IBD & Intestinal Disorders

Increased competition when new tumor necrosis factor inhibitors entered the market did not translate into price reductions during 2009-2016, according to a new analysis of Medicare claims data and wholesale acquisition costs published online in JAMA Internal Medicine.

utah778/Thinkstock

A research team led by Alvaro San-Juan-Rodriguez, PharmD, of the University of Pittsburgh said their analysis illustrates “a market failure contributing to the rising costs of prescription drugs.”

Before 2009, etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira) were the only tumor necrosis factor (TNF) inhibitors approved by the Food and Drug Administration for treating rheumatoid arthritis; infliximab and adalimumab are also approved to treat inflammatory bowel disease. In 2009, subcutaneous golimumab (Simponi) and certolizumab pegol (Cimzia) entered the market, followed by intravenous golimumab (Simponi ARIA) in 2013.

The researchers used an interrupted time series analysis with a linear model that “regressed the annual cost of existing TNF inhibitors against a continuous variable for month, two indicator variables for each period after market entry of new drugs, and the interactions between them.”

Using estimates from this model, the researchers calculated the trends in costs that would have been expected if new anti-TNFs had not entered the market. They examined costs for TNF inhibitors typically reimbursed under Medicare Part D (Enbrel, Humira, Simponi, and Cimzia) and adjusted the data for increases in manufacturer rebates, but “owing to lack of data,” they could not “assess how purchasing prices for drugs typically reimbursed under Medicare Part B [Remicade and Simponi ARIA] changed over time.” All estimates for annual costs of treatment were based on dosing recommendations for a standard 80-kg patient with rheumatoid arthritis.

The annual treatment costs with existing TNF inhibitors increased after the three new agents entered the market. For example, when wholesale acquisition cost data was applied, annual treatment costs with existing TNF inhibitors increased by 144% from April 2009 to December 2016 after new drug entry (from $15.809 to $38,574). However, in the absence of new drugs’ entry, the researchers estimated that annual treatment costs would have increased by 34% (from $15,809 to $21,184).

Medicare annual treatment costs increased by 139% (from $14,901 to $35,613), compared with a 43% increase expected in the absence of new drugs’ entry (from $14,901 to $21,308). Medicare spending increased in parallel with increases in annual treatment costs, but out-of-pocket costs and manufacturer coverage gap discounts remained relatively constant over time.

The research team noted that if cost trends had not changed after the entry of new products, the costs of Enbrel, Remicade, and Humira in December 2016 would have been 40%-45% lower.

“These increases were born solely by Medicare, while patient out-of-pocket spending remained flat. In addition, these increases were not offset by manufacturer discounts in the Medicare Part D coverage gap. The rising costs of existing products may reflect manufacturers’ opportunism in response to payers’ increased willingness to pay for TNF inhibitors after market entry of new, more expensive agents,” the research team noted.

The study was funded in part by the Myers Family Foundation and one author reported funding from the National Heart, Lung, and Blood Institute.

SOURCE: San-Juan-Rodriguez A et al. JAMA Intern Med. 2019 Feb 18. doi: 10.1001/jamainternmed.2018.7656

Increased competition when new tumor necrosis factor inhibitors entered the market did not translate into price reductions during 2009-2016, according to a new analysis of Medicare claims data and wholesale acquisition costs published online in JAMA Internal Medicine.

utah778/Thinkstock

A research team led by Alvaro San-Juan-Rodriguez, PharmD, of the University of Pittsburgh said their analysis illustrates “a market failure contributing to the rising costs of prescription drugs.”

Before 2009, etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira) were the only tumor necrosis factor (TNF) inhibitors approved by the Food and Drug Administration for treating rheumatoid arthritis; infliximab and adalimumab are also approved to treat inflammatory bowel disease. In 2009, subcutaneous golimumab (Simponi) and certolizumab pegol (Cimzia) entered the market, followed by intravenous golimumab (Simponi ARIA) in 2013.

The researchers used an interrupted time series analysis with a linear model that “regressed the annual cost of existing TNF inhibitors against a continuous variable for month, two indicator variables for each period after market entry of new drugs, and the interactions between them.”

Using estimates from this model, the researchers calculated the trends in costs that would have been expected if new anti-TNFs had not entered the market. They examined costs for TNF inhibitors typically reimbursed under Medicare Part D (Enbrel, Humira, Simponi, and Cimzia) and adjusted the data for increases in manufacturer rebates, but “owing to lack of data,” they could not “assess how purchasing prices for drugs typically reimbursed under Medicare Part B [Remicade and Simponi ARIA] changed over time.” All estimates for annual costs of treatment were based on dosing recommendations for a standard 80-kg patient with rheumatoid arthritis.

The annual treatment costs with existing TNF inhibitors increased after the three new agents entered the market. For example, when wholesale acquisition cost data was applied, annual treatment costs with existing TNF inhibitors increased by 144% from April 2009 to December 2016 after new drug entry (from $15.809 to $38,574). However, in the absence of new drugs’ entry, the researchers estimated that annual treatment costs would have increased by 34% (from $15,809 to $21,184).

Medicare annual treatment costs increased by 139% (from $14,901 to $35,613), compared with a 43% increase expected in the absence of new drugs’ entry (from $14,901 to $21,308). Medicare spending increased in parallel with increases in annual treatment costs, but out-of-pocket costs and manufacturer coverage gap discounts remained relatively constant over time.

The research team noted that if cost trends had not changed after the entry of new products, the costs of Enbrel, Remicade, and Humira in December 2016 would have been 40%-45% lower.

“These increases were born solely by Medicare, while patient out-of-pocket spending remained flat. In addition, these increases were not offset by manufacturer discounts in the Medicare Part D coverage gap. The rising costs of existing products may reflect manufacturers’ opportunism in response to payers’ increased willingness to pay for TNF inhibitors after market entry of new, more expensive agents,” the research team noted.

The study was funded in part by the Myers Family Foundation and one author reported funding from the National Heart, Lung, and Blood Institute.

SOURCE: San-Juan-Rodriguez A et al. JAMA Intern Med. 2019 Feb 18. doi: 10.1001/jamainternmed.2018.7656

Increased competition when new tumor necrosis factor inhibitors entered the market did not translate into price reductions during 2009-2016, according to a new analysis of Medicare claims data and wholesale acquisition costs published online in JAMA Internal Medicine.

utah778/Thinkstock

A research team led by Alvaro San-Juan-Rodriguez, PharmD, of the University of Pittsburgh said their analysis illustrates “a market failure contributing to the rising costs of prescription drugs.”

Before 2009, etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira) were the only tumor necrosis factor (TNF) inhibitors approved by the Food and Drug Administration for treating rheumatoid arthritis; infliximab and adalimumab are also approved to treat inflammatory bowel disease. In 2009, subcutaneous golimumab (Simponi) and certolizumab pegol (Cimzia) entered the market, followed by intravenous golimumab (Simponi ARIA) in 2013.

The researchers used an interrupted time series analysis with a linear model that “regressed the annual cost of existing TNF inhibitors against a continuous variable for month, two indicator variables for each period after market entry of new drugs, and the interactions between them.”

Using estimates from this model, the researchers calculated the trends in costs that would have been expected if new anti-TNFs had not entered the market. They examined costs for TNF inhibitors typically reimbursed under Medicare Part D (Enbrel, Humira, Simponi, and Cimzia) and adjusted the data for increases in manufacturer rebates, but “owing to lack of data,” they could not “assess how purchasing prices for drugs typically reimbursed under Medicare Part B [Remicade and Simponi ARIA] changed over time.” All estimates for annual costs of treatment were based on dosing recommendations for a standard 80-kg patient with rheumatoid arthritis.

The annual treatment costs with existing TNF inhibitors increased after the three new agents entered the market. For example, when wholesale acquisition cost data was applied, annual treatment costs with existing TNF inhibitors increased by 144% from April 2009 to December 2016 after new drug entry (from $15.809 to $38,574). However, in the absence of new drugs’ entry, the researchers estimated that annual treatment costs would have increased by 34% (from $15,809 to $21,184).

Medicare annual treatment costs increased by 139% (from $14,901 to $35,613), compared with a 43% increase expected in the absence of new drugs’ entry (from $14,901 to $21,308). Medicare spending increased in parallel with increases in annual treatment costs, but out-of-pocket costs and manufacturer coverage gap discounts remained relatively constant over time.

The research team noted that if cost trends had not changed after the entry of new products, the costs of Enbrel, Remicade, and Humira in December 2016 would have been 40%-45% lower.

“These increases were born solely by Medicare, while patient out-of-pocket spending remained flat. In addition, these increases were not offset by manufacturer discounts in the Medicare Part D coverage gap. The rising costs of existing products may reflect manufacturers’ opportunism in response to payers’ increased willingness to pay for TNF inhibitors after market entry of new, more expensive agents,” the research team noted.

The study was funded in part by the Myers Family Foundation and one author reported funding from the National Heart, Lung, and Blood Institute.

SOURCE: San-Juan-Rodriguez A et al. JAMA Intern Med. 2019 Feb 18. doi: 10.1001/jamainternmed.2018.7656

Early enterovirus infections could be an underlying cause of celiac disease, according to a case-control study of Norwegian children with an at-risk genotype.

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“We found a significant association between exposure to enterovirus and subsequent risk of celiac disease,” wrote lead author Christian R. Kahrs of the University of Oslo and his coauthors, adding that “adenovirus was not associated with celiac disease.” The study was published in the BMJ.

From 2001 to 2007, 46,939 newborns in Norway were screened for the HLA-DQ2/DQ8 genotype, which is associated with an increased risk of celiac disease. The genotype was identified in 912 children, and blood and stool sample collection began at 3 months. Children who were still contributing blood samples by 2014-2016 were invited to be screened for celiac disease.

Of the 220 children screened, 25 were diagnosed with celiac disease. Enterovirus was detected in 370 (17%) of the 2,135 stool samples and was more frequent in children who developed celiac disease antibodies than in matched controls (adjusted odds ratio, 1.49; 95% confidence interval, 1.07-2.06; P = .02). There was a significant association between later development of celiac disease and the commonly identified enterovirus A (aOR, 1.62; 95% CI, 1.04-2.53; P = .03) and enterovirus B (aOR, 2.27; 95% CI, 1.33-3.88; P = .003). No adenovirus types were associated with development of celiac disease.

The authors acknowledged their study’s limitations, including the possibility that children might be diagnosed with celiac disease later than the study’s roughly 10-year follow-up and the limited number of children with the disease despite a large number of analyzed samples. They noted that, “given the limited number of cases, we call for corroboration in similar studies and preferably interventional studies to reach conclusions about causality.”

The study was funded by the Research Council of Norway, the Project for the Conceptual Development of Research Organization, and the Norwegian Coeliac Society. Two authors reported grant support from trusts and foundations in Norway and Switzerland; no conflicts of interest were reported.

SOURCE: Kahrs CR et al. BMJ. 2019 Feb 13. doi: 10.1136/bmj.l231.

Early enterovirus infections could be an underlying cause of celiac disease, according to a case-control study of Norwegian children with an at-risk genotype.

designer491/Thinkstock

“We found a significant association between exposure to enterovirus and subsequent risk of celiac disease,” wrote lead author Christian R. Kahrs of the University of Oslo and his coauthors, adding that “adenovirus was not associated with celiac disease.” The study was published in the BMJ.

From 2001 to 2007, 46,939 newborns in Norway were screened for the HLA-DQ2/DQ8 genotype, which is associated with an increased risk of celiac disease. The genotype was identified in 912 children, and blood and stool sample collection began at 3 months. Children who were still contributing blood samples by 2014-2016 were invited to be screened for celiac disease.

Of the 220 children screened, 25 were diagnosed with celiac disease. Enterovirus was detected in 370 (17%) of the 2,135 stool samples and was more frequent in children who developed celiac disease antibodies than in matched controls (adjusted odds ratio, 1.49; 95% confidence interval, 1.07-2.06; P = .02). There was a significant association between later development of celiac disease and the commonly identified enterovirus A (aOR, 1.62; 95% CI, 1.04-2.53; P = .03) and enterovirus B (aOR, 2.27; 95% CI, 1.33-3.88; P = .003). No adenovirus types were associated with development of celiac disease.

The authors acknowledged their study’s limitations, including the possibility that children might be diagnosed with celiac disease later than the study’s roughly 10-year follow-up and the limited number of children with the disease despite a large number of analyzed samples. They noted that, “given the limited number of cases, we call for corroboration in similar studies and preferably interventional studies to reach conclusions about causality.”

The study was funded by the Research Council of Norway, the Project for the Conceptual Development of Research Organization, and the Norwegian Coeliac Society. Two authors reported grant support from trusts and foundations in Norway and Switzerland; no conflicts of interest were reported.

SOURCE: Kahrs CR et al. BMJ. 2019 Feb 13. doi: 10.1136/bmj.l231.

Early enterovirus infections could be an underlying cause of celiac disease, according to a case-control study of Norwegian children with an at-risk genotype.

designer491/Thinkstock

“We found a significant association between exposure to enterovirus and subsequent risk of celiac disease,” wrote lead author Christian R. Kahrs of the University of Oslo and his coauthors, adding that “adenovirus was not associated with celiac disease.” The study was published in the BMJ.

From 2001 to 2007, 46,939 newborns in Norway were screened for the HLA-DQ2/DQ8 genotype, which is associated with an increased risk of celiac disease. The genotype was identified in 912 children, and blood and stool sample collection began at 3 months. Children who were still contributing blood samples by 2014-2016 were invited to be screened for celiac disease.

Of the 220 children screened, 25 were diagnosed with celiac disease. Enterovirus was detected in 370 (17%) of the 2,135 stool samples and was more frequent in children who developed celiac disease antibodies than in matched controls (adjusted odds ratio, 1.49; 95% confidence interval, 1.07-2.06; P = .02). There was a significant association between later development of celiac disease and the commonly identified enterovirus A (aOR, 1.62; 95% CI, 1.04-2.53; P = .03) and enterovirus B (aOR, 2.27; 95% CI, 1.33-3.88; P = .003). No adenovirus types were associated with development of celiac disease.

The authors acknowledged their study’s limitations, including the possibility that children might be diagnosed with celiac disease later than the study’s roughly 10-year follow-up and the limited number of children with the disease despite a large number of analyzed samples. They noted that, “given the limited number of cases, we call for corroboration in similar studies and preferably interventional studies to reach conclusions about causality.”

The study was funded by the Research Council of Norway, the Project for the Conceptual Development of Research Organization, and the Norwegian Coeliac Society. Two authors reported grant support from trusts and foundations in Norway and Switzerland; no conflicts of interest were reported.

SOURCE: Kahrs CR et al. BMJ. 2019 Feb 13. doi: 10.1136/bmj.l231.

LAS VEGAS – Delays in diagnosis of inflammatory bowel disease (IBD) appear to be very common and often extensive, a new survey of U.S. patients suggests. Nearly two-thirds said their diagnosis was delayed past symptom onset for more than a year, and almost half reported a delay of more than 2 years.

On average, patients who experienced diagnosis delays said they’d seen an average of 3.5 physicians. “Most patients reported that they received an uncertain or wrong diagnosis by their primary care physician or gastroenterologist,” said study coauthor Ryan C. Ungaro, MD, of Icahn School of Medicine at Mount Sinai, New York, in an interview prior to the presentation of the study findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

“Working at a tertiary care IBD center, we noticed that many patients tell us it took them a long time to get diagnosed with Crohn’s disease [CD] or ulcerative colitis [UC],” said Dr. Ungaro. “There are some studies on delay in diagnosis in Europe but none in the U.S. We hypothesized that diagnostic delay is a major issue for IBD patients in the U.S.”

The study authors offered a survey to 2,341 patients with IBD; 1,121 responded to the questions. Of those, 68% reported their diagnosis was delayed, with 64% reporting a delay of over 1 year and 48% reporting a delay over 2 years.

Compared with those with UC, patients with CD were more likely to report more than 1-year delays (70% vs. 48%; P less than .0001) and more than 2-year delays (52% vs. 37%; P = .0008).

Patients who reported delays said they saw an average of 3.5 physicians before getting an IBD diagnosis. The patients most commonly blamed their incorrect diagnosis on primary care providers (58%) and gastroenterologists (28%).

“Most likely, CD may be misdiagnosed because the common presenting symptoms – abdominal pain, diarrhea – are also seen in other common gastrointestinal conditions such as irritable bowel syndrome,” Dr. Ungaro said. “In contrast, most patients with UC present with rectal bleeding which is a ‘red flag’ symptom that is more likely to get worked up.”

In some cases, patients blamed themselves, reporting “that they personally did not feel their symptoms warranted work-up or were too embarrassed by their symptoms to tell anyone,” Dr. Ungaro said. “The other theme that was noted was access – delay or difficulty seeing a gastroenterologist.”

Going forward, “diagnostic delay may be improved through patient education regarding awareness of alarm symptoms for IBD,” said gastroenterologist and study lead author Zane Gallinger, MD, FRCPC, of the University of Toronto at Mount Sinai Hospital, in an interview. According to him, these symptoms include diarrhea, abdominal pain, weight loss, family history of CD, perianal abscess, and fistula and fever.

At the primary care level, Dr. Gallinger said that noninvasive tests such as fecal calprotectin can help identify patients with inflammatory conditions and that “more rapid access to gastroenterologists for earlier diagnosis of IBD can improve patient outcomes.”

The Crohn’s and Colitis Foundation funded the study. Dr. Gallinger reported relationships with Takeda and AbbVie.

SOURCE: Gallinger Z et al. Crohn’s & Colitis Congress, Abstract P030.

LAS VEGAS – Delays in diagnosis of inflammatory bowel disease (IBD) appear to be very common and often extensive, a new survey of U.S. patients suggests. Nearly two-thirds said their diagnosis was delayed past symptom onset for more than a year, and almost half reported a delay of more than 2 years.

On average, patients who experienced diagnosis delays said they’d seen an average of 3.5 physicians. “Most patients reported that they received an uncertain or wrong diagnosis by their primary care physician or gastroenterologist,” said study coauthor Ryan C. Ungaro, MD, of Icahn School of Medicine at Mount Sinai, New York, in an interview prior to the presentation of the study findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

“Working at a tertiary care IBD center, we noticed that many patients tell us it took them a long time to get diagnosed with Crohn’s disease [CD] or ulcerative colitis [UC],” said Dr. Ungaro. “There are some studies on delay in diagnosis in Europe but none in the U.S. We hypothesized that diagnostic delay is a major issue for IBD patients in the U.S.”

The study authors offered a survey to 2,341 patients with IBD; 1,121 responded to the questions. Of those, 68% reported their diagnosis was delayed, with 64% reporting a delay of over 1 year and 48% reporting a delay over 2 years.

Compared with those with UC, patients with CD were more likely to report more than 1-year delays (70% vs. 48%; P less than .0001) and more than 2-year delays (52% vs. 37%; P = .0008).

Patients who reported delays said they saw an average of 3.5 physicians before getting an IBD diagnosis. The patients most commonly blamed their incorrect diagnosis on primary care providers (58%) and gastroenterologists (28%).

“Most likely, CD may be misdiagnosed because the common presenting symptoms – abdominal pain, diarrhea – are also seen in other common gastrointestinal conditions such as irritable bowel syndrome,” Dr. Ungaro said. “In contrast, most patients with UC present with rectal bleeding which is a ‘red flag’ symptom that is more likely to get worked up.”

In some cases, patients blamed themselves, reporting “that they personally did not feel their symptoms warranted work-up or were too embarrassed by their symptoms to tell anyone,” Dr. Ungaro said. “The other theme that was noted was access – delay or difficulty seeing a gastroenterologist.”

Going forward, “diagnostic delay may be improved through patient education regarding awareness of alarm symptoms for IBD,” said gastroenterologist and study lead author Zane Gallinger, MD, FRCPC, of the University of Toronto at Mount Sinai Hospital, in an interview. According to him, these symptoms include diarrhea, abdominal pain, weight loss, family history of CD, perianal abscess, and fistula and fever.

At the primary care level, Dr. Gallinger said that noninvasive tests such as fecal calprotectin can help identify patients with inflammatory conditions and that “more rapid access to gastroenterologists for earlier diagnosis of IBD can improve patient outcomes.”

The Crohn’s and Colitis Foundation funded the study. Dr. Gallinger reported relationships with Takeda and AbbVie.

SOURCE: Gallinger Z et al. Crohn’s & Colitis Congress, Abstract P030.

LAS VEGAS – Delays in diagnosis of inflammatory bowel disease (IBD) appear to be very common and often extensive, a new survey of U.S. patients suggests. Nearly two-thirds said their diagnosis was delayed past symptom onset for more than a year, and almost half reported a delay of more than 2 years.

On average, patients who experienced diagnosis delays said they’d seen an average of 3.5 physicians. “Most patients reported that they received an uncertain or wrong diagnosis by their primary care physician or gastroenterologist,” said study coauthor Ryan C. Ungaro, MD, of Icahn School of Medicine at Mount Sinai, New York, in an interview prior to the presentation of the study findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

“Working at a tertiary care IBD center, we noticed that many patients tell us it took them a long time to get diagnosed with Crohn’s disease [CD] or ulcerative colitis [UC],” said Dr. Ungaro. “There are some studies on delay in diagnosis in Europe but none in the U.S. We hypothesized that diagnostic delay is a major issue for IBD patients in the U.S.”

The study authors offered a survey to 2,341 patients with IBD; 1,121 responded to the questions. Of those, 68% reported their diagnosis was delayed, with 64% reporting a delay of over 1 year and 48% reporting a delay over 2 years.

Compared with those with UC, patients with CD were more likely to report more than 1-year delays (70% vs. 48%; P less than .0001) and more than 2-year delays (52% vs. 37%; P = .0008).

Patients who reported delays said they saw an average of 3.5 physicians before getting an IBD diagnosis. The patients most commonly blamed their incorrect diagnosis on primary care providers (58%) and gastroenterologists (28%).

“Most likely, CD may be misdiagnosed because the common presenting symptoms – abdominal pain, diarrhea – are also seen in other common gastrointestinal conditions such as irritable bowel syndrome,” Dr. Ungaro said. “In contrast, most patients with UC present with rectal bleeding which is a ‘red flag’ symptom that is more likely to get worked up.”

In some cases, patients blamed themselves, reporting “that they personally did not feel their symptoms warranted work-up or were too embarrassed by their symptoms to tell anyone,” Dr. Ungaro said. “The other theme that was noted was access – delay or difficulty seeing a gastroenterologist.”

Going forward, “diagnostic delay may be improved through patient education regarding awareness of alarm symptoms for IBD,” said gastroenterologist and study lead author Zane Gallinger, MD, FRCPC, of the University of Toronto at Mount Sinai Hospital, in an interview. According to him, these symptoms include diarrhea, abdominal pain, weight loss, family history of CD, perianal abscess, and fistula and fever.

At the primary care level, Dr. Gallinger said that noninvasive tests such as fecal calprotectin can help identify patients with inflammatory conditions and that “more rapid access to gastroenterologists for earlier diagnosis of IBD can improve patient outcomes.”

The Crohn’s and Colitis Foundation funded the study. Dr. Gallinger reported relationships with Takeda and AbbVie.

SOURCE: Gallinger Z et al. Crohn’s & Colitis Congress, Abstract P030.

LAS VEGAS – Immunosuppressant thiopurine drugs are a common and often successful treatment for patients with inflammatory bowel disease (IBD), but they can cause serious side effects via myelosuppression. Now, a new study suggests that a racial gap may prevent minority patients from being promptly diagnosed with myelosuppressive side effects.

“We found that minority IBD patients – black, Hispanic, Asian/Pacific Islander – had significantly higher hospitalization rates that were due to myelosuppressive events compared to white IBD patients,” lead author Ryan Suk, MS, said in an interview. “Among those IBD patients who were hospitalized due to myelosuppression, black and Hispanic IBD patients had a significantly higher chance of getting admitted as urgent compared to white IBD patients.”

Ms. Suk, a health economics graduate student at the University of Texas, Houston, spoke in an interview prior to the presentation of her study’s findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

According to Ms. Suk, multiple studies have previously revealed racial and ethnic disparities in health care access and use by minority patients with IBD.

She pointed to a 2010 study that found black patients with IBD were much less likely than whites were to see a gastroenterologist or IBD specialist at least once a year. She also cited a 2009 study that found black patients with IBD were significantly less adherent than were white patients; researchers linked older age and higher trust in physicians to higher levels of adherence (Am J Gastroenterol. 2010 Oct;105[10]:2202-8; Inflamm Bowel Dis. 2009 Aug;15[8]:1233-9).

In light of these findings, she said, “we questioned what the possible results of thiopurine use could be in minority patients without proper and consistent routine IBD care.”

While thiopurine is considered a standard form of care for IBD patients, Ms. Suk said an estimated one-third of patients must stop the treatment because of side effects such as anemia, leukopenia/neutropenia, and thrombocytopenia.

For the new study, Ms. Suk and her colleagues tracked patients who were hospitalized with a primary diagnosis of IBD or IBD-related complications from 2003-2014 via the Nationwide Inpatient Sample. There were 249,253 white patients, 192,864 black patients, 28,956 Hispanic patients, 17,073 Asian/Pacific Islander patients, and 2,849 patients in the “other” category.

The researchers found higher odds of hospitalization for myelosuppression in minorities compared with non-Hispanic whites: Non-Hispanic blacks (adjusted odds ratio = 1.3; 95% confidence interval [1.2-1.4], vs. whites), Hispanics (aOR = 1.6; 95% CI [1.4-1.7], vs. whites), and Asian/Pacific Islanders (aOR = 2.3; 95% CI [1.9-2.8], vs. whites).

The researchers found that among patients diagnosed with myelosuppression, two groups – non-Hispanic blacks and Hispanics – had higher odds of being admitted urgently, compared with non-Hispanic whites (aOR = 1.7; 95% CI [1.2-2.3] and aOR = 1.6; 95% CI [1.1-2.2] vs. whites, respectively).

“Unlike Asian/Pacific Islander patients, black and Hispanic patients had a higher likelihood of getting hospitalized from myelosuppression and also higher likelihood to get admitted urgently compared to the white cohort,” Ms. Suk said. “It is possible that they have less access to thiopurine management and monitoring, leading to developing more severe adverse events and therefore having urgent myelosuppressive hospitalizations.”

As for Asian/Pacific Islander patients, she noted that they had the highest likelihood of myelosuppression hospitalization but did not have the highest chance of getting admitted as urgent. “We think that Asians have a higher risk of myelosuppression due to genetic factors, not from less access to care, and thus they had more elective hospitalizations,” she said.

The researchers also linked Medicaid, self-pay, and no-charge patients to higher levels of myelosuppression hospitalizations. “This shows that patients who have less access to care [need more] urgent admission from myelosuppressive events,” Ms. Suk said.

No funding was reported, and the study authors had no relevant disclosures.

SOURCE: Suk R et al. Crohn’s & Colitis Congress, Abstract P059.

LAS VEGAS – Immunosuppressant thiopurine drugs are a common and often successful treatment for patients with inflammatory bowel disease (IBD), but they can cause serious side effects via myelosuppression. Now, a new study suggests that a racial gap may prevent minority patients from being promptly diagnosed with myelosuppressive side effects.

“We found that minority IBD patients – black, Hispanic, Asian/Pacific Islander – had significantly higher hospitalization rates that were due to myelosuppressive events compared to white IBD patients,” lead author Ryan Suk, MS, said in an interview. “Among those IBD patients who were hospitalized due to myelosuppression, black and Hispanic IBD patients had a significantly higher chance of getting admitted as urgent compared to white IBD patients.”

Ms. Suk, a health economics graduate student at the University of Texas, Houston, spoke in an interview prior to the presentation of her study’s findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

According to Ms. Suk, multiple studies have previously revealed racial and ethnic disparities in health care access and use by minority patients with IBD.

She pointed to a 2010 study that found black patients with IBD were much less likely than whites were to see a gastroenterologist or IBD specialist at least once a year. She also cited a 2009 study that found black patients with IBD were significantly less adherent than were white patients; researchers linked older age and higher trust in physicians to higher levels of adherence (Am J Gastroenterol. 2010 Oct;105[10]:2202-8; Inflamm Bowel Dis. 2009 Aug;15[8]:1233-9).

In light of these findings, she said, “we questioned what the possible results of thiopurine use could be in minority patients without proper and consistent routine IBD care.”

While thiopurine is considered a standard form of care for IBD patients, Ms. Suk said an estimated one-third of patients must stop the treatment because of side effects such as anemia, leukopenia/neutropenia, and thrombocytopenia.

For the new study, Ms. Suk and her colleagues tracked patients who were hospitalized with a primary diagnosis of IBD or IBD-related complications from 2003-2014 via the Nationwide Inpatient Sample. There were 249,253 white patients, 192,864 black patients, 28,956 Hispanic patients, 17,073 Asian/Pacific Islander patients, and 2,849 patients in the “other” category.

The researchers found higher odds of hospitalization for myelosuppression in minorities compared with non-Hispanic whites: Non-Hispanic blacks (adjusted odds ratio = 1.3; 95% confidence interval [1.2-1.4], vs. whites), Hispanics (aOR = 1.6; 95% CI [1.4-1.7], vs. whites), and Asian/Pacific Islanders (aOR = 2.3; 95% CI [1.9-2.8], vs. whites).

The researchers found that among patients diagnosed with myelosuppression, two groups – non-Hispanic blacks and Hispanics – had higher odds of being admitted urgently, compared with non-Hispanic whites (aOR = 1.7; 95% CI [1.2-2.3] and aOR = 1.6; 95% CI [1.1-2.2] vs. whites, respectively).

“Unlike Asian/Pacific Islander patients, black and Hispanic patients had a higher likelihood of getting hospitalized from myelosuppression and also higher likelihood to get admitted urgently compared to the white cohort,” Ms. Suk said. “It is possible that they have less access to thiopurine management and monitoring, leading to developing more severe adverse events and therefore having urgent myelosuppressive hospitalizations.”

As for Asian/Pacific Islander patients, she noted that they had the highest likelihood of myelosuppression hospitalization but did not have the highest chance of getting admitted as urgent. “We think that Asians have a higher risk of myelosuppression due to genetic factors, not from less access to care, and thus they had more elective hospitalizations,” she said.

The researchers also linked Medicaid, self-pay, and no-charge patients to higher levels of myelosuppression hospitalizations. “This shows that patients who have less access to care [need more] urgent admission from myelosuppressive events,” Ms. Suk said.

No funding was reported, and the study authors had no relevant disclosures.

SOURCE: Suk R et al. Crohn’s & Colitis Congress, Abstract P059.

LAS VEGAS – Immunosuppressant thiopurine drugs are a common and often successful treatment for patients with inflammatory bowel disease (IBD), but they can cause serious side effects via myelosuppression. Now, a new study suggests that a racial gap may prevent minority patients from being promptly diagnosed with myelosuppressive side effects.

“We found that minority IBD patients – black, Hispanic, Asian/Pacific Islander – had significantly higher hospitalization rates that were due to myelosuppressive events compared to white IBD patients,” lead author Ryan Suk, MS, said in an interview. “Among those IBD patients who were hospitalized due to myelosuppression, black and Hispanic IBD patients had a significantly higher chance of getting admitted as urgent compared to white IBD patients.”

Ms. Suk, a health economics graduate student at the University of Texas, Houston, spoke in an interview prior to the presentation of her study’s findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

According to Ms. Suk, multiple studies have previously revealed racial and ethnic disparities in health care access and use by minority patients with IBD.

She pointed to a 2010 study that found black patients with IBD were much less likely than whites were to see a gastroenterologist or IBD specialist at least once a year. She also cited a 2009 study that found black patients with IBD were significantly less adherent than were white patients; researchers linked older age and higher trust in physicians to higher levels of adherence (Am J Gastroenterol. 2010 Oct;105[10]:2202-8; Inflamm Bowel Dis. 2009 Aug;15[8]:1233-9).

In light of these findings, she said, “we questioned what the possible results of thiopurine use could be in minority patients without proper and consistent routine IBD care.”

While thiopurine is considered a standard form of care for IBD patients, Ms. Suk said an estimated one-third of patients must stop the treatment because of side effects such as anemia, leukopenia/neutropenia, and thrombocytopenia.

For the new study, Ms. Suk and her colleagues tracked patients who were hospitalized with a primary diagnosis of IBD or IBD-related complications from 2003-2014 via the Nationwide Inpatient Sample. There were 249,253 white patients, 192,864 black patients, 28,956 Hispanic patients, 17,073 Asian/Pacific Islander patients, and 2,849 patients in the “other” category.

The researchers found higher odds of hospitalization for myelosuppression in minorities compared with non-Hispanic whites: Non-Hispanic blacks (adjusted odds ratio = 1.3; 95% confidence interval [1.2-1.4], vs. whites), Hispanics (aOR = 1.6; 95% CI [1.4-1.7], vs. whites), and Asian/Pacific Islanders (aOR = 2.3; 95% CI [1.9-2.8], vs. whites).

The researchers found that among patients diagnosed with myelosuppression, two groups – non-Hispanic blacks and Hispanics – had higher odds of being admitted urgently, compared with non-Hispanic whites (aOR = 1.7; 95% CI [1.2-2.3] and aOR = 1.6; 95% CI [1.1-2.2] vs. whites, respectively).

“Unlike Asian/Pacific Islander patients, black and Hispanic patients had a higher likelihood of getting hospitalized from myelosuppression and also higher likelihood to get admitted urgently compared to the white cohort,” Ms. Suk said. “It is possible that they have less access to thiopurine management and monitoring, leading to developing more severe adverse events and therefore having urgent myelosuppressive hospitalizations.”

As for Asian/Pacific Islander patients, she noted that they had the highest likelihood of myelosuppression hospitalization but did not have the highest chance of getting admitted as urgent. “We think that Asians have a higher risk of myelosuppression due to genetic factors, not from less access to care, and thus they had more elective hospitalizations,” she said.

The researchers also linked Medicaid, self-pay, and no-charge patients to higher levels of myelosuppression hospitalizations. “This shows that patients who have less access to care [need more] urgent admission from myelosuppressive events,” Ms. Suk said.

No funding was reported, and the study authors had no relevant disclosures.

SOURCE: Suk R et al. Crohn’s & Colitis Congress, Abstract P059.

LAS VEGAS – Inflammatory bowel disease (IBD) can disrupt both fertility and pregnancy, especially if it’s not fully controlled, and there’s a risk that the condition can be passed onto an unborn child. Still a new study suggests many patients with IBD don’t receive appropriate reproductive counseling.

Nearly two-thirds of 100 patients surveyed at a single center reported that no physician had talked to them about reproductive topics, and some said they’d considered not having children because of the condition. “Really fundamental subjects have not made their way into the interactions between patients and their care teams,” coauthor and gastroenterologist Sarah Streett, MD, AGAF, of Stanford (Calif.) University, said in an interview before the study was presented at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

IBD can lower fertility in both sexes and boost complications in pregnancy. “The good news is that almost all the medications used for IBD appear safe,” Dr. Streett said. “In fact, the safety risks for the baby and the pregnancy revolve around not having IBD under good control.”

Unfortunately, she said, misinformation is common. “Patients who become pregnant or are trying to become pregnant, and are worried about potential harm to the baby, will stop the medications due to incorrect information. Or they’ll be told by their health care team to stop their medications.”

Dr. Streett and study lead author Aarti Rao, MD, a gastroenterology fellow at Stanford, launched their study of IBD clinic patients to gain more understanding about patient knowledge. “We know from research already published that those with IBD have a lot of concerns about starting families and don’t have a lot of information to base their decision making on,” Dr. Streett said. “We wanted to evaluate that in our population and see how much people knew and what the need was.”

In 2018 and 2019, Dr. Streett and Dr. Rao gave an anonymous, validated 17-question survey to patients aged 18-45 with IBD. One hundred patients responded (median age = 30, 54% female, 59% white, 66% with incomes over $100,000, 52% with ulcerative colitis, 21% with prior IBD surgery, 71% with prior IBD hospitalization).

©Stuart Jenner/Thinkstock

With proper planning, care and coordination among treating health care providers via a multidisciplinary approach, women with IBD can have healthy pregnancies and healthy babies. Learn more at www.IBDParenthoodProject.org. 

SOURCE: Rao A et al. Crohn’s & Colitis Congress, Abstract P009.

LAS VEGAS – Inflammatory bowel disease (IBD) can disrupt both fertility and pregnancy, especially if it’s not fully controlled, and there’s a risk that the condition can be passed onto an unborn child. Still a new study suggests many patients with IBD don’t receive appropriate reproductive counseling.

Nearly two-thirds of 100 patients surveyed at a single center reported that no physician had talked to them about reproductive topics, and some said they’d considered not having children because of the condition. “Really fundamental subjects have not made their way into the interactions between patients and their care teams,” coauthor and gastroenterologist Sarah Streett, MD, AGAF, of Stanford (Calif.) University, said in an interview before the study was presented at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

IBD can lower fertility in both sexes and boost complications in pregnancy. “The good news is that almost all the medications used for IBD appear safe,” Dr. Streett said. “In fact, the safety risks for the baby and the pregnancy revolve around not having IBD under good control.”

Unfortunately, she said, misinformation is common. “Patients who become pregnant or are trying to become pregnant, and are worried about potential harm to the baby, will stop the medications due to incorrect information. Or they’ll be told by their health care team to stop their medications.”

Dr. Streett and study lead author Aarti Rao, MD, a gastroenterology fellow at Stanford, launched their study of IBD clinic patients to gain more understanding about patient knowledge. “We know from research already published that those with IBD have a lot of concerns about starting families and don’t have a lot of information to base their decision making on,” Dr. Streett said. “We wanted to evaluate that in our population and see how much people knew and what the need was.”

In 2018 and 2019, Dr. Streett and Dr. Rao gave an anonymous, validated 17-question survey to patients aged 18-45 with IBD. One hundred patients responded (median age = 30, 54% female, 59% white, 66% with incomes over $100,000, 52% with ulcerative colitis, 21% with prior IBD surgery, 71% with prior IBD hospitalization).

©Stuart Jenner/Thinkstock

With proper planning, care and coordination among treating health care providers via a multidisciplinary approach, women with IBD can have healthy pregnancies and healthy babies. Learn more at www.IBDParenthoodProject.org. 

SOURCE: Rao A et al. Crohn’s & Colitis Congress, Abstract P009.

LAS VEGAS – Inflammatory bowel disease (IBD) can disrupt both fertility and pregnancy, especially if it’s not fully controlled, and there’s a risk that the condition can be passed onto an unborn child. Still a new study suggests many patients with IBD don’t receive appropriate reproductive counseling.

Nearly two-thirds of 100 patients surveyed at a single center reported that no physician had talked to them about reproductive topics, and some said they’d considered not having children because of the condition. “Really fundamental subjects have not made their way into the interactions between patients and their care teams,” coauthor and gastroenterologist Sarah Streett, MD, AGAF, of Stanford (Calif.) University, said in an interview before the study was presented at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

IBD can lower fertility in both sexes and boost complications in pregnancy. “The good news is that almost all the medications used for IBD appear safe,” Dr. Streett said. “In fact, the safety risks for the baby and the pregnancy revolve around not having IBD under good control.”

Unfortunately, she said, misinformation is common. “Patients who become pregnant or are trying to become pregnant, and are worried about potential harm to the baby, will stop the medications due to incorrect information. Or they’ll be told by their health care team to stop their medications.”

Dr. Streett and study lead author Aarti Rao, MD, a gastroenterology fellow at Stanford, launched their study of IBD clinic patients to gain more understanding about patient knowledge. “We know from research already published that those with IBD have a lot of concerns about starting families and don’t have a lot of information to base their decision making on,” Dr. Streett said. “We wanted to evaluate that in our population and see how much people knew and what the need was.”

In 2018 and 2019, Dr. Streett and Dr. Rao gave an anonymous, validated 17-question survey to patients aged 18-45 with IBD. One hundred patients responded (median age = 30, 54% female, 59% white, 66% with incomes over $100,000, 52% with ulcerative colitis, 21% with prior IBD surgery, 71% with prior IBD hospitalization).

©Stuart Jenner/Thinkstock

With proper planning, care and coordination among treating health care providers via a multidisciplinary approach, women with IBD can have healthy pregnancies and healthy babies. Learn more at www.IBDParenthoodProject.org. 

SOURCE: Rao A et al. Crohn’s & Colitis Congress, Abstract P009.

Eight weeks of a mindfulness intervention known as acceptance and commitment therapy (ACT) significantly improved stress and depression among patients with inflammatory bowel disease, and these improvements persisted for at least 12 weeks after therapy ended, according to the results of a randomized, controlled trial.

Source: The American Gastroenterological Association

In the intention-to-treat analysis, stress symptoms, as measured by the Depression Anxiety and Stress Scales (DASS-21), improved by 39% at week 8 and by 45% at week 20, reported Brona Wynne, PhD, of University College Dublin together with her associates. These improvements were highly significant compared with baseline and treatment as usual (P = .001 for both comparisons). “Post hoc analyses indicated that baseline stress levels were similar in control and treatment groups,” the researchers wrote in Gastroenterology. “The results of the per protocol analysis were comparable, with a 43% and 49% reduction in stress in the treatment group from baseline to 8 and 20 weeks.”

Multiple studies have documented high levels of stress and psychological dysfunction among patients with Crohn’s disease and ulcerative colitis. Studies of various mindfulness therapy, relaxation, stress management, cognitive-behavioral therapy, and hypnotherapy interventions often failed to collect key clinical data or were underpowered, uncontrolled, and unrandomized. Acceptance and commitment therapy uses mindfulness to identify adverse thoughts and experiences, accept these as part of life, and recommit to “move towards values that have been identified and adopted by the individual,” the investigators wrote. “This can be defined as the ability to contact the present moment more fully as a conscious human being and to change, or persist in, behavior when doing so serves valued ends.”

Their single-center study, which they said was the first to evaluate ACT in IBD patients, included 79 individuals with stable or mildly active Crohn’s disease (38 patients) or ulcerative colitis (41 patients) who were randomly assigned to ACT (37 patients) or control treatment as usual (42 patients). The two comparison groups were demographically and clinically similar. The ACT program involved eight 90-minute, weekly sessions of groups of 14-16 individuals, led by a single psychologist who tailored the course material toward IBD with a focus on lowering stress. An independent psychologist observed each session to assess adherence to protocol.

Not only did ACT meet the primary study endpoint, it also produced a 25% decrease in perceived stress (on a 1-10 scale) by week 8 and a 27% decrease in perceived stress by week 20 (P less than .001 versus treatment as usual). Depression scores in the ACT group also fell by 47% by week 8 and by 45% at week 20 (P = .01 versus treatment as usual). Anxiety levels decreased by 29% at week 8 and by 31% at week 20, but these improvements did not significantly differ from those in the control group (P = .39).

Interestingly, ACT did not significantly improve symptom burden, activities of daily living, disease-related worry, general well-being, C-reactive protein (CRP) levels, fecal calprotectin levels, or scores on the version used of the Clinical Assessment of Depression (CAD) or the short Mayo assessment. Hair cortisol levels showed an association with baseline stress and anxiety, but not with treatment response.

Care programs for IBD increasingly emphasize mental health services despite a lack of robust trials to support these interventions, the investigators noted. Thus, their findings highlight “the need for researchers and clinicians to further develop and optimize the content and delivery of psychological programs for IBD patients.”

Tillotts Pharma and Boston Scientific provided partial funding, but had no other role in the study. The researchers reported having no relevant conflicts of interest.

SOURCE: Wynne B et al. Gastroenterology. 2018 Nov 16. doi: 10.1053/j.gastro.2018.11.030.

Eight weeks of a mindfulness intervention known as acceptance and commitment therapy (ACT) significantly improved stress and depression among patients with inflammatory bowel disease, and these improvements persisted for at least 12 weeks after therapy ended, according to the results of a randomized, controlled trial.

Source: The American Gastroenterological Association

In the intention-to-treat analysis, stress symptoms, as measured by the Depression Anxiety and Stress Scales (DASS-21), improved by 39% at week 8 and by 45% at week 20, reported Brona Wynne, PhD, of University College Dublin together with her associates. These improvements were highly significant compared with baseline and treatment as usual (P = .001 for both comparisons). “Post hoc analyses indicated that baseline stress levels were similar in control and treatment groups,” the researchers wrote in Gastroenterology. “The results of the per protocol analysis were comparable, with a 43% and 49% reduction in stress in the treatment group from baseline to 8 and 20 weeks.”

Multiple studies have documented high levels of stress and psychological dysfunction among patients with Crohn’s disease and ulcerative colitis. Studies of various mindfulness therapy, relaxation, stress management, cognitive-behavioral therapy, and hypnotherapy interventions often failed to collect key clinical data or were underpowered, uncontrolled, and unrandomized. Acceptance and commitment therapy uses mindfulness to identify adverse thoughts and experiences, accept these as part of life, and recommit to “move towards values that have been identified and adopted by the individual,” the investigators wrote. “This can be defined as the ability to contact the present moment more fully as a conscious human being and to change, or persist in, behavior when doing so serves valued ends.”

Their single-center study, which they said was the first to evaluate ACT in IBD patients, included 79 individuals with stable or mildly active Crohn’s disease (38 patients) or ulcerative colitis (41 patients) who were randomly assigned to ACT (37 patients) or control treatment as usual (42 patients). The two comparison groups were demographically and clinically similar. The ACT program involved eight 90-minute, weekly sessions of groups of 14-16 individuals, led by a single psychologist who tailored the course material toward IBD with a focus on lowering stress. An independent psychologist observed each session to assess adherence to protocol.

Not only did ACT meet the primary study endpoint, it also produced a 25% decrease in perceived stress (on a 1-10 scale) by week 8 and a 27% decrease in perceived stress by week 20 (P less than .001 versus treatment as usual). Depression scores in the ACT group also fell by 47% by week 8 and by 45% at week 20 (P = .01 versus treatment as usual). Anxiety levels decreased by 29% at week 8 and by 31% at week 20, but these improvements did not significantly differ from those in the control group (P = .39).

Interestingly, ACT did not significantly improve symptom burden, activities of daily living, disease-related worry, general well-being, C-reactive protein (CRP) levels, fecal calprotectin levels, or scores on the version used of the Clinical Assessment of Depression (CAD) or the short Mayo assessment. Hair cortisol levels showed an association with baseline stress and anxiety, but not with treatment response.

Care programs for IBD increasingly emphasize mental health services despite a lack of robust trials to support these interventions, the investigators noted. Thus, their findings highlight “the need for researchers and clinicians to further develop and optimize the content and delivery of psychological programs for IBD patients.”

Tillotts Pharma and Boston Scientific provided partial funding, but had no other role in the study. The researchers reported having no relevant conflicts of interest.

SOURCE: Wynne B et al. Gastroenterology. 2018 Nov 16. doi: 10.1053/j.gastro.2018.11.030.

Eight weeks of a mindfulness intervention known as acceptance and commitment therapy (ACT) significantly improved stress and depression among patients with inflammatory bowel disease, and these improvements persisted for at least 12 weeks after therapy ended, according to the results of a randomized, controlled trial.

Source: The American Gastroenterological Association

In the intention-to-treat analysis, stress symptoms, as measured by the Depression Anxiety and Stress Scales (DASS-21), improved by 39% at week 8 and by 45% at week 20, reported Brona Wynne, PhD, of University College Dublin together with her associates. These improvements were highly significant compared with baseline and treatment as usual (P = .001 for both comparisons). “Post hoc analyses indicated that baseline stress levels were similar in control and treatment groups,” the researchers wrote in Gastroenterology. “The results of the per protocol analysis were comparable, with a 43% and 49% reduction in stress in the treatment group from baseline to 8 and 20 weeks.”

Multiple studies have documented high levels of stress and psychological dysfunction among patients with Crohn’s disease and ulcerative colitis. Studies of various mindfulness therapy, relaxation, stress management, cognitive-behavioral therapy, and hypnotherapy interventions often failed to collect key clinical data or were underpowered, uncontrolled, and unrandomized. Acceptance and commitment therapy uses mindfulness to identify adverse thoughts and experiences, accept these as part of life, and recommit to “move towards values that have been identified and adopted by the individual,” the investigators wrote. “This can be defined as the ability to contact the present moment more fully as a conscious human being and to change, or persist in, behavior when doing so serves valued ends.”

Their single-center study, which they said was the first to evaluate ACT in IBD patients, included 79 individuals with stable or mildly active Crohn’s disease (38 patients) or ulcerative colitis (41 patients) who were randomly assigned to ACT (37 patients) or control treatment as usual (42 patients). The two comparison groups were demographically and clinically similar. The ACT program involved eight 90-minute, weekly sessions of groups of 14-16 individuals, led by a single psychologist who tailored the course material toward IBD with a focus on lowering stress. An independent psychologist observed each session to assess adherence to protocol.

Not only did ACT meet the primary study endpoint, it also produced a 25% decrease in perceived stress (on a 1-10 scale) by week 8 and a 27% decrease in perceived stress by week 20 (P less than .001 versus treatment as usual). Depression scores in the ACT group also fell by 47% by week 8 and by 45% at week 20 (P = .01 versus treatment as usual). Anxiety levels decreased by 29% at week 8 and by 31% at week 20, but these improvements did not significantly differ from those in the control group (P = .39).

Interestingly, ACT did not significantly improve symptom burden, activities of daily living, disease-related worry, general well-being, C-reactive protein (CRP) levels, fecal calprotectin levels, or scores on the version used of the Clinical Assessment of Depression (CAD) or the short Mayo assessment. Hair cortisol levels showed an association with baseline stress and anxiety, but not with treatment response.

Care programs for IBD increasingly emphasize mental health services despite a lack of robust trials to support these interventions, the investigators noted. Thus, their findings highlight “the need for researchers and clinicians to further develop and optimize the content and delivery of psychological programs for IBD patients.”

Tillotts Pharma and Boston Scientific provided partial funding, but had no other role in the study. The researchers reported having no relevant conflicts of interest.

SOURCE: Wynne B et al. Gastroenterology. 2018 Nov 16. doi: 10.1053/j.gastro.2018.11.030.

LAS VEGAS – Herpes zoster infection could pose a special risk for younger patients with inflammatory bowel disease who are on immunosuppressant or biologic therapies, a new study suggests.

About 3% of inflammatory bowel disease (IBD) patients developed herpes zoster (HZ) over a 5-year period at a single center, researchers found, and their average age was 37 years. The mean national age of HZ diagnosis is 59 years, and the latest guidelines from the Centers for Disease Control and Prevention do not recommend that people get vaccinated against HZ, or shingles, until age 50.

“Increased efforts should be made to administer herpes zoster vaccine in all eligible IBD patients, and there should be additional research focused on determining whether IBD patients under 50 years old, especially those on immunosuppressants or biologic therapy, would benefit from herpes zoster vaccination,” said gastroenterologist and study coauthor Marie L. Borum, MD, MPH, of George Washington University, Washington. She spoke in an interview before presenting the study findings at the the Crohn’s & Colitis Congress – a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

Dr. Borum and her associates launched the study, published in Inflammatory Bowel Diseases, after noticing an increase in HZ cases among patients with IBD. The authors retrospectively analyzed the medical charts of all patients with IBD who were treated at a single center from 2012 to 2017 (n = 393; 55% female; average age, 44 years). Nearly all had ulcerative colitis (71%) or Crohn’s disease (24%).

Over the 5-year period, 11 patients – 5 with ulcerative colitis, 5 with Crohn’s disease, and 1 patient with unspecified colitis – were diagnosed with HZ. All were taking immunosuppressant or biologic medications, and none had been vaccinated against HZ.

The difference in the average age of diagnosis of the infected patients versus the national mean age (37 years vs. 59 years) was statistically significant (P less than .0001).

The IBD patients with HZ often had postherpetic neuralgia, Dr. Borum said.

Previous studies also have linked IBD to higher rates of HZ. A 2018 retrospective study of veterans found that “the incidence rates of herpes zoster in all age groups and all IBD medication subgroups were substantially higher than that in the oldest group of patients without IBD [older than 60 years]” (Clin Gastroenterol Hepatol. 2018 Dec;16[12]:1919-27).

In 2017, researchers at the University of Wisconsin–Madison received a grant to study immunity to the varicella zoster virus in patients with IBD. A university press release said the results “could support recommendations for universal herpes zoster immunization for all IBD patients above the age of 40.”

Why might IBD boost the risk of HZ? “Individuals with IBD may have an increased risk of developing more episodes of herpes zoster due to immune dysregulation,” Dr. Borum said. “Those on immunosuppressants or biologic therapies have greater risk of more frequent and severe complications. It has been speculated that Janus kinase inhibitors may be associated with an increased risk for developing HZ.”

Dr. Borum noted that the study is limited by its size and single-center design. “However, it supports the recommendations that additional research is needed to fully understand the potential impact of HZ on IBD patients.”

The study authors reported no relevant disclosures.

SOURCE: Borum ML et al. Inflamm Bowel Dis. 2019 Feb 7. doi: 10.1093/ibd/izy393.073.

LAS VEGAS – Herpes zoster infection could pose a special risk for younger patients with inflammatory bowel disease who are on immunosuppressant or biologic therapies, a new study suggests.

About 3% of inflammatory bowel disease (IBD) patients developed herpes zoster (HZ) over a 5-year period at a single center, researchers found, and their average age was 37 years. The mean national age of HZ diagnosis is 59 years, and the latest guidelines from the Centers for Disease Control and Prevention do not recommend that people get vaccinated against HZ, or shingles, until age 50.

“Increased efforts should be made to administer herpes zoster vaccine in all eligible IBD patients, and there should be additional research focused on determining whether IBD patients under 50 years old, especially those on immunosuppressants or biologic therapy, would benefit from herpes zoster vaccination,” said gastroenterologist and study coauthor Marie L. Borum, MD, MPH, of George Washington University, Washington. She spoke in an interview before presenting the study findings at the the Crohn’s & Colitis Congress – a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

Dr. Borum and her associates launched the study, published in Inflammatory Bowel Diseases, after noticing an increase in HZ cases among patients with IBD. The authors retrospectively analyzed the medical charts of all patients with IBD who were treated at a single center from 2012 to 2017 (n = 393; 55% female; average age, 44 years). Nearly all had ulcerative colitis (71%) or Crohn’s disease (24%).

Over the 5-year period, 11 patients – 5 with ulcerative colitis, 5 with Crohn’s disease, and 1 patient with unspecified colitis – were diagnosed with HZ. All were taking immunosuppressant or biologic medications, and none had been vaccinated against HZ.

The difference in the average age of diagnosis of the infected patients versus the national mean age (37 years vs. 59 years) was statistically significant (P less than .0001).

The IBD patients with HZ often had postherpetic neuralgia, Dr. Borum said.

Previous studies also have linked IBD to higher rates of HZ. A 2018 retrospective study of veterans found that “the incidence rates of herpes zoster in all age groups and all IBD medication subgroups were substantially higher than that in the oldest group of patients without IBD [older than 60 years]” (Clin Gastroenterol Hepatol. 2018 Dec;16[12]:1919-27).

In 2017, researchers at the University of Wisconsin–Madison received a grant to study immunity to the varicella zoster virus in patients with IBD. A university press release said the results “could support recommendations for universal herpes zoster immunization for all IBD patients above the age of 40.”

Why might IBD boost the risk of HZ? “Individuals with IBD may have an increased risk of developing more episodes of herpes zoster due to immune dysregulation,” Dr. Borum said. “Those on immunosuppressants or biologic therapies have greater risk of more frequent and severe complications. It has been speculated that Janus kinase inhibitors may be associated with an increased risk for developing HZ.”

Dr. Borum noted that the study is limited by its size and single-center design. “However, it supports the recommendations that additional research is needed to fully understand the potential impact of HZ on IBD patients.”

The study authors reported no relevant disclosures.

SOURCE: Borum ML et al. Inflamm Bowel Dis. 2019 Feb 7. doi: 10.1093/ibd/izy393.073.

LAS VEGAS – Herpes zoster infection could pose a special risk for younger patients with inflammatory bowel disease who are on immunosuppressant or biologic therapies, a new study suggests.

About 3% of inflammatory bowel disease (IBD) patients developed herpes zoster (HZ) over a 5-year period at a single center, researchers found, and their average age was 37 years. The mean national age of HZ diagnosis is 59 years, and the latest guidelines from the Centers for Disease Control and Prevention do not recommend that people get vaccinated against HZ, or shingles, until age 50.

“Increased efforts should be made to administer herpes zoster vaccine in all eligible IBD patients, and there should be additional research focused on determining whether IBD patients under 50 years old, especially those on immunosuppressants or biologic therapy, would benefit from herpes zoster vaccination,” said gastroenterologist and study coauthor Marie L. Borum, MD, MPH, of George Washington University, Washington. She spoke in an interview before presenting the study findings at the the Crohn’s & Colitis Congress – a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.

Dr. Borum and her associates launched the study, published in Inflammatory Bowel Diseases, after noticing an increase in HZ cases among patients with IBD. The authors retrospectively analyzed the medical charts of all patients with IBD who were treated at a single center from 2012 to 2017 (n = 393; 55% female; average age, 44 years). Nearly all had ulcerative colitis (71%) or Crohn’s disease (24%).

Over the 5-year period, 11 patients – 5 with ulcerative colitis, 5 with Crohn’s disease, and 1 patient with unspecified colitis – were diagnosed with HZ. All were taking immunosuppressant or biologic medications, and none had been vaccinated against HZ.

The difference in the average age of diagnosis of the infected patients versus the national mean age (37 years vs. 59 years) was statistically significant (P less than .0001).

The IBD patients with HZ often had postherpetic neuralgia, Dr. Borum said.

Previous studies also have linked IBD to higher rates of HZ. A 2018 retrospective study of veterans found that “the incidence rates of herpes zoster in all age groups and all IBD medication subgroups were substantially higher than that in the oldest group of patients without IBD [older than 60 years]” (Clin Gastroenterol Hepatol. 2018 Dec;16[12]:1919-27).

In 2017, researchers at the University of Wisconsin–Madison received a grant to study immunity to the varicella zoster virus in patients with IBD. A university press release said the results “could support recommendations for universal herpes zoster immunization for all IBD patients above the age of 40.”

Why might IBD boost the risk of HZ? “Individuals with IBD may have an increased risk of developing more episodes of herpes zoster due to immune dysregulation,” Dr. Borum said. “Those on immunosuppressants or biologic therapies have greater risk of more frequent and severe complications. It has been speculated that Janus kinase inhibitors may be associated with an increased risk for developing HZ.”

Dr. Borum noted that the study is limited by its size and single-center design. “However, it supports the recommendations that additional research is needed to fully understand the potential impact of HZ on IBD patients.”

The study authors reported no relevant disclosures.

SOURCE: Borum ML et al. Inflamm Bowel Dis. 2019 Feb 7. doi: 10.1093/ibd/izy393.073.

The food additive maltodextrin may increase risk of inflammatory bowel disease, according to a recent study.

Compared with control subjects, mice given drinking water that contained 5% maltodextrin were significantly more likely to develop colitis and lose weight when challenged with dextran sodium sulfate (DSS), reported lead author Federica Laudisi, PhD, of the department of systems medicine at the University of Rome Tor Vergata in Rome, and her colleagues.

Further experiments with murine intestinal crypts and a human cell line echoed these results and offered mechanistic insight. Treatment with maltodextrin stressed the endoplasmic reticulum of goblet cells, predisposing the intestinal epithelium to mucus depletion and inflammation. With these results, maltodextrin joins polysorbate 80 and carboxymethylcellulose on a growing list of food additives in the Western diet with proinflammatory potential.

“Although the U.S. Food and Drug Administration recognizes these dietary elements as safe,” the investigators wrote in Cellular and Molecular Gastroenterology and Hepatology, “their use has been linked to the development of intestinal pathologies in both animals and human beings.

“It also has been shown that the polysaccharide maltodextrin, which is commonly used as a filler and thickener during food processing, can alter microbial phenotype and host antibacterial defenses. Maltodextrin expands the Escherichia coli population in the ileum and induces necrotizing enterocolitis in preterm piglets (Am J Physiol Gastrointest Liver Physiol. 2009 Dec;297:G1115-25).”

The present study began by administering three compounds dissolved in drinking water to wild-type Balb/c mice for 45 days: 5% maltodextrin, 0.5% propylene glycol, or 5 g/L animal gelatin. Control mice drank plain water. None of the treatments triggered clinical or histologic signs of colitis, and stool levels of lipocalin-2 (Lcn-2), a biomarker of intestinal inflammation, remained comparable with that of control mice. However, outcomes changed when mice were challenged with DSS (1.75% in drinking water) on days 35-45 or injected subcutaneously with indomethacin (5 mg/kg) on day 35 and sacrificed 24 hours later. When challenged with DSS, mice in the maltodextrin group developed severe colitis and lost 10%-15% of body weight, compared with minimal colitis and negligible weight loss in the other groups. In addition, compared with other mice, maltodextrin-fed mice had increased colon tissue expression of Lcn-2 and inflammatory cytokine interleukin (IL)-1beta. These initial findings suggested that dietary maltodextrin could increase susceptibility to clinical colitis.

To determine the pathophysiology of this phenomenon, the investigators performed microarray analysis of colonic samples. Multiple genes associated with carbohydrate and lipid metabolism were upregulated in maltodextrin-fed mice, including genes that controlled the unfolded protein response (UPR), a process in which unfolded proteins accumulate in the endoplasmic reticulum (ER) during ER stress. The most prominently expressed among the UPR-related genes was Ern-2, which regulates inositol-requiring enzyme 1beta, found exclusively in the ER of goblet cells in the small intestine and colon. When maltodextrin causes ER stress in goblet cells, it leads to misfolding of mucin glycoprotein Mucin-2 (Muc-2), a major component of gut mucus, causing gut mucus levels to drop. A diminished mucus barrier exposes the intestine to infection and damage, as demonstrated by higher rates of pathogenic bacteria in Muc-2–deficient mice than in control mice, and more severe intestinal damage than in controls when Muc-2 mice are deliberately infected with pathogens.

The investigators found that humans likely have similar responses to dietary maltodextrin. Treating the mucus-secreting HT29-methotrexate treated (HT29-MTX) cell line with 5% maltodextrin resulted in upregulation of Ern-2, which is the same mechanism observed in mice. Additional testing showed that this process was mediated by p38 mitogen-activated protein kinase, and pharmacologic inhibition or knockdown of p38 suppressed RNA expression of Ern-2. The investigators found that p38 was similarly involved in maltodextrin-fed mice.

To show that maltodextrin enhances susceptibility to inflammation via ER stress, the investigators used tauroursodeoxycholic acid (TUDCA) to inhibit ER stress. Indeed, inhibition led to reduced Ern-2 expression in HT29-MTX cells and in mice treated with maltodextrin. Giving TUDCA to maltodextrin-fed mice resulted in less weight loss, improved histology, and lower expression of Lcn-2 and IL-1beta.

The study concluded with three final experiments: The first showed that maltodextrin did not alter mucosa-associated microbiota; the second showed that mice fed 5% maltodextrin long term (for 10 weeks) had low-grade intestinal inflammation on histology, albeit without clinical colitis or weight loss; and the third showed that mice consuming maltodextrin long term had higher 15-hour fasting blood glycemic levels than control mice, supporting recent research suggesting that food additives can disrupt metabolism in a nonsusceptible host.

“In conclusion,” the investigators wrote, “this study shows that a maltodextrin-enriched diet reduces the intestinal content of Muc-2, thus making the host more sensitive to colitogenic stimuli. These data, together with the demonstration that maltodextrin can promote epithelial intestinal adhesion of pathogenic bacteria, supports the hypothesis that Western diets rich in maltodextrin can contribute to gut disease susceptibility.”

The study was funded by the Italian Ministry of Education, Universities, and Research. The authors reported no conflicts of interest.

SOURCE: Laudisi F et al. CMGH. 2019 Jan 18. doi: 10.1016/j.jcmgh.2018.09.002.

The food additive maltodextrin may increase risk of inflammatory bowel disease, according to a recent study.

Compared with control subjects, mice given drinking water that contained 5% maltodextrin were significantly more likely to develop colitis and lose weight when challenged with dextran sodium sulfate (DSS), reported lead author Federica Laudisi, PhD, of the department of systems medicine at the University of Rome Tor Vergata in Rome, and her colleagues.

Further experiments with murine intestinal crypts and a human cell line echoed these results and offered mechanistic insight. Treatment with maltodextrin stressed the endoplasmic reticulum of goblet cells, predisposing the intestinal epithelium to mucus depletion and inflammation. With these results, maltodextrin joins polysorbate 80 and carboxymethylcellulose on a growing list of food additives in the Western diet with proinflammatory potential.

“Although the U.S. Food and Drug Administration recognizes these dietary elements as safe,” the investigators wrote in Cellular and Molecular Gastroenterology and Hepatology, “their use has been linked to the development of intestinal pathologies in both animals and human beings.

“It also has been shown that the polysaccharide maltodextrin, which is commonly used as a filler and thickener during food processing, can alter microbial phenotype and host antibacterial defenses. Maltodextrin expands the Escherichia coli population in the ileum and induces necrotizing enterocolitis in preterm piglets (Am J Physiol Gastrointest Liver Physiol. 2009 Dec;297:G1115-25).”

The present study began by administering three compounds dissolved in drinking water to wild-type Balb/c mice for 45 days: 5% maltodextrin, 0.5% propylene glycol, or 5 g/L animal gelatin. Control mice drank plain water. None of the treatments triggered clinical or histologic signs of colitis, and stool levels of lipocalin-2 (Lcn-2), a biomarker of intestinal inflammation, remained comparable with that of control mice. However, outcomes changed when mice were challenged with DSS (1.75% in drinking water) on days 35-45 or injected subcutaneously with indomethacin (5 mg/kg) on day 35 and sacrificed 24 hours later. When challenged with DSS, mice in the maltodextrin group developed severe colitis and lost 10%-15% of body weight, compared with minimal colitis and negligible weight loss in the other groups. In addition, compared with other mice, maltodextrin-fed mice had increased colon tissue expression of Lcn-2 and inflammatory cytokine interleukin (IL)-1beta. These initial findings suggested that dietary maltodextrin could increase susceptibility to clinical colitis.

To determine the pathophysiology of this phenomenon, the investigators performed microarray analysis of colonic samples. Multiple genes associated with carbohydrate and lipid metabolism were upregulated in maltodextrin-fed mice, including genes that controlled the unfolded protein response (UPR), a process in which unfolded proteins accumulate in the endoplasmic reticulum (ER) during ER stress. The most prominently expressed among the UPR-related genes was Ern-2, which regulates inositol-requiring enzyme 1beta, found exclusively in the ER of goblet cells in the small intestine and colon. When maltodextrin causes ER stress in goblet cells, it leads to misfolding of mucin glycoprotein Mucin-2 (Muc-2), a major component of gut mucus, causing gut mucus levels to drop. A diminished mucus barrier exposes the intestine to infection and damage, as demonstrated by higher rates of pathogenic bacteria in Muc-2–deficient mice than in control mice, and more severe intestinal damage than in controls when Muc-2 mice are deliberately infected with pathogens.

The investigators found that humans likely have similar responses to dietary maltodextrin. Treating the mucus-secreting HT29-methotrexate treated (HT29-MTX) cell line with 5% maltodextrin resulted in upregulation of Ern-2, which is the same mechanism observed in mice. Additional testing showed that this process was mediated by p38 mitogen-activated protein kinase, and pharmacologic inhibition or knockdown of p38 suppressed RNA expression of Ern-2. The investigators found that p38 was similarly involved in maltodextrin-fed mice.

To show that maltodextrin enhances susceptibility to inflammation via ER stress, the investigators used tauroursodeoxycholic acid (TUDCA) to inhibit ER stress. Indeed, inhibition led to reduced Ern-2 expression in HT29-MTX cells and in mice treated with maltodextrin. Giving TUDCA to maltodextrin-fed mice resulted in less weight loss, improved histology, and lower expression of Lcn-2 and IL-1beta.

The study concluded with three final experiments: The first showed that maltodextrin did not alter mucosa-associated microbiota; the second showed that mice fed 5% maltodextrin long term (for 10 weeks) had low-grade intestinal inflammation on histology, albeit without clinical colitis or weight loss; and the third showed that mice consuming maltodextrin long term had higher 15-hour fasting blood glycemic levels than control mice, supporting recent research suggesting that food additives can disrupt metabolism in a nonsusceptible host.

“In conclusion,” the investigators wrote, “this study shows that a maltodextrin-enriched diet reduces the intestinal content of Muc-2, thus making the host more sensitive to colitogenic stimuli. These data, together with the demonstration that maltodextrin can promote epithelial intestinal adhesion of pathogenic bacteria, supports the hypothesis that Western diets rich in maltodextrin can contribute to gut disease susceptibility.”

The study was funded by the Italian Ministry of Education, Universities, and Research. The authors reported no conflicts of interest.

SOURCE: Laudisi F et al. CMGH. 2019 Jan 18. doi: 10.1016/j.jcmgh.2018.09.002.

The food additive maltodextrin may increase risk of inflammatory bowel disease, according to a recent study.

Compared with control subjects, mice given drinking water that contained 5% maltodextrin were significantly more likely to develop colitis and lose weight when challenged with dextran sodium sulfate (DSS), reported lead author Federica Laudisi, PhD, of the department of systems medicine at the University of Rome Tor Vergata in Rome, and her colleagues.

Further experiments with murine intestinal crypts and a human cell line echoed these results and offered mechanistic insight. Treatment with maltodextrin stressed the endoplasmic reticulum of goblet cells, predisposing the intestinal epithelium to mucus depletion and inflammation. With these results, maltodextrin joins polysorbate 80 and carboxymethylcellulose on a growing list of food additives in the Western diet with proinflammatory potential.

“Although the U.S. Food and Drug Administration recognizes these dietary elements as safe,” the investigators wrote in Cellular and Molecular Gastroenterology and Hepatology, “their use has been linked to the development of intestinal pathologies in both animals and human beings.

“It also has been shown that the polysaccharide maltodextrin, which is commonly used as a filler and thickener during food processing, can alter microbial phenotype and host antibacterial defenses. Maltodextrin expands the Escherichia coli population in the ileum and induces necrotizing enterocolitis in preterm piglets (Am J Physiol Gastrointest Liver Physiol. 2009 Dec;297:G1115-25).”

The present study began by administering three compounds dissolved in drinking water to wild-type Balb/c mice for 45 days: 5% maltodextrin, 0.5% propylene glycol, or 5 g/L animal gelatin. Control mice drank plain water. None of the treatments triggered clinical or histologic signs of colitis, and stool levels of lipocalin-2 (Lcn-2), a biomarker of intestinal inflammation, remained comparable with that of control mice. However, outcomes changed when mice were challenged with DSS (1.75% in drinking water) on days 35-45 or injected subcutaneously with indomethacin (5 mg/kg) on day 35 and sacrificed 24 hours later. When challenged with DSS, mice in the maltodextrin group developed severe colitis and lost 10%-15% of body weight, compared with minimal colitis and negligible weight loss in the other groups. In addition, compared with other mice, maltodextrin-fed mice had increased colon tissue expression of Lcn-2 and inflammatory cytokine interleukin (IL)-1beta. These initial findings suggested that dietary maltodextrin could increase susceptibility to clinical colitis.

To determine the pathophysiology of this phenomenon, the investigators performed microarray analysis of colonic samples. Multiple genes associated with carbohydrate and lipid metabolism were upregulated in maltodextrin-fed mice, including genes that controlled the unfolded protein response (UPR), a process in which unfolded proteins accumulate in the endoplasmic reticulum (ER) during ER stress. The most prominently expressed among the UPR-related genes was Ern-2, which regulates inositol-requiring enzyme 1beta, found exclusively in the ER of goblet cells in the small intestine and colon. When maltodextrin causes ER stress in goblet cells, it leads to misfolding of mucin glycoprotein Mucin-2 (Muc-2), a major component of gut mucus, causing gut mucus levels to drop. A diminished mucus barrier exposes the intestine to infection and damage, as demonstrated by higher rates of pathogenic bacteria in Muc-2–deficient mice than in control mice, and more severe intestinal damage than in controls when Muc-2 mice are deliberately infected with pathogens.

The investigators found that humans likely have similar responses to dietary maltodextrin. Treating the mucus-secreting HT29-methotrexate treated (HT29-MTX) cell line with 5% maltodextrin resulted in upregulation of Ern-2, which is the same mechanism observed in mice. Additional testing showed that this process was mediated by p38 mitogen-activated protein kinase, and pharmacologic inhibition or knockdown of p38 suppressed RNA expression of Ern-2. The investigators found that p38 was similarly involved in maltodextrin-fed mice.

To show that maltodextrin enhances susceptibility to inflammation via ER stress, the investigators used tauroursodeoxycholic acid (TUDCA) to inhibit ER stress. Indeed, inhibition led to reduced Ern-2 expression in HT29-MTX cells and in mice treated with maltodextrin. Giving TUDCA to maltodextrin-fed mice resulted in less weight loss, improved histology, and lower expression of Lcn-2 and IL-1beta.

The study concluded with three final experiments: The first showed that maltodextrin did not alter mucosa-associated microbiota; the second showed that mice fed 5% maltodextrin long term (for 10 weeks) had low-grade intestinal inflammation on histology, albeit without clinical colitis or weight loss; and the third showed that mice consuming maltodextrin long term had higher 15-hour fasting blood glycemic levels than control mice, supporting recent research suggesting that food additives can disrupt metabolism in a nonsusceptible host.

“In conclusion,” the investigators wrote, “this study shows that a maltodextrin-enriched diet reduces the intestinal content of Muc-2, thus making the host more sensitive to colitogenic stimuli. These data, together with the demonstration that maltodextrin can promote epithelial intestinal adhesion of pathogenic bacteria, supports the hypothesis that Western diets rich in maltodextrin can contribute to gut disease susceptibility.”

The study was funded by the Italian Ministry of Education, Universities, and Research. The authors reported no conflicts of interest.

SOURCE: Laudisi F et al. CMGH. 2019 Jan 18. doi: 10.1016/j.jcmgh.2018.09.002.

When patients with inflammatory bowel disease report persistent gastrointestinal symptoms, clinicians should perform a thorough clinical assessment and then take a stepwise approach to rule out ongoing inflammation, according to a clinical practice update from the American Gastroenterological Association.

A fecal calprotectin test can be useful because values under 50 mcg/mL may suggest endoscopic remission, which may, in turn, point to another etiology of gastrointestinal symptoms, wrote Jean-Frederic Colombel, MD, of the Icahn School of Medicine at Mount Sinai, New York, together with his associates in Clinical Gastroenterology and Hepatology.

However, a result between 50 and 250 mcg/mL is harder to interpret because the upper limit of normal varies and mild increases can occur secondary to nonspecific low-grade inflammation, according to the experts. For mild gastrointestinal symptoms, they suggested testing fecal calprotectin every 3-6 months to identify flares as early as possible. If a flare is suspected, they advised considering cross-sectional imaging or endoscopy with biopsy.

Imaging also is indicated for patients with obstructive symptoms such as abdominal pain, obstipation, or constipation, the practice update states. Such symptoms can indicate fecal stasis proximal to distal colitis in patients with ulcerative colitis, or intestinal stenosis in patients with Crohn’s disease.

Other pathophysiologies of gastrointestinal symptoms also should be considered based on constellations of symptoms. For example, steatorrhea with chronic abdominal pain may indicate pancreatic exocrine insufficiency, which fecal elastase testing can help confirm. Symptoms of diarrhea-predominant irritable bowel syndrome can result from bile acid diarrhea, for which several screening tests are available. Diarrhea, abdominal pain, and bloating may indicate carbohydrate malabsorption or small-intestinal bacterial overgrowth, which can be evaluated with breath testing.

If patients with inflammatory bowel disease have persistent gastrointestinal symptoms but lack objective evidence of ongoing inflammation or another etiology, then clinicians should increase their suspicion of an overlapping functional gastrointestinal disorder. These conditions actually “share many common pathophysiologic disturbances that, in some inflammatory bowel disease patients, may be a consequence of prior structural and functional bowel damage,” the experts wrote.

For patients with chronic constipation who do not have an underlying obstruction, they suggest osmotic or stimulant laxatives. For chronic diarrhea, they recommend hypomobility agents or bile-acid sequestrants. Patients with fecal symptoms of irritable bowel syndrome also should be evaluated for pelvic floor disorders, which may improve with biofeedback therapy, the experts state.

A low-FODMAP diet (a diet low in lactose, fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) also can improve symptoms of irritable bowel syndrome, including patients with inflammatory bowel disease. However, a dietitian always should deliver this restrictive diet because patients with inflammatory bowel disease already are at increased risk for undernutrition.

Patients with functional gastrointestinal pain may benefit from antispasmodics, neuropathic-directed agents, and antidepressants, but they should not receive opiates, the experts emphasized. Anxiety and depression are common in both inflammatory bowel disease and irritable bowel syndrome, and patients may benefit from psychotherapy (cognitive-behavioral therapy, hypnotherapy, and mindfulness therapy), antidepressants, anxiolytics, or combinations of these treatments. The practice update also recommends physical exercise, which has been shown to decrease the risk of recurrent active disease in the setting of inflammatory bowel disease.

Finally, persistent gut symptoms can indicate intestinal barrier dysfunction, even if endoscopy shows mucosal healing. Barrier dysfunction is a potential therapeutic target that needs further study in this setting, the experts noted. They also called for studies of the potential benefits and risks of probiotics and other alternative approaches, such as herbal treatments and supplements, yoga, acupuncture, and moxibustion. Until further evidence, however, they have recommended against complementary or alternative medicine or fecal microbiota transplantation.

Dr. Colombel has served as consultant, advisory board member, or speaker for AbbVie, Amgen, Boehringer-Ingelheim, Celgene Corporation, and many other pharmaceutical companies. He has received research grants from AbbVie, Takeda, and Janssen and Janssen.

SOURCE: Colombel J-F et al. Clin Gastroenterol Hepatol. 2018 Aug 9. doi: 10.1016/j.cgh.2018.08.001.

When patients with inflammatory bowel disease report persistent gastrointestinal symptoms, clinicians should perform a thorough clinical assessment and then take a stepwise approach to rule out ongoing inflammation, according to a clinical practice update from the American Gastroenterological Association.

A fecal calprotectin test can be useful because values under 50 mcg/mL may suggest endoscopic remission, which may, in turn, point to another etiology of gastrointestinal symptoms, wrote Jean-Frederic Colombel, MD, of the Icahn School of Medicine at Mount Sinai, New York, together with his associates in Clinical Gastroenterology and Hepatology.

However, a result between 50 and 250 mcg/mL is harder to interpret because the upper limit of normal varies and mild increases can occur secondary to nonspecific low-grade inflammation, according to the experts. For mild gastrointestinal symptoms, they suggested testing fecal calprotectin every 3-6 months to identify flares as early as possible. If a flare is suspected, they advised considering cross-sectional imaging or endoscopy with biopsy.

Imaging also is indicated for patients with obstructive symptoms such as abdominal pain, obstipation, or constipation, the practice update states. Such symptoms can indicate fecal stasis proximal to distal colitis in patients with ulcerative colitis, or intestinal stenosis in patients with Crohn’s disease.

Other pathophysiologies of gastrointestinal symptoms also should be considered based on constellations of symptoms. For example, steatorrhea with chronic abdominal pain may indicate pancreatic exocrine insufficiency, which fecal elastase testing can help confirm. Symptoms of diarrhea-predominant irritable bowel syndrome can result from bile acid diarrhea, for which several screening tests are available. Diarrhea, abdominal pain, and bloating may indicate carbohydrate malabsorption or small-intestinal bacterial overgrowth, which can be evaluated with breath testing.

If patients with inflammatory bowel disease have persistent gastrointestinal symptoms but lack objective evidence of ongoing inflammation or another etiology, then clinicians should increase their suspicion of an overlapping functional gastrointestinal disorder. These conditions actually “share many common pathophysiologic disturbances that, in some inflammatory bowel disease patients, may be a consequence of prior structural and functional bowel damage,” the experts wrote.

For patients with chronic constipation who do not have an underlying obstruction, they suggest osmotic or stimulant laxatives. For chronic diarrhea, they recommend hypomobility agents or bile-acid sequestrants. Patients with fecal symptoms of irritable bowel syndrome also should be evaluated for pelvic floor disorders, which may improve with biofeedback therapy, the experts state.

A low-FODMAP diet (a diet low in lactose, fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) also can improve symptoms of irritable bowel syndrome, including patients with inflammatory bowel disease. However, a dietitian always should deliver this restrictive diet because patients with inflammatory bowel disease already are at increased risk for undernutrition.

Patients with functional gastrointestinal pain may benefit from antispasmodics, neuropathic-directed agents, and antidepressants, but they should not receive opiates, the experts emphasized. Anxiety and depression are common in both inflammatory bowel disease and irritable bowel syndrome, and patients may benefit from psychotherapy (cognitive-behavioral therapy, hypnotherapy, and mindfulness therapy), antidepressants, anxiolytics, or combinations of these treatments. The practice update also recommends physical exercise, which has been shown to decrease the risk of recurrent active disease in the setting of inflammatory bowel disease.

Finally, persistent gut symptoms can indicate intestinal barrier dysfunction, even if endoscopy shows mucosal healing. Barrier dysfunction is a potential therapeutic target that needs further study in this setting, the experts noted. They also called for studies of the potential benefits and risks of probiotics and other alternative approaches, such as herbal treatments and supplements, yoga, acupuncture, and moxibustion. Until further evidence, however, they have recommended against complementary or alternative medicine or fecal microbiota transplantation.

Dr. Colombel has served as consultant, advisory board member, or speaker for AbbVie, Amgen, Boehringer-Ingelheim, Celgene Corporation, and many other pharmaceutical companies. He has received research grants from AbbVie, Takeda, and Janssen and Janssen.

SOURCE: Colombel J-F et al. Clin Gastroenterol Hepatol. 2018 Aug 9. doi: 10.1016/j.cgh.2018.08.001.

When patients with inflammatory bowel disease report persistent gastrointestinal symptoms, clinicians should perform a thorough clinical assessment and then take a stepwise approach to rule out ongoing inflammation, according to a clinical practice update from the American Gastroenterological Association.

A fecal calprotectin test can be useful because values under 50 mcg/mL may suggest endoscopic remission, which may, in turn, point to another etiology of gastrointestinal symptoms, wrote Jean-Frederic Colombel, MD, of the Icahn School of Medicine at Mount Sinai, New York, together with his associates in Clinical Gastroenterology and Hepatology.

However, a result between 50 and 250 mcg/mL is harder to interpret because the upper limit of normal varies and mild increases can occur secondary to nonspecific low-grade inflammation, according to the experts. For mild gastrointestinal symptoms, they suggested testing fecal calprotectin every 3-6 months to identify flares as early as possible. If a flare is suspected, they advised considering cross-sectional imaging or endoscopy with biopsy.

Imaging also is indicated for patients with obstructive symptoms such as abdominal pain, obstipation, or constipation, the practice update states. Such symptoms can indicate fecal stasis proximal to distal colitis in patients with ulcerative colitis, or intestinal stenosis in patients with Crohn’s disease.

Other pathophysiologies of gastrointestinal symptoms also should be considered based on constellations of symptoms. For example, steatorrhea with chronic abdominal pain may indicate pancreatic exocrine insufficiency, which fecal elastase testing can help confirm. Symptoms of diarrhea-predominant irritable bowel syndrome can result from bile acid diarrhea, for which several screening tests are available. Diarrhea, abdominal pain, and bloating may indicate carbohydrate malabsorption or small-intestinal bacterial overgrowth, which can be evaluated with breath testing.

If patients with inflammatory bowel disease have persistent gastrointestinal symptoms but lack objective evidence of ongoing inflammation or another etiology, then clinicians should increase their suspicion of an overlapping functional gastrointestinal disorder. These conditions actually “share many common pathophysiologic disturbances that, in some inflammatory bowel disease patients, may be a consequence of prior structural and functional bowel damage,” the experts wrote.

For patients with chronic constipation who do not have an underlying obstruction, they suggest osmotic or stimulant laxatives. For chronic diarrhea, they recommend hypomobility agents or bile-acid sequestrants. Patients with fecal symptoms of irritable bowel syndrome also should be evaluated for pelvic floor disorders, which may improve with biofeedback therapy, the experts state.

A low-FODMAP diet (a diet low in lactose, fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) also can improve symptoms of irritable bowel syndrome, including patients with inflammatory bowel disease. However, a dietitian always should deliver this restrictive diet because patients with inflammatory bowel disease already are at increased risk for undernutrition.

Patients with functional gastrointestinal pain may benefit from antispasmodics, neuropathic-directed agents, and antidepressants, but they should not receive opiates, the experts emphasized. Anxiety and depression are common in both inflammatory bowel disease and irritable bowel syndrome, and patients may benefit from psychotherapy (cognitive-behavioral therapy, hypnotherapy, and mindfulness therapy), antidepressants, anxiolytics, or combinations of these treatments. The practice update also recommends physical exercise, which has been shown to decrease the risk of recurrent active disease in the setting of inflammatory bowel disease.

Finally, persistent gut symptoms can indicate intestinal barrier dysfunction, even if endoscopy shows mucosal healing. Barrier dysfunction is a potential therapeutic target that needs further study in this setting, the experts noted. They also called for studies of the potential benefits and risks of probiotics and other alternative approaches, such as herbal treatments and supplements, yoga, acupuncture, and moxibustion. Until further evidence, however, they have recommended against complementary or alternative medicine or fecal microbiota transplantation.

Dr. Colombel has served as consultant, advisory board member, or speaker for AbbVie, Amgen, Boehringer-Ingelheim, Celgene Corporation, and many other pharmaceutical companies. He has received research grants from AbbVie, Takeda, and Janssen and Janssen.

SOURCE: Colombel J-F et al. Clin Gastroenterol Hepatol. 2018 Aug 9. doi: 10.1016/j.cgh.2018.08.001.

For patients with extensive mild to moderate ulcerative colitis, numerous randomized controlled trials support the use of either standard-dose mesalamine (2-3 grams per day) or diazo-bonded 5-aminosalicylic acid (ASA) instead of low-dose mesalamine, sulfasalazine, or no therapy, state new guidelines from the American Gastroenterological Association, published in Gastroenterology.

©selvanegra/thinkstockphotos.com

Sulfasalazine (2-4 grams per day) is less likely to be tolerated but remains a “reasonable option” for remitted patients who are already on it and for patients with prominent arthritis symptoms, especially if alternative treatments are cost prohibitive, wrote Cynthia W. Ko, MD, MS, of the University of Washington, Seattle, and her associates.

According to the guideline, patients with mild to moderate ulcerative colitis have less than four to six bowel movements per day, only mild or moderate rectal bleeding, no constitutional symptoms, and no high overall inflammatory burden or signs of high inflammatory activity on the Mayo Clinic score and Truelove and Witt’s criteria. These patients usually do not require colectomy, but this outcome is more likely when patients are diagnosed before age 40 years or have extensive disease or deep ulcers, extraintestinal manifestations, or elevated inflammatory markers. These higher-risk patients need more aggressive initial treatment and faster treatment intensification in cases of inadequate response, the guideline emphasizes. Even for cases of mild to moderate ulcerative colitis, treatment intensification is preferable to repeated courses of corticosteroids.

The guideline recommends adding rectal mesalamine to oral 5-ASA if patients have extensive or left-sided mild to moderate ulcerative colitis. In randomized controlled trials, this combination was significantly more likely to induce and maintain remission than was standard-dose oral mesalamine monotherapy, the authors noted. “In the maintenance trials, enemas were used twice per week or for 1 week per month. Both oral and topical mesalamine were well tolerated.”

For patients with moderate disease activity or a suboptimal response to standard-dose mesalamine or diazo-bonded 5-ASA, the guideline recommends adding rectal mesalamine to high-dose oral mesalamine (more than 3 grams daily). Combination therapy maximizes the delivery of mesalamine to the affected area of the colon, which optimizes the trial of 5-ASA before opting for treatment escalation, the authors noted. They recommend once-daily oral mesalamine dosing, since this is easier to adhere to and studies have found no benefit of more frequent dosing.

For inducing remission of mild to moderate ulcerative colitis, the guideline recommends standard-dose oral mesalamine or diazo-bonded 5-ASA over budesonide. “Overall, the budesonide preparations are not superior to mesalamine for induction of remission,” the authors wrote. Oral 5-ASAs are preferred, especially given the absence of data on the efficacy or safety of maintenance budesonide therapy.

SOURCE: Crocket SD et al.  Gastro 2019;156(2).  doi: org/10.1053/j.gastro.2018.12.009.

For patients with extensive mild to moderate ulcerative colitis, numerous randomized controlled trials support the use of either standard-dose mesalamine (2-3 grams per day) or diazo-bonded 5-aminosalicylic acid (ASA) instead of low-dose mesalamine, sulfasalazine, or no therapy, state new guidelines from the American Gastroenterological Association, published in Gastroenterology.

©selvanegra/thinkstockphotos.com

Sulfasalazine (2-4 grams per day) is less likely to be tolerated but remains a “reasonable option” for remitted patients who are already on it and for patients with prominent arthritis symptoms, especially if alternative treatments are cost prohibitive, wrote Cynthia W. Ko, MD, MS, of the University of Washington, Seattle, and her associates.

According to the guideline, patients with mild to moderate ulcerative colitis have less than four to six bowel movements per day, only mild or moderate rectal bleeding, no constitutional symptoms, and no high overall inflammatory burden or signs of high inflammatory activity on the Mayo Clinic score and Truelove and Witt’s criteria. These patients usually do not require colectomy, but this outcome is more likely when patients are diagnosed before age 40 years or have extensive disease or deep ulcers, extraintestinal manifestations, or elevated inflammatory markers. These higher-risk patients need more aggressive initial treatment and faster treatment intensification in cases of inadequate response, the guideline emphasizes. Even for cases of mild to moderate ulcerative colitis, treatment intensification is preferable to repeated courses of corticosteroids.

The guideline recommends adding rectal mesalamine to oral 5-ASA if patients have extensive or left-sided mild to moderate ulcerative colitis. In randomized controlled trials, this combination was significantly more likely to induce and maintain remission than was standard-dose oral mesalamine monotherapy, the authors noted. “In the maintenance trials, enemas were used twice per week or for 1 week per month. Both oral and topical mesalamine were well tolerated.”

For patients with moderate disease activity or a suboptimal response to standard-dose mesalamine or diazo-bonded 5-ASA, the guideline recommends adding rectal mesalamine to high-dose oral mesalamine (more than 3 grams daily). Combination therapy maximizes the delivery of mesalamine to the affected area of the colon, which optimizes the trial of 5-ASA before opting for treatment escalation, the authors noted. They recommend once-daily oral mesalamine dosing, since this is easier to adhere to and studies have found no benefit of more frequent dosing.

For inducing remission of mild to moderate ulcerative colitis, the guideline recommends standard-dose oral mesalamine or diazo-bonded 5-ASA over budesonide. “Overall, the budesonide preparations are not superior to mesalamine for induction of remission,” the authors wrote. Oral 5-ASAs are preferred, especially given the absence of data on the efficacy or safety of maintenance budesonide therapy.

SOURCE: Crocket SD et al.  Gastro 2019;156(2).  doi: org/10.1053/j.gastro.2018.12.009.

For patients with extensive mild to moderate ulcerative colitis, numerous randomized controlled trials support the use of either standard-dose mesalamine (2-3 grams per day) or diazo-bonded 5-aminosalicylic acid (ASA) instead of low-dose mesalamine, sulfasalazine, or no therapy, state new guidelines from the American Gastroenterological Association, published in Gastroenterology.

©selvanegra/thinkstockphotos.com

Sulfasalazine (2-4 grams per day) is less likely to be tolerated but remains a “reasonable option” for remitted patients who are already on it and for patients with prominent arthritis symptoms, especially if alternative treatments are cost prohibitive, wrote Cynthia W. Ko, MD, MS, of the University of Washington, Seattle, and her associates.

According to the guideline, patients with mild to moderate ulcerative colitis have less than four to six bowel movements per day, only mild or moderate rectal bleeding, no constitutional symptoms, and no high overall inflammatory burden or signs of high inflammatory activity on the Mayo Clinic score and Truelove and Witt’s criteria. These patients usually do not require colectomy, but this outcome is more likely when patients are diagnosed before age 40 years or have extensive disease or deep ulcers, extraintestinal manifestations, or elevated inflammatory markers. These higher-risk patients need more aggressive initial treatment and faster treatment intensification in cases of inadequate response, the guideline emphasizes. Even for cases of mild to moderate ulcerative colitis, treatment intensification is preferable to repeated courses of corticosteroids.

The guideline recommends adding rectal mesalamine to oral 5-ASA if patients have extensive or left-sided mild to moderate ulcerative colitis. In randomized controlled trials, this combination was significantly more likely to induce and maintain remission than was standard-dose oral mesalamine monotherapy, the authors noted. “In the maintenance trials, enemas were used twice per week or for 1 week per month. Both oral and topical mesalamine were well tolerated.”

For patients with moderate disease activity or a suboptimal response to standard-dose mesalamine or diazo-bonded 5-ASA, the guideline recommends adding rectal mesalamine to high-dose oral mesalamine (more than 3 grams daily). Combination therapy maximizes the delivery of mesalamine to the affected area of the colon, which optimizes the trial of 5-ASA before opting for treatment escalation, the authors noted. They recommend once-daily oral mesalamine dosing, since this is easier to adhere to and studies have found no benefit of more frequent dosing.

For inducing remission of mild to moderate ulcerative colitis, the guideline recommends standard-dose oral mesalamine or diazo-bonded 5-ASA over budesonide. “Overall, the budesonide preparations are not superior to mesalamine for induction of remission,” the authors wrote. Oral 5-ASAs are preferred, especially given the absence of data on the efficacy or safety of maintenance budesonide therapy.

SOURCE: Crocket SD et al.  Gastro 2019;156(2).  doi: org/10.1053/j.gastro.2018.12.009.