User login
Risk Stratification May Work Well for FIT-Based CRC Screening in Elderly
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
In particular, interval CRC risk can vary substantially based on the fecal hemoglobin (f-Hb) concentration in the patient’s last fecal immunochemical test (FIT), as well as the number of prior screening rounds.
“Less is known about what happens after the upper age limit has been reached and individuals are not invited to participate in more screening rounds. This is important as life expectancy is increasing, and it is increasingly important to consider the most efficient way of screening the elderly,” said lead author Brenda van Stigt, a PhD candidate focused on cancer screening at Erasmus University Medical Center in Rotterdam, the Netherlands.
In the Netherlands, adults between ages 55 and 75 are invited to participate in stool-based CRC screening every 2 years. Based on a fecal immunochemical testing (FIT) threshold of 47 μg Hb/g, those who test positive are referred to colonoscopy, and those who test negative are invited to participate again after a 2-year period.
FIT can play a major role in risk stratification, Ms. van Stigt noted, along with other factors that influence CRC risk, such as age, sex, and CRC screening history. Although this is documented for ages 55-75, she and colleagues wanted to know more about what happens after age 75.
Ms. Van Stigt and colleagues conducted a population-based study by analyzing Dutch national cancer registry data and FIT results around the final screening at age 75, looking at those who were diagnosed with CRC within 24 months of their last negative FIT. The researchers assessed interval CRC risk and cancer stage, accounting for sex, last f-Hb concentration, and the number of screening rounds.
Among 305,761 people with a complete 24-month follow-up after a negative FIT, 661 patients were diagnosed with interval CRC, indicating an overall interval CRC risk of 21.6 per 10,000 individuals with a negative FIT. There were no significant differences by sex.
However, there were differences by screening rounds, with those who had participated in three or four screening rounds having a lower risk than those who participated only once (HR, .49).
In addition, those with detectable f-Hb (>0 μg Hb/g) in their last screening round had a much higher interval CRC risk (HR, 4.87), at 65.8 per 10,000 negative FITs, compared with 13.8 per 10,000 among those without detectable f-Hb. Interval CRC risk also increased over time for those with detectable f-Hb.
About 15% of the total population had detectable f-Hb, whereas 46% of those with interval CRC had detectable f-Hb, Ms. van Stigt said, meaning that nearly half of patients who were diagnosed with interval CRC already had detectable f-Hb in their prior FIT.
In a survival analysis, there was no association between interval CRC risk and sex. However, those who participated in three or four screening rounds were half as likely to be diagnosed than those who participated once or twice, and those with detectable f-Hb were five times as likely to be diagnosed.
For late-stage CRC, there was no association with sex or the number of screening rounds. Detectable f-Hb was associated with not only a higher risk of interval CRC but also a late-stage diagnosis.
“These findings indicate that one uniform age to stop screening is suboptimal,” Ms. van Stigt said. “Personalized screening strategies should, therefore, also ideally incorporate a risk-stratified age to stop screening.”
The US Preventive Services Task Force recommends that clinicians personalize screening for ages 76-85, accounting for overall health, prior screening history, and patient preferences.
“But we have no clear guidance on how to quantify or weigh these factors. This interesting study highlights how one of these factors (prior screening history) and fecal hemoglobin level (an emerging factor) are powerful stratifiers of subsequent colorectal cancer risk,” said Sameer D. Saini, MD, AGAF, director and research investigator at the VA Ann Arbor Healthcare System’s Center for Clinical Management Research. Dr. Saini wasn’t involved with the study.
At the clinical level, Dr. Saini said, sophisticated modeling is needed to understand the interaction with competing risks and identify the optimal screening strategies for patients at varying levels of cancer risk and life expectancy. Models could also help to quantify the population benefits and cost-effectiveness of personalized screening.
“Finally, it is important to note that, in many health systems, access to quantitative FIT may be limited,” he said. “These data may be less informative if colonoscopy is the primary mode of screening.”
Ms. van Stigt and Dr. Saini reported no relevant disclosures.
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
In particular, interval CRC risk can vary substantially based on the fecal hemoglobin (f-Hb) concentration in the patient’s last fecal immunochemical test (FIT), as well as the number of prior screening rounds.
“Less is known about what happens after the upper age limit has been reached and individuals are not invited to participate in more screening rounds. This is important as life expectancy is increasing, and it is increasingly important to consider the most efficient way of screening the elderly,” said lead author Brenda van Stigt, a PhD candidate focused on cancer screening at Erasmus University Medical Center in Rotterdam, the Netherlands.
In the Netherlands, adults between ages 55 and 75 are invited to participate in stool-based CRC screening every 2 years. Based on a fecal immunochemical testing (FIT) threshold of 47 μg Hb/g, those who test positive are referred to colonoscopy, and those who test negative are invited to participate again after a 2-year period.
FIT can play a major role in risk stratification, Ms. van Stigt noted, along with other factors that influence CRC risk, such as age, sex, and CRC screening history. Although this is documented for ages 55-75, she and colleagues wanted to know more about what happens after age 75.
Ms. Van Stigt and colleagues conducted a population-based study by analyzing Dutch national cancer registry data and FIT results around the final screening at age 75, looking at those who were diagnosed with CRC within 24 months of their last negative FIT. The researchers assessed interval CRC risk and cancer stage, accounting for sex, last f-Hb concentration, and the number of screening rounds.
Among 305,761 people with a complete 24-month follow-up after a negative FIT, 661 patients were diagnosed with interval CRC, indicating an overall interval CRC risk of 21.6 per 10,000 individuals with a negative FIT. There were no significant differences by sex.
However, there were differences by screening rounds, with those who had participated in three or four screening rounds having a lower risk than those who participated only once (HR, .49).
In addition, those with detectable f-Hb (>0 μg Hb/g) in their last screening round had a much higher interval CRC risk (HR, 4.87), at 65.8 per 10,000 negative FITs, compared with 13.8 per 10,000 among those without detectable f-Hb. Interval CRC risk also increased over time for those with detectable f-Hb.
About 15% of the total population had detectable f-Hb, whereas 46% of those with interval CRC had detectable f-Hb, Ms. van Stigt said, meaning that nearly half of patients who were diagnosed with interval CRC already had detectable f-Hb in their prior FIT.
In a survival analysis, there was no association between interval CRC risk and sex. However, those who participated in three or four screening rounds were half as likely to be diagnosed than those who participated once or twice, and those with detectable f-Hb were five times as likely to be diagnosed.
For late-stage CRC, there was no association with sex or the number of screening rounds. Detectable f-Hb was associated with not only a higher risk of interval CRC but also a late-stage diagnosis.
“These findings indicate that one uniform age to stop screening is suboptimal,” Ms. van Stigt said. “Personalized screening strategies should, therefore, also ideally incorporate a risk-stratified age to stop screening.”
The US Preventive Services Task Force recommends that clinicians personalize screening for ages 76-85, accounting for overall health, prior screening history, and patient preferences.
“But we have no clear guidance on how to quantify or weigh these factors. This interesting study highlights how one of these factors (prior screening history) and fecal hemoglobin level (an emerging factor) are powerful stratifiers of subsequent colorectal cancer risk,” said Sameer D. Saini, MD, AGAF, director and research investigator at the VA Ann Arbor Healthcare System’s Center for Clinical Management Research. Dr. Saini wasn’t involved with the study.
At the clinical level, Dr. Saini said, sophisticated modeling is needed to understand the interaction with competing risks and identify the optimal screening strategies for patients at varying levels of cancer risk and life expectancy. Models could also help to quantify the population benefits and cost-effectiveness of personalized screening.
“Finally, it is important to note that, in many health systems, access to quantitative FIT may be limited,” he said. “These data may be less informative if colonoscopy is the primary mode of screening.”
Ms. van Stigt and Dr. Saini reported no relevant disclosures.
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
In particular, interval CRC risk can vary substantially based on the fecal hemoglobin (f-Hb) concentration in the patient’s last fecal immunochemical test (FIT), as well as the number of prior screening rounds.
“Less is known about what happens after the upper age limit has been reached and individuals are not invited to participate in more screening rounds. This is important as life expectancy is increasing, and it is increasingly important to consider the most efficient way of screening the elderly,” said lead author Brenda van Stigt, a PhD candidate focused on cancer screening at Erasmus University Medical Center in Rotterdam, the Netherlands.
In the Netherlands, adults between ages 55 and 75 are invited to participate in stool-based CRC screening every 2 years. Based on a fecal immunochemical testing (FIT) threshold of 47 μg Hb/g, those who test positive are referred to colonoscopy, and those who test negative are invited to participate again after a 2-year period.
FIT can play a major role in risk stratification, Ms. van Stigt noted, along with other factors that influence CRC risk, such as age, sex, and CRC screening history. Although this is documented for ages 55-75, she and colleagues wanted to know more about what happens after age 75.
Ms. Van Stigt and colleagues conducted a population-based study by analyzing Dutch national cancer registry data and FIT results around the final screening at age 75, looking at those who were diagnosed with CRC within 24 months of their last negative FIT. The researchers assessed interval CRC risk and cancer stage, accounting for sex, last f-Hb concentration, and the number of screening rounds.
Among 305,761 people with a complete 24-month follow-up after a negative FIT, 661 patients were diagnosed with interval CRC, indicating an overall interval CRC risk of 21.6 per 10,000 individuals with a negative FIT. There were no significant differences by sex.
However, there were differences by screening rounds, with those who had participated in three or four screening rounds having a lower risk than those who participated only once (HR, .49).
In addition, those with detectable f-Hb (>0 μg Hb/g) in their last screening round had a much higher interval CRC risk (HR, 4.87), at 65.8 per 10,000 negative FITs, compared with 13.8 per 10,000 among those without detectable f-Hb. Interval CRC risk also increased over time for those with detectable f-Hb.
About 15% of the total population had detectable f-Hb, whereas 46% of those with interval CRC had detectable f-Hb, Ms. van Stigt said, meaning that nearly half of patients who were diagnosed with interval CRC already had detectable f-Hb in their prior FIT.
In a survival analysis, there was no association between interval CRC risk and sex. However, those who participated in three or four screening rounds were half as likely to be diagnosed than those who participated once or twice, and those with detectable f-Hb were five times as likely to be diagnosed.
For late-stage CRC, there was no association with sex or the number of screening rounds. Detectable f-Hb was associated with not only a higher risk of interval CRC but also a late-stage diagnosis.
“These findings indicate that one uniform age to stop screening is suboptimal,” Ms. van Stigt said. “Personalized screening strategies should, therefore, also ideally incorporate a risk-stratified age to stop screening.”
The US Preventive Services Task Force recommends that clinicians personalize screening for ages 76-85, accounting for overall health, prior screening history, and patient preferences.
“But we have no clear guidance on how to quantify or weigh these factors. This interesting study highlights how one of these factors (prior screening history) and fecal hemoglobin level (an emerging factor) are powerful stratifiers of subsequent colorectal cancer risk,” said Sameer D. Saini, MD, AGAF, director and research investigator at the VA Ann Arbor Healthcare System’s Center for Clinical Management Research. Dr. Saini wasn’t involved with the study.
At the clinical level, Dr. Saini said, sophisticated modeling is needed to understand the interaction with competing risks and identify the optimal screening strategies for patients at varying levels of cancer risk and life expectancy. Models could also help to quantify the population benefits and cost-effectiveness of personalized screening.
“Finally, it is important to note that, in many health systems, access to quantitative FIT may be limited,” he said. “These data may be less informative if colonoscopy is the primary mode of screening.”
Ms. van Stigt and Dr. Saini reported no relevant disclosures.
FROM DDW 2024
Women with Autoimmune Liver Diseases Still Face Increased CVD Risks
WASHINGTON – , according to a study presented at the annual Digestive Disease Week® (DDW).
In particular, women with autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) appear to have higher risks than women without AIH or PBC. Those with primary sclerosing cholangitis (PSC) don’t seem to have increased risks.
“We know that cardiovascular disease remains the number one cause of death, but the mortality rate for women over the last decade has plateaued, whereas in men it’s actually declining due to interventions,” said lead author Rachel Redfield, MD, a transplant hepatology fellow at Thomas Jefferson University Hospital in Philadelphia.
“This is likely because we don’t have adequate risk stratification, especially for women,” she said. “We know that immune-mediated diseases — such as rheumatoid arthritis and psoriasis — carry a higher risk of cardiovascular disease, but there’s not a lot of data on our autoimmune liver disease patients.”
Although being a female can offer protection against some CVD risks, the atherosclerotic cardiovascular disease (ASCVD) 10-year risk score calculator recommended by the American College of Cardiology doesn’t include chronic inflammatory diseases associated with increased CVD risk, including AILD.
Dr. Redfield and colleagues conducted a multicenter, retrospective cohort study of patients with AIH, PBC, and PSC from 1999-2019. Using TriNetX data, the researchers looked at women with AILD who also had diabetes mellitus, hypertension, and hyperlipidemia, as well as a control group of men and women with these same disorders, excluding those who used biologics, immune modulators, and steroids or had other autoimmune disorders.
The research team used 1:1 propensity-score matching for women in the study group and in the control group based on age, race, ethnicity, ASCVD risk factors, and tobacco use. Women in the study group and men in the control group were matched for age, race, ethnicity, and tobacco use.
The primary outcome was summative cardiovascular risk, including unstable angina, acute myocardial infarction, presence of coronary angioplasty implant, coronary artery bypass, percutaneous coronary intervention, and cerebral infarction.
Overall, women with AIH had a significantly higher cardiovascular risk compared to women without AIH, at 25.4% versus 20.6% (P = .0007).
Specifically, women with PBC had a significantly higher cardiovascular risk compared to women without PBC, at 27.05% versus 20.9% (P < .0001).
There wasn’t a significant difference in risk between women with and without PSC, at 27.5% versus 21.8% (P = .27).
When compared to men without disease, women with AIH didn’t have a statistically significant higher risk, at 25.3% versus 24.2% (P = .44). Similarly, there didn’t appear to be a significant difference between women with PBC and men without PBC, at 26.9% versus 25.9% (P = .52), or between women with PSC and men without PSC, at 27.7% versus 26.2% (P = .78).
Dr. Redfield and colleagues then compared the ASCVD-calculated risk versus database risk, finding that in each group of women with AILD — including AIH, PBC, and PSC — the ASCVD-calculated risk was around 11%, compared with database risk scores of 25% for AIH, 27% for PBC, and 28% for PSC. These database risks appeared similar to both the ASCVD and database risk percentages for men.
“So potentially there’s an oversight in women with any kind of inflammatory disease, but specifically here, autoimmune liver diseases,” she said. “We really need to enhance our risk assessment strategies to take into account their risk and optimize patient outcomes.”
Dr. Redfield noted the limitations with using TriNetX data, including coding consistency among providers and healthcare organizations, unknown patient follow-up dates, and the inability to capture various inflammatory disease phenotypes, such as autoimmune hepatitis with multiple flares, which may be associated with higher cardiovascular risks.
As an attendee of the DDW session, Kenneth Kelson, MD, a gastroenterologist with Fremont Medical Group and Washington Hospital Healthcare System in Fremont, California, noted the importance of investigating the effects of different types of statins in these patients. Although the research team looked at top-level differences among statin users, finding that women with AILD were more likely to be on a statin, they didn’t incorporate statin therapy in the propensity-score matching model.
“Lipid-soluble statins are known to cause more liver trouble, even though it’s pretty low,” Dr. Kelson said. “Whereas the water-soluble statins have a lower incidence of liver issues.”
Dr. Redfield and Dr. Kelson reported no relevant disclosures.
WASHINGTON – , according to a study presented at the annual Digestive Disease Week® (DDW).
In particular, women with autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) appear to have higher risks than women without AIH or PBC. Those with primary sclerosing cholangitis (PSC) don’t seem to have increased risks.
“We know that cardiovascular disease remains the number one cause of death, but the mortality rate for women over the last decade has plateaued, whereas in men it’s actually declining due to interventions,” said lead author Rachel Redfield, MD, a transplant hepatology fellow at Thomas Jefferson University Hospital in Philadelphia.
“This is likely because we don’t have adequate risk stratification, especially for women,” she said. “We know that immune-mediated diseases — such as rheumatoid arthritis and psoriasis — carry a higher risk of cardiovascular disease, but there’s not a lot of data on our autoimmune liver disease patients.”
Although being a female can offer protection against some CVD risks, the atherosclerotic cardiovascular disease (ASCVD) 10-year risk score calculator recommended by the American College of Cardiology doesn’t include chronic inflammatory diseases associated with increased CVD risk, including AILD.
Dr. Redfield and colleagues conducted a multicenter, retrospective cohort study of patients with AIH, PBC, and PSC from 1999-2019. Using TriNetX data, the researchers looked at women with AILD who also had diabetes mellitus, hypertension, and hyperlipidemia, as well as a control group of men and women with these same disorders, excluding those who used biologics, immune modulators, and steroids or had other autoimmune disorders.
The research team used 1:1 propensity-score matching for women in the study group and in the control group based on age, race, ethnicity, ASCVD risk factors, and tobacco use. Women in the study group and men in the control group were matched for age, race, ethnicity, and tobacco use.
The primary outcome was summative cardiovascular risk, including unstable angina, acute myocardial infarction, presence of coronary angioplasty implant, coronary artery bypass, percutaneous coronary intervention, and cerebral infarction.
Overall, women with AIH had a significantly higher cardiovascular risk compared to women without AIH, at 25.4% versus 20.6% (P = .0007).
Specifically, women with PBC had a significantly higher cardiovascular risk compared to women without PBC, at 27.05% versus 20.9% (P < .0001).
There wasn’t a significant difference in risk between women with and without PSC, at 27.5% versus 21.8% (P = .27).
When compared to men without disease, women with AIH didn’t have a statistically significant higher risk, at 25.3% versus 24.2% (P = .44). Similarly, there didn’t appear to be a significant difference between women with PBC and men without PBC, at 26.9% versus 25.9% (P = .52), or between women with PSC and men without PSC, at 27.7% versus 26.2% (P = .78).
Dr. Redfield and colleagues then compared the ASCVD-calculated risk versus database risk, finding that in each group of women with AILD — including AIH, PBC, and PSC — the ASCVD-calculated risk was around 11%, compared with database risk scores of 25% for AIH, 27% for PBC, and 28% for PSC. These database risks appeared similar to both the ASCVD and database risk percentages for men.
“So potentially there’s an oversight in women with any kind of inflammatory disease, but specifically here, autoimmune liver diseases,” she said. “We really need to enhance our risk assessment strategies to take into account their risk and optimize patient outcomes.”
Dr. Redfield noted the limitations with using TriNetX data, including coding consistency among providers and healthcare organizations, unknown patient follow-up dates, and the inability to capture various inflammatory disease phenotypes, such as autoimmune hepatitis with multiple flares, which may be associated with higher cardiovascular risks.
As an attendee of the DDW session, Kenneth Kelson, MD, a gastroenterologist with Fremont Medical Group and Washington Hospital Healthcare System in Fremont, California, noted the importance of investigating the effects of different types of statins in these patients. Although the research team looked at top-level differences among statin users, finding that women with AILD were more likely to be on a statin, they didn’t incorporate statin therapy in the propensity-score matching model.
“Lipid-soluble statins are known to cause more liver trouble, even though it’s pretty low,” Dr. Kelson said. “Whereas the water-soluble statins have a lower incidence of liver issues.”
Dr. Redfield and Dr. Kelson reported no relevant disclosures.
WASHINGTON – , according to a study presented at the annual Digestive Disease Week® (DDW).
In particular, women with autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) appear to have higher risks than women without AIH or PBC. Those with primary sclerosing cholangitis (PSC) don’t seem to have increased risks.
“We know that cardiovascular disease remains the number one cause of death, but the mortality rate for women over the last decade has plateaued, whereas in men it’s actually declining due to interventions,” said lead author Rachel Redfield, MD, a transplant hepatology fellow at Thomas Jefferson University Hospital in Philadelphia.
“This is likely because we don’t have adequate risk stratification, especially for women,” she said. “We know that immune-mediated diseases — such as rheumatoid arthritis and psoriasis — carry a higher risk of cardiovascular disease, but there’s not a lot of data on our autoimmune liver disease patients.”
Although being a female can offer protection against some CVD risks, the atherosclerotic cardiovascular disease (ASCVD) 10-year risk score calculator recommended by the American College of Cardiology doesn’t include chronic inflammatory diseases associated with increased CVD risk, including AILD.
Dr. Redfield and colleagues conducted a multicenter, retrospective cohort study of patients with AIH, PBC, and PSC from 1999-2019. Using TriNetX data, the researchers looked at women with AILD who also had diabetes mellitus, hypertension, and hyperlipidemia, as well as a control group of men and women with these same disorders, excluding those who used biologics, immune modulators, and steroids or had other autoimmune disorders.
The research team used 1:1 propensity-score matching for women in the study group and in the control group based on age, race, ethnicity, ASCVD risk factors, and tobacco use. Women in the study group and men in the control group were matched for age, race, ethnicity, and tobacco use.
The primary outcome was summative cardiovascular risk, including unstable angina, acute myocardial infarction, presence of coronary angioplasty implant, coronary artery bypass, percutaneous coronary intervention, and cerebral infarction.
Overall, women with AIH had a significantly higher cardiovascular risk compared to women without AIH, at 25.4% versus 20.6% (P = .0007).
Specifically, women with PBC had a significantly higher cardiovascular risk compared to women without PBC, at 27.05% versus 20.9% (P < .0001).
There wasn’t a significant difference in risk between women with and without PSC, at 27.5% versus 21.8% (P = .27).
When compared to men without disease, women with AIH didn’t have a statistically significant higher risk, at 25.3% versus 24.2% (P = .44). Similarly, there didn’t appear to be a significant difference between women with PBC and men without PBC, at 26.9% versus 25.9% (P = .52), or between women with PSC and men without PSC, at 27.7% versus 26.2% (P = .78).
Dr. Redfield and colleagues then compared the ASCVD-calculated risk versus database risk, finding that in each group of women with AILD — including AIH, PBC, and PSC — the ASCVD-calculated risk was around 11%, compared with database risk scores of 25% for AIH, 27% for PBC, and 28% for PSC. These database risks appeared similar to both the ASCVD and database risk percentages for men.
“So potentially there’s an oversight in women with any kind of inflammatory disease, but specifically here, autoimmune liver diseases,” she said. “We really need to enhance our risk assessment strategies to take into account their risk and optimize patient outcomes.”
Dr. Redfield noted the limitations with using TriNetX data, including coding consistency among providers and healthcare organizations, unknown patient follow-up dates, and the inability to capture various inflammatory disease phenotypes, such as autoimmune hepatitis with multiple flares, which may be associated with higher cardiovascular risks.
As an attendee of the DDW session, Kenneth Kelson, MD, a gastroenterologist with Fremont Medical Group and Washington Hospital Healthcare System in Fremont, California, noted the importance of investigating the effects of different types of statins in these patients. Although the research team looked at top-level differences among statin users, finding that women with AILD were more likely to be on a statin, they didn’t incorporate statin therapy in the propensity-score matching model.
“Lipid-soluble statins are known to cause more liver trouble, even though it’s pretty low,” Dr. Kelson said. “Whereas the water-soluble statins have a lower incidence of liver issues.”
Dr. Redfield and Dr. Kelson reported no relevant disclosures.
FROM DDW 2024
Emerging Evidence Supports Dietary Management of MASLD Through Gut-Liver Axis
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
For instance, patients with MASLD had lower intake of fiber and omega-3 fatty acids but higher consumption of added sugars and ultraprocessed foods, which correlated with the associated bacterial species and functional pathways.
“MASLD is an escalating concern globally, which highlights the need for innovative targets for disease prevention and management,” said lead author Georgina Williams, PhD, a postdoctoral researcher in diet and gastroenterology at the University of Newcastle, Australia.
“Therapeutic options often rely on lifestyle modifications, with a focus on weight loss,” she said. “Diet is considered a key component of disease management.”
Although calorie restriction with a 3%-5% fat loss is associated with hepatic benefits in MASLD, Dr. Williams noted, researchers have considered whole dietary patterns and the best fit for patients. Aspects of the Mediterranean diet may be effective, as reflected in recommendations from the American Association for the Study of Liver Disease (AASLD), which highlight dietary components such as limited carbohydrates and saturated fat, along with high fiber and unsaturated fats. The gut microbiome may be essential to consider as well, she said, given MASLD-associated differences in bile acid metabolism, inflammation, and ethanol production.
Dr. Williams and colleagues conducted a retrospective case-control study in an outpatient liver clinic to understand diet and dysbiosis in MASLD, looking at differences in diet, gut microbiota composition, and functional pathways in those with and without MASLD. The researchers investigated daily average intake, serum, and stool samples among 50 people (25 per group) matched for age and gender, comparing fibrosis-4, MASLD severity scores, macronutrients, micronutrients, food groups, metagenomic sequencing, and inflammatory markers such as interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, cytokeratin (CK)-18, and high-sensitivity C-reactive protein (hsCRP).
Dietary Characteristics
At baseline, the groups differed by ethnicity, prescription medication use, and body mass index (BMI), where the MASLD group had greater ethnic diversity, medication use, and BMI. In addition, the MASLD group had a zero to mild score of fibrosis.
Overall, energy intake didn’t differ significantly between the two groups. The control group had higher alcohol intake, likely since the MASLD group was recommended to reduce alcohol intake, though the difference was about 5 grams per day. The MASLD group also had less caffeine intake than the control group, as well as slightly lower protein intake, though the differences weren’t statistically significant.
While consumption of total carbohydrates didn’t differ significantly between the groups, participants with MASLD consumed more calories from carbohydrates than did the controls. The MASLD group consumed more calories from added and free sugars and didn’t meet recommendations for dietary fiber.
With particular food groups, participants with MASLD ate significantly fewer whole grains, red and orange fruits, and leafy green vegetables. When consuming fruit, those with MASLD were more likely to drink juice than eat whole fruit. These findings could be relevant when considering high sugar intake and low dietary fiber, Dr. Williams said.
With dietary fat, there were no differences in total fat between the groups, but the fat profiles differed. The control group was significantly more likely to consume omega-3 fatty acids, including alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). The MASLD group was less likely to consume seafood, nuts, seeds, avocado, and olive oil.
With inflammatory markers, hsCRP and CK-18 were increased in MASLD, while IL-1ß was increased in controls, which was consistently associated with higher alcohol intake among the control group. IL-6 and TNF-α didn’t differ between the groups.
Notably, dietary fats were most consistently associated with inflammatory markers, Dr. Williams said, with inflammation being positively associated with saturated fats and negatively associated with unsaturated fats.
Looking at microbiota, the alpha diversity was no different, but the beta diversity was across 162 taxa. Per bacterial species, there was an inverse relationship between MASLD and associations with unsaturated fat, as well as positive indicators of high sugar and fructose intake and low unsaturated fat and dietary fiber intake.
Beyond that, the functional pathways enriched in MASLD were associated with increased sugar and carbohydrates, reduced fiber, and reduced unsaturated fat. Lower butyrate production in MASLD was associated with low intake of nuts, seeds, and unsaturated fat.
In Clinical Practice
Dr. Williams suggested reinforcing AASLD guidelines and looking at diet quality, not just diet quantity. Although an energy deficit remains relevant in MASLD, macronutrient consumption matters across dietary fats, fibers, and sugars.
Future avenues for research include metabolomic pathways related to bile acids and fatty acids, she said, as well as disentangling metabolic syndrome from MASLD outcomes.
Session moderator Olivier Barbier, PhD, professor of pharmacy at Laval University in Quebec, Canada, asked about microbiome differences across countries. Dr. Williams noted the limitations in this study of looking at differences across geography and ethnicity, particularly in Australia, but said the species identified were consistent with those found in most literature globally.
In response to other questions after the presentation, Dr. Williams said supplements (such as omega-3 fatty acids) were included in total intake, and those taking prebiotics or probiotics were excluded from the study. In an upcoming clinical trial, she and colleagues plan to control for household microbiomes as well.
“The premise is that microbiomes are shared between households, so when you’re doing these sorts of large-scale clinical studies, if you’re going to look at the microbiome, then you should control for one of the major confounding variables,” said Mark Sundrud, PhD, professor of medicine at the Dartmouth Center for Digestive Health in Lebanon, New Hampshire. Dr. Sundrud, who wasn’t involved with this study, presented on the role of bile acids in mucosal immune cell function at DDW.
“We’ve done a collaborative study looking at microbiomes and bile acids in inflammatory bowel disease (IBD) patients versus controls,” which included consideration of households, he said. “We were able to see more intrinsic disease-specific changes.”
Dr. Williams declared no relevant disclosures. Dr. Sundrud has served as a scientific adviser to Sage Therapeutics.
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
For instance, patients with MASLD had lower intake of fiber and omega-3 fatty acids but higher consumption of added sugars and ultraprocessed foods, which correlated with the associated bacterial species and functional pathways.
“MASLD is an escalating concern globally, which highlights the need for innovative targets for disease prevention and management,” said lead author Georgina Williams, PhD, a postdoctoral researcher in diet and gastroenterology at the University of Newcastle, Australia.
“Therapeutic options often rely on lifestyle modifications, with a focus on weight loss,” she said. “Diet is considered a key component of disease management.”
Although calorie restriction with a 3%-5% fat loss is associated with hepatic benefits in MASLD, Dr. Williams noted, researchers have considered whole dietary patterns and the best fit for patients. Aspects of the Mediterranean diet may be effective, as reflected in recommendations from the American Association for the Study of Liver Disease (AASLD), which highlight dietary components such as limited carbohydrates and saturated fat, along with high fiber and unsaturated fats. The gut microbiome may be essential to consider as well, she said, given MASLD-associated differences in bile acid metabolism, inflammation, and ethanol production.
Dr. Williams and colleagues conducted a retrospective case-control study in an outpatient liver clinic to understand diet and dysbiosis in MASLD, looking at differences in diet, gut microbiota composition, and functional pathways in those with and without MASLD. The researchers investigated daily average intake, serum, and stool samples among 50 people (25 per group) matched for age and gender, comparing fibrosis-4, MASLD severity scores, macronutrients, micronutrients, food groups, metagenomic sequencing, and inflammatory markers such as interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, cytokeratin (CK)-18, and high-sensitivity C-reactive protein (hsCRP).
Dietary Characteristics
At baseline, the groups differed by ethnicity, prescription medication use, and body mass index (BMI), where the MASLD group had greater ethnic diversity, medication use, and BMI. In addition, the MASLD group had a zero to mild score of fibrosis.
Overall, energy intake didn’t differ significantly between the two groups. The control group had higher alcohol intake, likely since the MASLD group was recommended to reduce alcohol intake, though the difference was about 5 grams per day. The MASLD group also had less caffeine intake than the control group, as well as slightly lower protein intake, though the differences weren’t statistically significant.
While consumption of total carbohydrates didn’t differ significantly between the groups, participants with MASLD consumed more calories from carbohydrates than did the controls. The MASLD group consumed more calories from added and free sugars and didn’t meet recommendations for dietary fiber.
With particular food groups, participants with MASLD ate significantly fewer whole grains, red and orange fruits, and leafy green vegetables. When consuming fruit, those with MASLD were more likely to drink juice than eat whole fruit. These findings could be relevant when considering high sugar intake and low dietary fiber, Dr. Williams said.
With dietary fat, there were no differences in total fat between the groups, but the fat profiles differed. The control group was significantly more likely to consume omega-3 fatty acids, including alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). The MASLD group was less likely to consume seafood, nuts, seeds, avocado, and olive oil.
With inflammatory markers, hsCRP and CK-18 were increased in MASLD, while IL-1ß was increased in controls, which was consistently associated with higher alcohol intake among the control group. IL-6 and TNF-α didn’t differ between the groups.
Notably, dietary fats were most consistently associated with inflammatory markers, Dr. Williams said, with inflammation being positively associated with saturated fats and negatively associated with unsaturated fats.
Looking at microbiota, the alpha diversity was no different, but the beta diversity was across 162 taxa. Per bacterial species, there was an inverse relationship between MASLD and associations with unsaturated fat, as well as positive indicators of high sugar and fructose intake and low unsaturated fat and dietary fiber intake.
Beyond that, the functional pathways enriched in MASLD were associated with increased sugar and carbohydrates, reduced fiber, and reduced unsaturated fat. Lower butyrate production in MASLD was associated with low intake of nuts, seeds, and unsaturated fat.
In Clinical Practice
Dr. Williams suggested reinforcing AASLD guidelines and looking at diet quality, not just diet quantity. Although an energy deficit remains relevant in MASLD, macronutrient consumption matters across dietary fats, fibers, and sugars.
Future avenues for research include metabolomic pathways related to bile acids and fatty acids, she said, as well as disentangling metabolic syndrome from MASLD outcomes.
Session moderator Olivier Barbier, PhD, professor of pharmacy at Laval University in Quebec, Canada, asked about microbiome differences across countries. Dr. Williams noted the limitations in this study of looking at differences across geography and ethnicity, particularly in Australia, but said the species identified were consistent with those found in most literature globally.
In response to other questions after the presentation, Dr. Williams said supplements (such as omega-3 fatty acids) were included in total intake, and those taking prebiotics or probiotics were excluded from the study. In an upcoming clinical trial, she and colleagues plan to control for household microbiomes as well.
“The premise is that microbiomes are shared between households, so when you’re doing these sorts of large-scale clinical studies, if you’re going to look at the microbiome, then you should control for one of the major confounding variables,” said Mark Sundrud, PhD, professor of medicine at the Dartmouth Center for Digestive Health in Lebanon, New Hampshire. Dr. Sundrud, who wasn’t involved with this study, presented on the role of bile acids in mucosal immune cell function at DDW.
“We’ve done a collaborative study looking at microbiomes and bile acids in inflammatory bowel disease (IBD) patients versus controls,” which included consideration of households, he said. “We were able to see more intrinsic disease-specific changes.”
Dr. Williams declared no relevant disclosures. Dr. Sundrud has served as a scientific adviser to Sage Therapeutics.
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
For instance, patients with MASLD had lower intake of fiber and omega-3 fatty acids but higher consumption of added sugars and ultraprocessed foods, which correlated with the associated bacterial species and functional pathways.
“MASLD is an escalating concern globally, which highlights the need for innovative targets for disease prevention and management,” said lead author Georgina Williams, PhD, a postdoctoral researcher in diet and gastroenterology at the University of Newcastle, Australia.
“Therapeutic options often rely on lifestyle modifications, with a focus on weight loss,” she said. “Diet is considered a key component of disease management.”
Although calorie restriction with a 3%-5% fat loss is associated with hepatic benefits in MASLD, Dr. Williams noted, researchers have considered whole dietary patterns and the best fit for patients. Aspects of the Mediterranean diet may be effective, as reflected in recommendations from the American Association for the Study of Liver Disease (AASLD), which highlight dietary components such as limited carbohydrates and saturated fat, along with high fiber and unsaturated fats. The gut microbiome may be essential to consider as well, she said, given MASLD-associated differences in bile acid metabolism, inflammation, and ethanol production.
Dr. Williams and colleagues conducted a retrospective case-control study in an outpatient liver clinic to understand diet and dysbiosis in MASLD, looking at differences in diet, gut microbiota composition, and functional pathways in those with and without MASLD. The researchers investigated daily average intake, serum, and stool samples among 50 people (25 per group) matched for age and gender, comparing fibrosis-4, MASLD severity scores, macronutrients, micronutrients, food groups, metagenomic sequencing, and inflammatory markers such as interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, cytokeratin (CK)-18, and high-sensitivity C-reactive protein (hsCRP).
Dietary Characteristics
At baseline, the groups differed by ethnicity, prescription medication use, and body mass index (BMI), where the MASLD group had greater ethnic diversity, medication use, and BMI. In addition, the MASLD group had a zero to mild score of fibrosis.
Overall, energy intake didn’t differ significantly between the two groups. The control group had higher alcohol intake, likely since the MASLD group was recommended to reduce alcohol intake, though the difference was about 5 grams per day. The MASLD group also had less caffeine intake than the control group, as well as slightly lower protein intake, though the differences weren’t statistically significant.
While consumption of total carbohydrates didn’t differ significantly between the groups, participants with MASLD consumed more calories from carbohydrates than did the controls. The MASLD group consumed more calories from added and free sugars and didn’t meet recommendations for dietary fiber.
With particular food groups, participants with MASLD ate significantly fewer whole grains, red and orange fruits, and leafy green vegetables. When consuming fruit, those with MASLD were more likely to drink juice than eat whole fruit. These findings could be relevant when considering high sugar intake and low dietary fiber, Dr. Williams said.
With dietary fat, there were no differences in total fat between the groups, but the fat profiles differed. The control group was significantly more likely to consume omega-3 fatty acids, including alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). The MASLD group was less likely to consume seafood, nuts, seeds, avocado, and olive oil.
With inflammatory markers, hsCRP and CK-18 were increased in MASLD, while IL-1ß was increased in controls, which was consistently associated with higher alcohol intake among the control group. IL-6 and TNF-α didn’t differ between the groups.
Notably, dietary fats were most consistently associated with inflammatory markers, Dr. Williams said, with inflammation being positively associated with saturated fats and negatively associated with unsaturated fats.
Looking at microbiota, the alpha diversity was no different, but the beta diversity was across 162 taxa. Per bacterial species, there was an inverse relationship between MASLD and associations with unsaturated fat, as well as positive indicators of high sugar and fructose intake and low unsaturated fat and dietary fiber intake.
Beyond that, the functional pathways enriched in MASLD were associated with increased sugar and carbohydrates, reduced fiber, and reduced unsaturated fat. Lower butyrate production in MASLD was associated with low intake of nuts, seeds, and unsaturated fat.
In Clinical Practice
Dr. Williams suggested reinforcing AASLD guidelines and looking at diet quality, not just diet quantity. Although an energy deficit remains relevant in MASLD, macronutrient consumption matters across dietary fats, fibers, and sugars.
Future avenues for research include metabolomic pathways related to bile acids and fatty acids, she said, as well as disentangling metabolic syndrome from MASLD outcomes.
Session moderator Olivier Barbier, PhD, professor of pharmacy at Laval University in Quebec, Canada, asked about microbiome differences across countries. Dr. Williams noted the limitations in this study of looking at differences across geography and ethnicity, particularly in Australia, but said the species identified were consistent with those found in most literature globally.
In response to other questions after the presentation, Dr. Williams said supplements (such as omega-3 fatty acids) were included in total intake, and those taking prebiotics or probiotics were excluded from the study. In an upcoming clinical trial, she and colleagues plan to control for household microbiomes as well.
“The premise is that microbiomes are shared between households, so when you’re doing these sorts of large-scale clinical studies, if you’re going to look at the microbiome, then you should control for one of the major confounding variables,” said Mark Sundrud, PhD, professor of medicine at the Dartmouth Center for Digestive Health in Lebanon, New Hampshire. Dr. Sundrud, who wasn’t involved with this study, presented on the role of bile acids in mucosal immune cell function at DDW.
“We’ve done a collaborative study looking at microbiomes and bile acids in inflammatory bowel disease (IBD) patients versus controls,” which included consideration of households, he said. “We were able to see more intrinsic disease-specific changes.”
Dr. Williams declared no relevant disclosures. Dr. Sundrud has served as a scientific adviser to Sage Therapeutics.
FROM DDW 2024
Colorectal Cancer Is Spiking Among Some Young Americans
WASHINGTON — Despite encouraging drops in overall colorectal cancer rates in the past two decades, one group stands out as an exception: Americans younger than 45.
, according to new research presented at the annual Digestive Disease Week®.
As high as those percentages appear, the number of people affected at these ages remains small compared with rates in Americans 45 and older, said Loren Laine, MD, AGAF, professor of medicine (digestive diseases) at Yale School of Medicine, who co-moderated a news briefing discussing the research.
“The trends are alarming [but] the actual numbers of colorectal cancer cases among children and teens are not high enough to suggest widespread screening,” agreed lead investigator Islam Mohamed, MD, an internal medicine resident at the University of Missouri-Kansas City.
For example, 1 out of every 333,000 15- to-19-year-olds developed colorectal cancer in 1999. Colorectal cancer became more common by 2020, when 1 out of every 77,000 teens developed it.
At the same time, the number of cases in young adults 20 to 24 increased from less than 1 to 2 per 100,000 in 2020.
Even if the risk is relatively low in terms of absolute numbers, experts are keeping an eye on why the rates are increasing. It’s also about raising awareness. If someone younger than 45 experiences colorectal cancer symptoms like blood in their stool, stomach pain, changes in bowel habits, or others, they should seek medical attention, Dr. Laine said.
“If you have symptoms like rectal bleeding, you shouldn’t take it lightly. It’s still pretty unlikely that they’re going to have colon cancer ... but obviously you should still not totally dismiss it,” Dr. Laine said.
“Colorectal cancer is no longer considered just a disease of the elderly population,” Dr. Mohamed said during the briefing. “It’s important that the public is aware of signs and symptoms of colorectal cancer.”
Dr. Mohamed and colleagues studied colorectal cancer cases using numbers from the CDC Wonder Database, a central database of public health information. They calculated increases by comparing rates in 1999 to 2020.
Colorectal cancer is a major cause of cancer-related death in the United States. It currently ranks third in terms of new cases and cancer-related deaths once some skin cancers are excluded, American Cancer Society data indicates.
Some Risk Factors Can Be Changed
The colorectal cancer rates in younger people “have been consistently rising. It might be related to the environmental factors, lifestyle factors, and genetic factors as well,” Dr. Mohamed said. “It also might mean that we are doing better. Maybe we’re screening patients more, and maybe we’re doing a greater job of picking patients who are at high risk of colorectal cancer in the younger population.”
“Adopting a healthy lifestyle would be a great approach to curb the rising incidence of colorectal cancer as we saw metabolic syndrome is a big [factor],” Dr. Mohamed added. Patients should be encouraged to maintain a balanced diet, engage in regular physical activity, and maybe limit alcohol consumption, he said.
On the other hand, up to one third of early-onset colorectal cancer cases are linked to factors that cannot be changed. A family history of colorectal cancer, presence of inflammatory bowel disease, and certain types of cancers linked to genetic mutations are examples. “When you think about it, most of those young people [with colorectal cancer] probably have genetic syndromes,” Dr. Laine said. “The big issue is, frankly, finding better ways to identify families that have genetic syndromes. That’s probably the biggest message.”
Risk Varied by Age
In addition to the increases in the 15- to 19-year-old and 20- to 24-year-old groups, the rates in 2020 compared with 1999 showed a
- 68% increase for ages 25 to 29.
- 71% increase for ages 30 to 34.
- 58% increase for ages 35 to 39.
- 45% increase for ages 40 to 44.
“These findings all emphasize the urgent needs for public awareness and personalized screening approaches,” Dr. Mohamed said, “particularly among younger populations who had the most substantial increase in colorectal cancer incidence we observed.”
The US Preventive Services Task Force lowered the recommended age for colorectal cancer screening from 50 to 45 in 2021. Dr. Mohamed suggested more targeted screening for people under 45 at higher risk.
“I think also staying informed about the rising incidence and the latest research and recommendations in terms of colorectal cancer prevention and screening will be really, really helpful.”
A version of this article appeared on WebMD Health News.
WASHINGTON — Despite encouraging drops in overall colorectal cancer rates in the past two decades, one group stands out as an exception: Americans younger than 45.
, according to new research presented at the annual Digestive Disease Week®.
As high as those percentages appear, the number of people affected at these ages remains small compared with rates in Americans 45 and older, said Loren Laine, MD, AGAF, professor of medicine (digestive diseases) at Yale School of Medicine, who co-moderated a news briefing discussing the research.
“The trends are alarming [but] the actual numbers of colorectal cancer cases among children and teens are not high enough to suggest widespread screening,” agreed lead investigator Islam Mohamed, MD, an internal medicine resident at the University of Missouri-Kansas City.
For example, 1 out of every 333,000 15- to-19-year-olds developed colorectal cancer in 1999. Colorectal cancer became more common by 2020, when 1 out of every 77,000 teens developed it.
At the same time, the number of cases in young adults 20 to 24 increased from less than 1 to 2 per 100,000 in 2020.
Even if the risk is relatively low in terms of absolute numbers, experts are keeping an eye on why the rates are increasing. It’s also about raising awareness. If someone younger than 45 experiences colorectal cancer symptoms like blood in their stool, stomach pain, changes in bowel habits, or others, they should seek medical attention, Dr. Laine said.
“If you have symptoms like rectal bleeding, you shouldn’t take it lightly. It’s still pretty unlikely that they’re going to have colon cancer ... but obviously you should still not totally dismiss it,” Dr. Laine said.
“Colorectal cancer is no longer considered just a disease of the elderly population,” Dr. Mohamed said during the briefing. “It’s important that the public is aware of signs and symptoms of colorectal cancer.”
Dr. Mohamed and colleagues studied colorectal cancer cases using numbers from the CDC Wonder Database, a central database of public health information. They calculated increases by comparing rates in 1999 to 2020.
Colorectal cancer is a major cause of cancer-related death in the United States. It currently ranks third in terms of new cases and cancer-related deaths once some skin cancers are excluded, American Cancer Society data indicates.
Some Risk Factors Can Be Changed
The colorectal cancer rates in younger people “have been consistently rising. It might be related to the environmental factors, lifestyle factors, and genetic factors as well,” Dr. Mohamed said. “It also might mean that we are doing better. Maybe we’re screening patients more, and maybe we’re doing a greater job of picking patients who are at high risk of colorectal cancer in the younger population.”
“Adopting a healthy lifestyle would be a great approach to curb the rising incidence of colorectal cancer as we saw metabolic syndrome is a big [factor],” Dr. Mohamed added. Patients should be encouraged to maintain a balanced diet, engage in regular physical activity, and maybe limit alcohol consumption, he said.
On the other hand, up to one third of early-onset colorectal cancer cases are linked to factors that cannot be changed. A family history of colorectal cancer, presence of inflammatory bowel disease, and certain types of cancers linked to genetic mutations are examples. “When you think about it, most of those young people [with colorectal cancer] probably have genetic syndromes,” Dr. Laine said. “The big issue is, frankly, finding better ways to identify families that have genetic syndromes. That’s probably the biggest message.”
Risk Varied by Age
In addition to the increases in the 15- to 19-year-old and 20- to 24-year-old groups, the rates in 2020 compared with 1999 showed a
- 68% increase for ages 25 to 29.
- 71% increase for ages 30 to 34.
- 58% increase for ages 35 to 39.
- 45% increase for ages 40 to 44.
“These findings all emphasize the urgent needs for public awareness and personalized screening approaches,” Dr. Mohamed said, “particularly among younger populations who had the most substantial increase in colorectal cancer incidence we observed.”
The US Preventive Services Task Force lowered the recommended age for colorectal cancer screening from 50 to 45 in 2021. Dr. Mohamed suggested more targeted screening for people under 45 at higher risk.
“I think also staying informed about the rising incidence and the latest research and recommendations in terms of colorectal cancer prevention and screening will be really, really helpful.”
A version of this article appeared on WebMD Health News.
WASHINGTON — Despite encouraging drops in overall colorectal cancer rates in the past two decades, one group stands out as an exception: Americans younger than 45.
, according to new research presented at the annual Digestive Disease Week®.
As high as those percentages appear, the number of people affected at these ages remains small compared with rates in Americans 45 and older, said Loren Laine, MD, AGAF, professor of medicine (digestive diseases) at Yale School of Medicine, who co-moderated a news briefing discussing the research.
“The trends are alarming [but] the actual numbers of colorectal cancer cases among children and teens are not high enough to suggest widespread screening,” agreed lead investigator Islam Mohamed, MD, an internal medicine resident at the University of Missouri-Kansas City.
For example, 1 out of every 333,000 15- to-19-year-olds developed colorectal cancer in 1999. Colorectal cancer became more common by 2020, when 1 out of every 77,000 teens developed it.
At the same time, the number of cases in young adults 20 to 24 increased from less than 1 to 2 per 100,000 in 2020.
Even if the risk is relatively low in terms of absolute numbers, experts are keeping an eye on why the rates are increasing. It’s also about raising awareness. If someone younger than 45 experiences colorectal cancer symptoms like blood in their stool, stomach pain, changes in bowel habits, or others, they should seek medical attention, Dr. Laine said.
“If you have symptoms like rectal bleeding, you shouldn’t take it lightly. It’s still pretty unlikely that they’re going to have colon cancer ... but obviously you should still not totally dismiss it,” Dr. Laine said.
“Colorectal cancer is no longer considered just a disease of the elderly population,” Dr. Mohamed said during the briefing. “It’s important that the public is aware of signs and symptoms of colorectal cancer.”
Dr. Mohamed and colleagues studied colorectal cancer cases using numbers from the CDC Wonder Database, a central database of public health information. They calculated increases by comparing rates in 1999 to 2020.
Colorectal cancer is a major cause of cancer-related death in the United States. It currently ranks third in terms of new cases and cancer-related deaths once some skin cancers are excluded, American Cancer Society data indicates.
Some Risk Factors Can Be Changed
The colorectal cancer rates in younger people “have been consistently rising. It might be related to the environmental factors, lifestyle factors, and genetic factors as well,” Dr. Mohamed said. “It also might mean that we are doing better. Maybe we’re screening patients more, and maybe we’re doing a greater job of picking patients who are at high risk of colorectal cancer in the younger population.”
“Adopting a healthy lifestyle would be a great approach to curb the rising incidence of colorectal cancer as we saw metabolic syndrome is a big [factor],” Dr. Mohamed added. Patients should be encouraged to maintain a balanced diet, engage in regular physical activity, and maybe limit alcohol consumption, he said.
On the other hand, up to one third of early-onset colorectal cancer cases are linked to factors that cannot be changed. A family history of colorectal cancer, presence of inflammatory bowel disease, and certain types of cancers linked to genetic mutations are examples. “When you think about it, most of those young people [with colorectal cancer] probably have genetic syndromes,” Dr. Laine said. “The big issue is, frankly, finding better ways to identify families that have genetic syndromes. That’s probably the biggest message.”
Risk Varied by Age
In addition to the increases in the 15- to 19-year-old and 20- to 24-year-old groups, the rates in 2020 compared with 1999 showed a
- 68% increase for ages 25 to 29.
- 71% increase for ages 30 to 34.
- 58% increase for ages 35 to 39.
- 45% increase for ages 40 to 44.
“These findings all emphasize the urgent needs for public awareness and personalized screening approaches,” Dr. Mohamed said, “particularly among younger populations who had the most substantial increase in colorectal cancer incidence we observed.”
The US Preventive Services Task Force lowered the recommended age for colorectal cancer screening from 50 to 45 in 2021. Dr. Mohamed suggested more targeted screening for people under 45 at higher risk.
“I think also staying informed about the rising incidence and the latest research and recommendations in terms of colorectal cancer prevention and screening will be really, really helpful.”
A version of this article appeared on WebMD Health News.
FROM DDW 2024
Mailed Outreach for CRC Screening Appeals Across Races and Ethnicities
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
In a comparison of four outreach approaches, sending a FIT kit to people between the ages of 45 and 49 via mail garnered better response rates than opt-in strategies to participate in FIT, inviting them to undergo colonoscopy, or asking them to choose between FIT or colonoscopy. At the same time, when given a choice between colonoscopy and FIT, colonoscopy was preferred across all racial and ethnic groups.
“It is well known that colorectal cancer is the second-leading cause of cancer-related deaths in the United States. The good news is that for the past several decades, we’ve seen a decline in colorectal cancer incidence and mortality in ages 50 and above. However, there has been a recent rise in incidence and mortality in people younger than 50,” said lead author Rebecca Ekeanyanwu, a third-year medical student at Meharry Medical College School of Medicine in Nashville, Tennessee. She was awarded the 2024 AGA Institute Council Healthcare Disparities Research Award for the top oral presentation for research in racial and ethnic health care disparities.
CRC incidence, screening rates, and mortality also vary by race and ethnicity, with higher incidence and mortality rates seen among non-Hispanic Black patients, more late-stage diagnoses among Hispanic patients, and lower screening rates among Asian patients.
“There’s no formal guidance on how to screen the population under age 50,” she said. “With the disparities in race and ethnicity, it remains unclear what would be the best population health strategy to optimize colorectal screening participation in young minorities.”
Ms. Ekeanyanwu and colleagues conducted a subanalysis of a 2022 randomized controlled trial at the University of California, Los Angeles, that looked at screening strategies for average-risk patients between ages 45 and 49. The study population included patients who were assigned to a primary care provider in the UCLA Health system and had active electronic portal use and excluded those with a personal or family history of adenoma or CRC, history of IBD or gastrointestinal cancer, and a prior FIT or colonoscopy.
In this study, the research team focused on the completion of any CRC screening at 26 weeks, stratified by race and ethnicity. They included four outreach scenarios: FIT invitation, colonoscopy invitation, a choice between FIT or colonoscopy invitation, or a default mailed FIT kit, which served as the control and typically is sent to UCLA patients overdue for screening among ages 50 and older. The researchers sent letters via US Postal Service and the online patient portal, as well as two texts about CRC screening.
Among 20,509 patients, 8918 were White (43.5%), 2757 were Hispanic (13.4%), 2613 were Asian (12.7%), and 797 were Black (3.9%).
The overall screening participation rate was 18.6%, with the lowest percentage among Black participants at 16.7% and the highest among Asian participants at 23.8%. These numbers varied significantly from the 20% seen among both White and Hispanic participants.
The default mailed outreach approach had the highest uptake with higher screening rates, at 26.2% overall, and had the highest participation in each racial and ethnic group. The rates were 28.7% among White patients, 20.1% among Black patients, 27.5% among Hispanic patients, and 31% among Asian patients.
Participation was lowest among the colonoscopy invitation group — as well as for White (14.8%), Hispanic (16%), and Asian (19.3%) patients. Among Black patients, participation was lowest in the FIT invitation group (12.8%).
Notably, in the choice group, more participants chose colonoscopy above FIT — across all racial and ethnic groups — at 12.1% versus 5.6% overall. In addition, among both FIT groups, there was significant crossover to colonoscopy, with about 7%-14% among the racial and ethnic groups preferring colonoscopy.
Ms. Ekeanyanwu noted the study may be limited by variations in sample size by race and ethnicity, as well as the socioeconomic status of typical patients at UCLA, who tend to fall in middle class and affluent groups. Demographic and socioeconomic factors may play a part in patients’ decision to get screened, she noted.
Patient participation in the digital portal may affect response rates as well, said Benjamin Lebwohl, MD, AGAF, an associate professor of medicine and epidemiology at Columbia University Medical Center, New York, who moderated the DDW session titled Reducing the Burden of GI Cancers Through Early Interventions.
“At least at my institution, we have a large number of such patients [not on the digital portal] who tend to be of lower socioeconomic status and tend to be at higher risk of not getting screened,” Dr. Lebwohl said. It would be important to consider “those who might need this intervention the most.”
Ms. Ekeanyanwu declared no relevant disclosures.
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
In a comparison of four outreach approaches, sending a FIT kit to people between the ages of 45 and 49 via mail garnered better response rates than opt-in strategies to participate in FIT, inviting them to undergo colonoscopy, or asking them to choose between FIT or colonoscopy. At the same time, when given a choice between colonoscopy and FIT, colonoscopy was preferred across all racial and ethnic groups.
“It is well known that colorectal cancer is the second-leading cause of cancer-related deaths in the United States. The good news is that for the past several decades, we’ve seen a decline in colorectal cancer incidence and mortality in ages 50 and above. However, there has been a recent rise in incidence and mortality in people younger than 50,” said lead author Rebecca Ekeanyanwu, a third-year medical student at Meharry Medical College School of Medicine in Nashville, Tennessee. She was awarded the 2024 AGA Institute Council Healthcare Disparities Research Award for the top oral presentation for research in racial and ethnic health care disparities.
CRC incidence, screening rates, and mortality also vary by race and ethnicity, with higher incidence and mortality rates seen among non-Hispanic Black patients, more late-stage diagnoses among Hispanic patients, and lower screening rates among Asian patients.
“There’s no formal guidance on how to screen the population under age 50,” she said. “With the disparities in race and ethnicity, it remains unclear what would be the best population health strategy to optimize colorectal screening participation in young minorities.”
Ms. Ekeanyanwu and colleagues conducted a subanalysis of a 2022 randomized controlled trial at the University of California, Los Angeles, that looked at screening strategies for average-risk patients between ages 45 and 49. The study population included patients who were assigned to a primary care provider in the UCLA Health system and had active electronic portal use and excluded those with a personal or family history of adenoma or CRC, history of IBD or gastrointestinal cancer, and a prior FIT or colonoscopy.
In this study, the research team focused on the completion of any CRC screening at 26 weeks, stratified by race and ethnicity. They included four outreach scenarios: FIT invitation, colonoscopy invitation, a choice between FIT or colonoscopy invitation, or a default mailed FIT kit, which served as the control and typically is sent to UCLA patients overdue for screening among ages 50 and older. The researchers sent letters via US Postal Service and the online patient portal, as well as two texts about CRC screening.
Among 20,509 patients, 8918 were White (43.5%), 2757 were Hispanic (13.4%), 2613 were Asian (12.7%), and 797 were Black (3.9%).
The overall screening participation rate was 18.6%, with the lowest percentage among Black participants at 16.7% and the highest among Asian participants at 23.8%. These numbers varied significantly from the 20% seen among both White and Hispanic participants.
The default mailed outreach approach had the highest uptake with higher screening rates, at 26.2% overall, and had the highest participation in each racial and ethnic group. The rates were 28.7% among White patients, 20.1% among Black patients, 27.5% among Hispanic patients, and 31% among Asian patients.
Participation was lowest among the colonoscopy invitation group — as well as for White (14.8%), Hispanic (16%), and Asian (19.3%) patients. Among Black patients, participation was lowest in the FIT invitation group (12.8%).
Notably, in the choice group, more participants chose colonoscopy above FIT — across all racial and ethnic groups — at 12.1% versus 5.6% overall. In addition, among both FIT groups, there was significant crossover to colonoscopy, with about 7%-14% among the racial and ethnic groups preferring colonoscopy.
Ms. Ekeanyanwu noted the study may be limited by variations in sample size by race and ethnicity, as well as the socioeconomic status of typical patients at UCLA, who tend to fall in middle class and affluent groups. Demographic and socioeconomic factors may play a part in patients’ decision to get screened, she noted.
Patient participation in the digital portal may affect response rates as well, said Benjamin Lebwohl, MD, AGAF, an associate professor of medicine and epidemiology at Columbia University Medical Center, New York, who moderated the DDW session titled Reducing the Burden of GI Cancers Through Early Interventions.
“At least at my institution, we have a large number of such patients [not on the digital portal] who tend to be of lower socioeconomic status and tend to be at higher risk of not getting screened,” Dr. Lebwohl said. It would be important to consider “those who might need this intervention the most.”
Ms. Ekeanyanwu declared no relevant disclosures.
WASHINGTON — , according to a study presented at the annual Digestive Disease Week® (DDW).
In a comparison of four outreach approaches, sending a FIT kit to people between the ages of 45 and 49 via mail garnered better response rates than opt-in strategies to participate in FIT, inviting them to undergo colonoscopy, or asking them to choose between FIT or colonoscopy. At the same time, when given a choice between colonoscopy and FIT, colonoscopy was preferred across all racial and ethnic groups.
“It is well known that colorectal cancer is the second-leading cause of cancer-related deaths in the United States. The good news is that for the past several decades, we’ve seen a decline in colorectal cancer incidence and mortality in ages 50 and above. However, there has been a recent rise in incidence and mortality in people younger than 50,” said lead author Rebecca Ekeanyanwu, a third-year medical student at Meharry Medical College School of Medicine in Nashville, Tennessee. She was awarded the 2024 AGA Institute Council Healthcare Disparities Research Award for the top oral presentation for research in racial and ethnic health care disparities.
CRC incidence, screening rates, and mortality also vary by race and ethnicity, with higher incidence and mortality rates seen among non-Hispanic Black patients, more late-stage diagnoses among Hispanic patients, and lower screening rates among Asian patients.
“There’s no formal guidance on how to screen the population under age 50,” she said. “With the disparities in race and ethnicity, it remains unclear what would be the best population health strategy to optimize colorectal screening participation in young minorities.”
Ms. Ekeanyanwu and colleagues conducted a subanalysis of a 2022 randomized controlled trial at the University of California, Los Angeles, that looked at screening strategies for average-risk patients between ages 45 and 49. The study population included patients who were assigned to a primary care provider in the UCLA Health system and had active electronic portal use and excluded those with a personal or family history of adenoma or CRC, history of IBD or gastrointestinal cancer, and a prior FIT or colonoscopy.
In this study, the research team focused on the completion of any CRC screening at 26 weeks, stratified by race and ethnicity. They included four outreach scenarios: FIT invitation, colonoscopy invitation, a choice between FIT or colonoscopy invitation, or a default mailed FIT kit, which served as the control and typically is sent to UCLA patients overdue for screening among ages 50 and older. The researchers sent letters via US Postal Service and the online patient portal, as well as two texts about CRC screening.
Among 20,509 patients, 8918 were White (43.5%), 2757 were Hispanic (13.4%), 2613 were Asian (12.7%), and 797 were Black (3.9%).
The overall screening participation rate was 18.6%, with the lowest percentage among Black participants at 16.7% and the highest among Asian participants at 23.8%. These numbers varied significantly from the 20% seen among both White and Hispanic participants.
The default mailed outreach approach had the highest uptake with higher screening rates, at 26.2% overall, and had the highest participation in each racial and ethnic group. The rates were 28.7% among White patients, 20.1% among Black patients, 27.5% among Hispanic patients, and 31% among Asian patients.
Participation was lowest among the colonoscopy invitation group — as well as for White (14.8%), Hispanic (16%), and Asian (19.3%) patients. Among Black patients, participation was lowest in the FIT invitation group (12.8%).
Notably, in the choice group, more participants chose colonoscopy above FIT — across all racial and ethnic groups — at 12.1% versus 5.6% overall. In addition, among both FIT groups, there was significant crossover to colonoscopy, with about 7%-14% among the racial and ethnic groups preferring colonoscopy.
Ms. Ekeanyanwu noted the study may be limited by variations in sample size by race and ethnicity, as well as the socioeconomic status of typical patients at UCLA, who tend to fall in middle class and affluent groups. Demographic and socioeconomic factors may play a part in patients’ decision to get screened, she noted.
Patient participation in the digital portal may affect response rates as well, said Benjamin Lebwohl, MD, AGAF, an associate professor of medicine and epidemiology at Columbia University Medical Center, New York, who moderated the DDW session titled Reducing the Burden of GI Cancers Through Early Interventions.
“At least at my institution, we have a large number of such patients [not on the digital portal] who tend to be of lower socioeconomic status and tend to be at higher risk of not getting screened,” Dr. Lebwohl said. It would be important to consider “those who might need this intervention the most.”
Ms. Ekeanyanwu declared no relevant disclosures.
FROM DDW 2024
Late-Night Eaters May Have Increased Risk for Colorectal Cancer
WASHINGTON — , according to the results of research presented at the annual Digestive Disease Week® (DDW).
Investigators in a new study questioned 664 people getting a colonoscopy to screen for cancer, and 42% said they were late eaters. This group was 46% more likely than non–late eaters to have an adenoma found during colonoscopy. An estimated 5% to 10% of them become cancerous over time.
“A lot of other studies are about what we eat but not when we eat,” said Edena Khoshaba, lead investigator and a medical student at Rush University Medical College in Chicago. “The common advice includes not eating red meat, eating more fruits and vegetables — which is great, of course — but we wanted to see if the timing affects us at all.”
Ms. Khoshaba and colleagues found it did. Late eaters were 5.5 times more likely to have three or more tubular adenomas compared to non–late eaters, even after adjusting for what people were eating. Tubular adenomas are the most common type of polyp found in the colon.
So, what’s the possible connection between late eating and the risk for colorectal cancer?
Resetting Your Internal Clock
Eating close to bedtime could be throwing off the body’s circadian rhythm. But in this case, it’s not the central circadian center located in the brain — the one that releases melatonin. Instead, late eating could disrupt the peripheral circadian rhythm, part of which is found in the GI tract. For example, if a person is eating late at night, the brain thinks it is nighttime while the gut thinks it is daytime, Ms. Khoshaba said in an interview.
This is an interesting study, said Amy Bragagnini, MS, RD, spokesperson for the Academy of Nutrition and Dietetics, when asked to comment on the research. “It is true that eating later at night can disrupt your circadian rhythm.”
“In addition, many of my patients have told me that when they do eat later at night, they don’t always make the healthiest food choices,” Ms. Bragagnini said. “Their late-night food choices are generally higher in added sugar and fat. This may cause them to consume far more calories than their body needs.” So, eating late at night can also lead to unwanted weight gain.
An unanswered question is if late eating is connected in any way at all to increasing rates of colorectal cancer seen in younger patients.
This was an observational study, and another possible limitation, Ms. Khoshaba said, is that people were asked to recall their diets over 24 hours, which may not always be accurate.
Some of the organisms in the gut have their own internal clocks that follow a daily rhythm, and what someone eat determines how many different kinds of these organisms are active, Ms. Bragagnini said.
“So, if your late-night eating consists of foods high in sugar and fat, you may be negatively impacting your microbiome.” she said.
The next step for Ms. Khoshaba and colleagues is a study examining the peripheral circadian rhythm, changes in the gut microbiome, and the risk for developing metabolic syndrome. Ms. Khoshaba and Ms. Bragagnini had no relevant disclosures.
A version of this article appeared on Medscape.com.
WASHINGTON — , according to the results of research presented at the annual Digestive Disease Week® (DDW).
Investigators in a new study questioned 664 people getting a colonoscopy to screen for cancer, and 42% said they were late eaters. This group was 46% more likely than non–late eaters to have an adenoma found during colonoscopy. An estimated 5% to 10% of them become cancerous over time.
“A lot of other studies are about what we eat but not when we eat,” said Edena Khoshaba, lead investigator and a medical student at Rush University Medical College in Chicago. “The common advice includes not eating red meat, eating more fruits and vegetables — which is great, of course — but we wanted to see if the timing affects us at all.”
Ms. Khoshaba and colleagues found it did. Late eaters were 5.5 times more likely to have three or more tubular adenomas compared to non–late eaters, even after adjusting for what people were eating. Tubular adenomas are the most common type of polyp found in the colon.
So, what’s the possible connection between late eating and the risk for colorectal cancer?
Resetting Your Internal Clock
Eating close to bedtime could be throwing off the body’s circadian rhythm. But in this case, it’s not the central circadian center located in the brain — the one that releases melatonin. Instead, late eating could disrupt the peripheral circadian rhythm, part of which is found in the GI tract. For example, if a person is eating late at night, the brain thinks it is nighttime while the gut thinks it is daytime, Ms. Khoshaba said in an interview.
This is an interesting study, said Amy Bragagnini, MS, RD, spokesperson for the Academy of Nutrition and Dietetics, when asked to comment on the research. “It is true that eating later at night can disrupt your circadian rhythm.”
“In addition, many of my patients have told me that when they do eat later at night, they don’t always make the healthiest food choices,” Ms. Bragagnini said. “Their late-night food choices are generally higher in added sugar and fat. This may cause them to consume far more calories than their body needs.” So, eating late at night can also lead to unwanted weight gain.
An unanswered question is if late eating is connected in any way at all to increasing rates of colorectal cancer seen in younger patients.
This was an observational study, and another possible limitation, Ms. Khoshaba said, is that people were asked to recall their diets over 24 hours, which may not always be accurate.
Some of the organisms in the gut have their own internal clocks that follow a daily rhythm, and what someone eat determines how many different kinds of these organisms are active, Ms. Bragagnini said.
“So, if your late-night eating consists of foods high in sugar and fat, you may be negatively impacting your microbiome.” she said.
The next step for Ms. Khoshaba and colleagues is a study examining the peripheral circadian rhythm, changes in the gut microbiome, and the risk for developing metabolic syndrome. Ms. Khoshaba and Ms. Bragagnini had no relevant disclosures.
A version of this article appeared on Medscape.com.
WASHINGTON — , according to the results of research presented at the annual Digestive Disease Week® (DDW).
Investigators in a new study questioned 664 people getting a colonoscopy to screen for cancer, and 42% said they were late eaters. This group was 46% more likely than non–late eaters to have an adenoma found during colonoscopy. An estimated 5% to 10% of them become cancerous over time.
“A lot of other studies are about what we eat but not when we eat,” said Edena Khoshaba, lead investigator and a medical student at Rush University Medical College in Chicago. “The common advice includes not eating red meat, eating more fruits and vegetables — which is great, of course — but we wanted to see if the timing affects us at all.”
Ms. Khoshaba and colleagues found it did. Late eaters were 5.5 times more likely to have three or more tubular adenomas compared to non–late eaters, even after adjusting for what people were eating. Tubular adenomas are the most common type of polyp found in the colon.
So, what’s the possible connection between late eating and the risk for colorectal cancer?
Resetting Your Internal Clock
Eating close to bedtime could be throwing off the body’s circadian rhythm. But in this case, it’s not the central circadian center located in the brain — the one that releases melatonin. Instead, late eating could disrupt the peripheral circadian rhythm, part of which is found in the GI tract. For example, if a person is eating late at night, the brain thinks it is nighttime while the gut thinks it is daytime, Ms. Khoshaba said in an interview.
This is an interesting study, said Amy Bragagnini, MS, RD, spokesperson for the Academy of Nutrition and Dietetics, when asked to comment on the research. “It is true that eating later at night can disrupt your circadian rhythm.”
“In addition, many of my patients have told me that when they do eat later at night, they don’t always make the healthiest food choices,” Ms. Bragagnini said. “Their late-night food choices are generally higher in added sugar and fat. This may cause them to consume far more calories than their body needs.” So, eating late at night can also lead to unwanted weight gain.
An unanswered question is if late eating is connected in any way at all to increasing rates of colorectal cancer seen in younger patients.
This was an observational study, and another possible limitation, Ms. Khoshaba said, is that people were asked to recall their diets over 24 hours, which may not always be accurate.
Some of the organisms in the gut have their own internal clocks that follow a daily rhythm, and what someone eat determines how many different kinds of these organisms are active, Ms. Bragagnini said.
“So, if your late-night eating consists of foods high in sugar and fat, you may be negatively impacting your microbiome.” she said.
The next step for Ms. Khoshaba and colleagues is a study examining the peripheral circadian rhythm, changes in the gut microbiome, and the risk for developing metabolic syndrome. Ms. Khoshaba and Ms. Bragagnini had no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM DDW 2024
GI Complications With GLP-1s for Weight Loss: Reexamining the Risks
WASHINGTON — In contrast with a previous study that found glucagon-like peptide 1 (GLP-1) receptor agonists associated with an increased risk for acute pancreatitis and bowel obstruction, a new retrospective study found no significant link to these complications.
One of the big differences from the previous study, published in JAMA in October 2023 by Sodhi and colleagues , is that the current research was able to account for initial body mass index (BMI), said Benjamin Liu, MD, a resident in internal medicine at Case Western Reserve University School of Medicine, Cleveland, Ohio.
This is important, he explained in his presentation (abstract 1074) at the annual Digestive Disease Week® 2024, because obesity on its own is associated with an increased risk for some of these gastrointestinal (GI) outcomes.
“They did an excellent study,” Dr. Liu said. “But their platform did not allow them to match participants for BMI.”
Another distinction between the two studies is that the JAMA study excluded people who had diabetes 90 days before or 30 days following the start of GLP-1 therapy.
Instead, Dr. Liu said, he and colleague Gengqing Song, MD, “just made it simple” and excluded anyone with diabetes or an A1c ≥ 6.5.
We didn’t want participants with diabetes because “we were looking at GLP-1s for weight loss,” Dr. Liu explained.
Although some clinical trials have already assessed adverse events of these medications, “clinical trials are not always a perfect representation of the real world,” Dr. Liu said in an interview. “So, it’s important to do real-world studies to see just what actually goes on.”
Reassessing GI Complications
In the current study, the researchers identified 105,793 patients from the TriNetX healthcare database taking a GLP-1, either semaglutide or liraglutide, for weight loss and 8794 patients taking 8 mg naltrexone/90 mg bupropion. After propensity matching, including for BMI, there were 8792 patients in each group.
They were identified in the database between 2011 and 2023. Researchers noted their first-ever occurrence of acute pancreatitis, bowel obstruction, gastroparesis, or biliary disease during the study period.
Participants had a BMI ≥ 30 kg/m2. In addition to BMI, propensity score matching included demographics, alcohol use, smoking, hyperlipidemia, and abdominal surgery. A second analysis specifically did not match participants for BMI.
The researchers found no significant association between GLP-1s and acute pancreatitis (adjusted hazard ratio [HR], 1.19; 95% CI, 0.66-2.14).
The labeling for semaglutide and liraglutide warns about an increased risk for acute pancreatitis, “but real-world studies and clinical trials are increasingly suggesting there is no increased risk,” Dr. Liu said.
They also did not find a significant association between GLP-1s and bowel obstruction (HR, 1.30; 95% CI, 0.69-2.18).
Despite the current findings, more research — especially prospective data — is needed to confirm pancreatitis as well as other GI risks like bowel obstruction potentially associated with GLP-1s, he added.
The study did, however, find an elevated risk for biliary disease (HR, 1.27; 95% CI, 1.02-1.59) in the BMI-matched cohorts.
This could be due to the rapidity of weight loss, Dr. Liu suggested. “We found that semaglutide caused more weight loss at 6 and 12 months than naltrexone/bupropion, and it did so at a faster rate. That falls in line with other data that suggest if you lose weight too fast, you actually have an increased risk of gallstones,” he said.
Rapid weight loss can release cholesterol into the body, which then collects in the bile ducts and causes gallstones. This risk for gallstone formation with rapid weight loss is also seen after bariatric surgery, Dr. Liu said.
Without BMI matching, he noted, the increased risk for biliary disease was no longer significant (HR, 1.21; 95% CI, 0.96-1.52).
The researchers also reported a significant association between GLP-1s and gastroparesis (HR, 2.30; 95% CI, 1.19-4.46), confirming the results of the JAMA study “but at a much lower incidence rate once we excluded all patients with diabetes,” said Dr. Liu. The JAMA study had a HR of 3.67 for gastroparesis (95% CI, 1.15-11.90).
Weighing in on the Results
“Overall, their study design looks sound,” said Mahyar Etminan, PharmD, associate professor of medicine at the University of British Columbia in Vancouver and an author of the JAMA study. He agreed that Dr. Liu’s research confirmed their findings about gastroparesis and biliary disease.
However, “I interpret the results with intestinal obstruction and pancreatitis as more inconclusive than no risk,” he added.
Session co-moderator and gastroenterologist and motility specialist with Stanford Health Care in California, Linda Anh Bui Nguyen, MD, AGAF, said that she thinks “it’s a promising study.
“But with any retrospective study where you’re looking at ICD-10 [International Classification of Diseases, Tenth Revision] codes, it really depends on the coders. The code could be subjective and could be wrong,” said Dr. Nguyen, clinical professor of medicine at Stanford Medical School, California.
For example, the diagnosis of gastroparesis requires a normal endoscopy and a gastric emptying test. “But we find that, frequently, patients are being given a diagnosis of gastroparesis without the test,” she said.
An unanswered question also remains regarding how pancreatitis or biliary disease is being diagnosed: “Was it imaging, lab testing, or symptoms?” she said in an interview. “For example, if patients had pain on the right side, did they call it biliary?”
Dr. Nguyen added that it is difficult to get this kind of detail in retrospective studies. She also agreed with Dr. Liu that prospective studies are warranted.
The study was independently supported. Dr. Liu, Dr. Etminan, and Dr. Nguyen had no relevant financial disclosures.
A version of this article appeared on Medscape.com.
WASHINGTON — In contrast with a previous study that found glucagon-like peptide 1 (GLP-1) receptor agonists associated with an increased risk for acute pancreatitis and bowel obstruction, a new retrospective study found no significant link to these complications.
One of the big differences from the previous study, published in JAMA in October 2023 by Sodhi and colleagues , is that the current research was able to account for initial body mass index (BMI), said Benjamin Liu, MD, a resident in internal medicine at Case Western Reserve University School of Medicine, Cleveland, Ohio.
This is important, he explained in his presentation (abstract 1074) at the annual Digestive Disease Week® 2024, because obesity on its own is associated with an increased risk for some of these gastrointestinal (GI) outcomes.
“They did an excellent study,” Dr. Liu said. “But their platform did not allow them to match participants for BMI.”
Another distinction between the two studies is that the JAMA study excluded people who had diabetes 90 days before or 30 days following the start of GLP-1 therapy.
Instead, Dr. Liu said, he and colleague Gengqing Song, MD, “just made it simple” and excluded anyone with diabetes or an A1c ≥ 6.5.
We didn’t want participants with diabetes because “we were looking at GLP-1s for weight loss,” Dr. Liu explained.
Although some clinical trials have already assessed adverse events of these medications, “clinical trials are not always a perfect representation of the real world,” Dr. Liu said in an interview. “So, it’s important to do real-world studies to see just what actually goes on.”
Reassessing GI Complications
In the current study, the researchers identified 105,793 patients from the TriNetX healthcare database taking a GLP-1, either semaglutide or liraglutide, for weight loss and 8794 patients taking 8 mg naltrexone/90 mg bupropion. After propensity matching, including for BMI, there were 8792 patients in each group.
They were identified in the database between 2011 and 2023. Researchers noted their first-ever occurrence of acute pancreatitis, bowel obstruction, gastroparesis, or biliary disease during the study period.
Participants had a BMI ≥ 30 kg/m2. In addition to BMI, propensity score matching included demographics, alcohol use, smoking, hyperlipidemia, and abdominal surgery. A second analysis specifically did not match participants for BMI.
The researchers found no significant association between GLP-1s and acute pancreatitis (adjusted hazard ratio [HR], 1.19; 95% CI, 0.66-2.14).
The labeling for semaglutide and liraglutide warns about an increased risk for acute pancreatitis, “but real-world studies and clinical trials are increasingly suggesting there is no increased risk,” Dr. Liu said.
They also did not find a significant association between GLP-1s and bowel obstruction (HR, 1.30; 95% CI, 0.69-2.18).
Despite the current findings, more research — especially prospective data — is needed to confirm pancreatitis as well as other GI risks like bowel obstruction potentially associated with GLP-1s, he added.
The study did, however, find an elevated risk for biliary disease (HR, 1.27; 95% CI, 1.02-1.59) in the BMI-matched cohorts.
This could be due to the rapidity of weight loss, Dr. Liu suggested. “We found that semaglutide caused more weight loss at 6 and 12 months than naltrexone/bupropion, and it did so at a faster rate. That falls in line with other data that suggest if you lose weight too fast, you actually have an increased risk of gallstones,” he said.
Rapid weight loss can release cholesterol into the body, which then collects in the bile ducts and causes gallstones. This risk for gallstone formation with rapid weight loss is also seen after bariatric surgery, Dr. Liu said.
Without BMI matching, he noted, the increased risk for biliary disease was no longer significant (HR, 1.21; 95% CI, 0.96-1.52).
The researchers also reported a significant association between GLP-1s and gastroparesis (HR, 2.30; 95% CI, 1.19-4.46), confirming the results of the JAMA study “but at a much lower incidence rate once we excluded all patients with diabetes,” said Dr. Liu. The JAMA study had a HR of 3.67 for gastroparesis (95% CI, 1.15-11.90).
Weighing in on the Results
“Overall, their study design looks sound,” said Mahyar Etminan, PharmD, associate professor of medicine at the University of British Columbia in Vancouver and an author of the JAMA study. He agreed that Dr. Liu’s research confirmed their findings about gastroparesis and biliary disease.
However, “I interpret the results with intestinal obstruction and pancreatitis as more inconclusive than no risk,” he added.
Session co-moderator and gastroenterologist and motility specialist with Stanford Health Care in California, Linda Anh Bui Nguyen, MD, AGAF, said that she thinks “it’s a promising study.
“But with any retrospective study where you’re looking at ICD-10 [International Classification of Diseases, Tenth Revision] codes, it really depends on the coders. The code could be subjective and could be wrong,” said Dr. Nguyen, clinical professor of medicine at Stanford Medical School, California.
For example, the diagnosis of gastroparesis requires a normal endoscopy and a gastric emptying test. “But we find that, frequently, patients are being given a diagnosis of gastroparesis without the test,” she said.
An unanswered question also remains regarding how pancreatitis or biliary disease is being diagnosed: “Was it imaging, lab testing, or symptoms?” she said in an interview. “For example, if patients had pain on the right side, did they call it biliary?”
Dr. Nguyen added that it is difficult to get this kind of detail in retrospective studies. She also agreed with Dr. Liu that prospective studies are warranted.
The study was independently supported. Dr. Liu, Dr. Etminan, and Dr. Nguyen had no relevant financial disclosures.
A version of this article appeared on Medscape.com.
WASHINGTON — In contrast with a previous study that found glucagon-like peptide 1 (GLP-1) receptor agonists associated with an increased risk for acute pancreatitis and bowel obstruction, a new retrospective study found no significant link to these complications.
One of the big differences from the previous study, published in JAMA in October 2023 by Sodhi and colleagues , is that the current research was able to account for initial body mass index (BMI), said Benjamin Liu, MD, a resident in internal medicine at Case Western Reserve University School of Medicine, Cleveland, Ohio.
This is important, he explained in his presentation (abstract 1074) at the annual Digestive Disease Week® 2024, because obesity on its own is associated with an increased risk for some of these gastrointestinal (GI) outcomes.
“They did an excellent study,” Dr. Liu said. “But their platform did not allow them to match participants for BMI.”
Another distinction between the two studies is that the JAMA study excluded people who had diabetes 90 days before or 30 days following the start of GLP-1 therapy.
Instead, Dr. Liu said, he and colleague Gengqing Song, MD, “just made it simple” and excluded anyone with diabetes or an A1c ≥ 6.5.
We didn’t want participants with diabetes because “we were looking at GLP-1s for weight loss,” Dr. Liu explained.
Although some clinical trials have already assessed adverse events of these medications, “clinical trials are not always a perfect representation of the real world,” Dr. Liu said in an interview. “So, it’s important to do real-world studies to see just what actually goes on.”
Reassessing GI Complications
In the current study, the researchers identified 105,793 patients from the TriNetX healthcare database taking a GLP-1, either semaglutide or liraglutide, for weight loss and 8794 patients taking 8 mg naltrexone/90 mg bupropion. After propensity matching, including for BMI, there were 8792 patients in each group.
They were identified in the database between 2011 and 2023. Researchers noted their first-ever occurrence of acute pancreatitis, bowel obstruction, gastroparesis, or biliary disease during the study period.
Participants had a BMI ≥ 30 kg/m2. In addition to BMI, propensity score matching included demographics, alcohol use, smoking, hyperlipidemia, and abdominal surgery. A second analysis specifically did not match participants for BMI.
The researchers found no significant association between GLP-1s and acute pancreatitis (adjusted hazard ratio [HR], 1.19; 95% CI, 0.66-2.14).
The labeling for semaglutide and liraglutide warns about an increased risk for acute pancreatitis, “but real-world studies and clinical trials are increasingly suggesting there is no increased risk,” Dr. Liu said.
They also did not find a significant association between GLP-1s and bowel obstruction (HR, 1.30; 95% CI, 0.69-2.18).
Despite the current findings, more research — especially prospective data — is needed to confirm pancreatitis as well as other GI risks like bowel obstruction potentially associated with GLP-1s, he added.
The study did, however, find an elevated risk for biliary disease (HR, 1.27; 95% CI, 1.02-1.59) in the BMI-matched cohorts.
This could be due to the rapidity of weight loss, Dr. Liu suggested. “We found that semaglutide caused more weight loss at 6 and 12 months than naltrexone/bupropion, and it did so at a faster rate. That falls in line with other data that suggest if you lose weight too fast, you actually have an increased risk of gallstones,” he said.
Rapid weight loss can release cholesterol into the body, which then collects in the bile ducts and causes gallstones. This risk for gallstone formation with rapid weight loss is also seen after bariatric surgery, Dr. Liu said.
Without BMI matching, he noted, the increased risk for biliary disease was no longer significant (HR, 1.21; 95% CI, 0.96-1.52).
The researchers also reported a significant association between GLP-1s and gastroparesis (HR, 2.30; 95% CI, 1.19-4.46), confirming the results of the JAMA study “but at a much lower incidence rate once we excluded all patients with diabetes,” said Dr. Liu. The JAMA study had a HR of 3.67 for gastroparesis (95% CI, 1.15-11.90).
Weighing in on the Results
“Overall, their study design looks sound,” said Mahyar Etminan, PharmD, associate professor of medicine at the University of British Columbia in Vancouver and an author of the JAMA study. He agreed that Dr. Liu’s research confirmed their findings about gastroparesis and biliary disease.
However, “I interpret the results with intestinal obstruction and pancreatitis as more inconclusive than no risk,” he added.
Session co-moderator and gastroenterologist and motility specialist with Stanford Health Care in California, Linda Anh Bui Nguyen, MD, AGAF, said that she thinks “it’s a promising study.
“But with any retrospective study where you’re looking at ICD-10 [International Classification of Diseases, Tenth Revision] codes, it really depends on the coders. The code could be subjective and could be wrong,” said Dr. Nguyen, clinical professor of medicine at Stanford Medical School, California.
For example, the diagnosis of gastroparesis requires a normal endoscopy and a gastric emptying test. “But we find that, frequently, patients are being given a diagnosis of gastroparesis without the test,” she said.
An unanswered question also remains regarding how pancreatitis or biliary disease is being diagnosed: “Was it imaging, lab testing, or symptoms?” she said in an interview. “For example, if patients had pain on the right side, did they call it biliary?”
Dr. Nguyen added that it is difficult to get this kind of detail in retrospective studies. She also agreed with Dr. Liu that prospective studies are warranted.
The study was independently supported. Dr. Liu, Dr. Etminan, and Dr. Nguyen had no relevant financial disclosures.
A version of this article appeared on Medscape.com.
FROM DDW 2024
In IBD Patients, Statin Use Associated with Lower Risk of Developing PSC
WASHINGTON — , according to a study presented at Digestive Disease Week® (DDW) 2024.
Statin use was associated with an 86% risk reduction, and only .09% of IBD patients who took statins developed PSC.
“We all take care of patients with liver disease, and we know what a significant burden PSC is. These patients have a significantly elevated risk of enhanced fibrosis and cirrhosis, multiple cancers, and cholangitis and sepsis,” said lead author Chiraag Kulkarni, MD, a gastroenterology fellow at Stanford (California) University Medical School.
“Despite this, we have to date no proven effective medical care for PSC,” he said. “However, over the last decade, there is growing evidence that statins may be beneficial in liver disease, and we see this evidence base stretching from basic science to clinical data.”
Dr. Kulkarni pointed to numerous studies that indicate statins may slow disease progression in steatotic liver disease, viral hepatitis, and cirrhosis. But could statins prevent the onset of PSC?
Because PSC incidence is low, Dr. Kulkarni and colleagues focused on a patient population with higher prevalence — those with IBD, who have an overall lifetime risk of 2% to 7%. The research team followed patients from the date of IBD diagnosis.
Among 33,813 patients with IBD in a national dataset from 2018 onward, 8813 used statins. Statin users tended to be older than non–statin users.
Overall, 181 patients developed new onset PSC during a median follow-up of about 45 months after initial IBD diagnosis. Only eight statin users (.09%) developed PSC, compared with 173 patients (.69%) in the control group.
In a propensity score-matched analysis, statin therapy was associated with a significantly lower risk of developing PSC (HR .14, P < .001). The associated E-value was 5.5, which suggested a robust finding and unlikely to be due to non-visible confounding.
The findings were consistent across secondary and sensitivity analyses, including by age, duration of statin use, and type of statin. For instance, for patients under age 50 where PSC is more likely to occur, statins were associated with a 90% reduction in PSC risk.
“We take away two things from this. First, it’s suggested that a protective effect occurs at ages where PSC is most likely to occur,” Dr. Kulkarni said. “Second, in combination with our propensity score-matched analysis, the results we are observing are not due to a survival bias, where the patients who survive to an age where statins are prescribed simply have a biologically different predilection for developing PSC.”
Statins also protected against PSC in both ulcerative colitis (HR .21) and Crohn’s disease (HR .15), as well as both women (HR .16) and men (HR .22).
Given the uncertainty about the optimal duration of statin therapy for a protective effect, Dr. Kulkarni and colleagues looked at a lag time of 12 months. They found statins were associated with an 84% risk reduction (HR .16), which was similar to the primary analysis.
The study was limited by the inability to capture dosage data or medication adherence. The findings raised several questions, Dr. Kulkarni said, such as the underlying mechanisms and clinical implications. For instance, the underlying mechanisms appear to be related to the pleiotropic effect of statins, modulation of gut inflammation, and alterations in bile acid profiles.
“This is really fascinating and interesting. I wonder about this as a primary prevention strategy in those who have normal cholesterol. Could this work or not?” said Gyongyi Szabo, MD, AGAF, chief academic officer at Beth Israel Deaconess Medical Center, Boston, who was a moderator for the Liver & Biliary Section Distinguished Abstract Plenary Session.
Dr. Kulkarni noted that these findings wouldn’t change clinical practice alone, but based on existing literature around statin hesitancy among patients with cardiovascular disease, the risk reduction for PSC could provide another reason to encourage patients to take them.
“To move this to a place where you can actually think about primary prevention, I think the biological mechanisms need to be teased out a little bit more,” Dr. Kulkarni said. “Then I think you probably still need to identify a higher-risk group than IBD alone.”
Dr. Kulkarni declared no disclosures.
WASHINGTON — , according to a study presented at Digestive Disease Week® (DDW) 2024.
Statin use was associated with an 86% risk reduction, and only .09% of IBD patients who took statins developed PSC.
“We all take care of patients with liver disease, and we know what a significant burden PSC is. These patients have a significantly elevated risk of enhanced fibrosis and cirrhosis, multiple cancers, and cholangitis and sepsis,” said lead author Chiraag Kulkarni, MD, a gastroenterology fellow at Stanford (California) University Medical School.
“Despite this, we have to date no proven effective medical care for PSC,” he said. “However, over the last decade, there is growing evidence that statins may be beneficial in liver disease, and we see this evidence base stretching from basic science to clinical data.”
Dr. Kulkarni pointed to numerous studies that indicate statins may slow disease progression in steatotic liver disease, viral hepatitis, and cirrhosis. But could statins prevent the onset of PSC?
Because PSC incidence is low, Dr. Kulkarni and colleagues focused on a patient population with higher prevalence — those with IBD, who have an overall lifetime risk of 2% to 7%. The research team followed patients from the date of IBD diagnosis.
Among 33,813 patients with IBD in a national dataset from 2018 onward, 8813 used statins. Statin users tended to be older than non–statin users.
Overall, 181 patients developed new onset PSC during a median follow-up of about 45 months after initial IBD diagnosis. Only eight statin users (.09%) developed PSC, compared with 173 patients (.69%) in the control group.
In a propensity score-matched analysis, statin therapy was associated with a significantly lower risk of developing PSC (HR .14, P < .001). The associated E-value was 5.5, which suggested a robust finding and unlikely to be due to non-visible confounding.
The findings were consistent across secondary and sensitivity analyses, including by age, duration of statin use, and type of statin. For instance, for patients under age 50 where PSC is more likely to occur, statins were associated with a 90% reduction in PSC risk.
“We take away two things from this. First, it’s suggested that a protective effect occurs at ages where PSC is most likely to occur,” Dr. Kulkarni said. “Second, in combination with our propensity score-matched analysis, the results we are observing are not due to a survival bias, where the patients who survive to an age where statins are prescribed simply have a biologically different predilection for developing PSC.”
Statins also protected against PSC in both ulcerative colitis (HR .21) and Crohn’s disease (HR .15), as well as both women (HR .16) and men (HR .22).
Given the uncertainty about the optimal duration of statin therapy for a protective effect, Dr. Kulkarni and colleagues looked at a lag time of 12 months. They found statins were associated with an 84% risk reduction (HR .16), which was similar to the primary analysis.
The study was limited by the inability to capture dosage data or medication adherence. The findings raised several questions, Dr. Kulkarni said, such as the underlying mechanisms and clinical implications. For instance, the underlying mechanisms appear to be related to the pleiotropic effect of statins, modulation of gut inflammation, and alterations in bile acid profiles.
“This is really fascinating and interesting. I wonder about this as a primary prevention strategy in those who have normal cholesterol. Could this work or not?” said Gyongyi Szabo, MD, AGAF, chief academic officer at Beth Israel Deaconess Medical Center, Boston, who was a moderator for the Liver & Biliary Section Distinguished Abstract Plenary Session.
Dr. Kulkarni noted that these findings wouldn’t change clinical practice alone, but based on existing literature around statin hesitancy among patients with cardiovascular disease, the risk reduction for PSC could provide another reason to encourage patients to take them.
“To move this to a place where you can actually think about primary prevention, I think the biological mechanisms need to be teased out a little bit more,” Dr. Kulkarni said. “Then I think you probably still need to identify a higher-risk group than IBD alone.”
Dr. Kulkarni declared no disclosures.
WASHINGTON — , according to a study presented at Digestive Disease Week® (DDW) 2024.
Statin use was associated with an 86% risk reduction, and only .09% of IBD patients who took statins developed PSC.
“We all take care of patients with liver disease, and we know what a significant burden PSC is. These patients have a significantly elevated risk of enhanced fibrosis and cirrhosis, multiple cancers, and cholangitis and sepsis,” said lead author Chiraag Kulkarni, MD, a gastroenterology fellow at Stanford (California) University Medical School.
“Despite this, we have to date no proven effective medical care for PSC,” he said. “However, over the last decade, there is growing evidence that statins may be beneficial in liver disease, and we see this evidence base stretching from basic science to clinical data.”
Dr. Kulkarni pointed to numerous studies that indicate statins may slow disease progression in steatotic liver disease, viral hepatitis, and cirrhosis. But could statins prevent the onset of PSC?
Because PSC incidence is low, Dr. Kulkarni and colleagues focused on a patient population with higher prevalence — those with IBD, who have an overall lifetime risk of 2% to 7%. The research team followed patients from the date of IBD diagnosis.
Among 33,813 patients with IBD in a national dataset from 2018 onward, 8813 used statins. Statin users tended to be older than non–statin users.
Overall, 181 patients developed new onset PSC during a median follow-up of about 45 months after initial IBD diagnosis. Only eight statin users (.09%) developed PSC, compared with 173 patients (.69%) in the control group.
In a propensity score-matched analysis, statin therapy was associated with a significantly lower risk of developing PSC (HR .14, P < .001). The associated E-value was 5.5, which suggested a robust finding and unlikely to be due to non-visible confounding.
The findings were consistent across secondary and sensitivity analyses, including by age, duration of statin use, and type of statin. For instance, for patients under age 50 where PSC is more likely to occur, statins were associated with a 90% reduction in PSC risk.
“We take away two things from this. First, it’s suggested that a protective effect occurs at ages where PSC is most likely to occur,” Dr. Kulkarni said. “Second, in combination with our propensity score-matched analysis, the results we are observing are not due to a survival bias, where the patients who survive to an age where statins are prescribed simply have a biologically different predilection for developing PSC.”
Statins also protected against PSC in both ulcerative colitis (HR .21) and Crohn’s disease (HR .15), as well as both women (HR .16) and men (HR .22).
Given the uncertainty about the optimal duration of statin therapy for a protective effect, Dr. Kulkarni and colleagues looked at a lag time of 12 months. They found statins were associated with an 84% risk reduction (HR .16), which was similar to the primary analysis.
The study was limited by the inability to capture dosage data or medication adherence. The findings raised several questions, Dr. Kulkarni said, such as the underlying mechanisms and clinical implications. For instance, the underlying mechanisms appear to be related to the pleiotropic effect of statins, modulation of gut inflammation, and alterations in bile acid profiles.
“This is really fascinating and interesting. I wonder about this as a primary prevention strategy in those who have normal cholesterol. Could this work or not?” said Gyongyi Szabo, MD, AGAF, chief academic officer at Beth Israel Deaconess Medical Center, Boston, who was a moderator for the Liver & Biliary Section Distinguished Abstract Plenary Session.
Dr. Kulkarni noted that these findings wouldn’t change clinical practice alone, but based on existing literature around statin hesitancy among patients with cardiovascular disease, the risk reduction for PSC could provide another reason to encourage patients to take them.
“To move this to a place where you can actually think about primary prevention, I think the biological mechanisms need to be teased out a little bit more,” Dr. Kulkarni said. “Then I think you probably still need to identify a higher-risk group than IBD alone.”
Dr. Kulkarni declared no disclosures.
FROM DDW 2024
Genetic Test Can Predict Response to Semaglutide for Weight Loss
TOPLINE:
, new evidence reveals.
METHODOLOGY:
- A machine learning genetic risk score can identify people with the hungry gut obesity phenotype, which has been found to be associated with greater weight loss with the glucagon-like peptide 1 receptor agonists (GLP-1 RA) liraglutide and exenatide.
- For this study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the GLP-1 RA semaglutide.
- Study participants were classified as the obesity phenotype hungry gut positive (n = 51) or hungry gut negative (n = 33).
- The researchers measured total body weight loss at 3, 6, 9, and 12 months and assessed the ability of the score to predict the response to semaglutide (defined as ≥ 5% of total body weight loss measured at 12 months).
TAKEAWAY:
- At 3 and 6 months, there were no significant differences in weight loss between the hungry gut positive and hungry gut negative groups.
- By 9 months, participants in the positive group lost 14.4% of their total body weight compared with 10.3% in case of participants in the negative group (P = .045).
- After a total of 12 months, the positive group lost 19.5% of their total body weight compared with 10.0% in case of participants in the negative group (P = .01).
- When used to predict the response to semaglutide, the area under the curve for the machine-learning genetic risk score was 0.76 (95% CI, 0.57-0.94; P = .04).
IN PRACTICE:
We can now tell with confidence who is going to respond to semaglutide, said Andres Acosta, MD, PhD, associate professor of medicine at Mayo Clinic. “For nonresponders, we can think about other interventions or medications that we have available.”
SOURCE:
This study was presented on May 20, 2024, at the annual Digestive Disease Week® (DDW) (Abstract 638).
LIMITATIONS:
Further prospective studies are needed to assess the validity of the test in a more diverse population and with different weight loss interventions.
DISCLOSURES:
This study was supported by a partnership between Mayo Clinic and Phenomix Sciences. Dr. Acosta is a cofounder of Phenomix Sciences.
A version of this article appeared on Medscape.com.
TOPLINE:
, new evidence reveals.
METHODOLOGY:
- A machine learning genetic risk score can identify people with the hungry gut obesity phenotype, which has been found to be associated with greater weight loss with the glucagon-like peptide 1 receptor agonists (GLP-1 RA) liraglutide and exenatide.
- For this study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the GLP-1 RA semaglutide.
- Study participants were classified as the obesity phenotype hungry gut positive (n = 51) or hungry gut negative (n = 33).
- The researchers measured total body weight loss at 3, 6, 9, and 12 months and assessed the ability of the score to predict the response to semaglutide (defined as ≥ 5% of total body weight loss measured at 12 months).
TAKEAWAY:
- At 3 and 6 months, there were no significant differences in weight loss between the hungry gut positive and hungry gut negative groups.
- By 9 months, participants in the positive group lost 14.4% of their total body weight compared with 10.3% in case of participants in the negative group (P = .045).
- After a total of 12 months, the positive group lost 19.5% of their total body weight compared with 10.0% in case of participants in the negative group (P = .01).
- When used to predict the response to semaglutide, the area under the curve for the machine-learning genetic risk score was 0.76 (95% CI, 0.57-0.94; P = .04).
IN PRACTICE:
We can now tell with confidence who is going to respond to semaglutide, said Andres Acosta, MD, PhD, associate professor of medicine at Mayo Clinic. “For nonresponders, we can think about other interventions or medications that we have available.”
SOURCE:
This study was presented on May 20, 2024, at the annual Digestive Disease Week® (DDW) (Abstract 638).
LIMITATIONS:
Further prospective studies are needed to assess the validity of the test in a more diverse population and with different weight loss interventions.
DISCLOSURES:
This study was supported by a partnership between Mayo Clinic and Phenomix Sciences. Dr. Acosta is a cofounder of Phenomix Sciences.
A version of this article appeared on Medscape.com.
TOPLINE:
, new evidence reveals.
METHODOLOGY:
- A machine learning genetic risk score can identify people with the hungry gut obesity phenotype, which has been found to be associated with greater weight loss with the glucagon-like peptide 1 receptor agonists (GLP-1 RA) liraglutide and exenatide.
- For this study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the GLP-1 RA semaglutide.
- Study participants were classified as the obesity phenotype hungry gut positive (n = 51) or hungry gut negative (n = 33).
- The researchers measured total body weight loss at 3, 6, 9, and 12 months and assessed the ability of the score to predict the response to semaglutide (defined as ≥ 5% of total body weight loss measured at 12 months).
TAKEAWAY:
- At 3 and 6 months, there were no significant differences in weight loss between the hungry gut positive and hungry gut negative groups.
- By 9 months, participants in the positive group lost 14.4% of their total body weight compared with 10.3% in case of participants in the negative group (P = .045).
- After a total of 12 months, the positive group lost 19.5% of their total body weight compared with 10.0% in case of participants in the negative group (P = .01).
- When used to predict the response to semaglutide, the area under the curve for the machine-learning genetic risk score was 0.76 (95% CI, 0.57-0.94; P = .04).
IN PRACTICE:
We can now tell with confidence who is going to respond to semaglutide, said Andres Acosta, MD, PhD, associate professor of medicine at Mayo Clinic. “For nonresponders, we can think about other interventions or medications that we have available.”
SOURCE:
This study was presented on May 20, 2024, at the annual Digestive Disease Week® (DDW) (Abstract 638).
LIMITATIONS:
Further prospective studies are needed to assess the validity of the test in a more diverse population and with different weight loss interventions.
DISCLOSURES:
This study was supported by a partnership between Mayo Clinic and Phenomix Sciences. Dr. Acosta is a cofounder of Phenomix Sciences.
A version of this article appeared on Medscape.com.
Mirikizumab Shows Promise for Moderate to Severe Crohn’s Disease
WASHINGTON — , according to results of the phase 3 randomized, double blind, treat-through VIVID-1 study.
Bruce E. Sands, MD, AGAF, chief of gastroenterology at the Icahn School of Medicine at Mount Sinai in New York, reported the findings in a poster (Abstract Su1801) at the annual Digestive Disease Week® (DDW).
The FDA approved mirikizumab (Omvoh, Eli Lilly) to treat moderate to severe ulcerative colitis in October 2023.
Dr. Sands and a team of US and international collaborators studied 1065 adults with Crohn’s disease or fistulizing Crohn’s disease for 3 months or more, with a mean duration of more than 7 years. At baseline, participants had a Simple Endoscopic Score for Crohn’s Disease (SES-CD) of 7 or more and reported an inadequate response, lost response, or intolerance to other therapy.
A total of 579 people were randomly assigned to mirikizumab and another 199 to placebo. Another 287 patients received ustekinumab; though they were not included in this current analysis, the findings were presented separately at DDW 2024.
Mean age of study participants was 30 years, and men comprised 57%-59% of the groups. Nearly half (49%) of each group previously failed biologic therapy.
A primary composite endpoint was clinical response at 12 weeks according to patient reported outcome and endoscopic response at 52 weeks measured with the SES-CD. A second primary endpoint was clinical response at 12 weeks by patient reported outcome combined with clinical remission on Crohn’s Disease Activity Index (CDAI) at 52 weeks.
Researchers also tracked 12 major secondary endpoints for mirikizumab vs placebo, including clinical response, endoscopic response, and clinical remission at week 12 and week 52.
Efficacy Findings
A higher percentage of participants in the mirikizumab group achieved 12-week secondary endpoints compared with placebo. In the treatment group, 32.5% reached endoscopic response vs 12.6% in the placebo group, a statistically significant difference (P < .000001). In addition, 17.6% achieved endoscopic remission in the treatment group vs 7.0% in the placebo group at 12 weeks (P < .000213).
The “treat-through” results at 52 weeks revealed that a higher proportion of the group taking mirikizumab met the co-primary endpoints compared with placebo. A total of 48.4% in the mirikizumab group vs 9.0% in the placebo group achieved endoscopic response (P < .000001). Similarly, a higher proportion met clinical remission on the CDAI, 54.1% in the treatment group vs 19.6% in the placebo group (P < .000001).
Overall, 38% of mirikizumab-treated patients vs 9% of the placebo group reached a composite endpoint of patient reported clinical response at week 12 and endoscopic response by SES-CD at week 52 (P < .000001).
Dr. Sands and colleagues also combined clinical response reported by patients at 12 weeks with CDAI findings for clinical remission at week 52. A total of 45.4% in the treatment group met the combined endpoint compared with 19.6% of the placebo group (P < .000001).
In an additional analysis, the researchers looked at this composite endpoint in patients in both groups who had failed or not failed a prior biologic for a total of 43.4% vs 12.4%, and 47.3% vs 26.5%, respectively.
“Mirikizumab demonstrated statistically significant and clinically meaningful improvements” in the study co-primary endpoints and secondary endpoints compared with placebo, the researchers concluded.
Safety Findings
Safety outcomes during the 52-week study were “consistent with the known safety profile” of mirikizumab, the researchers noted.
Treatment-emergent adverse events occurred in 78.6% of mirikizumab participants vs 73.0% of the placebo group. The most common were COVID-19, anemia, and arthralgia. Serious adverse events were reported in 10.3% of the mirikizumab group vs 17.1% of the placebo group. There were seven opportunistic infections in the treatment group, including herpes zoster and Candida, compared with none in the placebo group.
One person in the placebo cohort died of a pulmonary embolism; there were no deaths in the mirikizumab group.
People randomly assigned to placebo without a response at 12 weeks were switched over to mirikizumab. However, the findings from this group between 12 and 52 weeks were excluded from the 1-year data presented at DDW 2024, including one death from worsening Crohn’s disease during that time.
Mirikizumab looked particularly robust in this study, and it may turn out to be a critically important option for our patients, said Jordan Axelrad, MD, MPH, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health in New York City. Dr. Axelrad was not involved in this study.
Of importance, effect sizes were similar for “bio-naive and previously biologic-exposed patients,” he added.
These data “really underscore that therapies targeting IL-23 may be clinically useful for Crohn’s disease patients with prior biologic failure, representing a significant departure from our previous experience with other biologic classes,” Dr. Axelrad said.
The study was funded by Eli Lilly and Company. Dr. Sands is a consultant and receives grant funding from Lilly. Dr. Axelrad had no relevant disclosures.
A version of this article appeared on Medscape.com.
WASHINGTON — , according to results of the phase 3 randomized, double blind, treat-through VIVID-1 study.
Bruce E. Sands, MD, AGAF, chief of gastroenterology at the Icahn School of Medicine at Mount Sinai in New York, reported the findings in a poster (Abstract Su1801) at the annual Digestive Disease Week® (DDW).
The FDA approved mirikizumab (Omvoh, Eli Lilly) to treat moderate to severe ulcerative colitis in October 2023.
Dr. Sands and a team of US and international collaborators studied 1065 adults with Crohn’s disease or fistulizing Crohn’s disease for 3 months or more, with a mean duration of more than 7 years. At baseline, participants had a Simple Endoscopic Score for Crohn’s Disease (SES-CD) of 7 or more and reported an inadequate response, lost response, or intolerance to other therapy.
A total of 579 people were randomly assigned to mirikizumab and another 199 to placebo. Another 287 patients received ustekinumab; though they were not included in this current analysis, the findings were presented separately at DDW 2024.
Mean age of study participants was 30 years, and men comprised 57%-59% of the groups. Nearly half (49%) of each group previously failed biologic therapy.
A primary composite endpoint was clinical response at 12 weeks according to patient reported outcome and endoscopic response at 52 weeks measured with the SES-CD. A second primary endpoint was clinical response at 12 weeks by patient reported outcome combined with clinical remission on Crohn’s Disease Activity Index (CDAI) at 52 weeks.
Researchers also tracked 12 major secondary endpoints for mirikizumab vs placebo, including clinical response, endoscopic response, and clinical remission at week 12 and week 52.
Efficacy Findings
A higher percentage of participants in the mirikizumab group achieved 12-week secondary endpoints compared with placebo. In the treatment group, 32.5% reached endoscopic response vs 12.6% in the placebo group, a statistically significant difference (P < .000001). In addition, 17.6% achieved endoscopic remission in the treatment group vs 7.0% in the placebo group at 12 weeks (P < .000213).
The “treat-through” results at 52 weeks revealed that a higher proportion of the group taking mirikizumab met the co-primary endpoints compared with placebo. A total of 48.4% in the mirikizumab group vs 9.0% in the placebo group achieved endoscopic response (P < .000001). Similarly, a higher proportion met clinical remission on the CDAI, 54.1% in the treatment group vs 19.6% in the placebo group (P < .000001).
Overall, 38% of mirikizumab-treated patients vs 9% of the placebo group reached a composite endpoint of patient reported clinical response at week 12 and endoscopic response by SES-CD at week 52 (P < .000001).
Dr. Sands and colleagues also combined clinical response reported by patients at 12 weeks with CDAI findings for clinical remission at week 52. A total of 45.4% in the treatment group met the combined endpoint compared with 19.6% of the placebo group (P < .000001).
In an additional analysis, the researchers looked at this composite endpoint in patients in both groups who had failed or not failed a prior biologic for a total of 43.4% vs 12.4%, and 47.3% vs 26.5%, respectively.
“Mirikizumab demonstrated statistically significant and clinically meaningful improvements” in the study co-primary endpoints and secondary endpoints compared with placebo, the researchers concluded.
Safety Findings
Safety outcomes during the 52-week study were “consistent with the known safety profile” of mirikizumab, the researchers noted.
Treatment-emergent adverse events occurred in 78.6% of mirikizumab participants vs 73.0% of the placebo group. The most common were COVID-19, anemia, and arthralgia. Serious adverse events were reported in 10.3% of the mirikizumab group vs 17.1% of the placebo group. There were seven opportunistic infections in the treatment group, including herpes zoster and Candida, compared with none in the placebo group.
One person in the placebo cohort died of a pulmonary embolism; there were no deaths in the mirikizumab group.
People randomly assigned to placebo without a response at 12 weeks were switched over to mirikizumab. However, the findings from this group between 12 and 52 weeks were excluded from the 1-year data presented at DDW 2024, including one death from worsening Crohn’s disease during that time.
Mirikizumab looked particularly robust in this study, and it may turn out to be a critically important option for our patients, said Jordan Axelrad, MD, MPH, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health in New York City. Dr. Axelrad was not involved in this study.
Of importance, effect sizes were similar for “bio-naive and previously biologic-exposed patients,” he added.
These data “really underscore that therapies targeting IL-23 may be clinically useful for Crohn’s disease patients with prior biologic failure, representing a significant departure from our previous experience with other biologic classes,” Dr. Axelrad said.
The study was funded by Eli Lilly and Company. Dr. Sands is a consultant and receives grant funding from Lilly. Dr. Axelrad had no relevant disclosures.
A version of this article appeared on Medscape.com.
WASHINGTON — , according to results of the phase 3 randomized, double blind, treat-through VIVID-1 study.
Bruce E. Sands, MD, AGAF, chief of gastroenterology at the Icahn School of Medicine at Mount Sinai in New York, reported the findings in a poster (Abstract Su1801) at the annual Digestive Disease Week® (DDW).
The FDA approved mirikizumab (Omvoh, Eli Lilly) to treat moderate to severe ulcerative colitis in October 2023.
Dr. Sands and a team of US and international collaborators studied 1065 adults with Crohn’s disease or fistulizing Crohn’s disease for 3 months or more, with a mean duration of more than 7 years. At baseline, participants had a Simple Endoscopic Score for Crohn’s Disease (SES-CD) of 7 or more and reported an inadequate response, lost response, or intolerance to other therapy.
A total of 579 people were randomly assigned to mirikizumab and another 199 to placebo. Another 287 patients received ustekinumab; though they were not included in this current analysis, the findings were presented separately at DDW 2024.
Mean age of study participants was 30 years, and men comprised 57%-59% of the groups. Nearly half (49%) of each group previously failed biologic therapy.
A primary composite endpoint was clinical response at 12 weeks according to patient reported outcome and endoscopic response at 52 weeks measured with the SES-CD. A second primary endpoint was clinical response at 12 weeks by patient reported outcome combined with clinical remission on Crohn’s Disease Activity Index (CDAI) at 52 weeks.
Researchers also tracked 12 major secondary endpoints for mirikizumab vs placebo, including clinical response, endoscopic response, and clinical remission at week 12 and week 52.
Efficacy Findings
A higher percentage of participants in the mirikizumab group achieved 12-week secondary endpoints compared with placebo. In the treatment group, 32.5% reached endoscopic response vs 12.6% in the placebo group, a statistically significant difference (P < .000001). In addition, 17.6% achieved endoscopic remission in the treatment group vs 7.0% in the placebo group at 12 weeks (P < .000213).
The “treat-through” results at 52 weeks revealed that a higher proportion of the group taking mirikizumab met the co-primary endpoints compared with placebo. A total of 48.4% in the mirikizumab group vs 9.0% in the placebo group achieved endoscopic response (P < .000001). Similarly, a higher proportion met clinical remission on the CDAI, 54.1% in the treatment group vs 19.6% in the placebo group (P < .000001).
Overall, 38% of mirikizumab-treated patients vs 9% of the placebo group reached a composite endpoint of patient reported clinical response at week 12 and endoscopic response by SES-CD at week 52 (P < .000001).
Dr. Sands and colleagues also combined clinical response reported by patients at 12 weeks with CDAI findings for clinical remission at week 52. A total of 45.4% in the treatment group met the combined endpoint compared with 19.6% of the placebo group (P < .000001).
In an additional analysis, the researchers looked at this composite endpoint in patients in both groups who had failed or not failed a prior biologic for a total of 43.4% vs 12.4%, and 47.3% vs 26.5%, respectively.
“Mirikizumab demonstrated statistically significant and clinically meaningful improvements” in the study co-primary endpoints and secondary endpoints compared with placebo, the researchers concluded.
Safety Findings
Safety outcomes during the 52-week study were “consistent with the known safety profile” of mirikizumab, the researchers noted.
Treatment-emergent adverse events occurred in 78.6% of mirikizumab participants vs 73.0% of the placebo group. The most common were COVID-19, anemia, and arthralgia. Serious adverse events were reported in 10.3% of the mirikizumab group vs 17.1% of the placebo group. There were seven opportunistic infections in the treatment group, including herpes zoster and Candida, compared with none in the placebo group.
One person in the placebo cohort died of a pulmonary embolism; there were no deaths in the mirikizumab group.
People randomly assigned to placebo without a response at 12 weeks were switched over to mirikizumab. However, the findings from this group between 12 and 52 weeks were excluded from the 1-year data presented at DDW 2024, including one death from worsening Crohn’s disease during that time.
Mirikizumab looked particularly robust in this study, and it may turn out to be a critically important option for our patients, said Jordan Axelrad, MD, MPH, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health in New York City. Dr. Axelrad was not involved in this study.
Of importance, effect sizes were similar for “bio-naive and previously biologic-exposed patients,” he added.
These data “really underscore that therapies targeting IL-23 may be clinically useful for Crohn’s disease patients with prior biologic failure, representing a significant departure from our previous experience with other biologic classes,” Dr. Axelrad said.
The study was funded by Eli Lilly and Company. Dr. Sands is a consultant and receives grant funding from Lilly. Dr. Axelrad had no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM DDW 2024