan and large families who will be left bereft in having lost a parent.

More power to the team. We wish them well with the study, but again, this is a pointer to the future, one would hope, of modern genetic computational epidemiology. 

I’d be really interested in any ideas or comments that you might have. Are you in the field? Are you seeing more young patients? Do you have any ideas or hypotheses of your own around the microbiome and what bugs might be involved and so on?

Dr. Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford, England; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, has disclosed relevant financial relationships with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, Merck Serono, and Roche. 

A version of this article appeared on Medscape.com.

On December 4, UnitedHealthcare CEO Brian Thompson was assassinated in New York City outside of a hotel. As of the time of this writing, the shooter is still at large.

I suppose I could write about how this shows that Americans are fed up with the way modern commercial healthcare companies operate. Who gets care and who doesn’t.

I could write about how industry trends of “Delay, Deny, Defend” lead to the suffering of millions of people who need healthcare that they thought they were paying for.

 

I could write about the callousness of the way people online are celebrating the cold-blooded murder of a married man with two children.

I might write about how insurance companies intentionally, and routinely, drag out (or deny) reimbursements for physicians (including small solo practice ones, like myself) who are legitimately caring for their patients.

I suppose I could write something about how gun violence is so pervasive in our society that it scarcely merits a second glance at the news story. If the headline just said, “Unknown Assailant Kills Man Outside Hotel,” would you have even read beyond that?

I could write about how the lack of regulations, and accelerating attempts to scrap them, can lead to insider trading.

I could write about how having insurance companies and medical facilities more beholden to shareholders than to patients is a serious conflict of interest.

I could try to make points about how the widespread availability of firearms (in this case one with a built-in silencer) in America means that anyone with a vendetta, or serious mental illness, or just a short temper, can get one — and use it.

I could talk about how “greed is good” in healthcare settings rewards a few and hurts many — no matter how much the PR spinners try to make it sound like it’s a great win-win situation all-around.

I could argue that the jubilant “good riddance” and “eat the rich” responses of many — both medical and nonmedical people — to the killing shows that, as a society, we’re losing the qualities that make us human.

I could also argue that putting financial gain for executive bonuses and stockholder dividends ahead of the health and well-being of others shows that, as a society, we’re losing the qualities that make us human.

I could make a point that violence is never the answer, yet an increasing number of people in our country seem to think it is, provided the target is someone they have a difference of opinion with. Which is, honestly, pretty damn scary.

I could talk about how policies of arbitrarily changing the rules about anesthesia coverage, or letting a computer decide how long a hospital stay should be, or to deny rehabilitation care, are unethical, unjust, and just plain wrong.

I could write about a lot of things based on what happened outside that New York Hilton Midtown in early December.

But as I stare at my screen, I’m well aware that no matter what I write it won’t change any opinions, solve anything, or even lead to people trying to find a solution.

Because that’s just the world we live in.

Block has a solo neurology practice in Scottsdale, Arizona. 

On December 4, UnitedHealthcare CEO Brian Thompson was assassinated in New York City outside of a hotel. As of the time of this writing, the shooter is still at large.

I suppose I could write about how this shows that Americans are fed up with the way modern commercial healthcare companies operate. Who gets care and who doesn’t.

I could write about how industry trends of “Delay, Deny, Defend” lead to the suffering of millions of people who need healthcare that they thought they were paying for.

 

I could write about the callousness of the way people online are celebrating the cold-blooded murder of a married man with two children.

I might write about how insurance companies intentionally, and routinely, drag out (or deny) reimbursements for physicians (including small solo practice ones, like myself) who are legitimately caring for their patients.

I suppose I could write something about how gun violence is so pervasive in our society that it scarcely merits a second glance at the news story. If the headline just said, “Unknown Assailant Kills Man Outside Hotel,” would you have even read beyond that?

I could write about how the lack of regulations, and accelerating attempts to scrap them, can lead to insider trading.

I could write about how having insurance companies and medical facilities more beholden to shareholders than to patients is a serious conflict of interest.

I could try to make points about how the widespread availability of firearms (in this case one with a built-in silencer) in America means that anyone with a vendetta, or serious mental illness, or just a short temper, can get one — and use it.

I could talk about how “greed is good” in healthcare settings rewards a few and hurts many — no matter how much the PR spinners try to make it sound like it’s a great win-win situation all-around.

I could argue that the jubilant “good riddance” and “eat the rich” responses of many — both medical and nonmedical people — to the killing shows that, as a society, we’re losing the qualities that make us human.

I could also argue that putting financial gain for executive bonuses and stockholder dividends ahead of the health and well-being of others shows that, as a society, we’re losing the qualities that make us human.

I could make a point that violence is never the answer, yet an increasing number of people in our country seem to think it is, provided the target is someone they have a difference of opinion with. Which is, honestly, pretty damn scary.

I could talk about how policies of arbitrarily changing the rules about anesthesia coverage, or letting a computer decide how long a hospital stay should be, or to deny rehabilitation care, are unethical, unjust, and just plain wrong.

I could write about a lot of things based on what happened outside that New York Hilton Midtown in early December.

But as I stare at my screen, I’m well aware that no matter what I write it won’t change any opinions, solve anything, or even lead to people trying to find a solution.

Because that’s just the world we live in.

Block has a solo neurology practice in Scottsdale, Arizona. 

On December 4, UnitedHealthcare CEO Brian Thompson was assassinated in New York City outside of a hotel. As of the time of this writing, the shooter is still at large.

I suppose I could write about how this shows that Americans are fed up with the way modern commercial healthcare companies operate. Who gets care and who doesn’t.

I could write about how industry trends of “Delay, Deny, Defend” lead to the suffering of millions of people who need healthcare that they thought they were paying for.

 

I could write about the callousness of the way people online are celebrating the cold-blooded murder of a married man with two children.

I might write about how insurance companies intentionally, and routinely, drag out (or deny) reimbursements for physicians (including small solo practice ones, like myself) who are legitimately caring for their patients.

I suppose I could write something about how gun violence is so pervasive in our society that it scarcely merits a second glance at the news story. If the headline just said, “Unknown Assailant Kills Man Outside Hotel,” would you have even read beyond that?

I could write about how the lack of regulations, and accelerating attempts to scrap them, can lead to insider trading.

I could write about how having insurance companies and medical facilities more beholden to shareholders than to patients is a serious conflict of interest.

I could try to make points about how the widespread availability of firearms (in this case one with a built-in silencer) in America means that anyone with a vendetta, or serious mental illness, or just a short temper, can get one — and use it.

I could talk about how “greed is good” in healthcare settings rewards a few and hurts many — no matter how much the PR spinners try to make it sound like it’s a great win-win situation all-around.

I could argue that the jubilant “good riddance” and “eat the rich” responses of many — both medical and nonmedical people — to the killing shows that, as a society, we’re losing the qualities that make us human.

I could also argue that putting financial gain for executive bonuses and stockholder dividends ahead of the health and well-being of others shows that, as a society, we’re losing the qualities that make us human.

I could make a point that violence is never the answer, yet an increasing number of people in our country seem to think it is, provided the target is someone they have a difference of opinion with. Which is, honestly, pretty damn scary.

I could talk about how policies of arbitrarily changing the rules about anesthesia coverage, or letting a computer decide how long a hospital stay should be, or to deny rehabilitation care, are unethical, unjust, and just plain wrong.

I could write about a lot of things based on what happened outside that New York Hilton Midtown in early December.

But as I stare at my screen, I’m well aware that no matter what I write it won’t change any opinions, solve anything, or even lead to people trying to find a solution.

Because that’s just the world we live in.

Block has a solo neurology practice in Scottsdale, Arizona. 

The answer one gets often depends on how one crafts the question. For example, Jeffrey D. Johnson PhD, a professor of communications at Portland State University in Oregon has found that if patients are asked “Is there something else you would like to address today?” 80% had their unmet questions addressed. However, if the question was worded “Is there anything else ...?” Very few had their unmet concerns addressed.

I recently encountered two studies that provide another striking example of how differently structured questions aimed at same topic can result in dramatically different results. In this case both studies used one database, the UK Biobank cohort study which contains “de-identified genetic, lifestyle, and health information” collected from a half million adults in the UK. A subgroup of nearly 90,000 who had undergone a week long activity measurement using a wrist accelerometer was the focus of both groups of investigators who asked the same broad question “What is the relationship between physical activity and disease?”

 

The first study I found has already received some publicity in the lay press and dealt with those individuals who, for a variety of reasons, pack all of their exercise into just a few days, usually the weekend, aka weekend warriors. The investigators found that when compared with generally inactive individuals those who were able to achieve activity volumes that met current guidelines were at lower risk for more than 200 diseases, particularly those that were cardiac based. I guess that shouldn’t surprise us. The finding that has received most of the publicity to date in the lay press was that “Associations were similar whether the activity followed a weekend warrior pattern or was spread out evenly through the week.”

The second study, using the same database, found that those individuals who spent more than 10.6 hours per day sitting had 60% an increased risk of heart failure and cardiovascular related death. And, here’s the real news, that risk remained even in people who were otherwise physically active.

I suspect these two groups of investigators, both associated with Harvard-related institutions, knew of each other’s work and would agree that their findings are not incompatible. However, it is interesting that, when presented with the same database, one group chose to focus its attention on the exercise end of the spectrum while the other looked at the effect of inactivity. 

I have always tried to include a “healthy” amount of exercise in my day. However, more recently my professional interest has been drawn to the increasing number of studies I read that deal with the risks of inactivity and sedentarism. For example, just in the last 2 years I have written about a study in children that showed that sedentary time is responsible for 70% of the total increase in cholesterol as children advance into young adulthood. Another study in adults found that every 2-hour increase in sedentary behavior was associated with a 12% decrease in the patient’s likelihood of achieving healthy aging.

If I were asked to place relative values on these two studies, I would say that the study highlighting the risk of prolonged sitting is potentially far more relevant to the population at large, which is for the most part sedentary. Of course, while I have no data to support my contention, I see the weekend warrior population as a niche group.

So what are the take-home messages from these two studies? One is for the weekend warrior. “You can take some comfort in the results that support your exercise schedule but don’t feel too comfortable about it if most of the week you are sitting at a desk.” 

For the rest of us — whether we are pediatricians, family practitioners, or internists — the message is to ease off our messaging on exercise and spend more energy getting our patients off their rear ends. It’s beginning to feel like we should be including accelerometers in our regular diagnostic and therapeutic weaponry. Sending home patients with a Holter cardiac monitor has become commonplace. We should be sending more folks home with accelerometers or asking the more affluent to share the data from their smart watches. “You’ve been bragging about your “steps. Show me your sitting time.”

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

The answer one gets often depends on how one crafts the question. For example, Jeffrey D. Johnson PhD, a professor of communications at Portland State University in Oregon has found that if patients are asked “Is there something else you would like to address today?” 80% had their unmet questions addressed. However, if the question was worded “Is there anything else ...?” Very few had their unmet concerns addressed.

I recently encountered two studies that provide another striking example of how differently structured questions aimed at same topic can result in dramatically different results. In this case both studies used one database, the UK Biobank cohort study which contains “de-identified genetic, lifestyle, and health information” collected from a half million adults in the UK. A subgroup of nearly 90,000 who had undergone a week long activity measurement using a wrist accelerometer was the focus of both groups of investigators who asked the same broad question “What is the relationship between physical activity and disease?”

 

The first study I found has already received some publicity in the lay press and dealt with those individuals who, for a variety of reasons, pack all of their exercise into just a few days, usually the weekend, aka weekend warriors. The investigators found that when compared with generally inactive individuals those who were able to achieve activity volumes that met current guidelines were at lower risk for more than 200 diseases, particularly those that were cardiac based. I guess that shouldn’t surprise us. The finding that has received most of the publicity to date in the lay press was that “Associations were similar whether the activity followed a weekend warrior pattern or was spread out evenly through the week.”

The second study, using the same database, found that those individuals who spent more than 10.6 hours per day sitting had 60% an increased risk of heart failure and cardiovascular related death. And, here’s the real news, that risk remained even in people who were otherwise physically active.

I suspect these two groups of investigators, both associated with Harvard-related institutions, knew of each other’s work and would agree that their findings are not incompatible. However, it is interesting that, when presented with the same database, one group chose to focus its attention on the exercise end of the spectrum while the other looked at the effect of inactivity. 

I have always tried to include a “healthy” amount of exercise in my day. However, more recently my professional interest has been drawn to the increasing number of studies I read that deal with the risks of inactivity and sedentarism. For example, just in the last 2 years I have written about a study in children that showed that sedentary time is responsible for 70% of the total increase in cholesterol as children advance into young adulthood. Another study in adults found that every 2-hour increase in sedentary behavior was associated with a 12% decrease in the patient’s likelihood of achieving healthy aging.

If I were asked to place relative values on these two studies, I would say that the study highlighting the risk of prolonged sitting is potentially far more relevant to the population at large, which is for the most part sedentary. Of course, while I have no data to support my contention, I see the weekend warrior population as a niche group.

So what are the take-home messages from these two studies? One is for the weekend warrior. “You can take some comfort in the results that support your exercise schedule but don’t feel too comfortable about it if most of the week you are sitting at a desk.” 

For the rest of us — whether we are pediatricians, family practitioners, or internists — the message is to ease off our messaging on exercise and spend more energy getting our patients off their rear ends. It’s beginning to feel like we should be including accelerometers in our regular diagnostic and therapeutic weaponry. Sending home patients with a Holter cardiac monitor has become commonplace. We should be sending more folks home with accelerometers or asking the more affluent to share the data from their smart watches. “You’ve been bragging about your “steps. Show me your sitting time.”

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

The answer one gets often depends on how one crafts the question. For example, Jeffrey D. Johnson PhD, a professor of communications at Portland State University in Oregon has found that if patients are asked “Is there something else you would like to address today?” 80% had their unmet questions addressed. However, if the question was worded “Is there anything else ...?” Very few had their unmet concerns addressed.

I recently encountered two studies that provide another striking example of how differently structured questions aimed at same topic can result in dramatically different results. In this case both studies used one database, the UK Biobank cohort study which contains “de-identified genetic, lifestyle, and health information” collected from a half million adults in the UK. A subgroup of nearly 90,000 who had undergone a week long activity measurement using a wrist accelerometer was the focus of both groups of investigators who asked the same broad question “What is the relationship between physical activity and disease?”

 

The first study I found has already received some publicity in the lay press and dealt with those individuals who, for a variety of reasons, pack all of their exercise into just a few days, usually the weekend, aka weekend warriors. The investigators found that when compared with generally inactive individuals those who were able to achieve activity volumes that met current guidelines were at lower risk for more than 200 diseases, particularly those that were cardiac based. I guess that shouldn’t surprise us. The finding that has received most of the publicity to date in the lay press was that “Associations were similar whether the activity followed a weekend warrior pattern or was spread out evenly through the week.”

The second study, using the same database, found that those individuals who spent more than 10.6 hours per day sitting had 60% an increased risk of heart failure and cardiovascular related death. And, here’s the real news, that risk remained even in people who were otherwise physically active.

I suspect these two groups of investigators, both associated with Harvard-related institutions, knew of each other’s work and would agree that their findings are not incompatible. However, it is interesting that, when presented with the same database, one group chose to focus its attention on the exercise end of the spectrum while the other looked at the effect of inactivity. 

I have always tried to include a “healthy” amount of exercise in my day. However, more recently my professional interest has been drawn to the increasing number of studies I read that deal with the risks of inactivity and sedentarism. For example, just in the last 2 years I have written about a study in children that showed that sedentary time is responsible for 70% of the total increase in cholesterol as children advance into young adulthood. Another study in adults found that every 2-hour increase in sedentary behavior was associated with a 12% decrease in the patient’s likelihood of achieving healthy aging.

If I were asked to place relative values on these two studies, I would say that the study highlighting the risk of prolonged sitting is potentially far more relevant to the population at large, which is for the most part sedentary. Of course, while I have no data to support my contention, I see the weekend warrior population as a niche group.

So what are the take-home messages from these two studies? One is for the weekend warrior. “You can take some comfort in the results that support your exercise schedule but don’t feel too comfortable about it if most of the week you are sitting at a desk.” 

For the rest of us — whether we are pediatricians, family practitioners, or internists — the message is to ease off our messaging on exercise and spend more energy getting our patients off their rear ends. It’s beginning to feel like we should be including accelerometers in our regular diagnostic and therapeutic weaponry. Sending home patients with a Holter cardiac monitor has become commonplace. We should be sending more folks home with accelerometers or asking the more affluent to share the data from their smart watches. “You’ve been bragging about your “steps. Show me your sitting time.”

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

It has been three and a half years since the US Preventive Services Task Force (USPSTF) lowered the age to start colorectal cancer (CRC) screening from 50 to 45. As I mentioned in a previous commentary, two major medical groups — the American Academy of Family Physicians and the American College of Physicians — felt that the evidence was insufficient to support this change. 

Did doctors adjust their screening practices? A recent study suggests that they have. Comparing CRC screening rates in more than 10 million adults aged 45-49 during the 20 months preceding and 20 months following the USPSTF recommendation, researchers found significant increases during the latter time period, with the greatest increases among persons of high socioeconomic status or living in metropolitan areas.

Another study addressed concerns that younger adults may be less likely to follow up on positive screening results or more likely to have false positives on a fecal immunochemical test (FIT). Patients aged 45-49 years were slightly less likely to have a positive FIT result than 50-year-olds, but they had similar rates of colonoscopy completion and similar percentages of abnormal findings on colonoscopy.

Although the sensitivity and specificity of FIT varies quite a bit across different test brands, its overall effectiveness at reducing colorectal cancer deaths is well established. In 2024, the Food and Drug Administration approved three new screening options: a blood-based screening test (Shield), a next-generation multitarget stool DNA test (Cologuard Plus), and a multitarget stool RNA test (ColoSense) with similar performance characteristics as Cologuard Plus. The latter two tests will become available early next year.

This profusion of noninvasive options for CRC screening will challenge those tasked with developing the next iteration of the USPSTF recommendations. Not only must future guidelines establish what evidence threshold is sufficient to recommend a new screening strategy, but they also will need to consider the population-level consequences of relative utilization of different tests. For example, a cost-effectiveness analysis found that more CRC deaths would occur if people who would have otherwise accepted colonoscopy or fecal tests chose to be screened with Shield instead; however, this negative outcome could be offset if for every three of these test substitutions, two other people chose Shield who would otherwise have not been screened at all.

In the meantime, it is important for primary care clinicians to be familiar with evidence-based intervals for CRC screening tests and test eligibility criteria. A troubling study of patients who completed a multitarget stool DNA test in a Midwestern health system in 2021 found that more than one in five had the test ordered inappropriately, based on USPSTF guidelines. Reasons for inappropriate testing included having had a colonoscopy within the past 10 years, a family history of CRC, symptoms suggestive of possible CRC, age younger than 45, and a prior diagnosis of colonic adenomas. 

Just as a medication works best when the patient takes it as prescribed, a CRC screening test is most likely to yield more benefit than harm when it’s provided to the right patient at the right time.

Dr. Lin is Associate Director, Family Medicine Residency Program, at Lancaster General Hospital in Pennsylvania. He reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

It has been three and a half years since the US Preventive Services Task Force (USPSTF) lowered the age to start colorectal cancer (CRC) screening from 50 to 45. As I mentioned in a previous commentary, two major medical groups — the American Academy of Family Physicians and the American College of Physicians — felt that the evidence was insufficient to support this change. 

Did doctors adjust their screening practices? A recent study suggests that they have. Comparing CRC screening rates in more than 10 million adults aged 45-49 during the 20 months preceding and 20 months following the USPSTF recommendation, researchers found significant increases during the latter time period, with the greatest increases among persons of high socioeconomic status or living in metropolitan areas.

Another study addressed concerns that younger adults may be less likely to follow up on positive screening results or more likely to have false positives on a fecal immunochemical test (FIT). Patients aged 45-49 years were slightly less likely to have a positive FIT result than 50-year-olds, but they had similar rates of colonoscopy completion and similar percentages of abnormal findings on colonoscopy.

Although the sensitivity and specificity of FIT varies quite a bit across different test brands, its overall effectiveness at reducing colorectal cancer deaths is well established. In 2024, the Food and Drug Administration approved three new screening options: a blood-based screening test (Shield), a next-generation multitarget stool DNA test (Cologuard Plus), and a multitarget stool RNA test (ColoSense) with similar performance characteristics as Cologuard Plus. The latter two tests will become available early next year.

This profusion of noninvasive options for CRC screening will challenge those tasked with developing the next iteration of the USPSTF recommendations. Not only must future guidelines establish what evidence threshold is sufficient to recommend a new screening strategy, but they also will need to consider the population-level consequences of relative utilization of different tests. For example, a cost-effectiveness analysis found that more CRC deaths would occur if people who would have otherwise accepted colonoscopy or fecal tests chose to be screened with Shield instead; however, this negative outcome could be offset if for every three of these test substitutions, two other people chose Shield who would otherwise have not been screened at all.

In the meantime, it is important for primary care clinicians to be familiar with evidence-based intervals for CRC screening tests and test eligibility criteria. A troubling study of patients who completed a multitarget stool DNA test in a Midwestern health system in 2021 found that more than one in five had the test ordered inappropriately, based on USPSTF guidelines. Reasons for inappropriate testing included having had a colonoscopy within the past 10 years, a family history of CRC, symptoms suggestive of possible CRC, age younger than 45, and a prior diagnosis of colonic adenomas. 

Just as a medication works best when the patient takes it as prescribed, a CRC screening test is most likely to yield more benefit than harm when it’s provided to the right patient at the right time.

Dr. Lin is Associate Director, Family Medicine Residency Program, at Lancaster General Hospital in Pennsylvania. He reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

It has been three and a half years since the US Preventive Services Task Force (USPSTF) lowered the age to start colorectal cancer (CRC) screening from 50 to 45. As I mentioned in a previous commentary, two major medical groups — the American Academy of Family Physicians and the American College of Physicians — felt that the evidence was insufficient to support this change. 

Did doctors adjust their screening practices? A recent study suggests that they have. Comparing CRC screening rates in more than 10 million adults aged 45-49 during the 20 months preceding and 20 months following the USPSTF recommendation, researchers found significant increases during the latter time period, with the greatest increases among persons of high socioeconomic status or living in metropolitan areas.

Another study addressed concerns that younger adults may be less likely to follow up on positive screening results or more likely to have false positives on a fecal immunochemical test (FIT). Patients aged 45-49 years were slightly less likely to have a positive FIT result than 50-year-olds, but they had similar rates of colonoscopy completion and similar percentages of abnormal findings on colonoscopy.

Although the sensitivity and specificity of FIT varies quite a bit across different test brands, its overall effectiveness at reducing colorectal cancer deaths is well established. In 2024, the Food and Drug Administration approved three new screening options: a blood-based screening test (Shield), a next-generation multitarget stool DNA test (Cologuard Plus), and a multitarget stool RNA test (ColoSense) with similar performance characteristics as Cologuard Plus. The latter two tests will become available early next year.

This profusion of noninvasive options for CRC screening will challenge those tasked with developing the next iteration of the USPSTF recommendations. Not only must future guidelines establish what evidence threshold is sufficient to recommend a new screening strategy, but they also will need to consider the population-level consequences of relative utilization of different tests. For example, a cost-effectiveness analysis found that more CRC deaths would occur if people who would have otherwise accepted colonoscopy or fecal tests chose to be screened with Shield instead; however, this negative outcome could be offset if for every three of these test substitutions, two other people chose Shield who would otherwise have not been screened at all.

In the meantime, it is important for primary care clinicians to be familiar with evidence-based intervals for CRC screening tests and test eligibility criteria. A troubling study of patients who completed a multitarget stool DNA test in a Midwestern health system in 2021 found that more than one in five had the test ordered inappropriately, based on USPSTF guidelines. Reasons for inappropriate testing included having had a colonoscopy within the past 10 years, a family history of CRC, symptoms suggestive of possible CRC, age younger than 45, and a prior diagnosis of colonic adenomas. 

Just as a medication works best when the patient takes it as prescribed, a CRC screening test is most likely to yield more benefit than harm when it’s provided to the right patient at the right time.

Dr. Lin is Associate Director, Family Medicine Residency Program, at Lancaster General Hospital in Pennsylvania. He reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

This video transcript has been edited for clarity. 

Dear colleagues, I am Christoph Diener, from the Faculty of Medicine at the University Duisburg-Essen in Germany. In this video, I would like to cover six publications on stroke, which were published this fall. 

The Best Thrombolytic?

Let me start with systemic thrombolysis. We now have two thrombolytic agents available. One is the well-known alteplase, and newly approved for the treatment of stroke is tenecteplase. The ATTEST-2 study in the United Kingdom, published in The Lancet Neurology, compared tenecteplase 0.25 mg/kg body weight as a bolus with alteplase 0.9 mg/kg body weight as an infusion over 60 minutes in the 4.5-hour time window in 1777 patients with ischemic stroke.

There was no significant difference between the two thrombolytics for the primary endpoint of modified Rankin Scale score after 90 days. There was also no difference with respect to mortality, intracranial bleeding, or extracranial bleeding. 

We finally have 11 randomized controlled trials that compared tenecteplase and alteplase in acute ischemic stroke. A meta-analysis of these randomized trials was published in Neurology. The analysis included 3700 patients treated with tenecteplase and 3700 patients treated with alteplase. For the primary endpoint, excellent functional outcome defined as modified Rankin Scale score 0-1 after 90 days, there was a significant benefit for tenecteplase (relative risk, 1.05), but the absolute difference was very small, at 3%. There was no difference in mortality or bleeding complications. 

In conclusion, I think both substances are great. They are effective. Tenecteplase is most probably the drug which should be used in people who have to transfer from a primary stroke center to a dedicated stroke center that provides thrombectomy. Otherwise, I think it’s a choice of the physician as to which thrombolytic agent to use. 

 

Mobile Stroke Units

A highly debated topic is mobile stroke units. These stroke units have a CT scanner and laboratory on board, and this makes it possible to perform thrombolysis on the way to the hospital. A retrospective, observational study collected data between 2018 and 2023, and included 19,400 patients with acute stroke, of whom 1237, or 6.4%, were treated in a mobile stroke unit. This study was published in JAMA Neurology. 

The modified Rankin Scale score at the time of discharge was better in patients treated with a mobile stroke unit, but the absolute benefit was only 0.03 points on the modified Rankin Scale. The question is whether this is cost-effective, and can we really do this at times when there is a traumatic shortage of physicians and nursing staff in the hospital? 

 

DOAC Reversal Agents

Oral anticoagulation, as you know, is usually considered a contraindication for systemic thrombolysis. Idarucizumab, a monoclonal antibody, was developed to reverse the biological activity of dabigatran and then allow systemic thrombolysis.

A recent publication in Neurology analyzed 13 cohort studies with 553 stroke patients on dabigatran who received idarucizumab prior to systemic thrombolysis, and the rate of intracranial hemorrhage was 4%. This means it’s obviously possible to perform thrombolysis when the activity of dabigatran is neutralized by idarucizumab.

Unfortunately, until today, we have no data on whether this can also be done with andexanet alfa in people who are treated with a factor Xa inhibitor like, for example, apixaban, rivaroxaban, or edoxaban. 

 

Anticoagulation in ESUS 

My next topic is ESUS, or embolic stroke of undetermined source. We have four large randomized trials and three smaller trials that compared antiplatelet therapy with DOACs in patients with ESUS. A group in Neurology published a meta-analysis of seven randomized controlled studies with, altogether, 14,800 patients with ESUS. 

The comparison between antiplatelet therapy and anticoagulants showed no difference for recurrent ischemic stroke, and also not for major subgroups. This means that people with ESUS should receive antiplatelet therapy, most probably aspirin. 

 

Anticoagulation Post–Ischemic Stroke With AF 

My final topic is the optimal time to start anticoagulation in people with atrial fibrillation who suffer an ischemic stroke. The OPTIMAS study, published in The Lancet, randomized 3650 patients who were anticoagulated with DOACs early (which means less than 4 days) or delayed (between 7 and 14 days). There was no difference in the primary endpoint, which was recurrent ischemic stroke, intracranial hemorrhage, or systemic embolism at 90 days.

The conclusion is that, in most cases, we can probably initiate anticoagulation in people with ischemic stroke and atrial fibrillation within the first 4 days. 

Dear colleagues, this is an exciting time for the stroke field. I presented six new studies that have impact, I think, on the management of patients with ischemic stroke.

Dr. Diener is a professor in the Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen in Germany. He reported conflicts of interest with Abbott, AbbVie, Boehringer Ingelheim, Lundbeck, Novartis, Orion Pharma, Teva, WebMD, and The German Research Council. He also serves on the editorial boards of Cephalalgia, Lancet Neurology, and Drugs.

A version of this article first appeared on Medscape.com.

This video transcript has been edited for clarity. 

Dear colleagues, I am Christoph Diener, from the Faculty of Medicine at the University Duisburg-Essen in Germany. In this video, I would like to cover six publications on stroke, which were published this fall. 

The Best Thrombolytic?

Let me start with systemic thrombolysis. We now have two thrombolytic agents available. One is the well-known alteplase, and newly approved for the treatment of stroke is tenecteplase. The ATTEST-2 study in the United Kingdom, published in The Lancet Neurology, compared tenecteplase 0.25 mg/kg body weight as a bolus with alteplase 0.9 mg/kg body weight as an infusion over 60 minutes in the 4.5-hour time window in 1777 patients with ischemic stroke.

There was no significant difference between the two thrombolytics for the primary endpoint of modified Rankin Scale score after 90 days. There was also no difference with respect to mortality, intracranial bleeding, or extracranial bleeding. 

We finally have 11 randomized controlled trials that compared tenecteplase and alteplase in acute ischemic stroke. A meta-analysis of these randomized trials was published in Neurology. The analysis included 3700 patients treated with tenecteplase and 3700 patients treated with alteplase. For the primary endpoint, excellent functional outcome defined as modified Rankin Scale score 0-1 after 90 days, there was a significant benefit for tenecteplase (relative risk, 1.05), but the absolute difference was very small, at 3%. There was no difference in mortality or bleeding complications. 

In conclusion, I think both substances are great. They are effective. Tenecteplase is most probably the drug which should be used in people who have to transfer from a primary stroke center to a dedicated stroke center that provides thrombectomy. Otherwise, I think it’s a choice of the physician as to which thrombolytic agent to use. 

 

Mobile Stroke Units

A highly debated topic is mobile stroke units. These stroke units have a CT scanner and laboratory on board, and this makes it possible to perform thrombolysis on the way to the hospital. A retrospective, observational study collected data between 2018 and 2023, and included 19,400 patients with acute stroke, of whom 1237, or 6.4%, were treated in a mobile stroke unit. This study was published in JAMA Neurology. 

The modified Rankin Scale score at the time of discharge was better in patients treated with a mobile stroke unit, but the absolute benefit was only 0.03 points on the modified Rankin Scale. The question is whether this is cost-effective, and can we really do this at times when there is a traumatic shortage of physicians and nursing staff in the hospital? 

 

DOAC Reversal Agents

Oral anticoagulation, as you know, is usually considered a contraindication for systemic thrombolysis. Idarucizumab, a monoclonal antibody, was developed to reverse the biological activity of dabigatran and then allow systemic thrombolysis.

A recent publication in Neurology analyzed 13 cohort studies with 553 stroke patients on dabigatran who received idarucizumab prior to systemic thrombolysis, and the rate of intracranial hemorrhage was 4%. This means it’s obviously possible to perform thrombolysis when the activity of dabigatran is neutralized by idarucizumab.

Unfortunately, until today, we have no data on whether this can also be done with andexanet alfa in people who are treated with a factor Xa inhibitor like, for example, apixaban, rivaroxaban, or edoxaban. 

 

Anticoagulation in ESUS 

My next topic is ESUS, or embolic stroke of undetermined source. We have four large randomized trials and three smaller trials that compared antiplatelet therapy with DOACs in patients with ESUS. A group in Neurology published a meta-analysis of seven randomized controlled studies with, altogether, 14,800 patients with ESUS. 

The comparison between antiplatelet therapy and anticoagulants showed no difference for recurrent ischemic stroke, and also not for major subgroups. This means that people with ESUS should receive antiplatelet therapy, most probably aspirin. 

 

Anticoagulation Post–Ischemic Stroke With AF 

My final topic is the optimal time to start anticoagulation in people with atrial fibrillation who suffer an ischemic stroke. The OPTIMAS study, published in The Lancet, randomized 3650 patients who were anticoagulated with DOACs early (which means less than 4 days) or delayed (between 7 and 14 days). There was no difference in the primary endpoint, which was recurrent ischemic stroke, intracranial hemorrhage, or systemic embolism at 90 days.

The conclusion is that, in most cases, we can probably initiate anticoagulation in people with ischemic stroke and atrial fibrillation within the first 4 days. 

Dear colleagues, this is an exciting time for the stroke field. I presented six new studies that have impact, I think, on the management of patients with ischemic stroke.

Dr. Diener is a professor in the Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen in Germany. He reported conflicts of interest with Abbott, AbbVie, Boehringer Ingelheim, Lundbeck, Novartis, Orion Pharma, Teva, WebMD, and The German Research Council. He also serves on the editorial boards of Cephalalgia, Lancet Neurology, and Drugs.

A version of this article first appeared on Medscape.com.

This video transcript has been edited for clarity. 

Dear colleagues, I am Christoph Diener, from the Faculty of Medicine at the University Duisburg-Essen in Germany. In this video, I would like to cover six publications on stroke, which were published this fall. 

The Best Thrombolytic?

Let me start with systemic thrombolysis. We now have two thrombolytic agents available. One is the well-known alteplase, and newly approved for the treatment of stroke is tenecteplase. The ATTEST-2 study in the United Kingdom, published in The Lancet Neurology, compared tenecteplase 0.25 mg/kg body weight as a bolus with alteplase 0.9 mg/kg body weight as an infusion over 60 minutes in the 4.5-hour time window in 1777 patients with ischemic stroke.

There was no significant difference between the two thrombolytics for the primary endpoint of modified Rankin Scale score after 90 days. There was also no difference with respect to mortality, intracranial bleeding, or extracranial bleeding. 

We finally have 11 randomized controlled trials that compared tenecteplase and alteplase in acute ischemic stroke. A meta-analysis of these randomized trials was published in Neurology. The analysis included 3700 patients treated with tenecteplase and 3700 patients treated with alteplase. For the primary endpoint, excellent functional outcome defined as modified Rankin Scale score 0-1 after 90 days, there was a significant benefit for tenecteplase (relative risk, 1.05), but the absolute difference was very small, at 3%. There was no difference in mortality or bleeding complications. 

In conclusion, I think both substances are great. They are effective. Tenecteplase is most probably the drug which should be used in people who have to transfer from a primary stroke center to a dedicated stroke center that provides thrombectomy. Otherwise, I think it’s a choice of the physician as to which thrombolytic agent to use. 

 

Mobile Stroke Units

A highly debated topic is mobile stroke units. These stroke units have a CT scanner and laboratory on board, and this makes it possible to perform thrombolysis on the way to the hospital. A retrospective, observational study collected data between 2018 and 2023, and included 19,400 patients with acute stroke, of whom 1237, or 6.4%, were treated in a mobile stroke unit. This study was published in JAMA Neurology. 

The modified Rankin Scale score at the time of discharge was better in patients treated with a mobile stroke unit, but the absolute benefit was only 0.03 points on the modified Rankin Scale. The question is whether this is cost-effective, and can we really do this at times when there is a traumatic shortage of physicians and nursing staff in the hospital? 

 

DOAC Reversal Agents

Oral anticoagulation, as you know, is usually considered a contraindication for systemic thrombolysis. Idarucizumab, a monoclonal antibody, was developed to reverse the biological activity of dabigatran and then allow systemic thrombolysis.

A recent publication in Neurology analyzed 13 cohort studies with 553 stroke patients on dabigatran who received idarucizumab prior to systemic thrombolysis, and the rate of intracranial hemorrhage was 4%. This means it’s obviously possible to perform thrombolysis when the activity of dabigatran is neutralized by idarucizumab.

Unfortunately, until today, we have no data on whether this can also be done with andexanet alfa in people who are treated with a factor Xa inhibitor like, for example, apixaban, rivaroxaban, or edoxaban. 

 

Anticoagulation in ESUS 

My next topic is ESUS, or embolic stroke of undetermined source. We have four large randomized trials and three smaller trials that compared antiplatelet therapy with DOACs in patients with ESUS. A group in Neurology published a meta-analysis of seven randomized controlled studies with, altogether, 14,800 patients with ESUS. 

The comparison between antiplatelet therapy and anticoagulants showed no difference for recurrent ischemic stroke, and also not for major subgroups. This means that people with ESUS should receive antiplatelet therapy, most probably aspirin. 

 

Anticoagulation Post–Ischemic Stroke With AF 

My final topic is the optimal time to start anticoagulation in people with atrial fibrillation who suffer an ischemic stroke. The OPTIMAS study, published in The Lancet, randomized 3650 patients who were anticoagulated with DOACs early (which means less than 4 days) or delayed (between 7 and 14 days). There was no difference in the primary endpoint, which was recurrent ischemic stroke, intracranial hemorrhage, or systemic embolism at 90 days.

The conclusion is that, in most cases, we can probably initiate anticoagulation in people with ischemic stroke and atrial fibrillation within the first 4 days. 

Dear colleagues, this is an exciting time for the stroke field. I presented six new studies that have impact, I think, on the management of patients with ischemic stroke.

Dr. Diener is a professor in the Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen in Germany. He reported conflicts of interest with Abbott, AbbVie, Boehringer Ingelheim, Lundbeck, Novartis, Orion Pharma, Teva, WebMD, and The German Research Council. He also serves on the editorial boards of Cephalalgia, Lancet Neurology, and Drugs.

A version of this article first appeared on Medscape.com.