People who ate more plant-based and less meat-based foods — whether on a vegan, vegetarian, or omnivorous diet — had more favorable microbiome compositions than those who did not follow a healthy dietary pattern, new research suggested.

For example, red meat was a strong driver of omnivore microbiomes, with corresponding signature microbes that are negatively correlated with host cardiometabolic health.

In contrast, the signature microbes found in vegans’ gut microbiomes were correlated with favorable cardiometabolic markers and were enriched in omnivores who ate more plant-based foods.

“From the viewpoint of the impact of diet on the gut microbiome, what seems to be more important is the diversity of healthy plant-based foods that are consumed,” principal author Nicola Segata, PhD, University of Trento in Italy, said in an interview. “Whether this comes within a vegan or an omnivore diet is less crucial, as long as there is no specific overconsumption of unhealthy food categories, such as red meat.”

Excluding broad categories of foods also can have consequences, he added. “For example, we saw that the exclusion of dairy fermented foods is associated with decreased presence of potentially probiotic microbes that are constitutive of such foods. Avoiding meat or dairy products does not necessarily have a positive effect if it does not come with a variety of quality plant-based products.”

The study was published online in Nature Microbiology.

 

Diet Tied to Microbial Signature

The researchers analyzed biological samples from 21,561 individuals across five multi-national cohorts to map how differences in diet patterns (omnivore, vegetarian, and vegan) are reflected in gut microbiomes.

They found that the three diet patterns are highly distinguishable by their microbial profiles and that each diet has corresponding unique signature microbes, including those tied to digestion of specific types of food and sometimes those derived from food itself.

The microbiomes of omnivores had an increased presence of bacteria associated with meat digestion, such as Alistipes putredinis, which is involved in protein fermentation. Omnivores also had more bacteria associated with both inflammatory bowel disease and increased colon cancer risk, such as Ruminococcus torques and Bilophila wadsworthia.

The microbiomes of vegans had an abundance of bacteria involved in fiber fermentation, such as several species of Bacteroides and Firmicutes phyla, which help produce short-chain fatty acids. These compounds have beneficial effects on gut health by reducing inflammation and helping to maintain a better homeostatic balance between an individual’s metabolism and immune system.

The main difference between vegetarians and vegans was the presence in vegetarians’ microbiomes of Streptococcus thermophilus, a bacterium found mainly in dairy products and used in the production of yogurt.

Dietary factors within each diet pattern, such as the amount of plant-based food, shape the microbiome more than the type of diet and are important for gut health, according to the authors. For example, by eating more plant-based foods, people with an omnivorous diet can bring the proportion of beneficial signature microbes in their microbiomes more in line with the levels in people who are vegan or vegetarian.

“Since our data showed that omnivores on average ingest significantly fewer healthy plant-based foods than vegetarians or vegans, optimizing the quality of omnivore diets by increasing dietary plant diversity could lead to better gut health,” they wrote.

The ultimate goal, Segata said, is “a precision nutrition approach that recommends foods based on the configuration of the microbiome of patients and of the aspects of the microbiome one wants to enhance. We are not there yet, but it is nonetheless important to know which foods are usually boosting which types of members of the gut microbiome.”

His team is currently analyzing changes in the gut microbiome induced by diet changes among thousands of participants in various cohorts.

“This is one of the next steps toward unraveling causality along the diet-microbiome-health axis, together with the cultivation of specific microbiome members of interest for potential prebiotic and probiotic strategies,” he said.

 

Conventional Dietary Advice for Now

The findings are consistent with those of previous studies, Jack Gilbert, MD, director of the Microbiome and Metagenomics Center at the University of California, San Diego, and president of Applied Microbiology International, Cambridge, England, said in an interview.

“Future research needs to focus on whether the gut microbial signature can predict those that develop cardiovascular disease in each cohort — ie, the n-of-1 studies, whereby a vegan develops cardiovascular disease, or a carnivore does not,” said Gilbert, who was not involved in the study.

With more data, he said, “we can also start examining these trends over time to understand what might be going on with these ‘oddballs.’ ”

“There is not much you can do with the ‘eat a healthy balanced diet’ routine,” he noted. “If I got a microbiome signature, I could potentially tell you what to eat to optimize your blood glucose trends and your lipid panels but not to handle long-term disease risk, yet. So sticking with the guideline-recommended dietary advice seems best, until we can provide more nuanced advice for the patient.

“Importantly, I would also like to see time-resolved data,” he added. “Signatures can fluctuate over time, even over days, and so collecting a few weeks of stool samples would help us to better align the microbiome signatures to clinical endpoints.”

Segata is a consultant to and receives options from ZOE. Gilbert is a member of the scientific advisory boards of Holobiome, BiomeSense, EcoBiomics Canadian Research Program, MASTER EU, Sun Genomics, and Oath; the editorial advisory board for The Scientist; and the external advisory board for the Binational Early Asthma & Microbiome Study. He is also an adviser for Bened Life.

A version of this article appeared on Medscape.com.

People who ate more plant-based and less meat-based foods — whether on a vegan, vegetarian, or omnivorous diet — had more favorable microbiome compositions than those who did not follow a healthy dietary pattern, new research suggested.

For example, red meat was a strong driver of omnivore microbiomes, with corresponding signature microbes that are negatively correlated with host cardiometabolic health.

In contrast, the signature microbes found in vegans’ gut microbiomes were correlated with favorable cardiometabolic markers and were enriched in omnivores who ate more plant-based foods.

“From the viewpoint of the impact of diet on the gut microbiome, what seems to be more important is the diversity of healthy plant-based foods that are consumed,” principal author Nicola Segata, PhD, University of Trento in Italy, said in an interview. “Whether this comes within a vegan or an omnivore diet is less crucial, as long as there is no specific overconsumption of unhealthy food categories, such as red meat.”

Excluding broad categories of foods also can have consequences, he added. “For example, we saw that the exclusion of dairy fermented foods is associated with decreased presence of potentially probiotic microbes that are constitutive of such foods. Avoiding meat or dairy products does not necessarily have a positive effect if it does not come with a variety of quality plant-based products.”

The study was published online in Nature Microbiology.

 

Diet Tied to Microbial Signature

The researchers analyzed biological samples from 21,561 individuals across five multi-national cohorts to map how differences in diet patterns (omnivore, vegetarian, and vegan) are reflected in gut microbiomes.

They found that the three diet patterns are highly distinguishable by their microbial profiles and that each diet has corresponding unique signature microbes, including those tied to digestion of specific types of food and sometimes those derived from food itself.

The microbiomes of omnivores had an increased presence of bacteria associated with meat digestion, such as Alistipes putredinis, which is involved in protein fermentation. Omnivores also had more bacteria associated with both inflammatory bowel disease and increased colon cancer risk, such as Ruminococcus torques and Bilophila wadsworthia.

The microbiomes of vegans had an abundance of bacteria involved in fiber fermentation, such as several species of Bacteroides and Firmicutes phyla, which help produce short-chain fatty acids. These compounds have beneficial effects on gut health by reducing inflammation and helping to maintain a better homeostatic balance between an individual’s metabolism and immune system.

The main difference between vegetarians and vegans was the presence in vegetarians’ microbiomes of Streptococcus thermophilus, a bacterium found mainly in dairy products and used in the production of yogurt.

Dietary factors within each diet pattern, such as the amount of plant-based food, shape the microbiome more than the type of diet and are important for gut health, according to the authors. For example, by eating more plant-based foods, people with an omnivorous diet can bring the proportion of beneficial signature microbes in their microbiomes more in line with the levels in people who are vegan or vegetarian.

“Since our data showed that omnivores on average ingest significantly fewer healthy plant-based foods than vegetarians or vegans, optimizing the quality of omnivore diets by increasing dietary plant diversity could lead to better gut health,” they wrote.

The ultimate goal, Segata said, is “a precision nutrition approach that recommends foods based on the configuration of the microbiome of patients and of the aspects of the microbiome one wants to enhance. We are not there yet, but it is nonetheless important to know which foods are usually boosting which types of members of the gut microbiome.”

His team is currently analyzing changes in the gut microbiome induced by diet changes among thousands of participants in various cohorts.

“This is one of the next steps toward unraveling causality along the diet-microbiome-health axis, together with the cultivation of specific microbiome members of interest for potential prebiotic and probiotic strategies,” he said.

 

Conventional Dietary Advice for Now

The findings are consistent with those of previous studies, Jack Gilbert, MD, director of the Microbiome and Metagenomics Center at the University of California, San Diego, and president of Applied Microbiology International, Cambridge, England, said in an interview.

“Future research needs to focus on whether the gut microbial signature can predict those that develop cardiovascular disease in each cohort — ie, the n-of-1 studies, whereby a vegan develops cardiovascular disease, or a carnivore does not,” said Gilbert, who was not involved in the study.

With more data, he said, “we can also start examining these trends over time to understand what might be going on with these ‘oddballs.’ ”

“There is not much you can do with the ‘eat a healthy balanced diet’ routine,” he noted. “If I got a microbiome signature, I could potentially tell you what to eat to optimize your blood glucose trends and your lipid panels but not to handle long-term disease risk, yet. So sticking with the guideline-recommended dietary advice seems best, until we can provide more nuanced advice for the patient.

“Importantly, I would also like to see time-resolved data,” he added. “Signatures can fluctuate over time, even over days, and so collecting a few weeks of stool samples would help us to better align the microbiome signatures to clinical endpoints.”

Segata is a consultant to and receives options from ZOE. Gilbert is a member of the scientific advisory boards of Holobiome, BiomeSense, EcoBiomics Canadian Research Program, MASTER EU, Sun Genomics, and Oath; the editorial advisory board for The Scientist; and the external advisory board for the Binational Early Asthma & Microbiome Study. He is also an adviser for Bened Life.

A version of this article appeared on Medscape.com.

People who ate more plant-based and less meat-based foods — whether on a vegan, vegetarian, or omnivorous diet — had more favorable microbiome compositions than those who did not follow a healthy dietary pattern, new research suggested.

For example, red meat was a strong driver of omnivore microbiomes, with corresponding signature microbes that are negatively correlated with host cardiometabolic health.

In contrast, the signature microbes found in vegans’ gut microbiomes were correlated with favorable cardiometabolic markers and were enriched in omnivores who ate more plant-based foods.

“From the viewpoint of the impact of diet on the gut microbiome, what seems to be more important is the diversity of healthy plant-based foods that are consumed,” principal author Nicola Segata, PhD, University of Trento in Italy, said in an interview. “Whether this comes within a vegan or an omnivore diet is less crucial, as long as there is no specific overconsumption of unhealthy food categories, such as red meat.”

Excluding broad categories of foods also can have consequences, he added. “For example, we saw that the exclusion of dairy fermented foods is associated with decreased presence of potentially probiotic microbes that are constitutive of such foods. Avoiding meat or dairy products does not necessarily have a positive effect if it does not come with a variety of quality plant-based products.”

The study was published online in Nature Microbiology.

 

Diet Tied to Microbial Signature

The researchers analyzed biological samples from 21,561 individuals across five multi-national cohorts to map how differences in diet patterns (omnivore, vegetarian, and vegan) are reflected in gut microbiomes.

They found that the three diet patterns are highly distinguishable by their microbial profiles and that each diet has corresponding unique signature microbes, including those tied to digestion of specific types of food and sometimes those derived from food itself.

The microbiomes of omnivores had an increased presence of bacteria associated with meat digestion, such as Alistipes putredinis, which is involved in protein fermentation. Omnivores also had more bacteria associated with both inflammatory bowel disease and increased colon cancer risk, such as Ruminococcus torques and Bilophila wadsworthia.

The microbiomes of vegans had an abundance of bacteria involved in fiber fermentation, such as several species of Bacteroides and Firmicutes phyla, which help produce short-chain fatty acids. These compounds have beneficial effects on gut health by reducing inflammation and helping to maintain a better homeostatic balance between an individual’s metabolism and immune system.

The main difference between vegetarians and vegans was the presence in vegetarians’ microbiomes of Streptococcus thermophilus, a bacterium found mainly in dairy products and used in the production of yogurt.

Dietary factors within each diet pattern, such as the amount of plant-based food, shape the microbiome more than the type of diet and are important for gut health, according to the authors. For example, by eating more plant-based foods, people with an omnivorous diet can bring the proportion of beneficial signature microbes in their microbiomes more in line with the levels in people who are vegan or vegetarian.

“Since our data showed that omnivores on average ingest significantly fewer healthy plant-based foods than vegetarians or vegans, optimizing the quality of omnivore diets by increasing dietary plant diversity could lead to better gut health,” they wrote.

The ultimate goal, Segata said, is “a precision nutrition approach that recommends foods based on the configuration of the microbiome of patients and of the aspects of the microbiome one wants to enhance. We are not there yet, but it is nonetheless important to know which foods are usually boosting which types of members of the gut microbiome.”

His team is currently analyzing changes in the gut microbiome induced by diet changes among thousands of participants in various cohorts.

“This is one of the next steps toward unraveling causality along the diet-microbiome-health axis, together with the cultivation of specific microbiome members of interest for potential prebiotic and probiotic strategies,” he said.

 

Conventional Dietary Advice for Now

The findings are consistent with those of previous studies, Jack Gilbert, MD, director of the Microbiome and Metagenomics Center at the University of California, San Diego, and president of Applied Microbiology International, Cambridge, England, said in an interview.

“Future research needs to focus on whether the gut microbial signature can predict those that develop cardiovascular disease in each cohort — ie, the n-of-1 studies, whereby a vegan develops cardiovascular disease, or a carnivore does not,” said Gilbert, who was not involved in the study.

With more data, he said, “we can also start examining these trends over time to understand what might be going on with these ‘oddballs.’ ”

“There is not much you can do with the ‘eat a healthy balanced diet’ routine,” he noted. “If I got a microbiome signature, I could potentially tell you what to eat to optimize your blood glucose trends and your lipid panels but not to handle long-term disease risk, yet. So sticking with the guideline-recommended dietary advice seems best, until we can provide more nuanced advice for the patient.

“Importantly, I would also like to see time-resolved data,” he added. “Signatures can fluctuate over time, even over days, and so collecting a few weeks of stool samples would help us to better align the microbiome signatures to clinical endpoints.”

Segata is a consultant to and receives options from ZOE. Gilbert is a member of the scientific advisory boards of Holobiome, BiomeSense, EcoBiomics Canadian Research Program, MASTER EU, Sun Genomics, and Oath; the editorial advisory board for The Scientist; and the external advisory board for the Binational Early Asthma & Microbiome Study. He is also an adviser for Bened Life.

A version of this article appeared on Medscape.com.

Clinicians should be aware of how to manage certain gastrointestinal (GI) and liver conditions associated with pregnancy, such as hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, and acute fatty liver of pregnancy, according to a clinical practice update (CPU) from the American Gastroenterological Association.

Notably, procedures, medications, or other interventions intended to improve maternal health shouldn’t be withheld solely because the patient is pregnant, the authors wrote. Instead, treatments should be personalized based on a risk-benefit assessment.  

 

“Pregnancy causes significant physiological changes that can affect the GI tract and liver function. Some common conditions — such as nausea, vomiting, gastroesophageal reflux disease (GERD), and constipation — may be exacerbated, and underlying GI or liver diseases can behave differently during pregnancy,” said lead author Shivangi Kothari, MD, associate professor of medicine and associate director of endoscopy at the University of Rochester Medical Center and Strong Memorial Hospital, both in Rochester, New York.  

“These conditions can pose significant risks to both the mother and fetus, and their management requires a specialized, updated approach,” she said. “This clinical practice update stresses the need for coordinated, multidisciplinary care among obstetricians, gastroenterologists, hepatologists, and maternal-and-fetal medicine experts to ensure optimal outcomes, particularly in complex or high-risk cases.”  

The update was published online in Gastroenterology.  

 

Pregnancy-Related Concerns

The best path to optimal outcomes is to start early, the authors wrote. Before pregnancy, patients should consider preconception and contraceptive care counseling with a multidisciplinary team that can address GI and liver issues, especially among reproductive-age people who want to become pregnant.

Once pregnant, though, patients shouldn’t be deterred from receiving procedures, medications, or interventions just because they’re pregnant, the authors wrote. Instead, taking an individual approach will help clinicians decide what to do based on the risks and benefits.  

At the beginning of pregnancy, early treatment of nausea and vomiting can reduce progression to hyperemesis gravidarum, the authors wrote. Stepwise treatment can include vitamin B6, doxylamine, hydration, and adequate nutrition, followed by ondansetron, metoclopramide, promethazine, and intravenous glucocorticoids in moderate to severe cases.  

Constipation may also pose a problem because of hormonal, physiological, and medication-related changes. Treatment options can include dietary fiber, lactulose, and polyethylene glycol-based laxatives.  

Patients with certain conditions — such as complex inflammatory bowel disease (IBD), advanced cirrhosis, or liver transplant — should work with a multidisciplinary team to coordinate birth, preferably in a tertiary care center, the authors wrote.  

For patients with IBD, clinical remission helps to improve pregnancy outcomes, including before conception, during pregnancy, and throughout the postpartum period. Biologic agents should be used during pregnancy and postpartum, though methotrexate, thalidomide, and ozanimod should be stopped at least 6 months before conception.  

For patients with chronic hepatitis B, serum hepatitis B virus DNA and liver biochemical levels should be tested. Patients with a serum level > 200,000 IU/mL during the third trimester should be considered for treatment with tenofovir disoproxil fumarate.  

For patients on immunosuppressive therapy for chronic liver diseases or after liver transplantation, therapy should continue at the lowest effective dose. However, mycophenolate mofetil shouldn’t be administered during pregnancy.  

Intrahepatic cholestasis of pregnancy may be diagnosed during the second or third trimester based on pruritus and a serum bile acid level > 10 μmol/L. Treatment should include oral ursodeoxycholic acid, with a total daily dose of 10-15 mg/kg.  

Other pregnancy-related liver diseases — such as pre-eclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; and acute fatty liver of pregnancy — require careful birth planning and evaluation for possible liver transplantation. For certain high-risk patients, daily aspirin should start at week 12 of gestation.  

In addition, elective endoscopic procedures should wait until after birth, and nonemergent but necessary procedures should be performed during the second trimester. Patients with cirrhosis should undergo evaluation for esophageal varices, and upper endoscopy should happen during the second trimester to guide beta-blocker therapy or endoscopic variceal litigation.  

Endoscopic retrograde cholangiopancreatography can be performed for urgent indications, such as choledocholithiasis, cholangitis, and some gallstone pancreatitis cases, ideally during the second trimester.  

Cholecystectomy is considered safe during pregnancy, with a laparoscopic approach as the standard of care regardless of trimester, though the second trimester is ideal. 

Pregnancy-Related Updates in Practice

Ultimately, clinicians should familiarize themselves with the best practice advice to feel comfortable when counseling and managing pregnancy-related concerns, especially high-risk patients, said Eugenia Shmidt, MD, assistant professor of gastroenterology, hepatology, and nutrition, and founder of the IBD Preconception and Pregnancy Planning Clinic at the University of Minnesota, Minneapolis.

“Half of all patients with GI and liver disease are women, and oftentimes, they don’t have appropriate guidance regarding reproductive health in the context of their disease,” she said. “There exists a very large knowledge gap in this area, particularly because most clinical trials exclude pregnant people.”  

Most importantly, the advice statements can guide practitioners on how to help pregnant patients make informed reproductive decisions, she added.  

“This CPU makes it clear that preconception counseling and multidisciplinary care are key in optimizing reproductive health, regardless of the underlying GI or liver disease,” Shmidt said. “GI practitioners should be counseling women well in advance of pregnancy and recruiting all relevant stakeholders as early as possible, even prior to conception. This way, pregnancy care is not reactive, but instead proactive.”  

The authors received no specific funding for this update. Kothari and Shmidt reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Clinicians should be aware of how to manage certain gastrointestinal (GI) and liver conditions associated with pregnancy, such as hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, and acute fatty liver of pregnancy, according to a clinical practice update (CPU) from the American Gastroenterological Association.

Notably, procedures, medications, or other interventions intended to improve maternal health shouldn’t be withheld solely because the patient is pregnant, the authors wrote. Instead, treatments should be personalized based on a risk-benefit assessment.  

 

“Pregnancy causes significant physiological changes that can affect the GI tract and liver function. Some common conditions — such as nausea, vomiting, gastroesophageal reflux disease (GERD), and constipation — may be exacerbated, and underlying GI or liver diseases can behave differently during pregnancy,” said lead author Shivangi Kothari, MD, associate professor of medicine and associate director of endoscopy at the University of Rochester Medical Center and Strong Memorial Hospital, both in Rochester, New York.  

“These conditions can pose significant risks to both the mother and fetus, and their management requires a specialized, updated approach,” she said. “This clinical practice update stresses the need for coordinated, multidisciplinary care among obstetricians, gastroenterologists, hepatologists, and maternal-and-fetal medicine experts to ensure optimal outcomes, particularly in complex or high-risk cases.”  

The update was published online in Gastroenterology.  

 

Pregnancy-Related Concerns

The best path to optimal outcomes is to start early, the authors wrote. Before pregnancy, patients should consider preconception and contraceptive care counseling with a multidisciplinary team that can address GI and liver issues, especially among reproductive-age people who want to become pregnant.

Once pregnant, though, patients shouldn’t be deterred from receiving procedures, medications, or interventions just because they’re pregnant, the authors wrote. Instead, taking an individual approach will help clinicians decide what to do based on the risks and benefits.  

At the beginning of pregnancy, early treatment of nausea and vomiting can reduce progression to hyperemesis gravidarum, the authors wrote. Stepwise treatment can include vitamin B6, doxylamine, hydration, and adequate nutrition, followed by ondansetron, metoclopramide, promethazine, and intravenous glucocorticoids in moderate to severe cases.  

Constipation may also pose a problem because of hormonal, physiological, and medication-related changes. Treatment options can include dietary fiber, lactulose, and polyethylene glycol-based laxatives.  

Patients with certain conditions — such as complex inflammatory bowel disease (IBD), advanced cirrhosis, or liver transplant — should work with a multidisciplinary team to coordinate birth, preferably in a tertiary care center, the authors wrote.  

For patients with IBD, clinical remission helps to improve pregnancy outcomes, including before conception, during pregnancy, and throughout the postpartum period. Biologic agents should be used during pregnancy and postpartum, though methotrexate, thalidomide, and ozanimod should be stopped at least 6 months before conception.  

For patients with chronic hepatitis B, serum hepatitis B virus DNA and liver biochemical levels should be tested. Patients with a serum level > 200,000 IU/mL during the third trimester should be considered for treatment with tenofovir disoproxil fumarate.  

For patients on immunosuppressive therapy for chronic liver diseases or after liver transplantation, therapy should continue at the lowest effective dose. However, mycophenolate mofetil shouldn’t be administered during pregnancy.  

Intrahepatic cholestasis of pregnancy may be diagnosed during the second or third trimester based on pruritus and a serum bile acid level > 10 μmol/L. Treatment should include oral ursodeoxycholic acid, with a total daily dose of 10-15 mg/kg.  

Other pregnancy-related liver diseases — such as pre-eclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; and acute fatty liver of pregnancy — require careful birth planning and evaluation for possible liver transplantation. For certain high-risk patients, daily aspirin should start at week 12 of gestation.  

In addition, elective endoscopic procedures should wait until after birth, and nonemergent but necessary procedures should be performed during the second trimester. Patients with cirrhosis should undergo evaluation for esophageal varices, and upper endoscopy should happen during the second trimester to guide beta-blocker therapy or endoscopic variceal litigation.  

Endoscopic retrograde cholangiopancreatography can be performed for urgent indications, such as choledocholithiasis, cholangitis, and some gallstone pancreatitis cases, ideally during the second trimester.  

Cholecystectomy is considered safe during pregnancy, with a laparoscopic approach as the standard of care regardless of trimester, though the second trimester is ideal. 

Pregnancy-Related Updates in Practice

Ultimately, clinicians should familiarize themselves with the best practice advice to feel comfortable when counseling and managing pregnancy-related concerns, especially high-risk patients, said Eugenia Shmidt, MD, assistant professor of gastroenterology, hepatology, and nutrition, and founder of the IBD Preconception and Pregnancy Planning Clinic at the University of Minnesota, Minneapolis.

“Half of all patients with GI and liver disease are women, and oftentimes, they don’t have appropriate guidance regarding reproductive health in the context of their disease,” she said. “There exists a very large knowledge gap in this area, particularly because most clinical trials exclude pregnant people.”  

Most importantly, the advice statements can guide practitioners on how to help pregnant patients make informed reproductive decisions, she added.  

“This CPU makes it clear that preconception counseling and multidisciplinary care are key in optimizing reproductive health, regardless of the underlying GI or liver disease,” Shmidt said. “GI practitioners should be counseling women well in advance of pregnancy and recruiting all relevant stakeholders as early as possible, even prior to conception. This way, pregnancy care is not reactive, but instead proactive.”  

The authors received no specific funding for this update. Kothari and Shmidt reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Clinicians should be aware of how to manage certain gastrointestinal (GI) and liver conditions associated with pregnancy, such as hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, and acute fatty liver of pregnancy, according to a clinical practice update (CPU) from the American Gastroenterological Association.

Notably, procedures, medications, or other interventions intended to improve maternal health shouldn’t be withheld solely because the patient is pregnant, the authors wrote. Instead, treatments should be personalized based on a risk-benefit assessment.  

 

“Pregnancy causes significant physiological changes that can affect the GI tract and liver function. Some common conditions — such as nausea, vomiting, gastroesophageal reflux disease (GERD), and constipation — may be exacerbated, and underlying GI or liver diseases can behave differently during pregnancy,” said lead author Shivangi Kothari, MD, associate professor of medicine and associate director of endoscopy at the University of Rochester Medical Center and Strong Memorial Hospital, both in Rochester, New York.  

“These conditions can pose significant risks to both the mother and fetus, and their management requires a specialized, updated approach,” she said. “This clinical practice update stresses the need for coordinated, multidisciplinary care among obstetricians, gastroenterologists, hepatologists, and maternal-and-fetal medicine experts to ensure optimal outcomes, particularly in complex or high-risk cases.”  

The update was published online in Gastroenterology.  

 

Pregnancy-Related Concerns

The best path to optimal outcomes is to start early, the authors wrote. Before pregnancy, patients should consider preconception and contraceptive care counseling with a multidisciplinary team that can address GI and liver issues, especially among reproductive-age people who want to become pregnant.

Once pregnant, though, patients shouldn’t be deterred from receiving procedures, medications, or interventions just because they’re pregnant, the authors wrote. Instead, taking an individual approach will help clinicians decide what to do based on the risks and benefits.  

At the beginning of pregnancy, early treatment of nausea and vomiting can reduce progression to hyperemesis gravidarum, the authors wrote. Stepwise treatment can include vitamin B6, doxylamine, hydration, and adequate nutrition, followed by ondansetron, metoclopramide, promethazine, and intravenous glucocorticoids in moderate to severe cases.  

Constipation may also pose a problem because of hormonal, physiological, and medication-related changes. Treatment options can include dietary fiber, lactulose, and polyethylene glycol-based laxatives.  

Patients with certain conditions — such as complex inflammatory bowel disease (IBD), advanced cirrhosis, or liver transplant — should work with a multidisciplinary team to coordinate birth, preferably in a tertiary care center, the authors wrote.  

For patients with IBD, clinical remission helps to improve pregnancy outcomes, including before conception, during pregnancy, and throughout the postpartum period. Biologic agents should be used during pregnancy and postpartum, though methotrexate, thalidomide, and ozanimod should be stopped at least 6 months before conception.  

For patients with chronic hepatitis B, serum hepatitis B virus DNA and liver biochemical levels should be tested. Patients with a serum level > 200,000 IU/mL during the third trimester should be considered for treatment with tenofovir disoproxil fumarate.  

For patients on immunosuppressive therapy for chronic liver diseases or after liver transplantation, therapy should continue at the lowest effective dose. However, mycophenolate mofetil shouldn’t be administered during pregnancy.  

Intrahepatic cholestasis of pregnancy may be diagnosed during the second or third trimester based on pruritus and a serum bile acid level > 10 μmol/L. Treatment should include oral ursodeoxycholic acid, with a total daily dose of 10-15 mg/kg.  

Other pregnancy-related liver diseases — such as pre-eclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; and acute fatty liver of pregnancy — require careful birth planning and evaluation for possible liver transplantation. For certain high-risk patients, daily aspirin should start at week 12 of gestation.  

In addition, elective endoscopic procedures should wait until after birth, and nonemergent but necessary procedures should be performed during the second trimester. Patients with cirrhosis should undergo evaluation for esophageal varices, and upper endoscopy should happen during the second trimester to guide beta-blocker therapy or endoscopic variceal litigation.  

Endoscopic retrograde cholangiopancreatography can be performed for urgent indications, such as choledocholithiasis, cholangitis, and some gallstone pancreatitis cases, ideally during the second trimester.  

Cholecystectomy is considered safe during pregnancy, with a laparoscopic approach as the standard of care regardless of trimester, though the second trimester is ideal. 

Pregnancy-Related Updates in Practice

Ultimately, clinicians should familiarize themselves with the best practice advice to feel comfortable when counseling and managing pregnancy-related concerns, especially high-risk patients, said Eugenia Shmidt, MD, assistant professor of gastroenterology, hepatology, and nutrition, and founder of the IBD Preconception and Pregnancy Planning Clinic at the University of Minnesota, Minneapolis.

“Half of all patients with GI and liver disease are women, and oftentimes, they don’t have appropriate guidance regarding reproductive health in the context of their disease,” she said. “There exists a very large knowledge gap in this area, particularly because most clinical trials exclude pregnant people.”  

Most importantly, the advice statements can guide practitioners on how to help pregnant patients make informed reproductive decisions, she added.  

“This CPU makes it clear that preconception counseling and multidisciplinary care are key in optimizing reproductive health, regardless of the underlying GI or liver disease,” Shmidt said. “GI practitioners should be counseling women well in advance of pregnancy and recruiting all relevant stakeholders as early as possible, even prior to conception. This way, pregnancy care is not reactive, but instead proactive.”  

The authors received no specific funding for this update. Kothari and Shmidt reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Obesity appears to be associated with malignant progression of Barrett’s esophagus (BE), according to a recent systematic review and meta-analysis.

A dose-response relationship exists between body mass index (BMI) and esophageal adenocarcinoma (EAC) or high-grade dysplasia (HGD), the authors found.

“Obesity has been implicated in the pathogenesis of many reflux-related esophageal disorders such as gastroesophageal reflux disease (GERD), BE, and EAC,” said senior author Leo Alexandre, MRCP, PhD, a clinical associate professor and member of the Norwich Epidemiology Centre at the University of East Anglia and gastroenterologist with the Norfolk & Norwich University Hospital NHS Foundation Trust, both in Norwich, England.

“Guidelines advocate obesity as a criterion for targeted screening for BE in patients with chronic reflux symptoms,” he said. “While obesity is a recognized risk factor for both BE and EAC, it’s been unclear whether obesity is a risk factor for malignant progression.”

The study was published in Clinical Gastroenterology and Hepatology.

 

Analyzing Risk

BE, which is the only recognized precursor lesion to EAC, is associated with a 30-fold increase in the incidence of the aggressive cancer. Typically, malignant progression occurs when nondysplastic BE epithelium progresses to low-grade dysplasia (LGD) and then HGD, followed by invasive adenocarcinoma.

Current guidelines suggest that patients with BE undergo endoscopic surveillance for early detection of adenocarcinoma. However, clinical risk factors could help with risk stratification and a personalized approach to long-term BE management, the authors wrote.

Alexandre and colleagues reviewed case-control or cohort studies that reported on the effect of BMI on the progression of nondysplastic BE or LGD to EAC, HGD, or esophageal cancer (EC). Then they estimated the dose-response relationship with a two-stage dose-response meta-analysis.

Overall, 20 observational studies reported data on 38,565 adult patients, including 1684 patients who were diagnosed with EAC, HGD, or EC. The studies enrolled patients between 1976 and 2019 and were published between 2005 and 2022. Most were based in Europe or the United States, and 74.4% of participants were men.

Among 12 cohort studies with 19,223 patients who had baseline nondysplastic BE or LGD, 816 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .03%.

Among eight cohort studies with 6647 male patients who had baseline nondysplastic BE or LGD, 555 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .02%.

In addition, among 1992 female patients with baseline nondysplastic BE or LGD, 110 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .01%, which wasn’t a significant difference compared with the progression rate among male patients.

Based on meta-analyses, obesity was associated with a 4% increase in the risk for malignant progression among patients with BE (unadjusted odds ratio, 1.04; 95% CI, 1.00-1.07; P < .001).

Notably, each 5 unit increase in BMI was associated with a 6% increase in the risk of developing HGD or EAC (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001).

“Although the exact mechanisms by which obesity promotes esophageal carcinogenesis is not fully understood, several possible mechanisms may explain it,” Alexandre said. “The most obvious pathologic link is via GERD, with the mechanical effect of visceral obesity promoting the GERD directly, and the sequence of Barrett’s dysplasia to cancer indirectly. In addition, it has been demonstrated in experimental studies that gastric acid and bile acid drive malignant changes in esophageal epithelium through stimulation of proliferation, inhibition of apoptosis, and generation of free radicals.”

 

Considering Risk

This study highlights the importance of recognizing the association between obesity and cancer risks, said Prateek Sharma, MD, professor of medicine and director of gastrointestinal training at the University of Kansas School of Medicine, Kansas City, Kansas.

Sharma, who wasn’t involved with this study, coauthored an American Gastroenterological Association technical review on the management of BE.

“Obesity is a known risk factor for esophageal adenocarcinoma and may be a modifiable risk factor,” he said. “Showing that BMI is related to neoplastic progression in Barrett’s esophagus may impact surveillance intervals.”

Future research should look at additional obesity-related factors, such as visceral obesity and malignant progression of BE, as well as whether diet, lifestyle, and bariatric interventions can reduce the risk for progression.

“The next steps also include plugging BMI into risk scores and risk stratification models to enable targeted surveillance among high-risk groups,” Sharma said.

One of the study coauthors received funding as a National Institute for Health Research Academic clinical fellow. No other funding sources were declared. Alexandre and Sharma reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Obesity appears to be associated with malignant progression of Barrett’s esophagus (BE), according to a recent systematic review and meta-analysis.

A dose-response relationship exists between body mass index (BMI) and esophageal adenocarcinoma (EAC) or high-grade dysplasia (HGD), the authors found.

“Obesity has been implicated in the pathogenesis of many reflux-related esophageal disorders such as gastroesophageal reflux disease (GERD), BE, and EAC,” said senior author Leo Alexandre, MRCP, PhD, a clinical associate professor and member of the Norwich Epidemiology Centre at the University of East Anglia and gastroenterologist with the Norfolk & Norwich University Hospital NHS Foundation Trust, both in Norwich, England.

“Guidelines advocate obesity as a criterion for targeted screening for BE in patients with chronic reflux symptoms,” he said. “While obesity is a recognized risk factor for both BE and EAC, it’s been unclear whether obesity is a risk factor for malignant progression.”

The study was published in Clinical Gastroenterology and Hepatology.

 

Analyzing Risk

BE, which is the only recognized precursor lesion to EAC, is associated with a 30-fold increase in the incidence of the aggressive cancer. Typically, malignant progression occurs when nondysplastic BE epithelium progresses to low-grade dysplasia (LGD) and then HGD, followed by invasive adenocarcinoma.

Current guidelines suggest that patients with BE undergo endoscopic surveillance for early detection of adenocarcinoma. However, clinical risk factors could help with risk stratification and a personalized approach to long-term BE management, the authors wrote.

Alexandre and colleagues reviewed case-control or cohort studies that reported on the effect of BMI on the progression of nondysplastic BE or LGD to EAC, HGD, or esophageal cancer (EC). Then they estimated the dose-response relationship with a two-stage dose-response meta-analysis.

Overall, 20 observational studies reported data on 38,565 adult patients, including 1684 patients who were diagnosed with EAC, HGD, or EC. The studies enrolled patients between 1976 and 2019 and were published between 2005 and 2022. Most were based in Europe or the United States, and 74.4% of participants were men.

Among 12 cohort studies with 19,223 patients who had baseline nondysplastic BE or LGD, 816 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .03%.

Among eight cohort studies with 6647 male patients who had baseline nondysplastic BE or LGD, 555 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .02%.

In addition, among 1992 female patients with baseline nondysplastic BE or LGD, 110 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .01%, which wasn’t a significant difference compared with the progression rate among male patients.

Based on meta-analyses, obesity was associated with a 4% increase in the risk for malignant progression among patients with BE (unadjusted odds ratio, 1.04; 95% CI, 1.00-1.07; P < .001).

Notably, each 5 unit increase in BMI was associated with a 6% increase in the risk of developing HGD or EAC (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001).

“Although the exact mechanisms by which obesity promotes esophageal carcinogenesis is not fully understood, several possible mechanisms may explain it,” Alexandre said. “The most obvious pathologic link is via GERD, with the mechanical effect of visceral obesity promoting the GERD directly, and the sequence of Barrett’s dysplasia to cancer indirectly. In addition, it has been demonstrated in experimental studies that gastric acid and bile acid drive malignant changes in esophageal epithelium through stimulation of proliferation, inhibition of apoptosis, and generation of free radicals.”

 

Considering Risk

This study highlights the importance of recognizing the association between obesity and cancer risks, said Prateek Sharma, MD, professor of medicine and director of gastrointestinal training at the University of Kansas School of Medicine, Kansas City, Kansas.

Sharma, who wasn’t involved with this study, coauthored an American Gastroenterological Association technical review on the management of BE.

“Obesity is a known risk factor for esophageal adenocarcinoma and may be a modifiable risk factor,” he said. “Showing that BMI is related to neoplastic progression in Barrett’s esophagus may impact surveillance intervals.”

Future research should look at additional obesity-related factors, such as visceral obesity and malignant progression of BE, as well as whether diet, lifestyle, and bariatric interventions can reduce the risk for progression.

“The next steps also include plugging BMI into risk scores and risk stratification models to enable targeted surveillance among high-risk groups,” Sharma said.

One of the study coauthors received funding as a National Institute for Health Research Academic clinical fellow. No other funding sources were declared. Alexandre and Sharma reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Obesity appears to be associated with malignant progression of Barrett’s esophagus (BE), according to a recent systematic review and meta-analysis.

A dose-response relationship exists between body mass index (BMI) and esophageal adenocarcinoma (EAC) or high-grade dysplasia (HGD), the authors found.

“Obesity has been implicated in the pathogenesis of many reflux-related esophageal disorders such as gastroesophageal reflux disease (GERD), BE, and EAC,” said senior author Leo Alexandre, MRCP, PhD, a clinical associate professor and member of the Norwich Epidemiology Centre at the University of East Anglia and gastroenterologist with the Norfolk & Norwich University Hospital NHS Foundation Trust, both in Norwich, England.

“Guidelines advocate obesity as a criterion for targeted screening for BE in patients with chronic reflux symptoms,” he said. “While obesity is a recognized risk factor for both BE and EAC, it’s been unclear whether obesity is a risk factor for malignant progression.”

The study was published in Clinical Gastroenterology and Hepatology.

 

Analyzing Risk

BE, which is the only recognized precursor lesion to EAC, is associated with a 30-fold increase in the incidence of the aggressive cancer. Typically, malignant progression occurs when nondysplastic BE epithelium progresses to low-grade dysplasia (LGD) and then HGD, followed by invasive adenocarcinoma.

Current guidelines suggest that patients with BE undergo endoscopic surveillance for early detection of adenocarcinoma. However, clinical risk factors could help with risk stratification and a personalized approach to long-term BE management, the authors wrote.

Alexandre and colleagues reviewed case-control or cohort studies that reported on the effect of BMI on the progression of nondysplastic BE or LGD to EAC, HGD, or esophageal cancer (EC). Then they estimated the dose-response relationship with a two-stage dose-response meta-analysis.

Overall, 20 observational studies reported data on 38,565 adult patients, including 1684 patients who were diagnosed with EAC, HGD, or EC. The studies enrolled patients between 1976 and 2019 and were published between 2005 and 2022. Most were based in Europe or the United States, and 74.4% of participants were men.

Among 12 cohort studies with 19,223 patients who had baseline nondysplastic BE or LGD, 816 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .03%.

Among eight cohort studies with 6647 male patients who had baseline nondysplastic BE or LGD, 555 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .02%.

In addition, among 1992 female patients with baseline nondysplastic BE or LGD, 110 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .01%, which wasn’t a significant difference compared with the progression rate among male patients.

Based on meta-analyses, obesity was associated with a 4% increase in the risk for malignant progression among patients with BE (unadjusted odds ratio, 1.04; 95% CI, 1.00-1.07; P < .001).

Notably, each 5 unit increase in BMI was associated with a 6% increase in the risk of developing HGD or EAC (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001).

“Although the exact mechanisms by which obesity promotes esophageal carcinogenesis is not fully understood, several possible mechanisms may explain it,” Alexandre said. “The most obvious pathologic link is via GERD, with the mechanical effect of visceral obesity promoting the GERD directly, and the sequence of Barrett’s dysplasia to cancer indirectly. In addition, it has been demonstrated in experimental studies that gastric acid and bile acid drive malignant changes in esophageal epithelium through stimulation of proliferation, inhibition of apoptosis, and generation of free radicals.”

 

Considering Risk

This study highlights the importance of recognizing the association between obesity and cancer risks, said Prateek Sharma, MD, professor of medicine and director of gastrointestinal training at the University of Kansas School of Medicine, Kansas City, Kansas.

Sharma, who wasn’t involved with this study, coauthored an American Gastroenterological Association technical review on the management of BE.

“Obesity is a known risk factor for esophageal adenocarcinoma and may be a modifiable risk factor,” he said. “Showing that BMI is related to neoplastic progression in Barrett’s esophagus may impact surveillance intervals.”

Future research should look at additional obesity-related factors, such as visceral obesity and malignant progression of BE, as well as whether diet, lifestyle, and bariatric interventions can reduce the risk for progression.

“The next steps also include plugging BMI into risk scores and risk stratification models to enable targeted surveillance among high-risk groups,” Sharma said.

One of the study coauthors received funding as a National Institute for Health Research Academic clinical fellow. No other funding sources were declared. Alexandre and Sharma reported no relevant disclosures.

A version of this article appeared on Medscape.com.

A new prognostic model could potentially predict and stratify the risk for hepatocellular carcinoma (HCC) among patients with chronic hepatitis B (CHB) who are noncirrhotic and not indicated for antiviral treatment.

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.

A new prognostic model could potentially predict and stratify the risk for hepatocellular carcinoma (HCC) among patients with chronic hepatitis B (CHB) who are noncirrhotic and not indicated for antiviral treatment.

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.

A new prognostic model could potentially predict and stratify the risk for hepatocellular carcinoma (HCC) among patients with chronic hepatitis B (CHB) who are noncirrhotic and not indicated for antiviral treatment.

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.

In Fiscal Year (FY) 2023, > 40% of veterans enrolled by the US Department of Veterans Affairs (VA) received care from private practice, mainly for emergency services. Costs associated with that care have shifted from Medicare to the VA to the tune of billions of dollars, according to a recent study published in JAMA Health Forum.

The expenses are a result of the Maintaining Internal Systems and Strengthening Integrated Outside Networks (MISSION) Act of 2018, which established the Veterans Community Care Program (VCCP) and allowed the VA to contract with private clinicians. This provided veterans enrolled in both the Veterans Health Administration (VHA) and Medicare to have 2 government sources of health care financing. The VHA is billed if the veteran receives care at one of its facilities or is referred to a community facility; Medicare is billed only if the veteran is treated for a service not covered by VHA.

These shifts are concerning, according to Kenneth W. Kizer, MD, MPH, and Said Ibrahim, MD, MPH. In an accompanying editorial, they outline how the changes affect whether VHA care will have adequate funding to provide care for the additional 740,000 enrollees who have entered the system in the past 2 years. 

“This has created a $12 billion medical care budget shortfall for FY 2024,” Kizer and Ibrahim argue. The resulting “substantial budgetary tumult … is adversely impacting the front lines of care delivery at individual VA facilities, leading to delays in hiring caregivers and impeding access to VA care and timely care delivery, as well as greatly straining the traditional roles of VA staff and clinicians trying to manage the challenging cross-system referral processes.”

The study calculated the number of yearly emergency department (ED) visits per 1000 veterans in Medicare overall and by VA ED visits, VA-purchased community ED visits, and Medicare-purchased community ED visits. Estimated total costs shifted from Medicare to the VA after the MISSION Act between 2016 and 2021 were then calculated.

Of the 4,960,189 VA and Medicare enrollees in 2016, 37.0% presented to the ED at least once. Of the 4,837,436 dual enrollees in 2021, 37.6% presented to the ED at least once. ED visits increased 8%, from 820 per 1000 veterans in 2016, to 886 per 1000 veterans in 2019. The COVID-19 pandemic caused a dip in ED visits in 2020 by veterans (769 per 1000), but the number rose 2021 (852 per 1000 veterans).

Between 2016 and 2021, the percentage of VA-purchased community ED visits more than doubled, from 8.0% to 21.1%, while Medicare-purchased community ED visits dropped from 65.2% to 52.6%. Patterns were similar among veterans enrolled in traditional Medicare vs Medicare Advantage (MA). The study estimated that in 2021 at least $2 billion of VA community ED spending was due to payer shift from Medicare. 

The shift is “particularly concerning” among veterans enrolled in MA since insurance plans receive capitated payments regardless of actual use of VA- or Medicare-covered services. However, the study’s observational design “limited our ability to infer causality between MISSION Act implementation and payer change.”

The cost shifting is “symptomatic of the fiscally undisciplined implementation of the VCCP and the lack of financially sound policy on payment for VA-Medicare dual enrollees,” according to Drs. Kizer and Ibrahim. “Addressing this matter seems especially important in light of numerous studies showing that the quality of community care often may be inferior to VA care, as well as less timely.”

Kizer and Ibrahim point out that when a veteran who is jointly enrolled in VA and MA plans receives care from the VA, the VA incurs the cost of providing those services even though the MA plan is being paid to provide them. The VA is not allowed to recoup its costs from Medicare. Thus, the government pays twice for the care of the same person. 

A recent study reported > $78 billion in duplicate VA-MA spending between 2011 and 2020, with $12 billion in FY 2020. Kizer and Ibrahim suggest the current VA-MA duplicate spending is likely to be significantly more than the reported amounts.

“[No] evidence shows that this duplicate spending yields a demonstrable health benefit for veterans, although undoubtedly it benefits the financial well-being of the MA plans,” they write.

It’s a “challenging policy and programmatic conundrum,” the co-authors say, noting that eligible veterans often have military service-related conditions that the VA is uniquely experienced in treating.

“Policies and programs need to be designed and aligned to ensure that veterans have timely access to emergency and other services and that rising community care costs do not jeopardize veterans’ choice to access and use VA services, nor compromise the nationally vital roles of the VA in graduate medical education and other health professional training, research, and emergency preparedness.”

In Fiscal Year (FY) 2023, > 40% of veterans enrolled by the US Department of Veterans Affairs (VA) received care from private practice, mainly for emergency services. Costs associated with that care have shifted from Medicare to the VA to the tune of billions of dollars, according to a recent study published in JAMA Health Forum.

The expenses are a result of the Maintaining Internal Systems and Strengthening Integrated Outside Networks (MISSION) Act of 2018, which established the Veterans Community Care Program (VCCP) and allowed the VA to contract with private clinicians. This provided veterans enrolled in both the Veterans Health Administration (VHA) and Medicare to have 2 government sources of health care financing. The VHA is billed if the veteran receives care at one of its facilities or is referred to a community facility; Medicare is billed only if the veteran is treated for a service not covered by VHA.

These shifts are concerning, according to Kenneth W. Kizer, MD, MPH, and Said Ibrahim, MD, MPH. In an accompanying editorial, they outline how the changes affect whether VHA care will have adequate funding to provide care for the additional 740,000 enrollees who have entered the system in the past 2 years. 

“This has created a $12 billion medical care budget shortfall for FY 2024,” Kizer and Ibrahim argue. The resulting “substantial budgetary tumult … is adversely impacting the front lines of care delivery at individual VA facilities, leading to delays in hiring caregivers and impeding access to VA care and timely care delivery, as well as greatly straining the traditional roles of VA staff and clinicians trying to manage the challenging cross-system referral processes.”

The study calculated the number of yearly emergency department (ED) visits per 1000 veterans in Medicare overall and by VA ED visits, VA-purchased community ED visits, and Medicare-purchased community ED visits. Estimated total costs shifted from Medicare to the VA after the MISSION Act between 2016 and 2021 were then calculated.

Of the 4,960,189 VA and Medicare enrollees in 2016, 37.0% presented to the ED at least once. Of the 4,837,436 dual enrollees in 2021, 37.6% presented to the ED at least once. ED visits increased 8%, from 820 per 1000 veterans in 2016, to 886 per 1000 veterans in 2019. The COVID-19 pandemic caused a dip in ED visits in 2020 by veterans (769 per 1000), but the number rose 2021 (852 per 1000 veterans).

Between 2016 and 2021, the percentage of VA-purchased community ED visits more than doubled, from 8.0% to 21.1%, while Medicare-purchased community ED visits dropped from 65.2% to 52.6%. Patterns were similar among veterans enrolled in traditional Medicare vs Medicare Advantage (MA). The study estimated that in 2021 at least $2 billion of VA community ED spending was due to payer shift from Medicare. 

The shift is “particularly concerning” among veterans enrolled in MA since insurance plans receive capitated payments regardless of actual use of VA- or Medicare-covered services. However, the study’s observational design “limited our ability to infer causality between MISSION Act implementation and payer change.”

The cost shifting is “symptomatic of the fiscally undisciplined implementation of the VCCP and the lack of financially sound policy on payment for VA-Medicare dual enrollees,” according to Drs. Kizer and Ibrahim. “Addressing this matter seems especially important in light of numerous studies showing that the quality of community care often may be inferior to VA care, as well as less timely.”

Kizer and Ibrahim point out that when a veteran who is jointly enrolled in VA and MA plans receives care from the VA, the VA incurs the cost of providing those services even though the MA plan is being paid to provide them. The VA is not allowed to recoup its costs from Medicare. Thus, the government pays twice for the care of the same person. 

A recent study reported > $78 billion in duplicate VA-MA spending between 2011 and 2020, with $12 billion in FY 2020. Kizer and Ibrahim suggest the current VA-MA duplicate spending is likely to be significantly more than the reported amounts.

“[No] evidence shows that this duplicate spending yields a demonstrable health benefit for veterans, although undoubtedly it benefits the financial well-being of the MA plans,” they write.

It’s a “challenging policy and programmatic conundrum,” the co-authors say, noting that eligible veterans often have military service-related conditions that the VA is uniquely experienced in treating.

“Policies and programs need to be designed and aligned to ensure that veterans have timely access to emergency and other services and that rising community care costs do not jeopardize veterans’ choice to access and use VA services, nor compromise the nationally vital roles of the VA in graduate medical education and other health professional training, research, and emergency preparedness.”

In Fiscal Year (FY) 2023, > 40% of veterans enrolled by the US Department of Veterans Affairs (VA) received care from private practice, mainly for emergency services. Costs associated with that care have shifted from Medicare to the VA to the tune of billions of dollars, according to a recent study published in JAMA Health Forum.

The expenses are a result of the Maintaining Internal Systems and Strengthening Integrated Outside Networks (MISSION) Act of 2018, which established the Veterans Community Care Program (VCCP) and allowed the VA to contract with private clinicians. This provided veterans enrolled in both the Veterans Health Administration (VHA) and Medicare to have 2 government sources of health care financing. The VHA is billed if the veteran receives care at one of its facilities or is referred to a community facility; Medicare is billed only if the veteran is treated for a service not covered by VHA.

These shifts are concerning, according to Kenneth W. Kizer, MD, MPH, and Said Ibrahim, MD, MPH. In an accompanying editorial, they outline how the changes affect whether VHA care will have adequate funding to provide care for the additional 740,000 enrollees who have entered the system in the past 2 years. 

“This has created a $12 billion medical care budget shortfall for FY 2024,” Kizer and Ibrahim argue. The resulting “substantial budgetary tumult … is adversely impacting the front lines of care delivery at individual VA facilities, leading to delays in hiring caregivers and impeding access to VA care and timely care delivery, as well as greatly straining the traditional roles of VA staff and clinicians trying to manage the challenging cross-system referral processes.”

The study calculated the number of yearly emergency department (ED) visits per 1000 veterans in Medicare overall and by VA ED visits, VA-purchased community ED visits, and Medicare-purchased community ED visits. Estimated total costs shifted from Medicare to the VA after the MISSION Act between 2016 and 2021 were then calculated.

Of the 4,960,189 VA and Medicare enrollees in 2016, 37.0% presented to the ED at least once. Of the 4,837,436 dual enrollees in 2021, 37.6% presented to the ED at least once. ED visits increased 8%, from 820 per 1000 veterans in 2016, to 886 per 1000 veterans in 2019. The COVID-19 pandemic caused a dip in ED visits in 2020 by veterans (769 per 1000), but the number rose 2021 (852 per 1000 veterans).

Between 2016 and 2021, the percentage of VA-purchased community ED visits more than doubled, from 8.0% to 21.1%, while Medicare-purchased community ED visits dropped from 65.2% to 52.6%. Patterns were similar among veterans enrolled in traditional Medicare vs Medicare Advantage (MA). The study estimated that in 2021 at least $2 billion of VA community ED spending was due to payer shift from Medicare. 

The shift is “particularly concerning” among veterans enrolled in MA since insurance plans receive capitated payments regardless of actual use of VA- or Medicare-covered services. However, the study’s observational design “limited our ability to infer causality between MISSION Act implementation and payer change.”

The cost shifting is “symptomatic of the fiscally undisciplined implementation of the VCCP and the lack of financially sound policy on payment for VA-Medicare dual enrollees,” according to Drs. Kizer and Ibrahim. “Addressing this matter seems especially important in light of numerous studies showing that the quality of community care often may be inferior to VA care, as well as less timely.”

Kizer and Ibrahim point out that when a veteran who is jointly enrolled in VA and MA plans receives care from the VA, the VA incurs the cost of providing those services even though the MA plan is being paid to provide them. The VA is not allowed to recoup its costs from Medicare. Thus, the government pays twice for the care of the same person. 

A recent study reported > $78 billion in duplicate VA-MA spending between 2011 and 2020, with $12 billion in FY 2020. Kizer and Ibrahim suggest the current VA-MA duplicate spending is likely to be significantly more than the reported amounts.

“[No] evidence shows that this duplicate spending yields a demonstrable health benefit for veterans, although undoubtedly it benefits the financial well-being of the MA plans,” they write.

It’s a “challenging policy and programmatic conundrum,” the co-authors say, noting that eligible veterans often have military service-related conditions that the VA is uniquely experienced in treating.

“Policies and programs need to be designed and aligned to ensure that veterans have timely access to emergency and other services and that rising community care costs do not jeopardize veterans’ choice to access and use VA services, nor compromise the nationally vital roles of the VA in graduate medical education and other health professional training, research, and emergency preparedness.”

Hispanic adults in the US experience significantly higher risk of metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic dysfunction–associated steatohepatitis (MASH), compared with non-Hispanic adults, according to a new systematic review and meta-analysis.

These findings underscore worsening health disparities in MASLD management and outcomes in this patient population, Kaleb Tesfai, BS, of the University of California, San Diego, and colleagues reported.

Previously, a 2018 meta-analysis found that Hispanic individuals had a higher MASLD prevalence than non-Hispanic White and Black individuals, along with an elevated relative risk of MASH. 

“In the setting of the evolving obesity epidemic, prevalence of MASLD has increased and characteristics of patient populations of interest have changed since the time of this prior meta-analysis,” Mr. Tesfai and colleagues wrote in Clinical Gastroenterology and Hepatology. “Importantly, MASH has become a leading indication for liver transplant, thereby impacting long-term clinical outcomes. As such, accurate, updated prevalence rates and relative risk estimates of MASLD, MASH, advanced fibrosis/cirrhosis, and clinical outcomes for Hispanic adults in the US remain poorly characterized.”

The present meta-analysis focused specifically on Hispanic adults in the United States; it compared their disease prevalence, severity, and risk to non-Hispanic adults. Twenty-two studies, conducted between January 1, 2010, and December 31, 2023, were included, comprising 756,088 participants, of whom 62,072 were Hispanic. 

Study eligibility required reported data on the prevalence of MASLD, MASH, or advanced fibrosis, as well as racial or ethnic subgroup analyses. Studies were excluded if they did not use validated diagnostic methods, such as liver biopsy or imaging, or if they lacked stratification by Hispanic ethnicity. Prevalence estimates and relative risks were calculated using random-effects models. The analysis also accounted for potential confounding factors, including demographic characteristics, metabolic comorbidities, and social determinants of health (SDOH).

The pooled prevalence of MASLD among Hispanic adults was 41% (95% CI, 30%-52%), compared with 27% in non-Hispanic populations, reflecting a relative risk (RR) of 1.50 (95% CI, 1.32-1.69). For MASH, the pooled prevalence among Hispanic adults with MASLD was 61% (95% CI, 39%-82%), with an RR of 1.42 (95% CI, 1.04-1.93), compared with non-Hispanic adults.

“Our systematic review and meta-analysis highlights the worsening health disparities experienced by Hispanic adults in the US, with significant increase in the relative risk of MASLD and MASH in contemporary cohorts compared with prior estimates,” the investigators wrote. 

Despite these elevated risks for MASLD and MASH, advanced fibrosis and cirrhosis did not show statistically significant differences between Hispanic and non-Hispanic populations. 

The study also characterized the relationship between SDOH and detected health disparities. Adjustments for factors such as income, education, and health care access eliminated the independent association between Hispanic and MASLD risk, suggesting that these structural inequities play a meaningful role in disease disparities. 

Still, genetic factors, including PNPLA3 and TM6SF2 risk alleles, were identified as contributors to the higher disease burden in Hispanic populations.

Mr. Tesfai and colleagues called for prospective studies with standardized outcome definitions to better understand risks of advanced fibrosis and cirrhosis, as well as long-term clinical outcomes. In addition, they recommended further investigation of SDOH to determine optimal intervention targets.

“Public health initiatives focused on increasing screening for MASLD and MASH and enhancing health care delivery for this high-risk group are critically needed to optimize health outcomes for Hispanic adults in the US,” they concluded.This study was supported by various institutes at the National Institutes of Health, Gilead Sciences, and the SDSU-UCSD CREATE Partnership. The investigators disclosed additional relationships with Eli Lilly, Galmed, Pfizer, and others.

Hispanic adults in the US experience significantly higher risk of metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic dysfunction–associated steatohepatitis (MASH), compared with non-Hispanic adults, according to a new systematic review and meta-analysis.

These findings underscore worsening health disparities in MASLD management and outcomes in this patient population, Kaleb Tesfai, BS, of the University of California, San Diego, and colleagues reported.

Previously, a 2018 meta-analysis found that Hispanic individuals had a higher MASLD prevalence than non-Hispanic White and Black individuals, along with an elevated relative risk of MASH. 

“In the setting of the evolving obesity epidemic, prevalence of MASLD has increased and characteristics of patient populations of interest have changed since the time of this prior meta-analysis,” Mr. Tesfai and colleagues wrote in Clinical Gastroenterology and Hepatology. “Importantly, MASH has become a leading indication for liver transplant, thereby impacting long-term clinical outcomes. As such, accurate, updated prevalence rates and relative risk estimates of MASLD, MASH, advanced fibrosis/cirrhosis, and clinical outcomes for Hispanic adults in the US remain poorly characterized.”

The present meta-analysis focused specifically on Hispanic adults in the United States; it compared their disease prevalence, severity, and risk to non-Hispanic adults. Twenty-two studies, conducted between January 1, 2010, and December 31, 2023, were included, comprising 756,088 participants, of whom 62,072 were Hispanic. 

Study eligibility required reported data on the prevalence of MASLD, MASH, or advanced fibrosis, as well as racial or ethnic subgroup analyses. Studies were excluded if they did not use validated diagnostic methods, such as liver biopsy or imaging, or if they lacked stratification by Hispanic ethnicity. Prevalence estimates and relative risks were calculated using random-effects models. The analysis also accounted for potential confounding factors, including demographic characteristics, metabolic comorbidities, and social determinants of health (SDOH).

The pooled prevalence of MASLD among Hispanic adults was 41% (95% CI, 30%-52%), compared with 27% in non-Hispanic populations, reflecting a relative risk (RR) of 1.50 (95% CI, 1.32-1.69). For MASH, the pooled prevalence among Hispanic adults with MASLD was 61% (95% CI, 39%-82%), with an RR of 1.42 (95% CI, 1.04-1.93), compared with non-Hispanic adults.

“Our systematic review and meta-analysis highlights the worsening health disparities experienced by Hispanic adults in the US, with significant increase in the relative risk of MASLD and MASH in contemporary cohorts compared with prior estimates,” the investigators wrote. 

Despite these elevated risks for MASLD and MASH, advanced fibrosis and cirrhosis did not show statistically significant differences between Hispanic and non-Hispanic populations. 

The study also characterized the relationship between SDOH and detected health disparities. Adjustments for factors such as income, education, and health care access eliminated the independent association between Hispanic and MASLD risk, suggesting that these structural inequities play a meaningful role in disease disparities. 

Still, genetic factors, including PNPLA3 and TM6SF2 risk alleles, were identified as contributors to the higher disease burden in Hispanic populations.

Mr. Tesfai and colleagues called for prospective studies with standardized outcome definitions to better understand risks of advanced fibrosis and cirrhosis, as well as long-term clinical outcomes. In addition, they recommended further investigation of SDOH to determine optimal intervention targets.

“Public health initiatives focused on increasing screening for MASLD and MASH and enhancing health care delivery for this high-risk group are critically needed to optimize health outcomes for Hispanic adults in the US,” they concluded.This study was supported by various institutes at the National Institutes of Health, Gilead Sciences, and the SDSU-UCSD CREATE Partnership. The investigators disclosed additional relationships with Eli Lilly, Galmed, Pfizer, and others.

Hispanic adults in the US experience significantly higher risk of metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic dysfunction–associated steatohepatitis (MASH), compared with non-Hispanic adults, according to a new systematic review and meta-analysis.

These findings underscore worsening health disparities in MASLD management and outcomes in this patient population, Kaleb Tesfai, BS, of the University of California, San Diego, and colleagues reported.

Previously, a 2018 meta-analysis found that Hispanic individuals had a higher MASLD prevalence than non-Hispanic White and Black individuals, along with an elevated relative risk of MASH. 

“In the setting of the evolving obesity epidemic, prevalence of MASLD has increased and characteristics of patient populations of interest have changed since the time of this prior meta-analysis,” Mr. Tesfai and colleagues wrote in Clinical Gastroenterology and Hepatology. “Importantly, MASH has become a leading indication for liver transplant, thereby impacting long-term clinical outcomes. As such, accurate, updated prevalence rates and relative risk estimates of MASLD, MASH, advanced fibrosis/cirrhosis, and clinical outcomes for Hispanic adults in the US remain poorly characterized.”

The present meta-analysis focused specifically on Hispanic adults in the United States; it compared their disease prevalence, severity, and risk to non-Hispanic adults. Twenty-two studies, conducted between January 1, 2010, and December 31, 2023, were included, comprising 756,088 participants, of whom 62,072 were Hispanic. 

Study eligibility required reported data on the prevalence of MASLD, MASH, or advanced fibrosis, as well as racial or ethnic subgroup analyses. Studies were excluded if they did not use validated diagnostic methods, such as liver biopsy or imaging, or if they lacked stratification by Hispanic ethnicity. Prevalence estimates and relative risks were calculated using random-effects models. The analysis also accounted for potential confounding factors, including demographic characteristics, metabolic comorbidities, and social determinants of health (SDOH).

The pooled prevalence of MASLD among Hispanic adults was 41% (95% CI, 30%-52%), compared with 27% in non-Hispanic populations, reflecting a relative risk (RR) of 1.50 (95% CI, 1.32-1.69). For MASH, the pooled prevalence among Hispanic adults with MASLD was 61% (95% CI, 39%-82%), with an RR of 1.42 (95% CI, 1.04-1.93), compared with non-Hispanic adults.

“Our systematic review and meta-analysis highlights the worsening health disparities experienced by Hispanic adults in the US, with significant increase in the relative risk of MASLD and MASH in contemporary cohorts compared with prior estimates,” the investigators wrote. 

Despite these elevated risks for MASLD and MASH, advanced fibrosis and cirrhosis did not show statistically significant differences between Hispanic and non-Hispanic populations. 

The study also characterized the relationship between SDOH and detected health disparities. Adjustments for factors such as income, education, and health care access eliminated the independent association between Hispanic and MASLD risk, suggesting that these structural inequities play a meaningful role in disease disparities. 

Still, genetic factors, including PNPLA3 and TM6SF2 risk alleles, were identified as contributors to the higher disease burden in Hispanic populations.

Mr. Tesfai and colleagues called for prospective studies with standardized outcome definitions to better understand risks of advanced fibrosis and cirrhosis, as well as long-term clinical outcomes. In addition, they recommended further investigation of SDOH to determine optimal intervention targets.

“Public health initiatives focused on increasing screening for MASLD and MASH and enhancing health care delivery for this high-risk group are critically needed to optimize health outcomes for Hispanic adults in the US,” they concluded.This study was supported by various institutes at the National Institutes of Health, Gilead Sciences, and the SDSU-UCSD CREATE Partnership. The investigators disclosed additional relationships with Eli Lilly, Galmed, Pfizer, and others.

Clinicians generally shouldn’t use potassium-competitive acid blockers (P-CAB) as first-line therapy for acid-related conditions, nonerosive gastroesophageal reflux disease (GERD), or peptic ulcer disease, according to a recent clinical practice update from the American Gastroenterological Association (AGA).

However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs.

“P-CABs are a newer medication class now available in the US, associated with more rapid, potent, and prolonged gastric acid inhibition than PPI formulations,” said lead author Amit Patel, MD, a gastroenterologist at the Duke University School of Medicine and Durham Veterans Affairs Medical Center, Durham, North Carolina.

 

“P-CABs have potentially significant clinical benefits in the management of Helicobacter pylori infection and GERD, particularly more severe erosive esophagitis,” he said. “Emerging data are affording additional insights into the clinical benefits of P-CABs in settings such as on-demand therapy for reflux-associated symptoms, bleeding gastroduodenal ulcers, and endoscopic eradication therapy for Barrett’s esophagus.”

The update was published in Gastroenterology .

 

P-CAB Developments

For most patients, PPIs and histamine-2 receptor antagonists remain the primary way to inhibit gastric acid secretion for common upper gastrointestinal conditions, the authors wrote. However, P-CABs such as vonoprazan and tegoprazan may provide relief when PPIs have limitations.

Unlike PPIs, P-CABs are considered acid-stable, don’t require premeal dosing, aren’t prodrugs, and don’t require conversion to an active form to provide pharmacologic effects. They tend to have longer half-lives and more rapid onset. Serum gastrin levels typically remain higher with P-CABs.

In terms of safety, randomized trial data indicate that P-CABs are generally well tolerated and have short-term and medium-term safety similar to PPIs. Due to potent acid suppression, enteric infection risks remain higher, though long-term safety data is needed, the authors wrote.

Overall, P-CABs appear to be equally as potent or more potent than PPIs, though more potent acid inhibition isn’t necessarily associated with better outcomes, the authors wrote. For most foregut acid-related disorders — such as heartburn and prevention of nonsteroidal anti-inflammatory drug–associated ulcers — P-CABs can help when patients fail PPI therapy.

In general, though, nonclinical factors related to cost, barriers to obtaining medication, and limited long-term safety data may outweigh the advantages of P-CABs, especially if clinical superiority isn’t yet known, the authors wrote. 

For GERD, clinicians generally shouldn’t use P-CABs as first-line therapy for patients with uninvestigated heartburn symptoms or nonerosive reflux disease. However, P-CABs should be used for those with documented acid-related reflux who fail therapy with twice-daily PPIs. They may also be appropriate for on-demand heartburn therapy, although more evidence is needed.

For erosive esophagitis, P-CABs generally shouldn’t be used for milder cases but can be considered for patients with more severe cases that haven’t responded to PPIs, including refractory esophagitis.

For H pylori, P-CABs should be used in place of PPIs for eradication regimens, including among patients with clarithromycin-resistant strains. In contrast with most of the other indications in the update, the short-term duration of H pylori treatment reduced the authors’ concerns about P-CAB costs and safety.

For peptic ulcer disease, P-CABs generally shouldn’t be used as first-line treatment or prophylaxis. However, the rapid onset and potent acid inhibition could be useful for patients with bleeding gastroduodenal ulcers and high-risk stigmata.

“Emerging data will allow refinements in the populations and clinical settings for which P-CABs at various doses may be considered and advised — and may reveal more clinical scenarios in which they can provide meaningful benefit,” Patel said. “Further investigations, including additional populations and novel indicators, as well as evaluating long-term safety data and cost-effectiveness, are warranted, as P-CABs are incorporated more broadly into clinical practice worldwide.”
 
The authors received no specific funding for this update. Patel reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Clinicians generally shouldn’t use potassium-competitive acid blockers (P-CAB) as first-line therapy for acid-related conditions, nonerosive gastroesophageal reflux disease (GERD), or peptic ulcer disease, according to a recent clinical practice update from the American Gastroenterological Association (AGA).

However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs.

“P-CABs are a newer medication class now available in the US, associated with more rapid, potent, and prolonged gastric acid inhibition than PPI formulations,” said lead author Amit Patel, MD, a gastroenterologist at the Duke University School of Medicine and Durham Veterans Affairs Medical Center, Durham, North Carolina.

 

“P-CABs have potentially significant clinical benefits in the management of Helicobacter pylori infection and GERD, particularly more severe erosive esophagitis,” he said. “Emerging data are affording additional insights into the clinical benefits of P-CABs in settings such as on-demand therapy for reflux-associated symptoms, bleeding gastroduodenal ulcers, and endoscopic eradication therapy for Barrett’s esophagus.”

The update was published in Gastroenterology .

 

P-CAB Developments

For most patients, PPIs and histamine-2 receptor antagonists remain the primary way to inhibit gastric acid secretion for common upper gastrointestinal conditions, the authors wrote. However, P-CABs such as vonoprazan and tegoprazan may provide relief when PPIs have limitations.

Unlike PPIs, P-CABs are considered acid-stable, don’t require premeal dosing, aren’t prodrugs, and don’t require conversion to an active form to provide pharmacologic effects. They tend to have longer half-lives and more rapid onset. Serum gastrin levels typically remain higher with P-CABs.

In terms of safety, randomized trial data indicate that P-CABs are generally well tolerated and have short-term and medium-term safety similar to PPIs. Due to potent acid suppression, enteric infection risks remain higher, though long-term safety data is needed, the authors wrote.

Overall, P-CABs appear to be equally as potent or more potent than PPIs, though more potent acid inhibition isn’t necessarily associated with better outcomes, the authors wrote. For most foregut acid-related disorders — such as heartburn and prevention of nonsteroidal anti-inflammatory drug–associated ulcers — P-CABs can help when patients fail PPI therapy.

In general, though, nonclinical factors related to cost, barriers to obtaining medication, and limited long-term safety data may outweigh the advantages of P-CABs, especially if clinical superiority isn’t yet known, the authors wrote. 

For GERD, clinicians generally shouldn’t use P-CABs as first-line therapy for patients with uninvestigated heartburn symptoms or nonerosive reflux disease. However, P-CABs should be used for those with documented acid-related reflux who fail therapy with twice-daily PPIs. They may also be appropriate for on-demand heartburn therapy, although more evidence is needed.

For erosive esophagitis, P-CABs generally shouldn’t be used for milder cases but can be considered for patients with more severe cases that haven’t responded to PPIs, including refractory esophagitis.

For H pylori, P-CABs should be used in place of PPIs for eradication regimens, including among patients with clarithromycin-resistant strains. In contrast with most of the other indications in the update, the short-term duration of H pylori treatment reduced the authors’ concerns about P-CAB costs and safety.

For peptic ulcer disease, P-CABs generally shouldn’t be used as first-line treatment or prophylaxis. However, the rapid onset and potent acid inhibition could be useful for patients with bleeding gastroduodenal ulcers and high-risk stigmata.

“Emerging data will allow refinements in the populations and clinical settings for which P-CABs at various doses may be considered and advised — and may reveal more clinical scenarios in which they can provide meaningful benefit,” Patel said. “Further investigations, including additional populations and novel indicators, as well as evaluating long-term safety data and cost-effectiveness, are warranted, as P-CABs are incorporated more broadly into clinical practice worldwide.”
 
The authors received no specific funding for this update. Patel reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Clinicians generally shouldn’t use potassium-competitive acid blockers (P-CAB) as first-line therapy for acid-related conditions, nonerosive gastroesophageal reflux disease (GERD), or peptic ulcer disease, according to a recent clinical practice update from the American Gastroenterological Association (AGA).

However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs.

“P-CABs are a newer medication class now available in the US, associated with more rapid, potent, and prolonged gastric acid inhibition than PPI formulations,” said lead author Amit Patel, MD, a gastroenterologist at the Duke University School of Medicine and Durham Veterans Affairs Medical Center, Durham, North Carolina.

 

“P-CABs have potentially significant clinical benefits in the management of Helicobacter pylori infection and GERD, particularly more severe erosive esophagitis,” he said. “Emerging data are affording additional insights into the clinical benefits of P-CABs in settings such as on-demand therapy for reflux-associated symptoms, bleeding gastroduodenal ulcers, and endoscopic eradication therapy for Barrett’s esophagus.”

The update was published in Gastroenterology .

 

P-CAB Developments

For most patients, PPIs and histamine-2 receptor antagonists remain the primary way to inhibit gastric acid secretion for common upper gastrointestinal conditions, the authors wrote. However, P-CABs such as vonoprazan and tegoprazan may provide relief when PPIs have limitations.

Unlike PPIs, P-CABs are considered acid-stable, don’t require premeal dosing, aren’t prodrugs, and don’t require conversion to an active form to provide pharmacologic effects. They tend to have longer half-lives and more rapid onset. Serum gastrin levels typically remain higher with P-CABs.

In terms of safety, randomized trial data indicate that P-CABs are generally well tolerated and have short-term and medium-term safety similar to PPIs. Due to potent acid suppression, enteric infection risks remain higher, though long-term safety data is needed, the authors wrote.

Overall, P-CABs appear to be equally as potent or more potent than PPIs, though more potent acid inhibition isn’t necessarily associated with better outcomes, the authors wrote. For most foregut acid-related disorders — such as heartburn and prevention of nonsteroidal anti-inflammatory drug–associated ulcers — P-CABs can help when patients fail PPI therapy.

In general, though, nonclinical factors related to cost, barriers to obtaining medication, and limited long-term safety data may outweigh the advantages of P-CABs, especially if clinical superiority isn’t yet known, the authors wrote. 

For GERD, clinicians generally shouldn’t use P-CABs as first-line therapy for patients with uninvestigated heartburn symptoms or nonerosive reflux disease. However, P-CABs should be used for those with documented acid-related reflux who fail therapy with twice-daily PPIs. They may also be appropriate for on-demand heartburn therapy, although more evidence is needed.

For erosive esophagitis, P-CABs generally shouldn’t be used for milder cases but can be considered for patients with more severe cases that haven’t responded to PPIs, including refractory esophagitis.

For H pylori, P-CABs should be used in place of PPIs for eradication regimens, including among patients with clarithromycin-resistant strains. In contrast with most of the other indications in the update, the short-term duration of H pylori treatment reduced the authors’ concerns about P-CAB costs and safety.

For peptic ulcer disease, P-CABs generally shouldn’t be used as first-line treatment or prophylaxis. However, the rapid onset and potent acid inhibition could be useful for patients with bleeding gastroduodenal ulcers and high-risk stigmata.

“Emerging data will allow refinements in the populations and clinical settings for which P-CABs at various doses may be considered and advised — and may reveal more clinical scenarios in which they can provide meaningful benefit,” Patel said. “Further investigations, including additional populations and novel indicators, as well as evaluating long-term safety data and cost-effectiveness, are warranted, as P-CABs are incorporated more broadly into clinical practice worldwide.”
 
The authors received no specific funding for this update. Patel reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Liver stiffness measurement (LSM) using vibration-controlled transient elastography (VCTE) predicts long-term outcomes among pediatric patients with biliary atresia, according to investigators.

These findings suggest that LSM may serve as a noninvasive tool for risk stratification and treatment planning in this population, reported lead author Jean P. Molleston, MD, of Indiana University School of Medicine, Indianapolis, and colleagues.

 

“Biliary atresia is frequently complicated by hepatic fibrosis with progression to cirrhosis and portal hypertension manifested by ascites, hepatopulmonary syndrome, and variceal bleeding,” the investigators wrote in Gastroenterology. “The ability to predict these outcomes can inform clinical decision-making.”

To this end, VCTE has been gaining increasing support in the pediatric setting.

“Advantages of VCTE over liver biopsy include convenience, cost, sampling bias, and risk,” the investigators wrote. “VCTE potentially allows (1) fibrosis estimation, (2) prediction of portal hypertension complications/survival, and (3) ability to noninvasively monitor liver stiffness as a fibrosis surrogate.”

The present multicenter study aimed to gauge the prognostic utility of VCTE among 254 patients, aged 21 years or younger, with biliary atresia. All patients had a valid baseline LSM, plus longitudinal clinical and laboratory data drawn from studies by the Childhood Liver Disease Research Network (ChiLDReN). Liver stiffness was assessed noninvasively with FibroScan devices, adhering to protocols that required at least 10 valid measurements and a variability of less than 30%.

The primary outcomes were survival with native liver (SNL), defined as the time to liver transplantation or death, and a composite measure of liver-related events, including the first occurrence of transplantation, death, ascites, variceal bleeding, or hepatopulmonary syndrome. Secondary outcomes focused on the trajectory of platelet decline, a marker of disease progression. The study also explored the relationship between baseline LSM and conventional biomarkers, including platelet count, albumin, and bilirubin.

LSM was a strong predictor of long-term outcomes. Specifically, Kaplan-Meier analysis showed significant differences in 5-year SNL across LSM strata (P < .001). Children with LSM values less than 10 kPa had excellent 5-year SNL rates (LSM 10 to < 15 kPa, 88.9%; 95% CI, 75.1-95.3%), while those with LSM of at least 15 kPa exhibited substantially lower 5-year SNL (58.9%; 95% CI, 46.0-69.7%).

Similarly, event-free survival (EFS) rates declined as LSM values increased (P < .001). Participants with LSM less than 10 kPa had a 5-year EFS rate of 92.2% versus with 61.2% for those with LSM of at least 15 kPa.

LSM also predicted platelet decline. For every twofold increase in baseline LSM, platelet counts declined by an additional 4,000/mm³ per year (P < .001). This association was illustrated through predicted trajectories for participants with LSM values of 4, 7, 12, 18, and 42 kPa, corresponding to different percentiles of disease severity.

Cox proportional hazards analysis indicated that a two-fold increase in LSM was associated with a hazard ratio of 3.3 (P < .001) for liver transplant or death. While LSM had good discrimination on its own (C statistic = 0.83), it did not significantly improve predictive accuracy when added to models based on platelet count, albumin, and bilirubin.

“This noninvasive measurement could potentially be used to predict natural history, stratify patients for clinical trials, plan interventions, and provide anticipatory guidance,” Molleston and colleagues concluded. This study was supported by grants from the National Institute of Diabetes, Digestive and Kidney Diseases; National Institutes of Health; Childhood Liver Disease Research Network; and others. The investigators disclosed no conflicts of interest.

Liver stiffness measurement (LSM) using vibration-controlled transient elastography (VCTE) predicts long-term outcomes among pediatric patients with biliary atresia, according to investigators.

These findings suggest that LSM may serve as a noninvasive tool for risk stratification and treatment planning in this population, reported lead author Jean P. Molleston, MD, of Indiana University School of Medicine, Indianapolis, and colleagues.

 

“Biliary atresia is frequently complicated by hepatic fibrosis with progression to cirrhosis and portal hypertension manifested by ascites, hepatopulmonary syndrome, and variceal bleeding,” the investigators wrote in Gastroenterology. “The ability to predict these outcomes can inform clinical decision-making.”

To this end, VCTE has been gaining increasing support in the pediatric setting.

“Advantages of VCTE over liver biopsy include convenience, cost, sampling bias, and risk,” the investigators wrote. “VCTE potentially allows (1) fibrosis estimation, (2) prediction of portal hypertension complications/survival, and (3) ability to noninvasively monitor liver stiffness as a fibrosis surrogate.”

The present multicenter study aimed to gauge the prognostic utility of VCTE among 254 patients, aged 21 years or younger, with biliary atresia. All patients had a valid baseline LSM, plus longitudinal clinical and laboratory data drawn from studies by the Childhood Liver Disease Research Network (ChiLDReN). Liver stiffness was assessed noninvasively with FibroScan devices, adhering to protocols that required at least 10 valid measurements and a variability of less than 30%.

The primary outcomes were survival with native liver (SNL), defined as the time to liver transplantation or death, and a composite measure of liver-related events, including the first occurrence of transplantation, death, ascites, variceal bleeding, or hepatopulmonary syndrome. Secondary outcomes focused on the trajectory of platelet decline, a marker of disease progression. The study also explored the relationship between baseline LSM and conventional biomarkers, including platelet count, albumin, and bilirubin.

LSM was a strong predictor of long-term outcomes. Specifically, Kaplan-Meier analysis showed significant differences in 5-year SNL across LSM strata (P < .001). Children with LSM values less than 10 kPa had excellent 5-year SNL rates (LSM 10 to < 15 kPa, 88.9%; 95% CI, 75.1-95.3%), while those with LSM of at least 15 kPa exhibited substantially lower 5-year SNL (58.9%; 95% CI, 46.0-69.7%).

Similarly, event-free survival (EFS) rates declined as LSM values increased (P < .001). Participants with LSM less than 10 kPa had a 5-year EFS rate of 92.2% versus with 61.2% for those with LSM of at least 15 kPa.

LSM also predicted platelet decline. For every twofold increase in baseline LSM, platelet counts declined by an additional 4,000/mm³ per year (P < .001). This association was illustrated through predicted trajectories for participants with LSM values of 4, 7, 12, 18, and 42 kPa, corresponding to different percentiles of disease severity.

Cox proportional hazards analysis indicated that a two-fold increase in LSM was associated with a hazard ratio of 3.3 (P < .001) for liver transplant or death. While LSM had good discrimination on its own (C statistic = 0.83), it did not significantly improve predictive accuracy when added to models based on platelet count, albumin, and bilirubin.

“This noninvasive measurement could potentially be used to predict natural history, stratify patients for clinical trials, plan interventions, and provide anticipatory guidance,” Molleston and colleagues concluded. This study was supported by grants from the National Institute of Diabetes, Digestive and Kidney Diseases; National Institutes of Health; Childhood Liver Disease Research Network; and others. The investigators disclosed no conflicts of interest.

Liver stiffness measurement (LSM) using vibration-controlled transient elastography (VCTE) predicts long-term outcomes among pediatric patients with biliary atresia, according to investigators.

These findings suggest that LSM may serve as a noninvasive tool for risk stratification and treatment planning in this population, reported lead author Jean P. Molleston, MD, of Indiana University School of Medicine, Indianapolis, and colleagues.

 

“Biliary atresia is frequently complicated by hepatic fibrosis with progression to cirrhosis and portal hypertension manifested by ascites, hepatopulmonary syndrome, and variceal bleeding,” the investigators wrote in Gastroenterology. “The ability to predict these outcomes can inform clinical decision-making.”

To this end, VCTE has been gaining increasing support in the pediatric setting.

“Advantages of VCTE over liver biopsy include convenience, cost, sampling bias, and risk,” the investigators wrote. “VCTE potentially allows (1) fibrosis estimation, (2) prediction of portal hypertension complications/survival, and (3) ability to noninvasively monitor liver stiffness as a fibrosis surrogate.”

The present multicenter study aimed to gauge the prognostic utility of VCTE among 254 patients, aged 21 years or younger, with biliary atresia. All patients had a valid baseline LSM, plus longitudinal clinical and laboratory data drawn from studies by the Childhood Liver Disease Research Network (ChiLDReN). Liver stiffness was assessed noninvasively with FibroScan devices, adhering to protocols that required at least 10 valid measurements and a variability of less than 30%.

The primary outcomes were survival with native liver (SNL), defined as the time to liver transplantation or death, and a composite measure of liver-related events, including the first occurrence of transplantation, death, ascites, variceal bleeding, or hepatopulmonary syndrome. Secondary outcomes focused on the trajectory of platelet decline, a marker of disease progression. The study also explored the relationship between baseline LSM and conventional biomarkers, including platelet count, albumin, and bilirubin.

LSM was a strong predictor of long-term outcomes. Specifically, Kaplan-Meier analysis showed significant differences in 5-year SNL across LSM strata (P < .001). Children with LSM values less than 10 kPa had excellent 5-year SNL rates (LSM 10 to < 15 kPa, 88.9%; 95% CI, 75.1-95.3%), while those with LSM of at least 15 kPa exhibited substantially lower 5-year SNL (58.9%; 95% CI, 46.0-69.7%).

Similarly, event-free survival (EFS) rates declined as LSM values increased (P < .001). Participants with LSM less than 10 kPa had a 5-year EFS rate of 92.2% versus with 61.2% for those with LSM of at least 15 kPa.

LSM also predicted platelet decline. For every twofold increase in baseline LSM, platelet counts declined by an additional 4,000/mm³ per year (P < .001). This association was illustrated through predicted trajectories for participants with LSM values of 4, 7, 12, 18, and 42 kPa, corresponding to different percentiles of disease severity.

Cox proportional hazards analysis indicated that a two-fold increase in LSM was associated with a hazard ratio of 3.3 (P < .001) for liver transplant or death. While LSM had good discrimination on its own (C statistic = 0.83), it did not significantly improve predictive accuracy when added to models based on platelet count, albumin, and bilirubin.

“This noninvasive measurement could potentially be used to predict natural history, stratify patients for clinical trials, plan interventions, and provide anticipatory guidance,” Molleston and colleagues concluded. This study was supported by grants from the National Institute of Diabetes, Digestive and Kidney Diseases; National Institutes of Health; Childhood Liver Disease Research Network; and others. The investigators disclosed no conflicts of interest.

Lipophilic statins are associated with reduced risk of developing hepatocellular carcinoma (HCC) among patients with hepatic fibrosis and cirrhosis, according to investigators.

These findings also pave the way for new research into targeted therapies, personalized prevention strategies, and broader applications in high-risk populations, Erik Almazan, MD, and Raymond T. Chung, MD, of Harvard Medical School, Boston, Massachusetts, reported.

“Statins, metformin, and aspirin are low-cost medications often prescribed for the management of diseases associated with metabolic syndrome that have been associated with reduced HCC risk, the investigators wrote in Gastro Hep Advances. “Despite these findings, few studies have focused on populations in the US or without hepatitis B virus (HBV) or hepatitis C virus (HCV).”

To address this knowledge gap, Almazan and Chung retrospectively analyzed data from 3,677 patients with hepatic fibrosis and cirrhosis, drawn from the All of Us Controlled Tier Dataset v7, which spans May 2018 to July 2022. 

Within this population, 94 patients had HCC, while 3,583 served as controls. Lipophilic statin use was compared with hydrophilic statins, metformin, and aspirin. Multivariable logistic regression controlled for confounders including age, sex, race, and the presence of HBV or HCV.

Participants in the HCC cohort were older (mean age, 64 vs 58 years), more likely to be male (64.1% vs 50.0%), and had higher rates of chronic HBV (9.6% vs 2.5%) and chronic HCV (36.2% vs. 20.5%) compared to controls (P ≤ .01).

 

As a class, lipophilic statins were associated with a 36% reduced risk of HCC (odds ratio [OR], 0.64; 95% CI, 0.41-1.00; P < .05). Specifically, atorvastatin was associated with a 41% reduced risk (OR, 0.59; 95% CI, 0.37-0.93; P = .02), while simvastatin was associated with a 54% reduced risk (OR, 0.46; 95% CI, 0.22-0.97; P = .04). 

In contrast, hydrophilic statins, such as pravastatin and rosuvastatin, showed no significant association with HCC risk. Similarly, no protective association was observed for metformin or aspirin.

These findings suggest that lipophilic statins could provide a practical and cost-effective strategy for HCC prevention, particularly in patients with metabolic syndrome or alcohol-related liver disease, according to Almazan and Chung. These high-risk groups often lack accessible and noninvasive prevention options, further highlighting the clinical relevance of these results.

The investigators proposed that the chemopreventive effects of lipophilic statins may be linked to their ability to passively diffuse into cells and modulate pathways involved in cancer development, such as the mevalonate pathway. These potential mechanisms remain poorly understood.

Almazan and Chung also pointed out several study limitations, including lack of granular data on statin doses and treatment duration, absence of serologic and imaging confirmation of hepatic fibrosis and cirrhosis, and a study cohort drawn from populations historically underrepresented in medical research, potentially limiting generalizability to the broader US population. 

“Nevertheless, we believe that our study adds valuable information to the literature on statin use and its association with HCC with data from a US-based sample inclusive of individuals with risk factors other than HBV and HCV,” the investigators wrote. “These results provide further support for trials (such as NCT05028829) evaluating the utility of lipophilic statins for chemoprevention in HCC for persons at risk.”This study was supported by various National Institutes of Health grants. The investigators disclosed no conflicts of interest.

Lipophilic statins are associated with reduced risk of developing hepatocellular carcinoma (HCC) among patients with hepatic fibrosis and cirrhosis, according to investigators.

These findings also pave the way for new research into targeted therapies, personalized prevention strategies, and broader applications in high-risk populations, Erik Almazan, MD, and Raymond T. Chung, MD, of Harvard Medical School, Boston, Massachusetts, reported.

“Statins, metformin, and aspirin are low-cost medications often prescribed for the management of diseases associated with metabolic syndrome that have been associated with reduced HCC risk, the investigators wrote in Gastro Hep Advances. “Despite these findings, few studies have focused on populations in the US or without hepatitis B virus (HBV) or hepatitis C virus (HCV).”

To address this knowledge gap, Almazan and Chung retrospectively analyzed data from 3,677 patients with hepatic fibrosis and cirrhosis, drawn from the All of Us Controlled Tier Dataset v7, which spans May 2018 to July 2022. 

Within this population, 94 patients had HCC, while 3,583 served as controls. Lipophilic statin use was compared with hydrophilic statins, metformin, and aspirin. Multivariable logistic regression controlled for confounders including age, sex, race, and the presence of HBV or HCV.

Participants in the HCC cohort were older (mean age, 64 vs 58 years), more likely to be male (64.1% vs 50.0%), and had higher rates of chronic HBV (9.6% vs 2.5%) and chronic HCV (36.2% vs. 20.5%) compared to controls (P ≤ .01).

 

As a class, lipophilic statins were associated with a 36% reduced risk of HCC (odds ratio [OR], 0.64; 95% CI, 0.41-1.00; P < .05). Specifically, atorvastatin was associated with a 41% reduced risk (OR, 0.59; 95% CI, 0.37-0.93; P = .02), while simvastatin was associated with a 54% reduced risk (OR, 0.46; 95% CI, 0.22-0.97; P = .04). 

In contrast, hydrophilic statins, such as pravastatin and rosuvastatin, showed no significant association with HCC risk. Similarly, no protective association was observed for metformin or aspirin.

These findings suggest that lipophilic statins could provide a practical and cost-effective strategy for HCC prevention, particularly in patients with metabolic syndrome or alcohol-related liver disease, according to Almazan and Chung. These high-risk groups often lack accessible and noninvasive prevention options, further highlighting the clinical relevance of these results.

The investigators proposed that the chemopreventive effects of lipophilic statins may be linked to their ability to passively diffuse into cells and modulate pathways involved in cancer development, such as the mevalonate pathway. These potential mechanisms remain poorly understood.

Almazan and Chung also pointed out several study limitations, including lack of granular data on statin doses and treatment duration, absence of serologic and imaging confirmation of hepatic fibrosis and cirrhosis, and a study cohort drawn from populations historically underrepresented in medical research, potentially limiting generalizability to the broader US population. 

“Nevertheless, we believe that our study adds valuable information to the literature on statin use and its association with HCC with data from a US-based sample inclusive of individuals with risk factors other than HBV and HCV,” the investigators wrote. “These results provide further support for trials (such as NCT05028829) evaluating the utility of lipophilic statins for chemoprevention in HCC for persons at risk.”This study was supported by various National Institutes of Health grants. The investigators disclosed no conflicts of interest.

Lipophilic statins are associated with reduced risk of developing hepatocellular carcinoma (HCC) among patients with hepatic fibrosis and cirrhosis, according to investigators.

These findings also pave the way for new research into targeted therapies, personalized prevention strategies, and broader applications in high-risk populations, Erik Almazan, MD, and Raymond T. Chung, MD, of Harvard Medical School, Boston, Massachusetts, reported.

“Statins, metformin, and aspirin are low-cost medications often prescribed for the management of diseases associated with metabolic syndrome that have been associated with reduced HCC risk, the investigators wrote in Gastro Hep Advances. “Despite these findings, few studies have focused on populations in the US or without hepatitis B virus (HBV) or hepatitis C virus (HCV).”

To address this knowledge gap, Almazan and Chung retrospectively analyzed data from 3,677 patients with hepatic fibrosis and cirrhosis, drawn from the All of Us Controlled Tier Dataset v7, which spans May 2018 to July 2022. 

Within this population, 94 patients had HCC, while 3,583 served as controls. Lipophilic statin use was compared with hydrophilic statins, metformin, and aspirin. Multivariable logistic regression controlled for confounders including age, sex, race, and the presence of HBV or HCV.

Participants in the HCC cohort were older (mean age, 64 vs 58 years), more likely to be male (64.1% vs 50.0%), and had higher rates of chronic HBV (9.6% vs 2.5%) and chronic HCV (36.2% vs. 20.5%) compared to controls (P ≤ .01).

 

As a class, lipophilic statins were associated with a 36% reduced risk of HCC (odds ratio [OR], 0.64; 95% CI, 0.41-1.00; P < .05). Specifically, atorvastatin was associated with a 41% reduced risk (OR, 0.59; 95% CI, 0.37-0.93; P = .02), while simvastatin was associated with a 54% reduced risk (OR, 0.46; 95% CI, 0.22-0.97; P = .04). 

In contrast, hydrophilic statins, such as pravastatin and rosuvastatin, showed no significant association with HCC risk. Similarly, no protective association was observed for metformin or aspirin.

These findings suggest that lipophilic statins could provide a practical and cost-effective strategy for HCC prevention, particularly in patients with metabolic syndrome or alcohol-related liver disease, according to Almazan and Chung. These high-risk groups often lack accessible and noninvasive prevention options, further highlighting the clinical relevance of these results.

The investigators proposed that the chemopreventive effects of lipophilic statins may be linked to their ability to passively diffuse into cells and modulate pathways involved in cancer development, such as the mevalonate pathway. These potential mechanisms remain poorly understood.

Almazan and Chung also pointed out several study limitations, including lack of granular data on statin doses and treatment duration, absence of serologic and imaging confirmation of hepatic fibrosis and cirrhosis, and a study cohort drawn from populations historically underrepresented in medical research, potentially limiting generalizability to the broader US population. 

“Nevertheless, we believe that our study adds valuable information to the literature on statin use and its association with HCC with data from a US-based sample inclusive of individuals with risk factors other than HBV and HCV,” the investigators wrote. “These results provide further support for trials (such as NCT05028829) evaluating the utility of lipophilic statins for chemoprevention in HCC for persons at risk.”This study was supported by various National Institutes of Health grants. The investigators disclosed no conflicts of interest.