Key clinical point: Intradermal (ID) hepatitis B virus (HBV) vaccination with topical imiquimod pretreatment (ID-Imq) to the injection site was safe and provided superior seroprotection compared with intramuscular (IM) HBV vaccination with aqueous cream pretreatment (IM-Aq) in patients with inflammatory bowel disease (IBD).

Major finding: Patients who received ID-Imq vs. IM-Aq showed a significantly higher seroprotection rate at 12 months (91% vs. 69%; P = .005). Overall, 59% and 55% of patients in the ID-Imq and IM-Aq groups reported any adverse events, respectively, with local reactions being more common in the ID-Imq group.

Study details: Findings are from a phase 2 and 3 trial including 104 patients with IBD and no evidence of HBV infection or immunity who were randomly assigned to receive ID-Imq (n = 53) or IM-Aq (n = 51) at 0, 1, and 6 months.

Disclosures: This study was partly funded by a Young Investigator Research Grant from the Hong Kong College of Physicians. WK Leung reported serving as a speaker for Ferring, Janssen, and Takeda.

Source: Ko K-L et al. Clinical trial: Intra-dermal hepatitis B vaccination with topical imiquimod versus intra-muscular hepatitis B vaccination in inflammatory bowel disease patients. Aliment Pharmacol Ther. 2022 (May 11).  Doi: 10.1111/apt.16970

Key clinical point: Intradermal (ID) hepatitis B virus (HBV) vaccination with topical imiquimod pretreatment (ID-Imq) to the injection site was safe and provided superior seroprotection compared with intramuscular (IM) HBV vaccination with aqueous cream pretreatment (IM-Aq) in patients with inflammatory bowel disease (IBD).

Major finding: Patients who received ID-Imq vs. IM-Aq showed a significantly higher seroprotection rate at 12 months (91% vs. 69%; P = .005). Overall, 59% and 55% of patients in the ID-Imq and IM-Aq groups reported any adverse events, respectively, with local reactions being more common in the ID-Imq group.

Study details: Findings are from a phase 2 and 3 trial including 104 patients with IBD and no evidence of HBV infection or immunity who were randomly assigned to receive ID-Imq (n = 53) or IM-Aq (n = 51) at 0, 1, and 6 months.

Disclosures: This study was partly funded by a Young Investigator Research Grant from the Hong Kong College of Physicians. WK Leung reported serving as a speaker for Ferring, Janssen, and Takeda.

Source: Ko K-L et al. Clinical trial: Intra-dermal hepatitis B vaccination with topical imiquimod versus intra-muscular hepatitis B vaccination in inflammatory bowel disease patients. Aliment Pharmacol Ther. 2022 (May 11).  Doi: 10.1111/apt.16970

Key clinical point: Intradermal (ID) hepatitis B virus (HBV) vaccination with topical imiquimod pretreatment (ID-Imq) to the injection site was safe and provided superior seroprotection compared with intramuscular (IM) HBV vaccination with aqueous cream pretreatment (IM-Aq) in patients with inflammatory bowel disease (IBD).

Major finding: Patients who received ID-Imq vs. IM-Aq showed a significantly higher seroprotection rate at 12 months (91% vs. 69%; P = .005). Overall, 59% and 55% of patients in the ID-Imq and IM-Aq groups reported any adverse events, respectively, with local reactions being more common in the ID-Imq group.

Study details: Findings are from a phase 2 and 3 trial including 104 patients with IBD and no evidence of HBV infection or immunity who were randomly assigned to receive ID-Imq (n = 53) or IM-Aq (n = 51) at 0, 1, and 6 months.

Disclosures: This study was partly funded by a Young Investigator Research Grant from the Hong Kong College of Physicians. WK Leung reported serving as a speaker for Ferring, Janssen, and Takeda.

Source: Ko K-L et al. Clinical trial: Intra-dermal hepatitis B vaccination with topical imiquimod versus intra-muscular hepatitis B vaccination in inflammatory bowel disease patients. Aliment Pharmacol Ther. 2022 (May 11).  Doi: 10.1111/apt.16970

Key clinical point: Excess exposure to steroids has a significant negative impact on patients with inflammatory bowel disease (IBD).

Major finding: Steroid excess was observed in 15% of patients. The risks for ≥1 hospitalizations for IBD (odds ratio [OR] 12.33; 95% CI 8.89-17.11) and infections (OR 2.89; 95% CI 1.82-4.61) and ≥1 courses of general practitioner-prescribed antibiotics (OR 1.41; 95% CI 1.07-1.86) were significantly higher in patients with steroid excess vs. those without steroid exposure.

Study details: Findings are from a retrospective study including 2246 patients with IBD and primary care information.

Disclosures: This study was supported by a research grant from AbbVie. T Raine and CP Selinger declared receiving research/educational grants or speaker/consultation fees from various sources, including AbbVie.

Source: Rosiou K et al. Sources of excess steroid prescriptions and clinical adverse outcomes associated with steroid excess in patients with inflammatory bowel disease: The Leeds IBD Steroids study. Aliment Pharmacol Ther. 2022 (May 24). Doi: 10.1111/apt.17039

Key clinical point: Excess exposure to steroids has a significant negative impact on patients with inflammatory bowel disease (IBD).

Major finding: Steroid excess was observed in 15% of patients. The risks for ≥1 hospitalizations for IBD (odds ratio [OR] 12.33; 95% CI 8.89-17.11) and infections (OR 2.89; 95% CI 1.82-4.61) and ≥1 courses of general practitioner-prescribed antibiotics (OR 1.41; 95% CI 1.07-1.86) were significantly higher in patients with steroid excess vs. those without steroid exposure.

Study details: Findings are from a retrospective study including 2246 patients with IBD and primary care information.

Disclosures: This study was supported by a research grant from AbbVie. T Raine and CP Selinger declared receiving research/educational grants or speaker/consultation fees from various sources, including AbbVie.

Source: Rosiou K et al. Sources of excess steroid prescriptions and clinical adverse outcomes associated with steroid excess in patients with inflammatory bowel disease: The Leeds IBD Steroids study. Aliment Pharmacol Ther. 2022 (May 24). Doi: 10.1111/apt.17039

Key clinical point: Excess exposure to steroids has a significant negative impact on patients with inflammatory bowel disease (IBD).

Major finding: Steroid excess was observed in 15% of patients. The risks for ≥1 hospitalizations for IBD (odds ratio [OR] 12.33; 95% CI 8.89-17.11) and infections (OR 2.89; 95% CI 1.82-4.61) and ≥1 courses of general practitioner-prescribed antibiotics (OR 1.41; 95% CI 1.07-1.86) were significantly higher in patients with steroid excess vs. those without steroid exposure.

Study details: Findings are from a retrospective study including 2246 patients with IBD and primary care information.

Disclosures: This study was supported by a research grant from AbbVie. T Raine and CP Selinger declared receiving research/educational grants or speaker/consultation fees from various sources, including AbbVie.

Source: Rosiou K et al. Sources of excess steroid prescriptions and clinical adverse outcomes associated with steroid excess in patients with inflammatory bowel disease: The Leeds IBD Steroids study. Aliment Pharmacol Ther. 2022 (May 24). Doi: 10.1111/apt.17039

I can dimly recall watching Queen Elizabeth’s coronation on a very small black and white television screen. Even in monochrome it was a riveting event. Recently, the Queen celebrated her Platinum Jubilee, marking her 70-year reign. Apparently it was a multiday event with all the trappings, floating above an undercurrent of scandal and intrigue. I had better things to do than I did as a 7-year-old entranced by the novelty of a neighbor’s television set.

But, it turns out that I had missed the opportunity to see live and in color a royal meltdown starring the Queen’s great-grandson, 4-year-old Prince Louis. Not to worry. It remains on video archives for our education and pleasure ad infinitum. His performance was no more dramatic than what you have seen numerous times in the checkout line of the grocery store. However, this meltdown was on the world stage in the front row of the royal box and performed in various venues on each day of a 4-day event.

As long as you weren’t his parents, Kate Middleton and Prince William, the meltdown had its moments of hilarity. Louis made full use of his youthful and plastic face, creating a wide variety of taunts and responses to his mother’s praiseworthy and understated attempts at regaining control. Of course, the British press and every armchair parent with a Twitter account had a field day contributing their explanations and advice.

For example, here’s the headline on an international news website that caught my eye: “Royal reveals why Prince Louis was so ‘mischievous’ during the Jubilee”. In the article, a fellow royal and former rugby star who was sitting directly behind the little Prince during one of his performances chalked up the 4-year-old’s behavior to a “sugar high” resulting from the ample supply of sweets available behind the royal box.

Nowhere in the article is there a question of whether the “sugar high” is a science-based phenomenon. In fact, the reporter assumes we all know it exists and writes that “parents across the globe can probably [read: definitely] relate.”

I’m curious: How do you respond when a parent in the office explains the child’s behavior as the result of a “sugar high”? Or when you’re at a cookout and someone makes a comment that makes it obvious that they believe that “sugar highs” are real? Do you immediately pause the conversation and launch into a short but tasteful observation that you know of no scientific studies that sugar can cause a high? Or, figuring that in the face of an overwhelming burden of old wives’ tales it’s not worth mounting a rebuttal, do you pretend you didn’t hear the comment?

Or am I completely off base because your experience has left you convinced that despite the lack of supporting studies the “sugar high” phenomenon exists? Maybe you even include it on your list of explanations and remedies for pediatric misbehaviors. I am ready to listen, but it will take some heavy lifting to convince me.

I suspect your response to offhand comments about “sugar highs” is similar to mine. It depends on the situation. If I think there are obvious and correctable causes for the child’s misbehavior such as sleep deprivation or a mismatch between parental expectation and the child’s tolerance for a stimulating environment I will include in my parenting advice the comment, “Sugar highs probably don’t exist.”

On the other hand, if I’m tired and think my observation will fall on deaf ears I let the conversation drift. I worry that my silence will be interpreted as a confirmation of an old wives’ tale. What I really don’t want to do is perpetuate a myth that may prevent some children from getting the care they need.

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

I can dimly recall watching Queen Elizabeth’s coronation on a very small black and white television screen. Even in monochrome it was a riveting event. Recently, the Queen celebrated her Platinum Jubilee, marking her 70-year reign. Apparently it was a multiday event with all the trappings, floating above an undercurrent of scandal and intrigue. I had better things to do than I did as a 7-year-old entranced by the novelty of a neighbor’s television set.

But, it turns out that I had missed the opportunity to see live and in color a royal meltdown starring the Queen’s great-grandson, 4-year-old Prince Louis. Not to worry. It remains on video archives for our education and pleasure ad infinitum. His performance was no more dramatic than what you have seen numerous times in the checkout line of the grocery store. However, this meltdown was on the world stage in the front row of the royal box and performed in various venues on each day of a 4-day event.

As long as you weren’t his parents, Kate Middleton and Prince William, the meltdown had its moments of hilarity. Louis made full use of his youthful and plastic face, creating a wide variety of taunts and responses to his mother’s praiseworthy and understated attempts at regaining control. Of course, the British press and every armchair parent with a Twitter account had a field day contributing their explanations and advice.

For example, here’s the headline on an international news website that caught my eye: “Royal reveals why Prince Louis was so ‘mischievous’ during the Jubilee”. In the article, a fellow royal and former rugby star who was sitting directly behind the little Prince during one of his performances chalked up the 4-year-old’s behavior to a “sugar high” resulting from the ample supply of sweets available behind the royal box.

Nowhere in the article is there a question of whether the “sugar high” is a science-based phenomenon. In fact, the reporter assumes we all know it exists and writes that “parents across the globe can probably [read: definitely] relate.”

I’m curious: How do you respond when a parent in the office explains the child’s behavior as the result of a “sugar high”? Or when you’re at a cookout and someone makes a comment that makes it obvious that they believe that “sugar highs” are real? Do you immediately pause the conversation and launch into a short but tasteful observation that you know of no scientific studies that sugar can cause a high? Or, figuring that in the face of an overwhelming burden of old wives’ tales it’s not worth mounting a rebuttal, do you pretend you didn’t hear the comment?

Or am I completely off base because your experience has left you convinced that despite the lack of supporting studies the “sugar high” phenomenon exists? Maybe you even include it on your list of explanations and remedies for pediatric misbehaviors. I am ready to listen, but it will take some heavy lifting to convince me.

I suspect your response to offhand comments about “sugar highs” is similar to mine. It depends on the situation. If I think there are obvious and correctable causes for the child’s misbehavior such as sleep deprivation or a mismatch between parental expectation and the child’s tolerance for a stimulating environment I will include in my parenting advice the comment, “Sugar highs probably don’t exist.”

On the other hand, if I’m tired and think my observation will fall on deaf ears I let the conversation drift. I worry that my silence will be interpreted as a confirmation of an old wives’ tale. What I really don’t want to do is perpetuate a myth that may prevent some children from getting the care they need.

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

I can dimly recall watching Queen Elizabeth’s coronation on a very small black and white television screen. Even in monochrome it was a riveting event. Recently, the Queen celebrated her Platinum Jubilee, marking her 70-year reign. Apparently it was a multiday event with all the trappings, floating above an undercurrent of scandal and intrigue. I had better things to do than I did as a 7-year-old entranced by the novelty of a neighbor’s television set.

But, it turns out that I had missed the opportunity to see live and in color a royal meltdown starring the Queen’s great-grandson, 4-year-old Prince Louis. Not to worry. It remains on video archives for our education and pleasure ad infinitum. His performance was no more dramatic than what you have seen numerous times in the checkout line of the grocery store. However, this meltdown was on the world stage in the front row of the royal box and performed in various venues on each day of a 4-day event.

As long as you weren’t his parents, Kate Middleton and Prince William, the meltdown had its moments of hilarity. Louis made full use of his youthful and plastic face, creating a wide variety of taunts and responses to his mother’s praiseworthy and understated attempts at regaining control. Of course, the British press and every armchair parent with a Twitter account had a field day contributing their explanations and advice.

For example, here’s the headline on an international news website that caught my eye: “Royal reveals why Prince Louis was so ‘mischievous’ during the Jubilee”. In the article, a fellow royal and former rugby star who was sitting directly behind the little Prince during one of his performances chalked up the 4-year-old’s behavior to a “sugar high” resulting from the ample supply of sweets available behind the royal box.

Nowhere in the article is there a question of whether the “sugar high” is a science-based phenomenon. In fact, the reporter assumes we all know it exists and writes that “parents across the globe can probably [read: definitely] relate.”

I’m curious: How do you respond when a parent in the office explains the child’s behavior as the result of a “sugar high”? Or when you’re at a cookout and someone makes a comment that makes it obvious that they believe that “sugar highs” are real? Do you immediately pause the conversation and launch into a short but tasteful observation that you know of no scientific studies that sugar can cause a high? Or, figuring that in the face of an overwhelming burden of old wives’ tales it’s not worth mounting a rebuttal, do you pretend you didn’t hear the comment?

Or am I completely off base because your experience has left you convinced that despite the lack of supporting studies the “sugar high” phenomenon exists? Maybe you even include it on your list of explanations and remedies for pediatric misbehaviors. I am ready to listen, but it will take some heavy lifting to convince me.

I suspect your response to offhand comments about “sugar highs” is similar to mine. It depends on the situation. If I think there are obvious and correctable causes for the child’s misbehavior such as sleep deprivation or a mismatch between parental expectation and the child’s tolerance for a stimulating environment I will include in my parenting advice the comment, “Sugar highs probably don’t exist.”

On the other hand, if I’m tired and think my observation will fall on deaf ears I let the conversation drift. I worry that my silence will be interpreted as a confirmation of an old wives’ tale. What I really don’t want to do is perpetuate a myth that may prevent some children from getting the care they need.

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

Key clinical point: Induction therapy with tofacitinib or prednisone significantly increased serum lipid levels in patients with inflammatory bowel disease (IBD), whereas no changes were observed with immunomodulators or biologics.

Major finding: At 10 weeks, the total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels increased significantly in patients who initiated tofacitinib (+20%, +25%, and +26%, respectively; all P < .05) or prednisone (+26%, +31%, and +12%, respectively; all P < .05) therapy. The changes in lipid levels were not significant with other biologics or immunomodulators.

Study details: This was a prospective study that included 198 patients with ulcerative colitis (n = 61), Crohn’s disease (n = 137), or unclassified IBD (n = 8) who initiated prednisone, thiopurine, methotrexate, an anti-tumor necrosis factor alpha agent, ustekinumab, vedolizumab, or tofacitinib.

Disclosures: This study did not receive any funding. AC de Vries and CJ van der Woude declared receiving research funding and serving as advisory board members for various sources.

Source: Sleutjes JAM et al. Lipid changes after induction therapy in patients with inflammatory bowel disease: Effect of different drug classes and inflammation. Inflamm Bowel Dis. 2022 (May 19). Doi: 10.1093/ibd/izac100

Key clinical point: Induction therapy with tofacitinib or prednisone significantly increased serum lipid levels in patients with inflammatory bowel disease (IBD), whereas no changes were observed with immunomodulators or biologics.

Major finding: At 10 weeks, the total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels increased significantly in patients who initiated tofacitinib (+20%, +25%, and +26%, respectively; all P < .05) or prednisone (+26%, +31%, and +12%, respectively; all P < .05) therapy. The changes in lipid levels were not significant with other biologics or immunomodulators.

Study details: This was a prospective study that included 198 patients with ulcerative colitis (n = 61), Crohn’s disease (n = 137), or unclassified IBD (n = 8) who initiated prednisone, thiopurine, methotrexate, an anti-tumor necrosis factor alpha agent, ustekinumab, vedolizumab, or tofacitinib.

Disclosures: This study did not receive any funding. AC de Vries and CJ van der Woude declared receiving research funding and serving as advisory board members for various sources.

Source: Sleutjes JAM et al. Lipid changes after induction therapy in patients with inflammatory bowel disease: Effect of different drug classes and inflammation. Inflamm Bowel Dis. 2022 (May 19). Doi: 10.1093/ibd/izac100

Key clinical point: Induction therapy with tofacitinib or prednisone significantly increased serum lipid levels in patients with inflammatory bowel disease (IBD), whereas no changes were observed with immunomodulators or biologics.

Major finding: At 10 weeks, the total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels increased significantly in patients who initiated tofacitinib (+20%, +25%, and +26%, respectively; all P < .05) or prednisone (+26%, +31%, and +12%, respectively; all P < .05) therapy. The changes in lipid levels were not significant with other biologics or immunomodulators.

Study details: This was a prospective study that included 198 patients with ulcerative colitis (n = 61), Crohn’s disease (n = 137), or unclassified IBD (n = 8) who initiated prednisone, thiopurine, methotrexate, an anti-tumor necrosis factor alpha agent, ustekinumab, vedolizumab, or tofacitinib.

Disclosures: This study did not receive any funding. AC de Vries and CJ van der Woude declared receiving research funding and serving as advisory board members for various sources.

Source: Sleutjes JAM et al. Lipid changes after induction therapy in patients with inflammatory bowel disease: Effect of different drug classes and inflammation. Inflamm Bowel Dis. 2022 (May 19). Doi: 10.1093/ibd/izac100

Key clinical point: Vedolizumab can be considered a safe and valid option for elderly patients with inflammatory bowel disease, with efficacy being unaffected by age in Crohn’s disease (CD), but slightly reduced in elderly vs. nonelderly patients with ulcerative colitis (UC).

Major finding: Nonelderly vs. elderly patients with UC showed significantly higher clinical remission at 24 months (47.3% vs. 34.3%; P < .05) and persistence (67.6% vs. 51.4%; P = .02), both of which were not significantly different between elderly and nonelderly patients with CD. Adverse events were comparable among elderly and nonelderly patients.

Study details: This was a retrospective-prospective study that included 198 elderly patients aged ≥ 65 years with UC (n = 108) or CD (n = 90) and 396 matched nonelderly patients with UC (n = 205) or CD (n = 191), all of whom received vedolizumab.

Disclosures: This study was funded by Takeda. Some authors reported receiving consulting, lecture, or speakers’ fees, or serving as advisory board members for various sources, including Takeda.

Source: Pugliese D et al. Effectiveness and safety of vedolizumab in a matched cohort of elderly and nonelderly patients with inflammatory bowel disease: The IG-IBD LIVE study. Aliment Pharmacol Ther. 2022;56(1):95-109 (May 12). Doi: 10.1111/apt.16923

Key clinical point: Vedolizumab can be considered a safe and valid option for elderly patients with inflammatory bowel disease, with efficacy being unaffected by age in Crohn’s disease (CD), but slightly reduced in elderly vs. nonelderly patients with ulcerative colitis (UC).

Major finding: Nonelderly vs. elderly patients with UC showed significantly higher clinical remission at 24 months (47.3% vs. 34.3%; P < .05) and persistence (67.6% vs. 51.4%; P = .02), both of which were not significantly different between elderly and nonelderly patients with CD. Adverse events were comparable among elderly and nonelderly patients.

Study details: This was a retrospective-prospective study that included 198 elderly patients aged ≥ 65 years with UC (n = 108) or CD (n = 90) and 396 matched nonelderly patients with UC (n = 205) or CD (n = 191), all of whom received vedolizumab.

Disclosures: This study was funded by Takeda. Some authors reported receiving consulting, lecture, or speakers’ fees, or serving as advisory board members for various sources, including Takeda.

Source: Pugliese D et al. Effectiveness and safety of vedolizumab in a matched cohort of elderly and nonelderly patients with inflammatory bowel disease: The IG-IBD LIVE study. Aliment Pharmacol Ther. 2022;56(1):95-109 (May 12). Doi: 10.1111/apt.16923

Key clinical point: Vedolizumab can be considered a safe and valid option for elderly patients with inflammatory bowel disease, with efficacy being unaffected by age in Crohn’s disease (CD), but slightly reduced in elderly vs. nonelderly patients with ulcerative colitis (UC).

Major finding: Nonelderly vs. elderly patients with UC showed significantly higher clinical remission at 24 months (47.3% vs. 34.3%; P < .05) and persistence (67.6% vs. 51.4%; P = .02), both of which were not significantly different between elderly and nonelderly patients with CD. Adverse events were comparable among elderly and nonelderly patients.

Study details: This was a retrospective-prospective study that included 198 elderly patients aged ≥ 65 years with UC (n = 108) or CD (n = 90) and 396 matched nonelderly patients with UC (n = 205) or CD (n = 191), all of whom received vedolizumab.

Disclosures: This study was funded by Takeda. Some authors reported receiving consulting, lecture, or speakers’ fees, or serving as advisory board members for various sources, including Takeda.

Source: Pugliese D et al. Effectiveness and safety of vedolizumab in a matched cohort of elderly and nonelderly patients with inflammatory bowel disease: The IG-IBD LIVE study. Aliment Pharmacol Ther. 2022;56(1):95-109 (May 12). Doi: 10.1111/apt.16923

Key clinical point: Early treatment with postoperative biological therapy decreased endoscopic recurrence rates and improved long-term outcomes in patients who underwent Crohn’s disease (CD)-related surgery.

Major finding: The rate of endoscopic recurrence was higher in patients not treated vs. treated with early postoperative biological therapy (80.8% vs. 45.2%; P < .000024), with the risk of experiencing hospitalization or surgery at 5 years being 23.3% higher (P = .02221) and the rate of medical therapy escalation being significantly higher (66.0% vs. 14.0%; P < .00001) in the no-treatment vs. treatment group.

Study details: Findings are from a retrospective cohort study including 141 patients with CD who underwent surgery and colonoscopy at 6-12 months postoperatively.

Disclosures: This study did not receive any funding. Some authors declared receiving consulting fees, lecture fees, speaker’s fees, grants, or serving as advisory board members for various sources.

Source: D'Amico F et al. Early biological therapy in operated Crohn’s disease patients is associated with a lower rate of endoscopic recurrence and improved long-term outcomes: A single-center experience. Inflamm Bowel Dis. 2022 (May 28). Doi: 10.1093/ibd/izac110

Key clinical point: Early treatment with postoperative biological therapy decreased endoscopic recurrence rates and improved long-term outcomes in patients who underwent Crohn’s disease (CD)-related surgery.

Major finding: The rate of endoscopic recurrence was higher in patients not treated vs. treated with early postoperative biological therapy (80.8% vs. 45.2%; P < .000024), with the risk of experiencing hospitalization or surgery at 5 years being 23.3% higher (P = .02221) and the rate of medical therapy escalation being significantly higher (66.0% vs. 14.0%; P < .00001) in the no-treatment vs. treatment group.

Study details: Findings are from a retrospective cohort study including 141 patients with CD who underwent surgery and colonoscopy at 6-12 months postoperatively.

Disclosures: This study did not receive any funding. Some authors declared receiving consulting fees, lecture fees, speaker’s fees, grants, or serving as advisory board members for various sources.

Source: D'Amico F et al. Early biological therapy in operated Crohn’s disease patients is associated with a lower rate of endoscopic recurrence and improved long-term outcomes: A single-center experience. Inflamm Bowel Dis. 2022 (May 28). Doi: 10.1093/ibd/izac110

Key clinical point: Early treatment with postoperative biological therapy decreased endoscopic recurrence rates and improved long-term outcomes in patients who underwent Crohn’s disease (CD)-related surgery.

Major finding: The rate of endoscopic recurrence was higher in patients not treated vs. treated with early postoperative biological therapy (80.8% vs. 45.2%; P < .000024), with the risk of experiencing hospitalization or surgery at 5 years being 23.3% higher (P = .02221) and the rate of medical therapy escalation being significantly higher (66.0% vs. 14.0%; P < .00001) in the no-treatment vs. treatment group.

Study details: Findings are from a retrospective cohort study including 141 patients with CD who underwent surgery and colonoscopy at 6-12 months postoperatively.

Disclosures: This study did not receive any funding. Some authors declared receiving consulting fees, lecture fees, speaker’s fees, grants, or serving as advisory board members for various sources.

Source: D'Amico F et al. Early biological therapy in operated Crohn’s disease patients is associated with a lower rate of endoscopic recurrence and improved long-term outcomes: A single-center experience. Inflamm Bowel Dis. 2022 (May 28). Doi: 10.1093/ibd/izac110

LONDON – A low-carbohydrate, high-fat (LCHF) diet reduced the progression of nonalcoholic fatty liver disease (NAFLD), and despite no calorie restriction, participants with both NAFLD and type 2 diabetes lost 5.8% of their body weight, according to a randomized controlled study.

“Based on these results, the LCHF diet may be recommended to people with NAFLD and type 2 diabetes,” said Camilla Dalby Hansen, MD, department of gastroenterology and hepatology, Odense University Hospital, Denmark, who presented the data at the International Liver Congress (ILC) 2022.  

“Basically, if you have fat in your liver, you will benefit from eating fat,” she said.

The LCHF diet was compared with a low-fat, high-carbohydrate diet more typically followed for these conditions. The low-fat diet was also found to reduce the progression of NAFLD, but to a lesser extent than the LCHF diet.

Dr. Dalby Hansen called their study one of the most extensive investigations of the LCHF diet in patients with type 2 diabetes and fatty liver disease.

“Combining this [reduction in NAFLD score] with the huge weight loss, the lower HbA1c [blood sugar], the lowering of blood pressure in women, the rise in HDL levels, and reduction in triglycerides – all in all, this diet is very promising,” she said.

Stephen Harrison, MD, visiting professor, University of Oxford, United Kingdom, medical director of Pinnacle Clinical Research and president of Summit Clinical Research, San Antonio, commended Dr. Dalby Hansen on her methodology, which included before-and-after liver biopsies. “It’s a heinous effort to do paired liver biopsies in a lifestyle modification trial. That’s huge.”

“This study tells me that the way we manage patients doesn’t change – it is still lifestyle modification,” said Dr. Harrison, who was not involved with the study. “It’s eat less [rather] than more. It’s exercise and try to lose weight. In the long term, we give patients benefit, and we show that the disease has improved, and we offer something that means they can maintain a healthy life.”

He added that the relatively small and short trial was informative.

“They improved the NAFLD activity score [NAS],” he said. “I don’t know by how much. There was no change in fibrosis, but we wouldn’t expect this at 6 months.”

“It’s provocative work, and it gives us healthy information about how we can help manage our patients from a lifestyle perspective,” he concluded.
 

‘Do not lose weight. Eat until you are full’

In the study, 110 participants with type 2 diabetes and NAFLD, aged 18-78 years, were allocated to the LCHF diet, and 55 were allocated to the low-fat diet for 6 months.

The researchers performed liver biopsies at baseline and 6 months, which were blinded for scoring.  

Participants had ongoing dietitian consultations, with follow-up visits at 3 and 6 months. Compliance was reported continuously through an online food diary platform.

The primary endpoint was change in glycemic control as measured by A1c level over 6 months. The secondary endpoints comprised the proportion of participants with changes in the NAS of at least 2 points over 6 months. Both these measures were compared between the two dietary groups.

The two groups were matched at baseline, with a mean age of 55-57 years, 58% were women, 89% with metabolic syndrome, and a mean BMI 34 kg/m².

In baseline liver disease, F1 level fibrosis was the most common (58%), followed by hepatic steatosis (S1, 47%; S2, 32%), with a median NAS of 3, and 19% had nonalcoholic steatohepatitis.

The special thing about these diets was that participants were told to “not lose weight, but eat until you are full,” remarked Dr. Dalby Hansen.

Those on the LCHF diet consumed an average of 61% energy from fat, 13% from carbohydrates, and 23% from protein, compared with the low-fat diet, which comprised an average of 29% energy from fat, 46% from carbohydrates, and 21% from protein.

“It’s a lot of fat and corresponds to a quarter of a liter of olive oil per day,” said Dr. Dalby Hansen. “They really had to change their mindset a lot, because it was difficult for them to start eating all these fats, especially since we’ve all been told for decades that it isn’t good. But we supported them, and they got into it.”

The LCHF diet was primarily comprised of unsaturated fats – for example, avocado, oil, nuts, and seeds – but also included saturated fats, such as cheese, cream, and high-fat dairy products. Participants were free to eat unsaturated and saturated fats, but Dr. Dalby Hansen and her team advised participants that “good” unsaturated fats were preferable.

“Also, this diet contained vegetables but no bread, no potatoes, no rice, and no pasta. It was low in carbohydrates, below 20%,” she added.
 

Improved glycemic control, reduced liver fat

“We found that the LCHF diet improved diabetes control, it reduced the fat in the liver, and, even though they’re eating as many calories as they were used to until they were full, they lost 5.8% of body weight,” said Dr. Dalby Hansen in reporting the results. Participants in the low-fat group lost only 1.8% of body weight.

However, mean calorie intake dropped in both groups, by –2.2% in the LCHF group and –8.7% in the low-fat group. 

“The LCHF diet improved the primary outcome of A1c by 9.5 mmol/mol, which is similar to some anti-diabetic medications, such as DPP-4 inhibitors and SGLT2 inhibitors,” she said.

The low-fat group reduced A1c by 3.4 mmol/mol, resulting in a between-group difference of 6.1 mmol/mol.

“Upon follow-up of 3 months, after stopping the diets, on average the participants in both groups returned their HbA1c levels to nearly baseline values,” she said. Results were adjusted for weight loss and baseline values.

Both diets also improved the NAS. The proportion of participants who improved their NAS score by 2 or more points was 22% in the LCHF group versus 17% in the low-fat group (P = 0.58). Additionally, in the LCHF group, 70% of participants improved their score by 1 or more points, compared with 49% in the low-fat group and fewer in the LCHF group experienced a worsening of their score (1% vs. 23%, respectively).

One participant on LCHF had high triglycerides of 12 mmol/L after 3 months. Overall, the low-density lipoprotein increased marginally by 0.2 mmol per liter in the high-fat group, said Dr. Dalby Hansen.

Dr. Dalby Hansen noted some limitations. The findings might not be applicable in more severe NAFLD, dietary assessment relied on self-reporting, no food was provided, and participants had to cook themselves. It was also an open-label study because of the nature of the intervention.
 

Some hope for more sustainable dieting

Many diets are difficult to adhere to, remarked Dr. Dalby Hansen. “We thought this [diet] might be easier to comply with in the longer term, and we hope that these results might provide patients with more options.”

She added that most people who started the diet adapted and complied with it. “However, it might not be for everyone, but I think we can say that if people try, and it fits into their lives, then they go for it.”

However, “it is not about going out and eating whatever fat and how much of it you want. It’s important that you cut the carbohydrates too,” she said. “With this approach, we really saw amazing results.”

Dr. Dalby Hansen added that having various diets available, including the LCHF one, meant that as clinicians they could empower patients to take control of their metabolic health.

“We can ask them directly, ‘What would fit into their life?’” she said. “We know that one size does not fit at all, and I believe that if we could engage patients more, then they can take control of their own situation.”

Asked whether these findings were enough to change guidelines, Zobair Younossi, MD, professor and chairman, department of medicine, Inova Fairfax Medical Campus, Falls Church, Va., remarked that it was the sugar at work here.

“Dietary fat – it’s not the same as fat in the liver, and this diet has more to do with the sugar levels,” he said.

“I’m always reluctant to take results from a short-term study without long-term follow-up,” Dr. Younossi said. “I want to know will patients live longer, and long-term data are needed for this. Until I have that strong evidence that outcomes are going to change, or at least some sign that the outcome is going to change, it is too early to change any guidelines.”

Dr. Dalby Hansen reports no relevant financial relationships. Dr. Harrison reported financial relationships with numerous pharmaceutical companies. Dr. Younossi reports the following financial relationships: research funds and/or consultant to Abbott, Allergan, Bristol Myers Squibb, Echosens, Genfit, Gilead Sciences, Intercept, Madrigal, Merck, and Novo Nordisk.

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

LONDON – A low-carbohydrate, high-fat (LCHF) diet reduced the progression of nonalcoholic fatty liver disease (NAFLD), and despite no calorie restriction, participants with both NAFLD and type 2 diabetes lost 5.8% of their body weight, according to a randomized controlled study.

“Based on these results, the LCHF diet may be recommended to people with NAFLD and type 2 diabetes,” said Camilla Dalby Hansen, MD, department of gastroenterology and hepatology, Odense University Hospital, Denmark, who presented the data at the International Liver Congress (ILC) 2022.  

“Basically, if you have fat in your liver, you will benefit from eating fat,” she said.

The LCHF diet was compared with a low-fat, high-carbohydrate diet more typically followed for these conditions. The low-fat diet was also found to reduce the progression of NAFLD, but to a lesser extent than the LCHF diet.

Dr. Dalby Hansen called their study one of the most extensive investigations of the LCHF diet in patients with type 2 diabetes and fatty liver disease.

“Combining this [reduction in NAFLD score] with the huge weight loss, the lower HbA1c [blood sugar], the lowering of blood pressure in women, the rise in HDL levels, and reduction in triglycerides – all in all, this diet is very promising,” she said.

Stephen Harrison, MD, visiting professor, University of Oxford, United Kingdom, medical director of Pinnacle Clinical Research and president of Summit Clinical Research, San Antonio, commended Dr. Dalby Hansen on her methodology, which included before-and-after liver biopsies. “It’s a heinous effort to do paired liver biopsies in a lifestyle modification trial. That’s huge.”

“This study tells me that the way we manage patients doesn’t change – it is still lifestyle modification,” said Dr. Harrison, who was not involved with the study. “It’s eat less [rather] than more. It’s exercise and try to lose weight. In the long term, we give patients benefit, and we show that the disease has improved, and we offer something that means they can maintain a healthy life.”

He added that the relatively small and short trial was informative.

“They improved the NAFLD activity score [NAS],” he said. “I don’t know by how much. There was no change in fibrosis, but we wouldn’t expect this at 6 months.”

“It’s provocative work, and it gives us healthy information about how we can help manage our patients from a lifestyle perspective,” he concluded.
 

‘Do not lose weight. Eat until you are full’

In the study, 110 participants with type 2 diabetes and NAFLD, aged 18-78 years, were allocated to the LCHF diet, and 55 were allocated to the low-fat diet for 6 months.

The researchers performed liver biopsies at baseline and 6 months, which were blinded for scoring.  

Participants had ongoing dietitian consultations, with follow-up visits at 3 and 6 months. Compliance was reported continuously through an online food diary platform.

The primary endpoint was change in glycemic control as measured by A1c level over 6 months. The secondary endpoints comprised the proportion of participants with changes in the NAS of at least 2 points over 6 months. Both these measures were compared between the two dietary groups.

The two groups were matched at baseline, with a mean age of 55-57 years, 58% were women, 89% with metabolic syndrome, and a mean BMI 34 kg/m².

In baseline liver disease, F1 level fibrosis was the most common (58%), followed by hepatic steatosis (S1, 47%; S2, 32%), with a median NAS of 3, and 19% had nonalcoholic steatohepatitis.

The special thing about these diets was that participants were told to “not lose weight, but eat until you are full,” remarked Dr. Dalby Hansen.

Those on the LCHF diet consumed an average of 61% energy from fat, 13% from carbohydrates, and 23% from protein, compared with the low-fat diet, which comprised an average of 29% energy from fat, 46% from carbohydrates, and 21% from protein.

“It’s a lot of fat and corresponds to a quarter of a liter of olive oil per day,” said Dr. Dalby Hansen. “They really had to change their mindset a lot, because it was difficult for them to start eating all these fats, especially since we’ve all been told for decades that it isn’t good. But we supported them, and they got into it.”

The LCHF diet was primarily comprised of unsaturated fats – for example, avocado, oil, nuts, and seeds – but also included saturated fats, such as cheese, cream, and high-fat dairy products. Participants were free to eat unsaturated and saturated fats, but Dr. Dalby Hansen and her team advised participants that “good” unsaturated fats were preferable.

“Also, this diet contained vegetables but no bread, no potatoes, no rice, and no pasta. It was low in carbohydrates, below 20%,” she added.
 

Improved glycemic control, reduced liver fat

“We found that the LCHF diet improved diabetes control, it reduced the fat in the liver, and, even though they’re eating as many calories as they were used to until they were full, they lost 5.8% of body weight,” said Dr. Dalby Hansen in reporting the results. Participants in the low-fat group lost only 1.8% of body weight.

However, mean calorie intake dropped in both groups, by –2.2% in the LCHF group and –8.7% in the low-fat group. 

“The LCHF diet improved the primary outcome of A1c by 9.5 mmol/mol, which is similar to some anti-diabetic medications, such as DPP-4 inhibitors and SGLT2 inhibitors,” she said.

The low-fat group reduced A1c by 3.4 mmol/mol, resulting in a between-group difference of 6.1 mmol/mol.

“Upon follow-up of 3 months, after stopping the diets, on average the participants in both groups returned their HbA1c levels to nearly baseline values,” she said. Results were adjusted for weight loss and baseline values.

Both diets also improved the NAS. The proportion of participants who improved their NAS score by 2 or more points was 22% in the LCHF group versus 17% in the low-fat group (P = 0.58). Additionally, in the LCHF group, 70% of participants improved their score by 1 or more points, compared with 49% in the low-fat group and fewer in the LCHF group experienced a worsening of their score (1% vs. 23%, respectively).

One participant on LCHF had high triglycerides of 12 mmol/L after 3 months. Overall, the low-density lipoprotein increased marginally by 0.2 mmol per liter in the high-fat group, said Dr. Dalby Hansen.

Dr. Dalby Hansen noted some limitations. The findings might not be applicable in more severe NAFLD, dietary assessment relied on self-reporting, no food was provided, and participants had to cook themselves. It was also an open-label study because of the nature of the intervention.
 

Some hope for more sustainable dieting

Many diets are difficult to adhere to, remarked Dr. Dalby Hansen. “We thought this [diet] might be easier to comply with in the longer term, and we hope that these results might provide patients with more options.”

She added that most people who started the diet adapted and complied with it. “However, it might not be for everyone, but I think we can say that if people try, and it fits into their lives, then they go for it.”

However, “it is not about going out and eating whatever fat and how much of it you want. It’s important that you cut the carbohydrates too,” she said. “With this approach, we really saw amazing results.”

Dr. Dalby Hansen added that having various diets available, including the LCHF one, meant that as clinicians they could empower patients to take control of their metabolic health.

“We can ask them directly, ‘What would fit into their life?’” she said. “We know that one size does not fit at all, and I believe that if we could engage patients more, then they can take control of their own situation.”

Asked whether these findings were enough to change guidelines, Zobair Younossi, MD, professor and chairman, department of medicine, Inova Fairfax Medical Campus, Falls Church, Va., remarked that it was the sugar at work here.

“Dietary fat – it’s not the same as fat in the liver, and this diet has more to do with the sugar levels,” he said.

“I’m always reluctant to take results from a short-term study without long-term follow-up,” Dr. Younossi said. “I want to know will patients live longer, and long-term data are needed for this. Until I have that strong evidence that outcomes are going to change, or at least some sign that the outcome is going to change, it is too early to change any guidelines.”

Dr. Dalby Hansen reports no relevant financial relationships. Dr. Harrison reported financial relationships with numerous pharmaceutical companies. Dr. Younossi reports the following financial relationships: research funds and/or consultant to Abbott, Allergan, Bristol Myers Squibb, Echosens, Genfit, Gilead Sciences, Intercept, Madrigal, Merck, and Novo Nordisk.

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

LONDON – A low-carbohydrate, high-fat (LCHF) diet reduced the progression of nonalcoholic fatty liver disease (NAFLD), and despite no calorie restriction, participants with both NAFLD and type 2 diabetes lost 5.8% of their body weight, according to a randomized controlled study.

“Based on these results, the LCHF diet may be recommended to people with NAFLD and type 2 diabetes,” said Camilla Dalby Hansen, MD, department of gastroenterology and hepatology, Odense University Hospital, Denmark, who presented the data at the International Liver Congress (ILC) 2022.  

“Basically, if you have fat in your liver, you will benefit from eating fat,” she said.

The LCHF diet was compared with a low-fat, high-carbohydrate diet more typically followed for these conditions. The low-fat diet was also found to reduce the progression of NAFLD, but to a lesser extent than the LCHF diet.

Dr. Dalby Hansen called their study one of the most extensive investigations of the LCHF diet in patients with type 2 diabetes and fatty liver disease.

“Combining this [reduction in NAFLD score] with the huge weight loss, the lower HbA1c [blood sugar], the lowering of blood pressure in women, the rise in HDL levels, and reduction in triglycerides – all in all, this diet is very promising,” she said.

Stephen Harrison, MD, visiting professor, University of Oxford, United Kingdom, medical director of Pinnacle Clinical Research and president of Summit Clinical Research, San Antonio, commended Dr. Dalby Hansen on her methodology, which included before-and-after liver biopsies. “It’s a heinous effort to do paired liver biopsies in a lifestyle modification trial. That’s huge.”

“This study tells me that the way we manage patients doesn’t change – it is still lifestyle modification,” said Dr. Harrison, who was not involved with the study. “It’s eat less [rather] than more. It’s exercise and try to lose weight. In the long term, we give patients benefit, and we show that the disease has improved, and we offer something that means they can maintain a healthy life.”

He added that the relatively small and short trial was informative.

“They improved the NAFLD activity score [NAS],” he said. “I don’t know by how much. There was no change in fibrosis, but we wouldn’t expect this at 6 months.”

“It’s provocative work, and it gives us healthy information about how we can help manage our patients from a lifestyle perspective,” he concluded.
 

‘Do not lose weight. Eat until you are full’

In the study, 110 participants with type 2 diabetes and NAFLD, aged 18-78 years, were allocated to the LCHF diet, and 55 were allocated to the low-fat diet for 6 months.

The researchers performed liver biopsies at baseline and 6 months, which were blinded for scoring.  

Participants had ongoing dietitian consultations, with follow-up visits at 3 and 6 months. Compliance was reported continuously through an online food diary platform.

The primary endpoint was change in glycemic control as measured by A1c level over 6 months. The secondary endpoints comprised the proportion of participants with changes in the NAS of at least 2 points over 6 months. Both these measures were compared between the two dietary groups.

The two groups were matched at baseline, with a mean age of 55-57 years, 58% were women, 89% with metabolic syndrome, and a mean BMI 34 kg/m².

In baseline liver disease, F1 level fibrosis was the most common (58%), followed by hepatic steatosis (S1, 47%; S2, 32%), with a median NAS of 3, and 19% had nonalcoholic steatohepatitis.

The special thing about these diets was that participants were told to “not lose weight, but eat until you are full,” remarked Dr. Dalby Hansen.

Those on the LCHF diet consumed an average of 61% energy from fat, 13% from carbohydrates, and 23% from protein, compared with the low-fat diet, which comprised an average of 29% energy from fat, 46% from carbohydrates, and 21% from protein.

“It’s a lot of fat and corresponds to a quarter of a liter of olive oil per day,” said Dr. Dalby Hansen. “They really had to change their mindset a lot, because it was difficult for them to start eating all these fats, especially since we’ve all been told for decades that it isn’t good. But we supported them, and they got into it.”

The LCHF diet was primarily comprised of unsaturated fats – for example, avocado, oil, nuts, and seeds – but also included saturated fats, such as cheese, cream, and high-fat dairy products. Participants were free to eat unsaturated and saturated fats, but Dr. Dalby Hansen and her team advised participants that “good” unsaturated fats were preferable.

“Also, this diet contained vegetables but no bread, no potatoes, no rice, and no pasta. It was low in carbohydrates, below 20%,” she added.
 

Improved glycemic control, reduced liver fat

“We found that the LCHF diet improved diabetes control, it reduced the fat in the liver, and, even though they’re eating as many calories as they were used to until they were full, they lost 5.8% of body weight,” said Dr. Dalby Hansen in reporting the results. Participants in the low-fat group lost only 1.8% of body weight.

However, mean calorie intake dropped in both groups, by –2.2% in the LCHF group and –8.7% in the low-fat group. 

“The LCHF diet improved the primary outcome of A1c by 9.5 mmol/mol, which is similar to some anti-diabetic medications, such as DPP-4 inhibitors and SGLT2 inhibitors,” she said.

The low-fat group reduced A1c by 3.4 mmol/mol, resulting in a between-group difference of 6.1 mmol/mol.

“Upon follow-up of 3 months, after stopping the diets, on average the participants in both groups returned their HbA1c levels to nearly baseline values,” she said. Results were adjusted for weight loss and baseline values.

Both diets also improved the NAS. The proportion of participants who improved their NAS score by 2 or more points was 22% in the LCHF group versus 17% in the low-fat group (P = 0.58). Additionally, in the LCHF group, 70% of participants improved their score by 1 or more points, compared with 49% in the low-fat group and fewer in the LCHF group experienced a worsening of their score (1% vs. 23%, respectively).

One participant on LCHF had high triglycerides of 12 mmol/L after 3 months. Overall, the low-density lipoprotein increased marginally by 0.2 mmol per liter in the high-fat group, said Dr. Dalby Hansen.

Dr. Dalby Hansen noted some limitations. The findings might not be applicable in more severe NAFLD, dietary assessment relied on self-reporting, no food was provided, and participants had to cook themselves. It was also an open-label study because of the nature of the intervention.
 

Some hope for more sustainable dieting

Many diets are difficult to adhere to, remarked Dr. Dalby Hansen. “We thought this [diet] might be easier to comply with in the longer term, and we hope that these results might provide patients with more options.”

She added that most people who started the diet adapted and complied with it. “However, it might not be for everyone, but I think we can say that if people try, and it fits into their lives, then they go for it.”

However, “it is not about going out and eating whatever fat and how much of it you want. It’s important that you cut the carbohydrates too,” she said. “With this approach, we really saw amazing results.”

Dr. Dalby Hansen added that having various diets available, including the LCHF one, meant that as clinicians they could empower patients to take control of their metabolic health.

“We can ask them directly, ‘What would fit into their life?’” she said. “We know that one size does not fit at all, and I believe that if we could engage patients more, then they can take control of their own situation.”

Asked whether these findings were enough to change guidelines, Zobair Younossi, MD, professor and chairman, department of medicine, Inova Fairfax Medical Campus, Falls Church, Va., remarked that it was the sugar at work here.

“Dietary fat – it’s not the same as fat in the liver, and this diet has more to do with the sugar levels,” he said.

“I’m always reluctant to take results from a short-term study without long-term follow-up,” Dr. Younossi said. “I want to know will patients live longer, and long-term data are needed for this. Until I have that strong evidence that outcomes are going to change, or at least some sign that the outcome is going to change, it is too early to change any guidelines.”

Dr. Dalby Hansen reports no relevant financial relationships. Dr. Harrison reported financial relationships with numerous pharmaceutical companies. Dr. Younossi reports the following financial relationships: research funds and/or consultant to Abbott, Allergan, Bristol Myers Squibb, Echosens, Genfit, Gilead Sciences, Intercept, Madrigal, Merck, and Novo Nordisk.

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

Key clinical point: Risk for overall cancer was 17% higher and cancer-specific mortality 26% higher in patients with inflammatory bowel disease (IBD) compared with non-IBD individuals.

Major finding: Risk for overall cancer (adjusted hazard ratio [aHR] 1.17; P < .001), particularly digestive cancer (aHR 1.33; P = .001), skin cancer (aHR 1.25; P < .001), and male genital cancer (aHR 1.29; P = .003), and cancer-specific mortality (aHR 1.26; P < .001) was significantly higher among patients with IBD vs. non-IBD individuals.

Study details: Findings are from a prospective study that included 5142 patients with ulcerative colitis (n = 3258), Crohn’s disease (n = 1449), or unclassified IBD (n = 435) and who were compared with 450,785 non-IBD reference individuals from the UK Biobank cohort.

Disclosures: The study was supported by the National Natural Science Foundation of China. The authors declared no conflicts of interest.

Source: Wu S et al. Inflammatory bowel disease and long-term risk of cancer: A prospective cohort study among half a million adults in UK Biobank. Inflamm Bowel Dis. 2022 (May 27). Doi:  10.1093/ibd/izac096

Key clinical point: Risk for overall cancer was 17% higher and cancer-specific mortality 26% higher in patients with inflammatory bowel disease (IBD) compared with non-IBD individuals.

Major finding: Risk for overall cancer (adjusted hazard ratio [aHR] 1.17; P < .001), particularly digestive cancer (aHR 1.33; P = .001), skin cancer (aHR 1.25; P < .001), and male genital cancer (aHR 1.29; P = .003), and cancer-specific mortality (aHR 1.26; P < .001) was significantly higher among patients with IBD vs. non-IBD individuals.

Study details: Findings are from a prospective study that included 5142 patients with ulcerative colitis (n = 3258), Crohn’s disease (n = 1449), or unclassified IBD (n = 435) and who were compared with 450,785 non-IBD reference individuals from the UK Biobank cohort.

Disclosures: The study was supported by the National Natural Science Foundation of China. The authors declared no conflicts of interest.

Source: Wu S et al. Inflammatory bowel disease and long-term risk of cancer: A prospective cohort study among half a million adults in UK Biobank. Inflamm Bowel Dis. 2022 (May 27). Doi:  10.1093/ibd/izac096

Key clinical point: Risk for overall cancer was 17% higher and cancer-specific mortality 26% higher in patients with inflammatory bowel disease (IBD) compared with non-IBD individuals.

Major finding: Risk for overall cancer (adjusted hazard ratio [aHR] 1.17; P < .001), particularly digestive cancer (aHR 1.33; P = .001), skin cancer (aHR 1.25; P < .001), and male genital cancer (aHR 1.29; P = .003), and cancer-specific mortality (aHR 1.26; P < .001) was significantly higher among patients with IBD vs. non-IBD individuals.

Study details: Findings are from a prospective study that included 5142 patients with ulcerative colitis (n = 3258), Crohn’s disease (n = 1449), or unclassified IBD (n = 435) and who were compared with 450,785 non-IBD reference individuals from the UK Biobank cohort.

Disclosures: The study was supported by the National Natural Science Foundation of China. The authors declared no conflicts of interest.

Source: Wu S et al. Inflammatory bowel disease and long-term risk of cancer: A prospective cohort study among half a million adults in UK Biobank. Inflamm Bowel Dis. 2022 (May 27). Doi:  10.1093/ibd/izac096

Key Clinical Point: Maintenance therapy with subcutaneous risankizumab showed superior efficacy than withdrawal from risankizumab to receive subcutaneous placebo in patients with moderate-to-severe Crohn’s disease (CD). It also had a tolerable safety profile.

Major finding: At week 52, patients receiving maintenance 360 mg risankizumab vs. placebo showed higher rates of Crohn’s Disease Activity Index clinical remission (adjusted difference [Δ] 15%; 95% CI 4%-25%) and endoscopic response (Δ 28%; 95% CI 19%-37%), with findings being similar for 180 mg risankizumab. The incidence of adverse events was similar across treatment groups.

Study details: Findings are from the phase 3 FORTIFY trial including 542 patients with moderate-to-severe CD who showed a clinical response to risankizumab in the ADVANCE and MOTIVATE induction trials and were randomly assigned to receive subcutaneous risankizumab (180 or 360 mg) or placebo.

Disclosures: This study was funded by AbbVie. Some authors declared being employees or holding stocks at AbbVie, and other authors reported receiving grants, speakers’ fees, consulting fees, or serving as advisory board members for various sources, including AbbVie.

Source: Ferrante M et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: Results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046 (May 28). Doi: 10.1016/S0140-6736(22)00466-4

Key Clinical Point: Maintenance therapy with subcutaneous risankizumab showed superior efficacy than withdrawal from risankizumab to receive subcutaneous placebo in patients with moderate-to-severe Crohn’s disease (CD). It also had a tolerable safety profile.

Major finding: At week 52, patients receiving maintenance 360 mg risankizumab vs. placebo showed higher rates of Crohn’s Disease Activity Index clinical remission (adjusted difference [Δ] 15%; 95% CI 4%-25%) and endoscopic response (Δ 28%; 95% CI 19%-37%), with findings being similar for 180 mg risankizumab. The incidence of adverse events was similar across treatment groups.

Study details: Findings are from the phase 3 FORTIFY trial including 542 patients with moderate-to-severe CD who showed a clinical response to risankizumab in the ADVANCE and MOTIVATE induction trials and were randomly assigned to receive subcutaneous risankizumab (180 or 360 mg) or placebo.

Disclosures: This study was funded by AbbVie. Some authors declared being employees or holding stocks at AbbVie, and other authors reported receiving grants, speakers’ fees, consulting fees, or serving as advisory board members for various sources, including AbbVie.

Source: Ferrante M et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: Results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046 (May 28). Doi: 10.1016/S0140-6736(22)00466-4

Key Clinical Point: Maintenance therapy with subcutaneous risankizumab showed superior efficacy than withdrawal from risankizumab to receive subcutaneous placebo in patients with moderate-to-severe Crohn’s disease (CD). It also had a tolerable safety profile.

Major finding: At week 52, patients receiving maintenance 360 mg risankizumab vs. placebo showed higher rates of Crohn’s Disease Activity Index clinical remission (adjusted difference [Δ] 15%; 95% CI 4%-25%) and endoscopic response (Δ 28%; 95% CI 19%-37%), with findings being similar for 180 mg risankizumab. The incidence of adverse events was similar across treatment groups.

Study details: Findings are from the phase 3 FORTIFY trial including 542 patients with moderate-to-severe CD who showed a clinical response to risankizumab in the ADVANCE and MOTIVATE induction trials and were randomly assigned to receive subcutaneous risankizumab (180 or 360 mg) or placebo.

Disclosures: This study was funded by AbbVie. Some authors declared being employees or holding stocks at AbbVie, and other authors reported receiving grants, speakers’ fees, consulting fees, or serving as advisory board members for various sources, including AbbVie.

Source: Ferrante M et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: Results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046 (May 28). Doi: 10.1016/S0140-6736(22)00466-4

Key Clinical Point: Maintenance therapy with subcutaneous risankizumab showed superior efficacy than withdrawal from risankizumab to receive subcutaneous placebo in patients with moderate-to-severe Crohn’s disease (CD). It also had a tolerable safety profile.

Major finding: At week 52, patients receiving maintenance 360 mg risankizumab vs. placebo showed higher rates of Crohn’s Disease Activity Index clinical remission (adjusted difference [Δ] 15%; 95% CI 4%-25%) and endoscopic response (Δ 28%; 95% CI 19%-37%), with findings being similar for 180 mg risankizumab. The incidence of adverse events was similar across treatment groups.

Study details: Findings are from the phase 3 FORTIFY trial including 542 patients with moderate-to-severe CD who showed a clinical response to risankizumab in the ADVANCE and MOTIVATE induction trials and were randomly assigned to receive subcutaneous risankizumab (180 or 360 mg) or placebo.

Disclosures: This study was funded by AbbVie. Some authors declared being employees or holding stocks at AbbVie, and other authors reported receiving grants, speakers’ fees, consulting fees, or serving as advisory board members for various sources, including AbbVie.

Source: Ferrante M et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: Results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046 (May 28). Doi: 10.1016/S0140-6736(22)00466-4

Key Clinical Point: Maintenance therapy with subcutaneous risankizumab showed superior efficacy than withdrawal from risankizumab to receive subcutaneous placebo in patients with moderate-to-severe Crohn’s disease (CD). It also had a tolerable safety profile.

Major finding: At week 52, patients receiving maintenance 360 mg risankizumab vs. placebo showed higher rates of Crohn’s Disease Activity Index clinical remission (adjusted difference [Δ] 15%; 95% CI 4%-25%) and endoscopic response (Δ 28%; 95% CI 19%-37%), with findings being similar for 180 mg risankizumab. The incidence of adverse events was similar across treatment groups.

Study details: Findings are from the phase 3 FORTIFY trial including 542 patients with moderate-to-severe CD who showed a clinical response to risankizumab in the ADVANCE and MOTIVATE induction trials and were randomly assigned to receive subcutaneous risankizumab (180 or 360 mg) or placebo.

Disclosures: This study was funded by AbbVie. Some authors declared being employees or holding stocks at AbbVie, and other authors reported receiving grants, speakers’ fees, consulting fees, or serving as advisory board members for various sources, including AbbVie.

Source: Ferrante M et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: Results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046 (May 28). Doi: 10.1016/S0140-6736(22)00466-4

Key Clinical Point: Maintenance therapy with subcutaneous risankizumab showed superior efficacy than withdrawal from risankizumab to receive subcutaneous placebo in patients with moderate-to-severe Crohn’s disease (CD). It also had a tolerable safety profile.

Major finding: At week 52, patients receiving maintenance 360 mg risankizumab vs. placebo showed higher rates of Crohn’s Disease Activity Index clinical remission (adjusted difference [Δ] 15%; 95% CI 4%-25%) and endoscopic response (Δ 28%; 95% CI 19%-37%), with findings being similar for 180 mg risankizumab. The incidence of adverse events was similar across treatment groups.

Study details: Findings are from the phase 3 FORTIFY trial including 542 patients with moderate-to-severe CD who showed a clinical response to risankizumab in the ADVANCE and MOTIVATE induction trials and were randomly assigned to receive subcutaneous risankizumab (180 or 360 mg) or placebo.

Disclosures: This study was funded by AbbVie. Some authors declared being employees or holding stocks at AbbVie, and other authors reported receiving grants, speakers’ fees, consulting fees, or serving as advisory board members for various sources, including AbbVie.

Source: Ferrante M et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: Results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046 (May 28). Doi: 10.1016/S0140-6736(22)00466-4