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AGA Data Trends 2025: MASLD
New and Emerging Treatments for MASLD/MASH
- Hu Y, Sun C, Chen Y, Liu Y-D, Fan J-G. Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease. J Clin Transl Hepatol. 2024;12(9):802-814. doi:10.14218/JCTH.2024.00123
- Petta S, Targher G, Romeo S, et al. The first MASH drug therapy on the horizon: Current perspectives of resmetirom. Liver Int. 2024;44(7):1526-1536. doi:10.14218/JCTH.2024.00123doi:10.1111/liv.15930
- Ciardullo S, Muraca E, Vergani M, Invernizzi P, Perseghin G. Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions. Gastroenterol Rep (Oxf). 2024;12:goae029. doi:10.1093/gastro/goae029
- Chen VL, Morgan TR, Rotman Y, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312-320. doi:10.1097/HEP.0000000000001112
- Economist Impact 2024. MASLD/MASH in the US: A liver disease country profile. Published 2024. Accessed January 22, 2025. https://impact.economist.com/perspectives/sites/default/files/download/liver-disease-country-profile_united_states_final.pdf
- Tincopa MA, Anstee QM, Loomba R. New and emerging treatments for metabolic dysfunction-associated steatohepatitis. Cell Metab. 2024;36(5):912-926. doi:10.1016/j.cmet.2024.03.011
- Carpi S, Daniele S, de Almeida JFM, Gabbia D. Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC. Int J Mol Sci. 2024;25(22):12229. https://www.mdpi.com/1422-0067/25/22/1222
- Wong RJ. Epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-related liver disease (ALD). Metab Target Organ Damage. 2024;4:35. http://dx.doi.org/10.20517/mtod.2024.57
- Younossi ZM, Kalligeros M, Henry L. Epidemiology of Metabolic Dysfunction-Associated Steatotic Liver Disease. Clin Mol Hepatol. 2024. doi:10.3350/cmh.2024.0431
- Jozst L. Estimating the True Prevalence of MASH and MASLD in the US. AJMC. Published October 17, 2024. Accessed January 22, 2025. https://www.ajmc.com/view/estimating-the-true-prevalence-of-mash-and-masld-in-the-us
- Mayo Clinic website. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). Published October 4, 2023. Accessed January 22, 2025. https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493
- Younossi ZM. Economic burden of MASLD/MASH. Conference report for NATAP. EASL 2024. Published June 5-8, 2024. Accessed January 22, 2025. https://www.natap.org/2024/EASL/EASL_41.htm
- Loomba R, Noureddin M, Kowdley KV, et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH. Hepatol. 202;73(2):625-643. doi:10.1002/hep.31622
- Nicastro E. D’Antiga L. Nutritional Interventions, Probiotics, Synbiotics and Fecal Microbiota Transplantation in Steatoic Liver Disease. Advances in experimental medicine and Biology. Published online January 1. 202:113-133. doi:https://doi.org.10.1007/978-3-031-58572-2_7
- Shera S, Katzka W, Yang JC, et al. Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system. Front Microbiol. 2024;15:1407555. doi:10.3389/fmicb.2024.1407555
- Globe Newswire website. Akero Therapeutics Reports Second Quarter 2024 Financial Results and Provides Business Update [press release]. Published August 9, 2024. Accessed January 22, 2025. https://www.globenewswire.com/en/news-release/2024/08/09/2927685/0/en/Akero-Therapeutics-Reports-Second-Quarter-2024-Financial-Results-and-Provides-Business-Update.html
- Akero website. Clinical Trials Overview. We are currently enrolling three clinical trials as part of a Phase 3 SYNCHRONY program evaluating EFX for the treatment of pre-cirrhotic MASH (F2-F3) and compensated cirrhosis (F4) due to MASH [press release]. Published 2024. Accessed January 22, 2025. https://akerotx.com/clinical-trials/
- 89bio website. 89bio Initiates Phase 3 ENLIGHTEN-Fibrosis Trial of Pegozafermin in Non-Cirrhotic Metabolic Dysfunction-Associated Steatohepatitis (MASH) Patients with Fibrosis [press release]. Published March 12, 2024. Accessed January 22, 2025. https://www.89bio.com/news/89bio-initiates-phase-3-enlighten-fibrosis-trial-of-pegozafermin-in-non-cirrhotic-metabolic-dysfunction-associated-steatohepatitis-mash-patients-with-fibrosis/
- 89bio website. 89bio Reaches Alignment with the FDA and EMA on Phase 3 Program for Pegozafermin in Nonalcoholic Steatohepatitis (NASH); Program Initiation Planned in the First Half of 2024 [press release]. Published December 4, 2023. Accessed January 22, 2025. https://www.89bio.com/news/89bio-reaches-alignment-with-the-fda-and-ema-on-phase-3-program-for-pegozafermin-in-nonalcoholic-steatohepatitis-nash-program-initiation-planned-in-the-first-half-of-2024/
- Boehringer Ingelheim website. Boehringer receives U.S. FDA Breakthrough Therapy designation and initiates two phase III trials in MASH for survodutide [press release]. Published October 8, 2024. Accessed January 22, 2025. https://www.boehringer-ingelheim.com/human-health/metabolic-diseases/survodutide-us-fda-breakthrough-therapy-phase-3-trials-mash
- Hu Y, Sun C, Chen Y, Liu Y-D, Fan J-G. Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease. J Clin Transl Hepatol. 2024;12(9):802-814. doi:10.14218/JCTH.2024.00123
- Petta S, Targher G, Romeo S, et al. The first MASH drug therapy on the horizon: Current perspectives of resmetirom. Liver Int. 2024;44(7):1526-1536. doi:10.14218/JCTH.2024.00123doi:10.1111/liv.15930
- Ciardullo S, Muraca E, Vergani M, Invernizzi P, Perseghin G. Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions. Gastroenterol Rep (Oxf). 2024;12:goae029. doi:10.1093/gastro/goae029
- Chen VL, Morgan TR, Rotman Y, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312-320. doi:10.1097/HEP.0000000000001112
- Economist Impact 2024. MASLD/MASH in the US: A liver disease country profile. Published 2024. Accessed January 22, 2025. https://impact.economist.com/perspectives/sites/default/files/download/liver-disease-country-profile_united_states_final.pdf
- Tincopa MA, Anstee QM, Loomba R. New and emerging treatments for metabolic dysfunction-associated steatohepatitis. Cell Metab. 2024;36(5):912-926. doi:10.1016/j.cmet.2024.03.011
- Carpi S, Daniele S, de Almeida JFM, Gabbia D. Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC. Int J Mol Sci. 2024;25(22):12229. https://www.mdpi.com/1422-0067/25/22/1222
- Wong RJ. Epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-related liver disease (ALD). Metab Target Organ Damage. 2024;4:35. http://dx.doi.org/10.20517/mtod.2024.57
- Younossi ZM, Kalligeros M, Henry L. Epidemiology of Metabolic Dysfunction-Associated Steatotic Liver Disease. Clin Mol Hepatol. 2024. doi:10.3350/cmh.2024.0431
- Jozst L. Estimating the True Prevalence of MASH and MASLD in the US. AJMC. Published October 17, 2024. Accessed January 22, 2025. https://www.ajmc.com/view/estimating-the-true-prevalence-of-mash-and-masld-in-the-us
- Mayo Clinic website. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). Published October 4, 2023. Accessed January 22, 2025. https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493
- Younossi ZM. Economic burden of MASLD/MASH. Conference report for NATAP. EASL 2024. Published June 5-8, 2024. Accessed January 22, 2025. https://www.natap.org/2024/EASL/EASL_41.htm
- Loomba R, Noureddin M, Kowdley KV, et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH. Hepatol. 202;73(2):625-643. doi:10.1002/hep.31622
- Nicastro E. D’Antiga L. Nutritional Interventions, Probiotics, Synbiotics and Fecal Microbiota Transplantation in Steatoic Liver Disease. Advances in experimental medicine and Biology. Published online January 1. 202:113-133. doi:https://doi.org.10.1007/978-3-031-58572-2_7
- Shera S, Katzka W, Yang JC, et al. Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system. Front Microbiol. 2024;15:1407555. doi:10.3389/fmicb.2024.1407555
- Globe Newswire website. Akero Therapeutics Reports Second Quarter 2024 Financial Results and Provides Business Update [press release]. Published August 9, 2024. Accessed January 22, 2025. https://www.globenewswire.com/en/news-release/2024/08/09/2927685/0/en/Akero-Therapeutics-Reports-Second-Quarter-2024-Financial-Results-and-Provides-Business-Update.html
- Akero website. Clinical Trials Overview. We are currently enrolling three clinical trials as part of a Phase 3 SYNCHRONY program evaluating EFX for the treatment of pre-cirrhotic MASH (F2-F3) and compensated cirrhosis (F4) due to MASH [press release]. Published 2024. Accessed January 22, 2025. https://akerotx.com/clinical-trials/
- 89bio website. 89bio Initiates Phase 3 ENLIGHTEN-Fibrosis Trial of Pegozafermin in Non-Cirrhotic Metabolic Dysfunction-Associated Steatohepatitis (MASH) Patients with Fibrosis [press release]. Published March 12, 2024. Accessed January 22, 2025. https://www.89bio.com/news/89bio-initiates-phase-3-enlighten-fibrosis-trial-of-pegozafermin-in-non-cirrhotic-metabolic-dysfunction-associated-steatohepatitis-mash-patients-with-fibrosis/
- 89bio website. 89bio Reaches Alignment with the FDA and EMA on Phase 3 Program for Pegozafermin in Nonalcoholic Steatohepatitis (NASH); Program Initiation Planned in the First Half of 2024 [press release]. Published December 4, 2023. Accessed January 22, 2025. https://www.89bio.com/news/89bio-reaches-alignment-with-the-fda-and-ema-on-phase-3-program-for-pegozafermin-in-nonalcoholic-steatohepatitis-nash-program-initiation-planned-in-the-first-half-of-2024/
- Boehringer Ingelheim website. Boehringer receives U.S. FDA Breakthrough Therapy designation and initiates two phase III trials in MASH for survodutide [press release]. Published October 8, 2024. Accessed January 22, 2025. https://www.boehringer-ingelheim.com/human-health/metabolic-diseases/survodutide-us-fda-breakthrough-therapy-phase-3-trials-mash
- Hu Y, Sun C, Chen Y, Liu Y-D, Fan J-G. Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease. J Clin Transl Hepatol. 2024;12(9):802-814. doi:10.14218/JCTH.2024.00123
- Petta S, Targher G, Romeo S, et al. The first MASH drug therapy on the horizon: Current perspectives of resmetirom. Liver Int. 2024;44(7):1526-1536. doi:10.14218/JCTH.2024.00123doi:10.1111/liv.15930
- Ciardullo S, Muraca E, Vergani M, Invernizzi P, Perseghin G. Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions. Gastroenterol Rep (Oxf). 2024;12:goae029. doi:10.1093/gastro/goae029
- Chen VL, Morgan TR, Rotman Y, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312-320. doi:10.1097/HEP.0000000000001112
- Economist Impact 2024. MASLD/MASH in the US: A liver disease country profile. Published 2024. Accessed January 22, 2025. https://impact.economist.com/perspectives/sites/default/files/download/liver-disease-country-profile_united_states_final.pdf
- Tincopa MA, Anstee QM, Loomba R. New and emerging treatments for metabolic dysfunction-associated steatohepatitis. Cell Metab. 2024;36(5):912-926. doi:10.1016/j.cmet.2024.03.011
- Carpi S, Daniele S, de Almeida JFM, Gabbia D. Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC. Int J Mol Sci. 2024;25(22):12229. https://www.mdpi.com/1422-0067/25/22/1222
- Wong RJ. Epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-related liver disease (ALD). Metab Target Organ Damage. 2024;4:35. http://dx.doi.org/10.20517/mtod.2024.57
- Younossi ZM, Kalligeros M, Henry L. Epidemiology of Metabolic Dysfunction-Associated Steatotic Liver Disease. Clin Mol Hepatol. 2024. doi:10.3350/cmh.2024.0431
- Jozst L. Estimating the True Prevalence of MASH and MASLD in the US. AJMC. Published October 17, 2024. Accessed January 22, 2025. https://www.ajmc.com/view/estimating-the-true-prevalence-of-mash-and-masld-in-the-us
- Mayo Clinic website. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). Published October 4, 2023. Accessed January 22, 2025. https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493
- Younossi ZM. Economic burden of MASLD/MASH. Conference report for NATAP. EASL 2024. Published June 5-8, 2024. Accessed January 22, 2025. https://www.natap.org/2024/EASL/EASL_41.htm
- Loomba R, Noureddin M, Kowdley KV, et al. Combination Therapies Including Cilofexor and Firsocostat for Bridging Fibrosis and Cirrhosis Attributable to NASH. Hepatol. 202;73(2):625-643. doi:10.1002/hep.31622
- Nicastro E. D’Antiga L. Nutritional Interventions, Probiotics, Synbiotics and Fecal Microbiota Transplantation in Steatoic Liver Disease. Advances in experimental medicine and Biology. Published online January 1. 202:113-133. doi:https://doi.org.10.1007/978-3-031-58572-2_7
- Shera S, Katzka W, Yang JC, et al. Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system. Front Microbiol. 2024;15:1407555. doi:10.3389/fmicb.2024.1407555
- Globe Newswire website. Akero Therapeutics Reports Second Quarter 2024 Financial Results and Provides Business Update [press release]. Published August 9, 2024. Accessed January 22, 2025. https://www.globenewswire.com/en/news-release/2024/08/09/2927685/0/en/Akero-Therapeutics-Reports-Second-Quarter-2024-Financial-Results-and-Provides-Business-Update.html
- Akero website. Clinical Trials Overview. We are currently enrolling three clinical trials as part of a Phase 3 SYNCHRONY program evaluating EFX for the treatment of pre-cirrhotic MASH (F2-F3) and compensated cirrhosis (F4) due to MASH [press release]. Published 2024. Accessed January 22, 2025. https://akerotx.com/clinical-trials/
- 89bio website. 89bio Initiates Phase 3 ENLIGHTEN-Fibrosis Trial of Pegozafermin in Non-Cirrhotic Metabolic Dysfunction-Associated Steatohepatitis (MASH) Patients with Fibrosis [press release]. Published March 12, 2024. Accessed January 22, 2025. https://www.89bio.com/news/89bio-initiates-phase-3-enlighten-fibrosis-trial-of-pegozafermin-in-non-cirrhotic-metabolic-dysfunction-associated-steatohepatitis-mash-patients-with-fibrosis/
- 89bio website. 89bio Reaches Alignment with the FDA and EMA on Phase 3 Program for Pegozafermin in Nonalcoholic Steatohepatitis (NASH); Program Initiation Planned in the First Half of 2024 [press release]. Published December 4, 2023. Accessed January 22, 2025. https://www.89bio.com/news/89bio-reaches-alignment-with-the-fda-and-ema-on-phase-3-program-for-pegozafermin-in-nonalcoholic-steatohepatitis-nash-program-initiation-planned-in-the-first-half-of-2024/
- Boehringer Ingelheim website. Boehringer receives U.S. FDA Breakthrough Therapy designation and initiates two phase III trials in MASH for survodutide [press release]. Published October 8, 2024. Accessed January 22, 2025. https://www.boehringer-ingelheim.com/human-health/metabolic-diseases/survodutide-us-fda-breakthrough-therapy-phase-3-trials-mash
New and Emerging Treatments for MASLD/MASH
New and Emerging Treatments for MASLD/MASH
New Model Estimates Hepatocellular Carcinoma Risk in Patients With Chronic Hepatitis B
The model, called Revised REACH-B or reREACH-B, stems from cohort studies in Hong Kong, South Korea, and Taiwan, and looks at the nonlinear parabolic association between serum hepatitis B virus (HBV) DNA levels and HCC risk.
“Current clinical practice guidelines don’t advocate antiviral treatment for patients with CHB who don’t show elevated alanine aminotransferase (ALT) levels, even in those with high HBV viral loads,” said coauthor Young-Suk Lim, MD, PhD, professor of gastroenterology at the University of Ulsan College of Medicine and Asan Medical Center in Seoul, South Korea.
“This stance is rooted in the notion that patients in the immune-tolerant phase are at very low risk for developing HCC,” Lim said. “However, the immune-tolerant phase includes patients with HBV DNA levels who face the highest risk for HCC, and many patients with moderate HBV viremia fall into an undefined gray zone.”
The study was published in Annals of Internal Medicine.
Validating reREACH-B
During a course of CHB, HBV viral loads and HCC risks evolve over time because of viral replication and host immune responses, Lim explained. Most patients typically move to seroclearance and an “inactive hepatitis” phase, but about 10%-20% can progress to a “reactivation” phase, where HBV DNA levels and ALT levels increase, which can increase HCC risk as well.
In a previous cohort study in Taiwan, a prognostic model called Risk Estimation for HCC in CHB — or REACH-B — found the risk for HCC increases tenfold with increasing levels of HBV DNA up to 5 log10IU/mL in noncirrhotic patients with CHB, regardless of ALT levels. Another cohort study in South Korea found a nonlinear parabolic association between HCC risk and HBV DNA levels up to 9 log10 IU/mL, with the highest risks found for moderate HBV DNA levels around 6 log10 IU/mL.
In this study, Lim and colleagues developed a prognostic model to integrate the nonlinear relationship and validated it externally, as well as compared it with the previous REACH-B model. The Revised REACH-B model incorporates six variables: age, sex, platelet count, HBV DNA level, ALT, and hepatitis B e-antigen (HBeAg).
The study included 14,378 treatment-naive, noncirrhotic adults with CHB and serum ALT levels < two times the upper limit of normal for at least 1 year and serum hepatitis B surface antigen for at least 6 months. The internal validation cohort included 6,949 patients from Asan Medical Center, and the external validation cohort included 7,429 patients from previous studies in Hong Kong, South Korea, and Taiwan.
Among the Asan cohort, the mean age was 45 years, 29.9% were HBeAg positive, median HBV DNA levels were 3.1 log10 IU/mL, and the median ALT level was 25 U/L. In the external cohort, the mean age was 46 years, 21% were HBeAg positive, median HBV DNA levels were 3.4 log10 IU/mL, and the median ALT level was 20 U/L.
In the Asan cohort, 435 patients (6.3%) developed HCC during a median follow-up of 10 years. The annual HCC incidence rate was 0.63 per 100 person-years, and the estimated cumulative probability of developing HCC at 10 years was 6.4%.
In the external cohort, 467 patients (6.3%) developed HCC during a median follow-up of 12 years. The annual HCC incidence rate was 0.42 per 100 person-years, and the estimated cumulative probability of developing HCC at 10 years was 3.1%.
Overall, the association between HBV viral load and HCC risk was linear in the HBeAg-negative groups and inverse in the HBeAg-positive groups, with the association between HBV viral load and HCC risk showing a nonlinear parabolic pattern.
Across both cohorts, patients with HBV DNA levels between 5 and 6 log10 IU/mL had the highest risk for HCC in both the HBeAg-negative and HBeAg-positive groups, which was more than eight times higher than those HBV DNA levels ≤ 3 log10 IU/mL.
For internal validation, the Revised REACH-B model had a c-statistic of 0.844 and 5-year area under the curve of 0.864. For external validation across the three external cohorts, the reREACH-B had c-statistics of 0.804, 0.808, and 0.813, and 5-year area under the curve of 0.839, 0.860, and 0.865.
In addition, the revised model yielded a greater positive net benefit than the REACH-B model in the threshold probability range between 0% and 18%.
“These analyses indicate the reREACH-B model can be a valuable tool in clinical practice, aiding in timely management decisions,” Lim said.
Considering Prognostic Models
This study highlights the importance of recognizing that the association between HBV DNA viral load and HCC risk isn’t linear, said Norah Terrault, MD, chief of Gastroenterology and Hepatology at the Keck School of Medicine at the University of Southern California, Los Angeles.
“In contrast to most chronic liver diseases where liver cancer develops only among those with advanced fibrosis/cirrhosis, people with chronic hepatitis B are at risk prior to the development of cirrhosis,” she said. “Risk prediction scores for HCC can be a useful means of identifying those without cirrhosis who should be enrolled in HCC surveillance programs.”
For instance, patients with HBV DNA levels < 3 log10 IU/mL or > 8 log10 IU/mL don’t have an increased risk, Terrault noted. However, the highest risk group appears to be around 5-6 log10 IU/mL.
“Future risk prediction models should acknowledge that relationship in modeling HCC risk,” she said. “The re-REACH-B provides modest improvement over the REACH-B, but further validation of this score in more diverse cohorts is essential.”
The study received financial support from the Korean government and grants from the Patient-Centered Clinical Research Coordinating Center of the National Evidence-based Healthcare Collaborating Agency and the National R&D Program for Cancer Control through the National Cancer Center, which is funded by Korea’s Ministry of Health and Welfare. Lim and Terrault reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
The model, called Revised REACH-B or reREACH-B, stems from cohort studies in Hong Kong, South Korea, and Taiwan, and looks at the nonlinear parabolic association between serum hepatitis B virus (HBV) DNA levels and HCC risk.
“Current clinical practice guidelines don’t advocate antiviral treatment for patients with CHB who don’t show elevated alanine aminotransferase (ALT) levels, even in those with high HBV viral loads,” said coauthor Young-Suk Lim, MD, PhD, professor of gastroenterology at the University of Ulsan College of Medicine and Asan Medical Center in Seoul, South Korea.
“This stance is rooted in the notion that patients in the immune-tolerant phase are at very low risk for developing HCC,” Lim said. “However, the immune-tolerant phase includes patients with HBV DNA levels who face the highest risk for HCC, and many patients with moderate HBV viremia fall into an undefined gray zone.”
The study was published in Annals of Internal Medicine.
Validating reREACH-B
During a course of CHB, HBV viral loads and HCC risks evolve over time because of viral replication and host immune responses, Lim explained. Most patients typically move to seroclearance and an “inactive hepatitis” phase, but about 10%-20% can progress to a “reactivation” phase, where HBV DNA levels and ALT levels increase, which can increase HCC risk as well.
In a previous cohort study in Taiwan, a prognostic model called Risk Estimation for HCC in CHB — or REACH-B — found the risk for HCC increases tenfold with increasing levels of HBV DNA up to 5 log10IU/mL in noncirrhotic patients with CHB, regardless of ALT levels. Another cohort study in South Korea found a nonlinear parabolic association between HCC risk and HBV DNA levels up to 9 log10 IU/mL, with the highest risks found for moderate HBV DNA levels around 6 log10 IU/mL.
In this study, Lim and colleagues developed a prognostic model to integrate the nonlinear relationship and validated it externally, as well as compared it with the previous REACH-B model. The Revised REACH-B model incorporates six variables: age, sex, platelet count, HBV DNA level, ALT, and hepatitis B e-antigen (HBeAg).
The study included 14,378 treatment-naive, noncirrhotic adults with CHB and serum ALT levels < two times the upper limit of normal for at least 1 year and serum hepatitis B surface antigen for at least 6 months. The internal validation cohort included 6,949 patients from Asan Medical Center, and the external validation cohort included 7,429 patients from previous studies in Hong Kong, South Korea, and Taiwan.
Among the Asan cohort, the mean age was 45 years, 29.9% were HBeAg positive, median HBV DNA levels were 3.1 log10 IU/mL, and the median ALT level was 25 U/L. In the external cohort, the mean age was 46 years, 21% were HBeAg positive, median HBV DNA levels were 3.4 log10 IU/mL, and the median ALT level was 20 U/L.
In the Asan cohort, 435 patients (6.3%) developed HCC during a median follow-up of 10 years. The annual HCC incidence rate was 0.63 per 100 person-years, and the estimated cumulative probability of developing HCC at 10 years was 6.4%.
In the external cohort, 467 patients (6.3%) developed HCC during a median follow-up of 12 years. The annual HCC incidence rate was 0.42 per 100 person-years, and the estimated cumulative probability of developing HCC at 10 years was 3.1%.
Overall, the association between HBV viral load and HCC risk was linear in the HBeAg-negative groups and inverse in the HBeAg-positive groups, with the association between HBV viral load and HCC risk showing a nonlinear parabolic pattern.
Across both cohorts, patients with HBV DNA levels between 5 and 6 log10 IU/mL had the highest risk for HCC in both the HBeAg-negative and HBeAg-positive groups, which was more than eight times higher than those HBV DNA levels ≤ 3 log10 IU/mL.
For internal validation, the Revised REACH-B model had a c-statistic of 0.844 and 5-year area under the curve of 0.864. For external validation across the three external cohorts, the reREACH-B had c-statistics of 0.804, 0.808, and 0.813, and 5-year area under the curve of 0.839, 0.860, and 0.865.
In addition, the revised model yielded a greater positive net benefit than the REACH-B model in the threshold probability range between 0% and 18%.
“These analyses indicate the reREACH-B model can be a valuable tool in clinical practice, aiding in timely management decisions,” Lim said.
Considering Prognostic Models
This study highlights the importance of recognizing that the association between HBV DNA viral load and HCC risk isn’t linear, said Norah Terrault, MD, chief of Gastroenterology and Hepatology at the Keck School of Medicine at the University of Southern California, Los Angeles.
“In contrast to most chronic liver diseases where liver cancer develops only among those with advanced fibrosis/cirrhosis, people with chronic hepatitis B are at risk prior to the development of cirrhosis,” she said. “Risk prediction scores for HCC can be a useful means of identifying those without cirrhosis who should be enrolled in HCC surveillance programs.”
For instance, patients with HBV DNA levels < 3 log10 IU/mL or > 8 log10 IU/mL don’t have an increased risk, Terrault noted. However, the highest risk group appears to be around 5-6 log10 IU/mL.
“Future risk prediction models should acknowledge that relationship in modeling HCC risk,” she said. “The re-REACH-B provides modest improvement over the REACH-B, but further validation of this score in more diverse cohorts is essential.”
The study received financial support from the Korean government and grants from the Patient-Centered Clinical Research Coordinating Center of the National Evidence-based Healthcare Collaborating Agency and the National R&D Program for Cancer Control through the National Cancer Center, which is funded by Korea’s Ministry of Health and Welfare. Lim and Terrault reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
The model, called Revised REACH-B or reREACH-B, stems from cohort studies in Hong Kong, South Korea, and Taiwan, and looks at the nonlinear parabolic association between serum hepatitis B virus (HBV) DNA levels and HCC risk.
“Current clinical practice guidelines don’t advocate antiviral treatment for patients with CHB who don’t show elevated alanine aminotransferase (ALT) levels, even in those with high HBV viral loads,” said coauthor Young-Suk Lim, MD, PhD, professor of gastroenterology at the University of Ulsan College of Medicine and Asan Medical Center in Seoul, South Korea.
“This stance is rooted in the notion that patients in the immune-tolerant phase are at very low risk for developing HCC,” Lim said. “However, the immune-tolerant phase includes patients with HBV DNA levels who face the highest risk for HCC, and many patients with moderate HBV viremia fall into an undefined gray zone.”
The study was published in Annals of Internal Medicine.
Validating reREACH-B
During a course of CHB, HBV viral loads and HCC risks evolve over time because of viral replication and host immune responses, Lim explained. Most patients typically move to seroclearance and an “inactive hepatitis” phase, but about 10%-20% can progress to a “reactivation” phase, where HBV DNA levels and ALT levels increase, which can increase HCC risk as well.
In a previous cohort study in Taiwan, a prognostic model called Risk Estimation for HCC in CHB — or REACH-B — found the risk for HCC increases tenfold with increasing levels of HBV DNA up to 5 log10IU/mL in noncirrhotic patients with CHB, regardless of ALT levels. Another cohort study in South Korea found a nonlinear parabolic association between HCC risk and HBV DNA levels up to 9 log10 IU/mL, with the highest risks found for moderate HBV DNA levels around 6 log10 IU/mL.
In this study, Lim and colleagues developed a prognostic model to integrate the nonlinear relationship and validated it externally, as well as compared it with the previous REACH-B model. The Revised REACH-B model incorporates six variables: age, sex, platelet count, HBV DNA level, ALT, and hepatitis B e-antigen (HBeAg).
The study included 14,378 treatment-naive, noncirrhotic adults with CHB and serum ALT levels < two times the upper limit of normal for at least 1 year and serum hepatitis B surface antigen for at least 6 months. The internal validation cohort included 6,949 patients from Asan Medical Center, and the external validation cohort included 7,429 patients from previous studies in Hong Kong, South Korea, and Taiwan.
Among the Asan cohort, the mean age was 45 years, 29.9% were HBeAg positive, median HBV DNA levels were 3.1 log10 IU/mL, and the median ALT level was 25 U/L. In the external cohort, the mean age was 46 years, 21% were HBeAg positive, median HBV DNA levels were 3.4 log10 IU/mL, and the median ALT level was 20 U/L.
In the Asan cohort, 435 patients (6.3%) developed HCC during a median follow-up of 10 years. The annual HCC incidence rate was 0.63 per 100 person-years, and the estimated cumulative probability of developing HCC at 10 years was 6.4%.
In the external cohort, 467 patients (6.3%) developed HCC during a median follow-up of 12 years. The annual HCC incidence rate was 0.42 per 100 person-years, and the estimated cumulative probability of developing HCC at 10 years was 3.1%.
Overall, the association between HBV viral load and HCC risk was linear in the HBeAg-negative groups and inverse in the HBeAg-positive groups, with the association between HBV viral load and HCC risk showing a nonlinear parabolic pattern.
Across both cohorts, patients with HBV DNA levels between 5 and 6 log10 IU/mL had the highest risk for HCC in both the HBeAg-negative and HBeAg-positive groups, which was more than eight times higher than those HBV DNA levels ≤ 3 log10 IU/mL.
For internal validation, the Revised REACH-B model had a c-statistic of 0.844 and 5-year area under the curve of 0.864. For external validation across the three external cohorts, the reREACH-B had c-statistics of 0.804, 0.808, and 0.813, and 5-year area under the curve of 0.839, 0.860, and 0.865.
In addition, the revised model yielded a greater positive net benefit than the REACH-B model in the threshold probability range between 0% and 18%.
“These analyses indicate the reREACH-B model can be a valuable tool in clinical practice, aiding in timely management decisions,” Lim said.
Considering Prognostic Models
This study highlights the importance of recognizing that the association between HBV DNA viral load and HCC risk isn’t linear, said Norah Terrault, MD, chief of Gastroenterology and Hepatology at the Keck School of Medicine at the University of Southern California, Los Angeles.
“In contrast to most chronic liver diseases where liver cancer develops only among those with advanced fibrosis/cirrhosis, people with chronic hepatitis B are at risk prior to the development of cirrhosis,” she said. “Risk prediction scores for HCC can be a useful means of identifying those without cirrhosis who should be enrolled in HCC surveillance programs.”
For instance, patients with HBV DNA levels < 3 log10 IU/mL or > 8 log10 IU/mL don’t have an increased risk, Terrault noted. However, the highest risk group appears to be around 5-6 log10 IU/mL.
“Future risk prediction models should acknowledge that relationship in modeling HCC risk,” she said. “The re-REACH-B provides modest improvement over the REACH-B, but further validation of this score in more diverse cohorts is essential.”
The study received financial support from the Korean government and grants from the Patient-Centered Clinical Research Coordinating Center of the National Evidence-based Healthcare Collaborating Agency and the National R&D Program for Cancer Control through the National Cancer Center, which is funded by Korea’s Ministry of Health and Welfare. Lim and Terrault reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM ANNALS OF INTERNAL MEDICINE
Broken Sleep Linked to MASLD
TOPLINE:
Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.
METHODOLOGY:
- Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
- Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
- All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
- A standardized sleep hygiene education session was conducted at week 2.
TAKEAWAY:
- Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
- However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
- Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
- Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
- The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.
IN PRACTICE:
“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.
SOURCE:
The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.
LIMITATIONS:
The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.
DISCLOSURES:
This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
A version of this article first appeared on Medscape.com.
TOPLINE:
Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.
METHODOLOGY:
- Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
- Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
- All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
- A standardized sleep hygiene education session was conducted at week 2.
TAKEAWAY:
- Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
- However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
- Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
- Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
- The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.
IN PRACTICE:
“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.
SOURCE:
The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.
LIMITATIONS:
The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.
DISCLOSURES:
This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
A version of this article first appeared on Medscape.com.
TOPLINE:
Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.
METHODOLOGY:
- Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
- Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
- All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
- A standardized sleep hygiene education session was conducted at week 2.
TAKEAWAY:
- Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
- However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
- Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
- Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
- The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.
IN PRACTICE:
“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.
SOURCE:
The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.
LIMITATIONS:
The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.
DISCLOSURES:
This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
A version of this article first appeared on Medscape.com.
GLP-1 RAs: When Not to Prescribe
December 31, 2024
This transcript has been edited for clarity.
I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe.
It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people.
They include the following:
Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.
Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs.
Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.
Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m2, excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing.
And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.
GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.
Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
December 31, 2024
This transcript has been edited for clarity.
I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe.
It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people.
They include the following:
Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.
Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs.
Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.
Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m2, excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing.
And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.
GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.
Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
December 31, 2024
This transcript has been edited for clarity.
I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe.
It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people.
They include the following:
Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.
Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs.
Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.
Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m2, excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing.
And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.
GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.
Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Hepatocellular Carcinoma: Leading Causes of Mortality Predicted
TOPLINE:
Alcohol-associated liver disease (ALD) will likely become the leading cause of HCC-related mortality by 2026, and metabolic dysfunction–associated steatotic liver disease (MASLD) is projected to become the second leading cause by 2032, a new analysis found.
METHODOLOGY:
- HCC accounts for 75%-85% of primary liver cancers and most liver cancer deaths. Researchers have observed an upward trend in the incidence of and mortality from HCC in the past 2 decades.
- This cross-sectional study analyzed 188,280 HCC-related deaths among adults aged 25 and older to determine trends in mortality rates and project age-standardized mortality rates through 2040. Data came from the National Vital Statistics System database from 2006 to 2022.
- Researchers stratified mortality data by etiology of liver disease (ALD, hepatitis B virus, hepatitis C virus, and MASLD), age groups (25-64 or 65 and older years), sex, and race/ethnicity.
- Demographic data showed that 77.4% of deaths occurred in men, 55.6% in individuals aged 65 years or older, and 62.3% in White individuals.
TAKEAWAY:
- Overall, the age-standardized mortality rate for HCC-related deaths increased from 3.65 per 100,000 persons in 2006 to 5.03 in 2022 and was projected to increase to 6.39 per 100,000 persons by 2040.
- Sex- and age-related disparities were substantial. Men had much higher rates of HCC-related mortality than women (8.15 vs 2.33 per 100,000 persons), with a projected rate among men of 9.78 per 100,000 persons by 2040. HCC-related mortality rates for people aged 65 years or older were 10 times higher than for those aged 25-64 years (18.37 vs 1.79 per 100,000 persons) in 2022 and was projected to reach 32.81 per 100,000 persons by 2040 in the older group.
- Although hepatitis C virus–related deaths were projected to decline from 0.69 to 0.03 per 100,000 persons by 2034, ALD- and MASLD-related deaths showed increasing trends, with both projected to become the two leading causes of HCC-related mortality in the next few years.
- Racial disparities were also evident. By 2040, the American Indian/Alaska Native population showed the highest increase in projected HCC-related mortality rates, which went from 5.46 per 100,000 persons in 2006 to a project increase to 14.71 per 100,000 persons.
IN PRACTICE:
“HCC mortality was projected to continue increasing in the US, primarily due to rising rates of deaths attributable to ALD and MASLD,” the authors wrote.
This “study highlights the importance of addressing these conditions to decrease the burden of liver disease and liver disease mortality in the future,” Emad Qayed, MD, MPH, Emory University School of Medicine, Atlanta, wrote in an accompanying editorial.
SOURCE:
The study was led by Sikai Qiu, MM, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China, and was published online in JAMA Network Open.
LIMITATIONS:
The National Vital Statistics System database used in this study captured only mortality data without access to detailed clinical records or individual medical histories. Researchers could not analyze socioeconomic factors or individual-level risk factors owing to data anonymization requirements. Additionally, the inclusion of the COVID-19 pandemic period could have influenced observed trends and reliability of future projections.
DISCLOSURES:
This study was supported by grants from the National Natural Science Foundation of China. Several authors reported receiving consulting fees, speaking fees, or research support from various sources.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
Alcohol-associated liver disease (ALD) will likely become the leading cause of HCC-related mortality by 2026, and metabolic dysfunction–associated steatotic liver disease (MASLD) is projected to become the second leading cause by 2032, a new analysis found.
METHODOLOGY:
- HCC accounts for 75%-85% of primary liver cancers and most liver cancer deaths. Researchers have observed an upward trend in the incidence of and mortality from HCC in the past 2 decades.
- This cross-sectional study analyzed 188,280 HCC-related deaths among adults aged 25 and older to determine trends in mortality rates and project age-standardized mortality rates through 2040. Data came from the National Vital Statistics System database from 2006 to 2022.
- Researchers stratified mortality data by etiology of liver disease (ALD, hepatitis B virus, hepatitis C virus, and MASLD), age groups (25-64 or 65 and older years), sex, and race/ethnicity.
- Demographic data showed that 77.4% of deaths occurred in men, 55.6% in individuals aged 65 years or older, and 62.3% in White individuals.
TAKEAWAY:
- Overall, the age-standardized mortality rate for HCC-related deaths increased from 3.65 per 100,000 persons in 2006 to 5.03 in 2022 and was projected to increase to 6.39 per 100,000 persons by 2040.
- Sex- and age-related disparities were substantial. Men had much higher rates of HCC-related mortality than women (8.15 vs 2.33 per 100,000 persons), with a projected rate among men of 9.78 per 100,000 persons by 2040. HCC-related mortality rates for people aged 65 years or older were 10 times higher than for those aged 25-64 years (18.37 vs 1.79 per 100,000 persons) in 2022 and was projected to reach 32.81 per 100,000 persons by 2040 in the older group.
- Although hepatitis C virus–related deaths were projected to decline from 0.69 to 0.03 per 100,000 persons by 2034, ALD- and MASLD-related deaths showed increasing trends, with both projected to become the two leading causes of HCC-related mortality in the next few years.
- Racial disparities were also evident. By 2040, the American Indian/Alaska Native population showed the highest increase in projected HCC-related mortality rates, which went from 5.46 per 100,000 persons in 2006 to a project increase to 14.71 per 100,000 persons.
IN PRACTICE:
“HCC mortality was projected to continue increasing in the US, primarily due to rising rates of deaths attributable to ALD and MASLD,” the authors wrote.
This “study highlights the importance of addressing these conditions to decrease the burden of liver disease and liver disease mortality in the future,” Emad Qayed, MD, MPH, Emory University School of Medicine, Atlanta, wrote in an accompanying editorial.
SOURCE:
The study was led by Sikai Qiu, MM, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China, and was published online in JAMA Network Open.
LIMITATIONS:
The National Vital Statistics System database used in this study captured only mortality data without access to detailed clinical records or individual medical histories. Researchers could not analyze socioeconomic factors or individual-level risk factors owing to data anonymization requirements. Additionally, the inclusion of the COVID-19 pandemic period could have influenced observed trends and reliability of future projections.
DISCLOSURES:
This study was supported by grants from the National Natural Science Foundation of China. Several authors reported receiving consulting fees, speaking fees, or research support from various sources.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
Alcohol-associated liver disease (ALD) will likely become the leading cause of HCC-related mortality by 2026, and metabolic dysfunction–associated steatotic liver disease (MASLD) is projected to become the second leading cause by 2032, a new analysis found.
METHODOLOGY:
- HCC accounts for 75%-85% of primary liver cancers and most liver cancer deaths. Researchers have observed an upward trend in the incidence of and mortality from HCC in the past 2 decades.
- This cross-sectional study analyzed 188,280 HCC-related deaths among adults aged 25 and older to determine trends in mortality rates and project age-standardized mortality rates through 2040. Data came from the National Vital Statistics System database from 2006 to 2022.
- Researchers stratified mortality data by etiology of liver disease (ALD, hepatitis B virus, hepatitis C virus, and MASLD), age groups (25-64 or 65 and older years), sex, and race/ethnicity.
- Demographic data showed that 77.4% of deaths occurred in men, 55.6% in individuals aged 65 years or older, and 62.3% in White individuals.
TAKEAWAY:
- Overall, the age-standardized mortality rate for HCC-related deaths increased from 3.65 per 100,000 persons in 2006 to 5.03 in 2022 and was projected to increase to 6.39 per 100,000 persons by 2040.
- Sex- and age-related disparities were substantial. Men had much higher rates of HCC-related mortality than women (8.15 vs 2.33 per 100,000 persons), with a projected rate among men of 9.78 per 100,000 persons by 2040. HCC-related mortality rates for people aged 65 years or older were 10 times higher than for those aged 25-64 years (18.37 vs 1.79 per 100,000 persons) in 2022 and was projected to reach 32.81 per 100,000 persons by 2040 in the older group.
- Although hepatitis C virus–related deaths were projected to decline from 0.69 to 0.03 per 100,000 persons by 2034, ALD- and MASLD-related deaths showed increasing trends, with both projected to become the two leading causes of HCC-related mortality in the next few years.
- Racial disparities were also evident. By 2040, the American Indian/Alaska Native population showed the highest increase in projected HCC-related mortality rates, which went from 5.46 per 100,000 persons in 2006 to a project increase to 14.71 per 100,000 persons.
IN PRACTICE:
“HCC mortality was projected to continue increasing in the US, primarily due to rising rates of deaths attributable to ALD and MASLD,” the authors wrote.
This “study highlights the importance of addressing these conditions to decrease the burden of liver disease and liver disease mortality in the future,” Emad Qayed, MD, MPH, Emory University School of Medicine, Atlanta, wrote in an accompanying editorial.
SOURCE:
The study was led by Sikai Qiu, MM, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China, and was published online in JAMA Network Open.
LIMITATIONS:
The National Vital Statistics System database used in this study captured only mortality data without access to detailed clinical records or individual medical histories. Researchers could not analyze socioeconomic factors or individual-level risk factors owing to data anonymization requirements. Additionally, the inclusion of the COVID-19 pandemic period could have influenced observed trends and reliability of future projections.
DISCLOSURES:
This study was supported by grants from the National Natural Science Foundation of China. Several authors reported receiving consulting fees, speaking fees, or research support from various sources.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Health Impacts of Micro- and Nanoplastics
In preparation for a future international treaty aimed at reducing plastic pollution, the French Parliamentary Office for the Evaluation of Scientific and Technological Choices presented the conclusions of a public hearing on the impact of plastics on various aspects of human health.
Increased Global Plastic Production
Philippe Bolo, a member of the French Democratic Party and the rapporteur for the public mission on the health impacts of plastics, spoke about the latest round of treaty negotiations, held from November 25 to December 1 in South Korea, attended by leading French and global experts about the impact of plastics on human health.
The hearing highlighted a sharp increase in plastic production. “It has doubled in the last 20 years and is expected to exceed 500 million tons in 2024,” Bolo said. This is about 60 kg per person. According to projections from the Organization for Economic Co-operation and Development, on its current trajectory, plastic production will reach 750 million tons by 2040 and surpass 1 billion tons before 2050, he said.
Minimal Plastic Waste Recycling
Around one third (32%) of plastics are used for packaging. “Therefore, most plastic production is still intended for single-use purposes,” he said. Plastic waste follows a similar growth trajectory, with volumes expected to rise from 360 million tons in 2020 to 617 million tons by 2040 unless action is taken. Very little of this waste is recycled, even in the most countries that are most advanced in terms of collection, sorting, and processing.
In France, for example, in 2018, only 0.6 million tons of the 3.6 million tons of plastic waste produced was truly recycled. This is less than one fifth (17%). Globally, less than 10% of plastic waste is recycled. In 2020, plastic waste that ended up in the environment represented 81 million tons, or 22% of the total. “Beyond waste, this leads to pollution by microplastics and nanoplastics, resulting from their fragmentation. All environments are affected: Seas, rivers, soils, air, and even living organisms,” Bolo said.
Methodological Challenges
However, measuring the impact of plastics on health faces methodological difficulties due to the wide variety of composition, size, and shape of plastics. Nevertheless, the French Standardization Association (Association Française de Normalisation) has conducted work to establish a characterization standard for microplastics in water, which serves as an international reference.
“It is also very difficult to know what we are ingesting,” Bolo said. “A study conducted in 2019 estimated that the average human absorbs 5 grams of plastics per week, the equivalent of a credit card.» Since then, other studies have revised this estimate downward, but no consensus has been reached.
A recent study across 109 countries, both industrialized and developing, found significant exposure, estimated at 500 mg/d, particularly in Southeast Asian countries, where it was due mainly to seafood consumption.
A study concluded that plastic water bottles contain 240,000 particles per liter, 90% of which are nanoplastics. These nanoparticles can pass through the intestinal barrier to enter the bloodstream and reach several organs including the heart, brain, and placenta, as well as the fetus.
Changes to the Microbiome
Microplastics also accumulate in organs. Thus, the amount of plastic in the lungs increases with age, suggesting that particles may persist in the body without being eliminated. The health consequences of this are still poorly understood, but exposure to plastics appears to cause changes in the composition of the intestinal microbiota. Pathobionts (commensal bacteria with harmful potential) have been found in both adults and children, which could contribute to dysbiosis of the gut microbiome. Furthermore, a decrease in butyrate, a short-chain fatty acid beneficial to health, has been observed in children’s intestines.
Inhaled nanoplastics may disrupt the mucociliary clearance mechanisms of the respiratory system. The toxicity of inhaled plastic particles was demonstrated as early as the 1970s among workers in the flocking industry. Some developed lung function impairments, shortness of breath, inflammation, fibrosis, and even lung cancer. Similar symptoms have been observed in workers in the textile and polyvinyl chloride industries.
A study published recently in The New England Journal of Medicine measured the amount of microplastics collected from carotid plaque of more than 300 patients who had undergone carotid endarterectomy for asymptomatic carotid artery disease. It found a 4.53 times higher risk for the primary endpoint, a composite of myocardial infarction, stroke, and all-cause mortality, among individuals with microplastics and nanoplastics in plaque compared with those without.
Health Affects High
The danger of plastics is also directly linked to the chemical substances they contain. A general scientific review looked at the health impacts of three chemicals used almost exclusively in plastics: Polybromodiphenyl ethers (PBDEs), used as flame retardants in textiles or electronics; bisphenol A (BPA), used in the lining of cans and bottles; and phthalates, particularly diethylhexyl phthalate (DEHP), used to make plastics more flexible.
The review highlighted strong epidemiological evidence linking fetal exposure to PBDEs during pregnancy to low birth weight and later exposure to delayed or impaired cognitive development in children and even a loss of IQ. Statistically significant evidence of disruption of thyroid function in adults was also found.
BPA is linked to genital malformations in female newborns exposed to BPA in utero, type 2 diabetes in adults, insulin resistance, and polycystic ovary syndrome in women. BPA exposure also increases the risk for obesity and hypertension in both children and adults, as well as the risk for cardiovascular disease in adults.
Finally, the review established links between exposure to DEHP and miscarriages, genital malformations in male newborns, delayed or impaired cognitive development in children, loss of IQ, delayed psychomotor development, early puberty in young girls, and endometriosis in young women. DEHP exposure also has multiple effects on cardiometabolic health, including insulin resistance, obesity, and elevated blood pressure.
The economic costs associated with the health impacts of these three substances have been estimated at $675 billion in the United States.
Bolo said that the solution to this plastic pollution is necessarily international. “We need an ambitious and legally binding treaty to reduce plastic production,” he said. “The damage is already done; we need to act to protect human health,” he concluded. The parliamentary office has made nine recommendations to the treaty negotiators.
This story was translated from Medscape’s French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
In preparation for a future international treaty aimed at reducing plastic pollution, the French Parliamentary Office for the Evaluation of Scientific and Technological Choices presented the conclusions of a public hearing on the impact of plastics on various aspects of human health.
Increased Global Plastic Production
Philippe Bolo, a member of the French Democratic Party and the rapporteur for the public mission on the health impacts of plastics, spoke about the latest round of treaty negotiations, held from November 25 to December 1 in South Korea, attended by leading French and global experts about the impact of plastics on human health.
The hearing highlighted a sharp increase in plastic production. “It has doubled in the last 20 years and is expected to exceed 500 million tons in 2024,” Bolo said. This is about 60 kg per person. According to projections from the Organization for Economic Co-operation and Development, on its current trajectory, plastic production will reach 750 million tons by 2040 and surpass 1 billion tons before 2050, he said.
Minimal Plastic Waste Recycling
Around one third (32%) of plastics are used for packaging. “Therefore, most plastic production is still intended for single-use purposes,” he said. Plastic waste follows a similar growth trajectory, with volumes expected to rise from 360 million tons in 2020 to 617 million tons by 2040 unless action is taken. Very little of this waste is recycled, even in the most countries that are most advanced in terms of collection, sorting, and processing.
In France, for example, in 2018, only 0.6 million tons of the 3.6 million tons of plastic waste produced was truly recycled. This is less than one fifth (17%). Globally, less than 10% of plastic waste is recycled. In 2020, plastic waste that ended up in the environment represented 81 million tons, or 22% of the total. “Beyond waste, this leads to pollution by microplastics and nanoplastics, resulting from their fragmentation. All environments are affected: Seas, rivers, soils, air, and even living organisms,” Bolo said.
Methodological Challenges
However, measuring the impact of plastics on health faces methodological difficulties due to the wide variety of composition, size, and shape of plastics. Nevertheless, the French Standardization Association (Association Française de Normalisation) has conducted work to establish a characterization standard for microplastics in water, which serves as an international reference.
“It is also very difficult to know what we are ingesting,” Bolo said. “A study conducted in 2019 estimated that the average human absorbs 5 grams of plastics per week, the equivalent of a credit card.» Since then, other studies have revised this estimate downward, but no consensus has been reached.
A recent study across 109 countries, both industrialized and developing, found significant exposure, estimated at 500 mg/d, particularly in Southeast Asian countries, where it was due mainly to seafood consumption.
A study concluded that plastic water bottles contain 240,000 particles per liter, 90% of which are nanoplastics. These nanoparticles can pass through the intestinal barrier to enter the bloodstream and reach several organs including the heart, brain, and placenta, as well as the fetus.
Changes to the Microbiome
Microplastics also accumulate in organs. Thus, the amount of plastic in the lungs increases with age, suggesting that particles may persist in the body without being eliminated. The health consequences of this are still poorly understood, but exposure to plastics appears to cause changes in the composition of the intestinal microbiota. Pathobionts (commensal bacteria with harmful potential) have been found in both adults and children, which could contribute to dysbiosis of the gut microbiome. Furthermore, a decrease in butyrate, a short-chain fatty acid beneficial to health, has been observed in children’s intestines.
Inhaled nanoplastics may disrupt the mucociliary clearance mechanisms of the respiratory system. The toxicity of inhaled plastic particles was demonstrated as early as the 1970s among workers in the flocking industry. Some developed lung function impairments, shortness of breath, inflammation, fibrosis, and even lung cancer. Similar symptoms have been observed in workers in the textile and polyvinyl chloride industries.
A study published recently in The New England Journal of Medicine measured the amount of microplastics collected from carotid plaque of more than 300 patients who had undergone carotid endarterectomy for asymptomatic carotid artery disease. It found a 4.53 times higher risk for the primary endpoint, a composite of myocardial infarction, stroke, and all-cause mortality, among individuals with microplastics and nanoplastics in plaque compared with those without.
Health Affects High
The danger of plastics is also directly linked to the chemical substances they contain. A general scientific review looked at the health impacts of three chemicals used almost exclusively in plastics: Polybromodiphenyl ethers (PBDEs), used as flame retardants in textiles or electronics; bisphenol A (BPA), used in the lining of cans and bottles; and phthalates, particularly diethylhexyl phthalate (DEHP), used to make plastics more flexible.
The review highlighted strong epidemiological evidence linking fetal exposure to PBDEs during pregnancy to low birth weight and later exposure to delayed or impaired cognitive development in children and even a loss of IQ. Statistically significant evidence of disruption of thyroid function in adults was also found.
BPA is linked to genital malformations in female newborns exposed to BPA in utero, type 2 diabetes in adults, insulin resistance, and polycystic ovary syndrome in women. BPA exposure also increases the risk for obesity and hypertension in both children and adults, as well as the risk for cardiovascular disease in adults.
Finally, the review established links between exposure to DEHP and miscarriages, genital malformations in male newborns, delayed or impaired cognitive development in children, loss of IQ, delayed psychomotor development, early puberty in young girls, and endometriosis in young women. DEHP exposure also has multiple effects on cardiometabolic health, including insulin resistance, obesity, and elevated blood pressure.
The economic costs associated with the health impacts of these three substances have been estimated at $675 billion in the United States.
Bolo said that the solution to this plastic pollution is necessarily international. “We need an ambitious and legally binding treaty to reduce plastic production,” he said. “The damage is already done; we need to act to protect human health,” he concluded. The parliamentary office has made nine recommendations to the treaty negotiators.
This story was translated from Medscape’s French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
In preparation for a future international treaty aimed at reducing plastic pollution, the French Parliamentary Office for the Evaluation of Scientific and Technological Choices presented the conclusions of a public hearing on the impact of plastics on various aspects of human health.
Increased Global Plastic Production
Philippe Bolo, a member of the French Democratic Party and the rapporteur for the public mission on the health impacts of plastics, spoke about the latest round of treaty negotiations, held from November 25 to December 1 in South Korea, attended by leading French and global experts about the impact of plastics on human health.
The hearing highlighted a sharp increase in plastic production. “It has doubled in the last 20 years and is expected to exceed 500 million tons in 2024,” Bolo said. This is about 60 kg per person. According to projections from the Organization for Economic Co-operation and Development, on its current trajectory, plastic production will reach 750 million tons by 2040 and surpass 1 billion tons before 2050, he said.
Minimal Plastic Waste Recycling
Around one third (32%) of plastics are used for packaging. “Therefore, most plastic production is still intended for single-use purposes,” he said. Plastic waste follows a similar growth trajectory, with volumes expected to rise from 360 million tons in 2020 to 617 million tons by 2040 unless action is taken. Very little of this waste is recycled, even in the most countries that are most advanced in terms of collection, sorting, and processing.
In France, for example, in 2018, only 0.6 million tons of the 3.6 million tons of plastic waste produced was truly recycled. This is less than one fifth (17%). Globally, less than 10% of plastic waste is recycled. In 2020, plastic waste that ended up in the environment represented 81 million tons, or 22% of the total. “Beyond waste, this leads to pollution by microplastics and nanoplastics, resulting from their fragmentation. All environments are affected: Seas, rivers, soils, air, and even living organisms,” Bolo said.
Methodological Challenges
However, measuring the impact of plastics on health faces methodological difficulties due to the wide variety of composition, size, and shape of plastics. Nevertheless, the French Standardization Association (Association Française de Normalisation) has conducted work to establish a characterization standard for microplastics in water, which serves as an international reference.
“It is also very difficult to know what we are ingesting,” Bolo said. “A study conducted in 2019 estimated that the average human absorbs 5 grams of plastics per week, the equivalent of a credit card.» Since then, other studies have revised this estimate downward, but no consensus has been reached.
A recent study across 109 countries, both industrialized and developing, found significant exposure, estimated at 500 mg/d, particularly in Southeast Asian countries, where it was due mainly to seafood consumption.
A study concluded that plastic water bottles contain 240,000 particles per liter, 90% of which are nanoplastics. These nanoparticles can pass through the intestinal barrier to enter the bloodstream and reach several organs including the heart, brain, and placenta, as well as the fetus.
Changes to the Microbiome
Microplastics also accumulate in organs. Thus, the amount of plastic in the lungs increases with age, suggesting that particles may persist in the body without being eliminated. The health consequences of this are still poorly understood, but exposure to plastics appears to cause changes in the composition of the intestinal microbiota. Pathobionts (commensal bacteria with harmful potential) have been found in both adults and children, which could contribute to dysbiosis of the gut microbiome. Furthermore, a decrease in butyrate, a short-chain fatty acid beneficial to health, has been observed in children’s intestines.
Inhaled nanoplastics may disrupt the mucociliary clearance mechanisms of the respiratory system. The toxicity of inhaled plastic particles was demonstrated as early as the 1970s among workers in the flocking industry. Some developed lung function impairments, shortness of breath, inflammation, fibrosis, and even lung cancer. Similar symptoms have been observed in workers in the textile and polyvinyl chloride industries.
A study published recently in The New England Journal of Medicine measured the amount of microplastics collected from carotid plaque of more than 300 patients who had undergone carotid endarterectomy for asymptomatic carotid artery disease. It found a 4.53 times higher risk for the primary endpoint, a composite of myocardial infarction, stroke, and all-cause mortality, among individuals with microplastics and nanoplastics in plaque compared with those without.
Health Affects High
The danger of plastics is also directly linked to the chemical substances they contain. A general scientific review looked at the health impacts of three chemicals used almost exclusively in plastics: Polybromodiphenyl ethers (PBDEs), used as flame retardants in textiles or electronics; bisphenol A (BPA), used in the lining of cans and bottles; and phthalates, particularly diethylhexyl phthalate (DEHP), used to make plastics more flexible.
The review highlighted strong epidemiological evidence linking fetal exposure to PBDEs during pregnancy to low birth weight and later exposure to delayed or impaired cognitive development in children and even a loss of IQ. Statistically significant evidence of disruption of thyroid function in adults was also found.
BPA is linked to genital malformations in female newborns exposed to BPA in utero, type 2 diabetes in adults, insulin resistance, and polycystic ovary syndrome in women. BPA exposure also increases the risk for obesity and hypertension in both children and adults, as well as the risk for cardiovascular disease in adults.
Finally, the review established links between exposure to DEHP and miscarriages, genital malformations in male newborns, delayed or impaired cognitive development in children, loss of IQ, delayed psychomotor development, early puberty in young girls, and endometriosis in young women. DEHP exposure also has multiple effects on cardiometabolic health, including insulin resistance, obesity, and elevated blood pressure.
The economic costs associated with the health impacts of these three substances have been estimated at $675 billion in the United States.
Bolo said that the solution to this plastic pollution is necessarily international. “We need an ambitious and legally binding treaty to reduce plastic production,” he said. “The damage is already done; we need to act to protect human health,” he concluded. The parliamentary office has made nine recommendations to the treaty negotiators.
This story was translated from Medscape’s French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Some Antihypertensives Linked to HCC Risk in Patients With MASLD and Cirrhosis
SAN DIEGO — according to new research.
In particular, the use of calcium channel blockers (CCBs), angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs) was associated with a higher risk of developing HCC, compared with not using these medications.
About half of patients with MASLD have hypertension, and the use of antihypertensives in these patients is beneficial to reduce the risk for cardiovascular disease and complications related to MASLD, said lead author Ahmed Elhariri, MD, a research fellow at the University of Texas MD Anderson Cancer Center, Houston, who conducted the study as a research assistant in gastroenterology and hepatology at the Baylor College of Medicine, also in Houston.
However, previous studies have suggested a possible link between these medications and cancer development, “especially CCBs and breast and lung cancer,” said Elhariri, who presented the findings at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD).
Analyzing Potential Risks
In a case-control study, Elhariri and colleagues analyzed antihypertensive medication use among patients with MASLD-induced HCC, as defined by histology or radiology based on the Liver Imaging Reporting & Data System, and control patients with MASLD but without HCC.
Between 2020 and 2024, the research team recruited 153 newly diagnosed HCC cases with different etiologies and 170 patients with MASLD but without HCC from Baylor College of Medicine’s outpatient clinics. For this study, they selected 47 age- and sex-matched pairs, all of whom had cirrhosis. Only those with a history of hypertension were included, however. Data on risk factors of metabolic syndrome (including diabetes) and HCC were collected, along with details about medication use such as metformin and statins.
A total of 42 patients with MASLD and HCC and 39 MASLD control individuals had a history of hypertension and were treated with antihypertensive medications. The mean age was 66.5 years for the HCC group and 63.5 years for the control group, and the mean body mass index (BMI) was 31.1 for the HCC group and 31.7 for the control group.
After adjusting for age, sex, BMI, Hispanic ethnicity, and use of other medications, patients taking CCBs had an increased HCC risk (odds ratio [OR], 2.76), compared with those not taking CCBs. Patients taking ACE inhibitors or ARBs also had an increased HCC risk (OR, 2.54), compared with those not taking ACE inhibitors or ARBs.
However, there wasn’t a statistically significant difference in HCC risk among patients taking beta-blockers (OR, 0.87).
“Patients with fatty liver in the presence of metabolic syndrome, especially in the presence of cirrhosis and antihypertensives, need to have stricter surveillance for liver cancer,” Elhariri said.
“We need to carefully review blood pressure medications in patients with MASLD and cirrhosis,” he said. CCBs, ACE inhibitors, and ARBs can be replaced with beta-blockers, “which have been shown to reduce progression of cirrhosis-related complications.”
Considering Clinical Implications
“Although our study showed some association between the use of some commonly used antihypertensives and the risk for HCC in this high-risk population, it is based on data collected retrospectively on a small number of selected patients with advanced liver disease,” Elhariri noted.
The associations and underlying mechanisms should be studied in larger populations and prospective trials, he said. “Until we have more data with a significantly larger sample size, it’s premature to raise the concern in the general population.”
“The cardiovascular benefits of controlling blood pressure far outweigh the risk of liver cancer in patients with metabolic syndrome,” Elhariri added.
In ongoing studies, researchers are investigating ways to improve patient outcomes and reduce the negative effects of cirrhosis-associated complications among patients with MASLD and metabolic dysfunction–associated steatohepatitis (MASH), Muhammad Ali Butt, MD, a hepatology fellow at Beth Israel Lahey Hospital & Medical Center in Burlington, Massachusetts, said in an interview.
Butt, who wasn’t involved with this study, presented separate research on statins in MASH patients with cirrhosis, which indicated statistically significant decreases in portal hypertension, thrombosis, hepatorenal syndrome, hepatic encephalopathy, and mortality.
“We know patients with MASLD- and MASH-associated cirrhosis commonly have other comorbidities, including high cardiovascular risks, diabetes, and hyperlipidemia,” he said. “All of these conditions indicate patients to be on other medications such as antihypertensives or statins. It’s important to know the role these medications play, especially given the high-risk profile of these patients.”
Elhariri and Butt reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
SAN DIEGO — according to new research.
In particular, the use of calcium channel blockers (CCBs), angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs) was associated with a higher risk of developing HCC, compared with not using these medications.
About half of patients with MASLD have hypertension, and the use of antihypertensives in these patients is beneficial to reduce the risk for cardiovascular disease and complications related to MASLD, said lead author Ahmed Elhariri, MD, a research fellow at the University of Texas MD Anderson Cancer Center, Houston, who conducted the study as a research assistant in gastroenterology and hepatology at the Baylor College of Medicine, also in Houston.
However, previous studies have suggested a possible link between these medications and cancer development, “especially CCBs and breast and lung cancer,” said Elhariri, who presented the findings at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD).
Analyzing Potential Risks
In a case-control study, Elhariri and colleagues analyzed antihypertensive medication use among patients with MASLD-induced HCC, as defined by histology or radiology based on the Liver Imaging Reporting & Data System, and control patients with MASLD but without HCC.
Between 2020 and 2024, the research team recruited 153 newly diagnosed HCC cases with different etiologies and 170 patients with MASLD but without HCC from Baylor College of Medicine’s outpatient clinics. For this study, they selected 47 age- and sex-matched pairs, all of whom had cirrhosis. Only those with a history of hypertension were included, however. Data on risk factors of metabolic syndrome (including diabetes) and HCC were collected, along with details about medication use such as metformin and statins.
A total of 42 patients with MASLD and HCC and 39 MASLD control individuals had a history of hypertension and were treated with antihypertensive medications. The mean age was 66.5 years for the HCC group and 63.5 years for the control group, and the mean body mass index (BMI) was 31.1 for the HCC group and 31.7 for the control group.
After adjusting for age, sex, BMI, Hispanic ethnicity, and use of other medications, patients taking CCBs had an increased HCC risk (odds ratio [OR], 2.76), compared with those not taking CCBs. Patients taking ACE inhibitors or ARBs also had an increased HCC risk (OR, 2.54), compared with those not taking ACE inhibitors or ARBs.
However, there wasn’t a statistically significant difference in HCC risk among patients taking beta-blockers (OR, 0.87).
“Patients with fatty liver in the presence of metabolic syndrome, especially in the presence of cirrhosis and antihypertensives, need to have stricter surveillance for liver cancer,” Elhariri said.
“We need to carefully review blood pressure medications in patients with MASLD and cirrhosis,” he said. CCBs, ACE inhibitors, and ARBs can be replaced with beta-blockers, “which have been shown to reduce progression of cirrhosis-related complications.”
Considering Clinical Implications
“Although our study showed some association between the use of some commonly used antihypertensives and the risk for HCC in this high-risk population, it is based on data collected retrospectively on a small number of selected patients with advanced liver disease,” Elhariri noted.
The associations and underlying mechanisms should be studied in larger populations and prospective trials, he said. “Until we have more data with a significantly larger sample size, it’s premature to raise the concern in the general population.”
“The cardiovascular benefits of controlling blood pressure far outweigh the risk of liver cancer in patients with metabolic syndrome,” Elhariri added.
In ongoing studies, researchers are investigating ways to improve patient outcomes and reduce the negative effects of cirrhosis-associated complications among patients with MASLD and metabolic dysfunction–associated steatohepatitis (MASH), Muhammad Ali Butt, MD, a hepatology fellow at Beth Israel Lahey Hospital & Medical Center in Burlington, Massachusetts, said in an interview.
Butt, who wasn’t involved with this study, presented separate research on statins in MASH patients with cirrhosis, which indicated statistically significant decreases in portal hypertension, thrombosis, hepatorenal syndrome, hepatic encephalopathy, and mortality.
“We know patients with MASLD- and MASH-associated cirrhosis commonly have other comorbidities, including high cardiovascular risks, diabetes, and hyperlipidemia,” he said. “All of these conditions indicate patients to be on other medications such as antihypertensives or statins. It’s important to know the role these medications play, especially given the high-risk profile of these patients.”
Elhariri and Butt reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
SAN DIEGO — according to new research.
In particular, the use of calcium channel blockers (CCBs), angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs) was associated with a higher risk of developing HCC, compared with not using these medications.
About half of patients with MASLD have hypertension, and the use of antihypertensives in these patients is beneficial to reduce the risk for cardiovascular disease and complications related to MASLD, said lead author Ahmed Elhariri, MD, a research fellow at the University of Texas MD Anderson Cancer Center, Houston, who conducted the study as a research assistant in gastroenterology and hepatology at the Baylor College of Medicine, also in Houston.
However, previous studies have suggested a possible link between these medications and cancer development, “especially CCBs and breast and lung cancer,” said Elhariri, who presented the findings at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD).
Analyzing Potential Risks
In a case-control study, Elhariri and colleagues analyzed antihypertensive medication use among patients with MASLD-induced HCC, as defined by histology or radiology based on the Liver Imaging Reporting & Data System, and control patients with MASLD but without HCC.
Between 2020 and 2024, the research team recruited 153 newly diagnosed HCC cases with different etiologies and 170 patients with MASLD but without HCC from Baylor College of Medicine’s outpatient clinics. For this study, they selected 47 age- and sex-matched pairs, all of whom had cirrhosis. Only those with a history of hypertension were included, however. Data on risk factors of metabolic syndrome (including diabetes) and HCC were collected, along with details about medication use such as metformin and statins.
A total of 42 patients with MASLD and HCC and 39 MASLD control individuals had a history of hypertension and were treated with antihypertensive medications. The mean age was 66.5 years for the HCC group and 63.5 years for the control group, and the mean body mass index (BMI) was 31.1 for the HCC group and 31.7 for the control group.
After adjusting for age, sex, BMI, Hispanic ethnicity, and use of other medications, patients taking CCBs had an increased HCC risk (odds ratio [OR], 2.76), compared with those not taking CCBs. Patients taking ACE inhibitors or ARBs also had an increased HCC risk (OR, 2.54), compared with those not taking ACE inhibitors or ARBs.
However, there wasn’t a statistically significant difference in HCC risk among patients taking beta-blockers (OR, 0.87).
“Patients with fatty liver in the presence of metabolic syndrome, especially in the presence of cirrhosis and antihypertensives, need to have stricter surveillance for liver cancer,” Elhariri said.
“We need to carefully review blood pressure medications in patients with MASLD and cirrhosis,” he said. CCBs, ACE inhibitors, and ARBs can be replaced with beta-blockers, “which have been shown to reduce progression of cirrhosis-related complications.”
Considering Clinical Implications
“Although our study showed some association between the use of some commonly used antihypertensives and the risk for HCC in this high-risk population, it is based on data collected retrospectively on a small number of selected patients with advanced liver disease,” Elhariri noted.
The associations and underlying mechanisms should be studied in larger populations and prospective trials, he said. “Until we have more data with a significantly larger sample size, it’s premature to raise the concern in the general population.”
“The cardiovascular benefits of controlling blood pressure far outweigh the risk of liver cancer in patients with metabolic syndrome,” Elhariri added.
In ongoing studies, researchers are investigating ways to improve patient outcomes and reduce the negative effects of cirrhosis-associated complications among patients with MASLD and metabolic dysfunction–associated steatohepatitis (MASH), Muhammad Ali Butt, MD, a hepatology fellow at Beth Israel Lahey Hospital & Medical Center in Burlington, Massachusetts, said in an interview.
Butt, who wasn’t involved with this study, presented separate research on statins in MASH patients with cirrhosis, which indicated statistically significant decreases in portal hypertension, thrombosis, hepatorenal syndrome, hepatic encephalopathy, and mortality.
“We know patients with MASLD- and MASH-associated cirrhosis commonly have other comorbidities, including high cardiovascular risks, diabetes, and hyperlipidemia,” he said. “All of these conditions indicate patients to be on other medications such as antihypertensives or statins. It’s important to know the role these medications play, especially given the high-risk profile of these patients.”
Elhariri and Butt reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM AASLD 2024
Tapering Corticosteroids in Severe Alcohol-Associated Hepatitis Appears Safe
SAN DIEGO — , according to new research.
“Although several drugs have been evaluated for severe alcohol-associated hepatitis, none have succeeded in practice. Corticosteroids remain the mainstay of treatment; however, infections remain a major concern in 25%-40% of cases,” said Anand Kulkarni, MD, senior consultant and director of critical care hepatology at the Asian Institute of Gastroenterology in Hyderabad, India.
“There are no standard society guidelines for steroid dosing, and our current practices stem from studies in the 1970s, so there’s a major knowledge gap around optimal dosing and if stepwise tapering helps,” said Kulkarni, who presented the findings at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD).
Assessing Tapered Doses
In a multicenter, open-label randomized controlled trial, 254 patients with SAH from four Indian centers and one Canadian center were randomized to receive either a fixed or tapering dose of 40 mg prednisolone daily for 4 weeks. The patients in the tapering group received a starting dose of 40 mg, which was reduced by 10 mg weekly over 4 weeks.
While taking corticosteroids, 66% of those in the fixed dose group and 55% of those in the tapering group also received prophylactic antibiotics.
The mean age of participants was 41.1 years, the median Model For End-Stage Liver Disease score was 25.6, and 98.4% were men.
The primary objective was to compare the incidence of drug-related adverse events, infections, hospitalization, and mortality through day 90.
The duration of corticosteroid therapy was 22 days in the fixed dose group and 23 days in the tapering dose group.
Overall, the proportion of steroid responders was similar in both groups, at 80.3% in the fixed dose group and 82.5% in the tapering dose group.
However, the incidence of drug-related adverse events was significantly higher in the fixed dose group (52%) than in the tapering dose group (36.2%). The most common adverse events in both groups were infection, hyperglycemia, and hematochezia.
At 90 days, the incidence of infection was significantly lower in the tapering group (19.7%) than in the fixed dose group (33.1%). In both groups, the most common infection sites were the lungs (28.3%) and urinary tract (22.4%).
In terms of liver-related outcomes, some patients developed hepatic encephalopathy (11.8% in fixed dose vs 6.3% in tapering dose) and acute variceal bleed (3.1% in each group), as well as acute kidney injury (26.8% in fixed dose vs 18.9% in tapering dose).
Hospitalization within 90 days was required in 44.1% of the fixed dose group and 33.1% of the tapering dose group.
Survival at day 90 was 83.5% in the fixed dose group and 86.6% in the tapering dose group. Four patients in the fixed dose group and three patients in the tapering dose group underwent living donor liver transplantation by day 90.
Relapse of alcohol use by day 90 occurred in 13.4% of the fixed dose group and 12.6% of the tapering dose group.
“Rapid tapering in severe alcohol-associated hepatitis reduces infections and hospitalizations but doesn’t have a significant impact on survival,” Kulkarni concluded.
Considering Alternative Therapies
Given the high risk for infection in patients with SAH and limited certainty around benefits, the data may also call into question whether to give steroids to these patients at all, said session co-moderator Aleksander Krag, MD, professor of clinical medicine at the University of Southern Denmark, Odense, Denmark, and secretary general of the European Association for the Study of Liver 2023-2025.
“Since there are no other treatments available as of now, we’ll still continue to give steroids,” Kulkarni noted. But “tapering the dose should be beneficial.”
Although steroid therapy has been considered the “mainstay treatment” for SAH for 50 years, it doesn’t always lead to long-term improvement in liver values or survival, said Prasun Jalal, MD, the Stan and Sue Partee Endowed Chair in Hepatology at Baylor College of Medicine, Houston, who wasn’t involved with the study.
Researchers are looking to other connections, such as the gut microbiome, to find treatments for advanced alcoholic liver disease, Jalal said in an interview. In a small pilot study, he and colleagues found that intestinal microbiota transplantation (IMT) appears to be safe and effective for these patients.
“Early analyses suggest that IMT has a favorable outcome on the prognosis of patients with severe alcohol-associated hepatitis and is safe,” Jalal said. “A longer follow-up study with a larger sample size is in progress.”
Kulkarni and Krag reported no relevant disclosures. Jalal has speaking and teaching relationships with AbbVie and Madrigal.
A version of this article appeared on Medscape.com.
SAN DIEGO — , according to new research.
“Although several drugs have been evaluated for severe alcohol-associated hepatitis, none have succeeded in practice. Corticosteroids remain the mainstay of treatment; however, infections remain a major concern in 25%-40% of cases,” said Anand Kulkarni, MD, senior consultant and director of critical care hepatology at the Asian Institute of Gastroenterology in Hyderabad, India.
“There are no standard society guidelines for steroid dosing, and our current practices stem from studies in the 1970s, so there’s a major knowledge gap around optimal dosing and if stepwise tapering helps,” said Kulkarni, who presented the findings at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD).
Assessing Tapered Doses
In a multicenter, open-label randomized controlled trial, 254 patients with SAH from four Indian centers and one Canadian center were randomized to receive either a fixed or tapering dose of 40 mg prednisolone daily for 4 weeks. The patients in the tapering group received a starting dose of 40 mg, which was reduced by 10 mg weekly over 4 weeks.
While taking corticosteroids, 66% of those in the fixed dose group and 55% of those in the tapering group also received prophylactic antibiotics.
The mean age of participants was 41.1 years, the median Model For End-Stage Liver Disease score was 25.6, and 98.4% were men.
The primary objective was to compare the incidence of drug-related adverse events, infections, hospitalization, and mortality through day 90.
The duration of corticosteroid therapy was 22 days in the fixed dose group and 23 days in the tapering dose group.
Overall, the proportion of steroid responders was similar in both groups, at 80.3% in the fixed dose group and 82.5% in the tapering dose group.
However, the incidence of drug-related adverse events was significantly higher in the fixed dose group (52%) than in the tapering dose group (36.2%). The most common adverse events in both groups were infection, hyperglycemia, and hematochezia.
At 90 days, the incidence of infection was significantly lower in the tapering group (19.7%) than in the fixed dose group (33.1%). In both groups, the most common infection sites were the lungs (28.3%) and urinary tract (22.4%).
In terms of liver-related outcomes, some patients developed hepatic encephalopathy (11.8% in fixed dose vs 6.3% in tapering dose) and acute variceal bleed (3.1% in each group), as well as acute kidney injury (26.8% in fixed dose vs 18.9% in tapering dose).
Hospitalization within 90 days was required in 44.1% of the fixed dose group and 33.1% of the tapering dose group.
Survival at day 90 was 83.5% in the fixed dose group and 86.6% in the tapering dose group. Four patients in the fixed dose group and three patients in the tapering dose group underwent living donor liver transplantation by day 90.
Relapse of alcohol use by day 90 occurred in 13.4% of the fixed dose group and 12.6% of the tapering dose group.
“Rapid tapering in severe alcohol-associated hepatitis reduces infections and hospitalizations but doesn’t have a significant impact on survival,” Kulkarni concluded.
Considering Alternative Therapies
Given the high risk for infection in patients with SAH and limited certainty around benefits, the data may also call into question whether to give steroids to these patients at all, said session co-moderator Aleksander Krag, MD, professor of clinical medicine at the University of Southern Denmark, Odense, Denmark, and secretary general of the European Association for the Study of Liver 2023-2025.
“Since there are no other treatments available as of now, we’ll still continue to give steroids,” Kulkarni noted. But “tapering the dose should be beneficial.”
Although steroid therapy has been considered the “mainstay treatment” for SAH for 50 years, it doesn’t always lead to long-term improvement in liver values or survival, said Prasun Jalal, MD, the Stan and Sue Partee Endowed Chair in Hepatology at Baylor College of Medicine, Houston, who wasn’t involved with the study.
Researchers are looking to other connections, such as the gut microbiome, to find treatments for advanced alcoholic liver disease, Jalal said in an interview. In a small pilot study, he and colleagues found that intestinal microbiota transplantation (IMT) appears to be safe and effective for these patients.
“Early analyses suggest that IMT has a favorable outcome on the prognosis of patients with severe alcohol-associated hepatitis and is safe,” Jalal said. “A longer follow-up study with a larger sample size is in progress.”
Kulkarni and Krag reported no relevant disclosures. Jalal has speaking and teaching relationships with AbbVie and Madrigal.
A version of this article appeared on Medscape.com.
SAN DIEGO — , according to new research.
“Although several drugs have been evaluated for severe alcohol-associated hepatitis, none have succeeded in practice. Corticosteroids remain the mainstay of treatment; however, infections remain a major concern in 25%-40% of cases,” said Anand Kulkarni, MD, senior consultant and director of critical care hepatology at the Asian Institute of Gastroenterology in Hyderabad, India.
“There are no standard society guidelines for steroid dosing, and our current practices stem from studies in the 1970s, so there’s a major knowledge gap around optimal dosing and if stepwise tapering helps,” said Kulkarni, who presented the findings at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD).
Assessing Tapered Doses
In a multicenter, open-label randomized controlled trial, 254 patients with SAH from four Indian centers and one Canadian center were randomized to receive either a fixed or tapering dose of 40 mg prednisolone daily for 4 weeks. The patients in the tapering group received a starting dose of 40 mg, which was reduced by 10 mg weekly over 4 weeks.
While taking corticosteroids, 66% of those in the fixed dose group and 55% of those in the tapering group also received prophylactic antibiotics.
The mean age of participants was 41.1 years, the median Model For End-Stage Liver Disease score was 25.6, and 98.4% were men.
The primary objective was to compare the incidence of drug-related adverse events, infections, hospitalization, and mortality through day 90.
The duration of corticosteroid therapy was 22 days in the fixed dose group and 23 days in the tapering dose group.
Overall, the proportion of steroid responders was similar in both groups, at 80.3% in the fixed dose group and 82.5% in the tapering dose group.
However, the incidence of drug-related adverse events was significantly higher in the fixed dose group (52%) than in the tapering dose group (36.2%). The most common adverse events in both groups were infection, hyperglycemia, and hematochezia.
At 90 days, the incidence of infection was significantly lower in the tapering group (19.7%) than in the fixed dose group (33.1%). In both groups, the most common infection sites were the lungs (28.3%) and urinary tract (22.4%).
In terms of liver-related outcomes, some patients developed hepatic encephalopathy (11.8% in fixed dose vs 6.3% in tapering dose) and acute variceal bleed (3.1% in each group), as well as acute kidney injury (26.8% in fixed dose vs 18.9% in tapering dose).
Hospitalization within 90 days was required in 44.1% of the fixed dose group and 33.1% of the tapering dose group.
Survival at day 90 was 83.5% in the fixed dose group and 86.6% in the tapering dose group. Four patients in the fixed dose group and three patients in the tapering dose group underwent living donor liver transplantation by day 90.
Relapse of alcohol use by day 90 occurred in 13.4% of the fixed dose group and 12.6% of the tapering dose group.
“Rapid tapering in severe alcohol-associated hepatitis reduces infections and hospitalizations but doesn’t have a significant impact on survival,” Kulkarni concluded.
Considering Alternative Therapies
Given the high risk for infection in patients with SAH and limited certainty around benefits, the data may also call into question whether to give steroids to these patients at all, said session co-moderator Aleksander Krag, MD, professor of clinical medicine at the University of Southern Denmark, Odense, Denmark, and secretary general of the European Association for the Study of Liver 2023-2025.
“Since there are no other treatments available as of now, we’ll still continue to give steroids,” Kulkarni noted. But “tapering the dose should be beneficial.”
Although steroid therapy has been considered the “mainstay treatment” for SAH for 50 years, it doesn’t always lead to long-term improvement in liver values or survival, said Prasun Jalal, MD, the Stan and Sue Partee Endowed Chair in Hepatology at Baylor College of Medicine, Houston, who wasn’t involved with the study.
Researchers are looking to other connections, such as the gut microbiome, to find treatments for advanced alcoholic liver disease, Jalal said in an interview. In a small pilot study, he and colleagues found that intestinal microbiota transplantation (IMT) appears to be safe and effective for these patients.
“Early analyses suggest that IMT has a favorable outcome on the prognosis of patients with severe alcohol-associated hepatitis and is safe,” Jalal said. “A longer follow-up study with a larger sample size is in progress.”
Kulkarni and Krag reported no relevant disclosures. Jalal has speaking and teaching relationships with AbbVie and Madrigal.
A version of this article appeared on Medscape.com.
FROM AASLD 2024
Bariatric Surgery Better Than Obesity Drugs for Some Patients With MASLD
SAN DIEGO — , new study results showed.
In a separate analysis of data from the same study, researchers also found that bariatric surgery alone had lower risks for major adverse cardiovascular events (MACEs) than GLP-1 or SGLT2 inhibitor use or a combination of surgery and medications.
“While weight loss medications have demonstrated notable success, especially in managing diabetes and aiding weight loss, bariatric surgery offers more significant and varied benefits for weight and metabolic health, making it a better option for some patients,” said Leith Ghani, DO, an internal medicine resident at The University of Arizona College of Medicine – Phoenix.
Ghani presented the findings about mortality at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD). His co-author and fellow internal medicine resident Qumber Ali, DO, presented the findings about MACEs.
These findings highlight “the need for personalized treatment plans, allowing the decision between surgery and medication to be customized according to each patient’s specific situation and health goals,” Ghani said. “It also emphasizes the importance of a multidisciplinary approach to patient management.”
Comparing Bariatric Interventions and Pharmacologic Treatments
The retrospective, multicenter study of hospital admissions data from the Banner Health system in Phoenix included more than 8600 patients who had MASLD-related diagnostic codes and metabolic criteria. Patients were divided into four groups according to the treatment they received: Bariatric surgery alone (5.8%), GLP-1 medications (39.3%), SGLT2 inhibitor medications (23.4%), or a combination of surgery and medications (31.5%).
In the mortality analysis, Ghani and colleagues looked at data for patients who died between 12 and 60 months after surgery or starting medication. They found that patients who underwent bariatric surgery had a significantly higher chance of survival at 5 years.
When compared to bariatric surgery, the adjusted hazard ratio (aHR) for GLP-1 medications was 2.99, followed by an aHR of 2.96 for SGLT2 inhibitor medications, and an aHR of 1.78 for a combination of treatments.
In the MACE analysis, Ali and colleagues looked at data for patients who were followed for 12 months or more after intervention or initiation of treatment, identifying MACE diagnostic codes for coronary artery disease, cerebrovascular disease, and congestive heart failure. They found that patients who underwent bariatric surgery alone had a significantly lower rate of MACEs.
When compared to bariatric surgery, the aHR was 1.83 for GLP-1 medications, 1.72 for SGLT2 inhibitor medications, and 1.91 for a combination of treatments.
Regarding both analyses, patients taking GLP-1 or SGLT2 inhibitor medications may face higher risks for mortality or serious heart problems due to existing metabolic disorders or heart disease, Ali said.
Future studies could look at other risk factors that make these patients more vulnerable, he added. For instance, factors related to body mass index, glucose control, other medications, different clinical settings, and race/ethnicity can contribute to different treatment responses, as could the decision to take medication or undergo surgery in the first place.
“This emphasizes the need for additional, prospective randomized clinical trial research to explore why these differences exist,” Ali said. “While progress has been made, there is still much to learn about the optimal management of patients with metabolic and cardiovascular disorders.”
Considering a Multidisciplinary Approach to MASLD Treatment
Ghani and Ali also called for personalized treatment plans for metabolic-related disorders such as MASLD, as well as strong communication among specialists and with patients about the benefits and risks of choosing certain medications and procedures.
“Bariatric surgery is not a universal solution, and not all patients are suitable for surgery,” Ghani said. “We also can’t say at this point that drug treatments are worse than bariatric surgery. The effectiveness of these therapies can vary greatly depending on a patient’s health, lifestyle, and preferences.”
Looking ahead, MASLD studies should investigate long-term weight loss seen with bariatric surgery and different medications, said Katherine Schwenger, PhD, RD, a scientific associate at Toronto General Hospital in Toronto, Ontario, Canada.
“GLP-1s are a hot topic right now,” said Schwenger, who wasn’t involved with the study. But “we need to look at factors such as the longevity of weight loss. It’s hard to beat the success and sustainability of bariatric surgery.”
Ghani, Ali, and Schwenger reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
SAN DIEGO — , new study results showed.
In a separate analysis of data from the same study, researchers also found that bariatric surgery alone had lower risks for major adverse cardiovascular events (MACEs) than GLP-1 or SGLT2 inhibitor use or a combination of surgery and medications.
“While weight loss medications have demonstrated notable success, especially in managing diabetes and aiding weight loss, bariatric surgery offers more significant and varied benefits for weight and metabolic health, making it a better option for some patients,” said Leith Ghani, DO, an internal medicine resident at The University of Arizona College of Medicine – Phoenix.
Ghani presented the findings about mortality at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD). His co-author and fellow internal medicine resident Qumber Ali, DO, presented the findings about MACEs.
These findings highlight “the need for personalized treatment plans, allowing the decision between surgery and medication to be customized according to each patient’s specific situation and health goals,” Ghani said. “It also emphasizes the importance of a multidisciplinary approach to patient management.”
Comparing Bariatric Interventions and Pharmacologic Treatments
The retrospective, multicenter study of hospital admissions data from the Banner Health system in Phoenix included more than 8600 patients who had MASLD-related diagnostic codes and metabolic criteria. Patients were divided into four groups according to the treatment they received: Bariatric surgery alone (5.8%), GLP-1 medications (39.3%), SGLT2 inhibitor medications (23.4%), or a combination of surgery and medications (31.5%).
In the mortality analysis, Ghani and colleagues looked at data for patients who died between 12 and 60 months after surgery or starting medication. They found that patients who underwent bariatric surgery had a significantly higher chance of survival at 5 years.
When compared to bariatric surgery, the adjusted hazard ratio (aHR) for GLP-1 medications was 2.99, followed by an aHR of 2.96 for SGLT2 inhibitor medications, and an aHR of 1.78 for a combination of treatments.
In the MACE analysis, Ali and colleagues looked at data for patients who were followed for 12 months or more after intervention or initiation of treatment, identifying MACE diagnostic codes for coronary artery disease, cerebrovascular disease, and congestive heart failure. They found that patients who underwent bariatric surgery alone had a significantly lower rate of MACEs.
When compared to bariatric surgery, the aHR was 1.83 for GLP-1 medications, 1.72 for SGLT2 inhibitor medications, and 1.91 for a combination of treatments.
Regarding both analyses, patients taking GLP-1 or SGLT2 inhibitor medications may face higher risks for mortality or serious heart problems due to existing metabolic disorders or heart disease, Ali said.
Future studies could look at other risk factors that make these patients more vulnerable, he added. For instance, factors related to body mass index, glucose control, other medications, different clinical settings, and race/ethnicity can contribute to different treatment responses, as could the decision to take medication or undergo surgery in the first place.
“This emphasizes the need for additional, prospective randomized clinical trial research to explore why these differences exist,” Ali said. “While progress has been made, there is still much to learn about the optimal management of patients with metabolic and cardiovascular disorders.”
Considering a Multidisciplinary Approach to MASLD Treatment
Ghani and Ali also called for personalized treatment plans for metabolic-related disorders such as MASLD, as well as strong communication among specialists and with patients about the benefits and risks of choosing certain medications and procedures.
“Bariatric surgery is not a universal solution, and not all patients are suitable for surgery,” Ghani said. “We also can’t say at this point that drug treatments are worse than bariatric surgery. The effectiveness of these therapies can vary greatly depending on a patient’s health, lifestyle, and preferences.”
Looking ahead, MASLD studies should investigate long-term weight loss seen with bariatric surgery and different medications, said Katherine Schwenger, PhD, RD, a scientific associate at Toronto General Hospital in Toronto, Ontario, Canada.
“GLP-1s are a hot topic right now,” said Schwenger, who wasn’t involved with the study. But “we need to look at factors such as the longevity of weight loss. It’s hard to beat the success and sustainability of bariatric surgery.”
Ghani, Ali, and Schwenger reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
SAN DIEGO — , new study results showed.
In a separate analysis of data from the same study, researchers also found that bariatric surgery alone had lower risks for major adverse cardiovascular events (MACEs) than GLP-1 or SGLT2 inhibitor use or a combination of surgery and medications.
“While weight loss medications have demonstrated notable success, especially in managing diabetes and aiding weight loss, bariatric surgery offers more significant and varied benefits for weight and metabolic health, making it a better option for some patients,” said Leith Ghani, DO, an internal medicine resident at The University of Arizona College of Medicine – Phoenix.
Ghani presented the findings about mortality at The Liver Meeting 2024: American Association for the Study of Liver Diseases (AASLD). His co-author and fellow internal medicine resident Qumber Ali, DO, presented the findings about MACEs.
These findings highlight “the need for personalized treatment plans, allowing the decision between surgery and medication to be customized according to each patient’s specific situation and health goals,” Ghani said. “It also emphasizes the importance of a multidisciplinary approach to patient management.”
Comparing Bariatric Interventions and Pharmacologic Treatments
The retrospective, multicenter study of hospital admissions data from the Banner Health system in Phoenix included more than 8600 patients who had MASLD-related diagnostic codes and metabolic criteria. Patients were divided into four groups according to the treatment they received: Bariatric surgery alone (5.8%), GLP-1 medications (39.3%), SGLT2 inhibitor medications (23.4%), or a combination of surgery and medications (31.5%).
In the mortality analysis, Ghani and colleagues looked at data for patients who died between 12 and 60 months after surgery or starting medication. They found that patients who underwent bariatric surgery had a significantly higher chance of survival at 5 years.
When compared to bariatric surgery, the adjusted hazard ratio (aHR) for GLP-1 medications was 2.99, followed by an aHR of 2.96 for SGLT2 inhibitor medications, and an aHR of 1.78 for a combination of treatments.
In the MACE analysis, Ali and colleagues looked at data for patients who were followed for 12 months or more after intervention or initiation of treatment, identifying MACE diagnostic codes for coronary artery disease, cerebrovascular disease, and congestive heart failure. They found that patients who underwent bariatric surgery alone had a significantly lower rate of MACEs.
When compared to bariatric surgery, the aHR was 1.83 for GLP-1 medications, 1.72 for SGLT2 inhibitor medications, and 1.91 for a combination of treatments.
Regarding both analyses, patients taking GLP-1 or SGLT2 inhibitor medications may face higher risks for mortality or serious heart problems due to existing metabolic disorders or heart disease, Ali said.
Future studies could look at other risk factors that make these patients more vulnerable, he added. For instance, factors related to body mass index, glucose control, other medications, different clinical settings, and race/ethnicity can contribute to different treatment responses, as could the decision to take medication or undergo surgery in the first place.
“This emphasizes the need for additional, prospective randomized clinical trial research to explore why these differences exist,” Ali said. “While progress has been made, there is still much to learn about the optimal management of patients with metabolic and cardiovascular disorders.”
Considering a Multidisciplinary Approach to MASLD Treatment
Ghani and Ali also called for personalized treatment plans for metabolic-related disorders such as MASLD, as well as strong communication among specialists and with patients about the benefits and risks of choosing certain medications and procedures.
“Bariatric surgery is not a universal solution, and not all patients are suitable for surgery,” Ghani said. “We also can’t say at this point that drug treatments are worse than bariatric surgery. The effectiveness of these therapies can vary greatly depending on a patient’s health, lifestyle, and preferences.”
Looking ahead, MASLD studies should investigate long-term weight loss seen with bariatric surgery and different medications, said Katherine Schwenger, PhD, RD, a scientific associate at Toronto General Hospital in Toronto, Ontario, Canada.
“GLP-1s are a hot topic right now,” said Schwenger, who wasn’t involved with the study. But “we need to look at factors such as the longevity of weight loss. It’s hard to beat the success and sustainability of bariatric surgery.”
Ghani, Ali, and Schwenger reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM AASLD 2024
2024 Rare Diseases Report: Hematology and Oncology
2024 Rare Diseases Report: Hematology and Oncology
National Organization for Rare Disorders: Strengthening Rare Cancer Advocacy
By Alli Ward
NORD's Rare Cancer Coalition has transformed advocacy and awareness efforts, offering education and fostering research to address the challenges of rare cancers.
Treatment of Glioblastoma: A Potential Shift in Paradigm
By Jeffrey N. Bruce, MD
Immunotherapies and molecular profiling are paving the way for more targeted approaches in treating glioblastoma.
Emerging Insights and Therapeutic Strategies for Large Cell Neuroendocrine Carcinoma of the Lung
By Robert A. Ramirez, DO, FACP, and Aman Chauhan, MD
New diagnostic tools and precision medicine approaches are addressing the unique challenges of this aggressive neuroendocrine cancer.
Advancements in the Treatment of Malignant PEComas with mTOR Inhibitors
By Richard F. Riedel, MD
The use of mTOR inhibitors marks significant progress in managing advanced malignant PEComas, offering new hope for patients.
Cutaneous T-Cell Lymphomas Update: Benefits of a Multidisciplinary Care Approach
By Jina Chung, MD, and Eric Mou, MD
A multidisciplinary care model ensures optimal outcomes for patients with cutaneous T-cell lymphomas, addressing both medical and emotional needs.
Optimizing Myelofibrosis Care in the Age of JAK Inhibitors
By Douglas Tremblay, MD
JAK inhibitors are central to myelofibrosis management, with personalized strategies helping to navigate resistance and improve quality of life.
Current Management and Future Directions in the Treatment of Gallbladder Cancer
By Ghassan K. Abou-Alfa, MD, MBA, JD, FASCO
Molecular profiling and immunotherapy are reshaping the treatment paradigm for gallbladder cancer, improving survival outcomes.
Improving Prognosis in Hepatoblastoma: Evolving Risk Stratification and Treatment Strategies
By Greg M. Tiao, MD
Risk stratification and individualized therapies are driving progress in treating hepatoblastoma, with promising advancements on the horizon.
National Organization for Rare Disorders: Strengthening Rare Cancer Advocacy
By Alli Ward
NORD's Rare Cancer Coalition has transformed advocacy and awareness efforts, offering education and fostering research to address the challenges of rare cancers.
Treatment of Glioblastoma: A Potential Shift in Paradigm
By Jeffrey N. Bruce, MD
Immunotherapies and molecular profiling are paving the way for more targeted approaches in treating glioblastoma.
Emerging Insights and Therapeutic Strategies for Large Cell Neuroendocrine Carcinoma of the Lung
By Robert A. Ramirez, DO, FACP, and Aman Chauhan, MD
New diagnostic tools and precision medicine approaches are addressing the unique challenges of this aggressive neuroendocrine cancer.
Advancements in the Treatment of Malignant PEComas with mTOR Inhibitors
By Richard F. Riedel, MD
The use of mTOR inhibitors marks significant progress in managing advanced malignant PEComas, offering new hope for patients.
Cutaneous T-Cell Lymphomas Update: Benefits of a Multidisciplinary Care Approach
By Jina Chung, MD, and Eric Mou, MD
A multidisciplinary care model ensures optimal outcomes for patients with cutaneous T-cell lymphomas, addressing both medical and emotional needs.
Optimizing Myelofibrosis Care in the Age of JAK Inhibitors
By Douglas Tremblay, MD
JAK inhibitors are central to myelofibrosis management, with personalized strategies helping to navigate resistance and improve quality of life.
Current Management and Future Directions in the Treatment of Gallbladder Cancer
By Ghassan K. Abou-Alfa, MD, MBA, JD, FASCO
Molecular profiling and immunotherapy are reshaping the treatment paradigm for gallbladder cancer, improving survival outcomes.
Improving Prognosis in Hepatoblastoma: Evolving Risk Stratification and Treatment Strategies
By Greg M. Tiao, MD
Risk stratification and individualized therapies are driving progress in treating hepatoblastoma, with promising advancements on the horizon.
National Organization for Rare Disorders: Strengthening Rare Cancer Advocacy
By Alli Ward
NORD's Rare Cancer Coalition has transformed advocacy and awareness efforts, offering education and fostering research to address the challenges of rare cancers.
Treatment of Glioblastoma: A Potential Shift in Paradigm
By Jeffrey N. Bruce, MD
Immunotherapies and molecular profiling are paving the way for more targeted approaches in treating glioblastoma.
Emerging Insights and Therapeutic Strategies for Large Cell Neuroendocrine Carcinoma of the Lung
By Robert A. Ramirez, DO, FACP, and Aman Chauhan, MD
New diagnostic tools and precision medicine approaches are addressing the unique challenges of this aggressive neuroendocrine cancer.
Advancements in the Treatment of Malignant PEComas with mTOR Inhibitors
By Richard F. Riedel, MD
The use of mTOR inhibitors marks significant progress in managing advanced malignant PEComas, offering new hope for patients.
Cutaneous T-Cell Lymphomas Update: Benefits of a Multidisciplinary Care Approach
By Jina Chung, MD, and Eric Mou, MD
A multidisciplinary care model ensures optimal outcomes for patients with cutaneous T-cell lymphomas, addressing both medical and emotional needs.
Optimizing Myelofibrosis Care in the Age of JAK Inhibitors
By Douglas Tremblay, MD
JAK inhibitors are central to myelofibrosis management, with personalized strategies helping to navigate resistance and improve quality of life.
Current Management and Future Directions in the Treatment of Gallbladder Cancer
By Ghassan K. Abou-Alfa, MD, MBA, JD, FASCO
Molecular profiling and immunotherapy are reshaping the treatment paradigm for gallbladder cancer, improving survival outcomes.
Improving Prognosis in Hepatoblastoma: Evolving Risk Stratification and Treatment Strategies
By Greg M. Tiao, MD
Risk stratification and individualized therapies are driving progress in treating hepatoblastoma, with promising advancements on the horizon.
2024 Rare Diseases Report: Hematology and Oncology
2024 Rare Diseases Report: Hematology and Oncology