Jennie Smith

Researchers in Japan report that infants with atopic dermatitis who are treated early and aggressively with corticosteroids develop fewer food allergies by age 2 years.

For their research published in the Journal of Allergy and Clinical Immunology: In Practice, Yumiko Miyaji, MD, PhD, of Japan’s National Center for Child Health and Development in Tokyo and colleagues looked at 3 years’ worth of records for 177 infants younger than 1 year of age seen at a hospital allergy center for eczema. Of these infants, 89 were treated with betamethasone valerate within 4 months of disease onset, and 88 were treated after 4 months of onset. Most (142) were followed-up at 22-24 months, when all were in complete remission or near remission from eczema.

At follow-up, clinicians collected information about anaphylactic reactions to food, administered specific food challenges, and tested serum immunoglobin E levels for food allergens. Dr. Miyaji and colleagues found a significant difference in the prevalence of allergies between the early-treated and late-treated groups to chicken egg, cow’s milk, wheat, peanuts, soy, or fish (25% vs. 46%, respectively; P equal to .013). For individual food allergies, only chicken egg was associated with a statistically significant difference in prevalence (15% vs 36%, P equal to .006).

“Our present study may be the first to demonstrate that early aggressive topical corticosteroid treatment to shorten the duration of eczema in infants was significantly associated with a decrease in later development of [food allergies],” Dr. Miyaji and colleagues wrote in their analysis.

The investigators acknowledged as limitations of their study some between-group differences at baseline, with characteristics such as Staphylococcus aureus infections and some inflammatory biomarkers higher in the early treatment group.

The Japan Agency for Medical Research and Development supported the study, and the investigators disclosed no conflicts of interest related to their findings.

SOURCE: Miyaji Y et al. J Allergy Clin Immunol Pract. 2019. doi: 10.1016/j.jaip.2019.11.036

Researchers in Japan report that infants with atopic dermatitis who are treated early and aggressively with corticosteroids develop fewer food allergies by age 2 years.

For their research published in the Journal of Allergy and Clinical Immunology: In Practice, Yumiko Miyaji, MD, PhD, of Japan’s National Center for Child Health and Development in Tokyo and colleagues looked at 3 years’ worth of records for 177 infants younger than 1 year of age seen at a hospital allergy center for eczema. Of these infants, 89 were treated with betamethasone valerate within 4 months of disease onset, and 88 were treated after 4 months of onset. Most (142) were followed-up at 22-24 months, when all were in complete remission or near remission from eczema.

At follow-up, clinicians collected information about anaphylactic reactions to food, administered specific food challenges, and tested serum immunoglobin E levels for food allergens. Dr. Miyaji and colleagues found a significant difference in the prevalence of allergies between the early-treated and late-treated groups to chicken egg, cow’s milk, wheat, peanuts, soy, or fish (25% vs. 46%, respectively; P equal to .013). For individual food allergies, only chicken egg was associated with a statistically significant difference in prevalence (15% vs 36%, P equal to .006).

“Our present study may be the first to demonstrate that early aggressive topical corticosteroid treatment to shorten the duration of eczema in infants was significantly associated with a decrease in later development of [food allergies],” Dr. Miyaji and colleagues wrote in their analysis.

The investigators acknowledged as limitations of their study some between-group differences at baseline, with characteristics such as Staphylococcus aureus infections and some inflammatory biomarkers higher in the early treatment group.

The Japan Agency for Medical Research and Development supported the study, and the investigators disclosed no conflicts of interest related to their findings.

SOURCE: Miyaji Y et al. J Allergy Clin Immunol Pract. 2019. doi: 10.1016/j.jaip.2019.11.036

Researchers in Japan report that infants with atopic dermatitis who are treated early and aggressively with corticosteroids develop fewer food allergies by age 2 years.

For their research published in the Journal of Allergy and Clinical Immunology: In Practice, Yumiko Miyaji, MD, PhD, of Japan’s National Center for Child Health and Development in Tokyo and colleagues looked at 3 years’ worth of records for 177 infants younger than 1 year of age seen at a hospital allergy center for eczema. Of these infants, 89 were treated with betamethasone valerate within 4 months of disease onset, and 88 were treated after 4 months of onset. Most (142) were followed-up at 22-24 months, when all were in complete remission or near remission from eczema.

At follow-up, clinicians collected information about anaphylactic reactions to food, administered specific food challenges, and tested serum immunoglobin E levels for food allergens. Dr. Miyaji and colleagues found a significant difference in the prevalence of allergies between the early-treated and late-treated groups to chicken egg, cow’s milk, wheat, peanuts, soy, or fish (25% vs. 46%, respectively; P equal to .013). For individual food allergies, only chicken egg was associated with a statistically significant difference in prevalence (15% vs 36%, P equal to .006).

“Our present study may be the first to demonstrate that early aggressive topical corticosteroid treatment to shorten the duration of eczema in infants was significantly associated with a decrease in later development of [food allergies],” Dr. Miyaji and colleagues wrote in their analysis.

The investigators acknowledged as limitations of their study some between-group differences at baseline, with characteristics such as Staphylococcus aureus infections and some inflammatory biomarkers higher in the early treatment group.

The Japan Agency for Medical Research and Development supported the study, and the investigators disclosed no conflicts of interest related to their findings.

SOURCE: Miyaji Y et al. J Allergy Clin Immunol Pract. 2019. doi: 10.1016/j.jaip.2019.11.036

Diagnosis and treatment for obstructive sleep apnea resulted in medical cost savings in a group of U.S. truck drivers.

welcomia/Getty Images

“Among the 1.87 million U.S. commercial drivers estimated by the Bureau of Labor Statistics to be operating non–farm-based heavy trucks (gross weight at least 26,000 pounds), 17%-28%, or 318,00 to 524,000, are expected to have at least mild [obstructive sleep apnea] based on prevalence studies on commercial drivers,” wrote Stephen V. Burks, PhD, of the University of Minnesota, Morris, and colleagues.

“If the larger population of the 4.0 million drivers estimated by the Federal Motor Carrier Safety Administration to be using commercial driver’s licenses in interstate and intrastate transportation is considered, 0.68 to 1.1 million drivers may have OSA. The majority of these drivers are thought to be undiagnosed and untreated. There is thus considerable scope for healthcare cost savings through treatment of OSA among commercial drivers,” they noted.

The study was published in Sleep.

In 2017, after industry complaints about costs, the federal government withdrew its proposal to mandate testing truckers for OSA. Yet some commercial fleets do require testing, and a new study looking at retrospective data from a large fleet’s health insurance program shows that drivers diagnosed and treated for OSA saw medical cost savings, compared with those considered likely to have OSA who had neither diagnosis nor treatment.

Dr. Burks and his colleagues looked at records for 1,516 drivers tested for OSA, of whom 1,224 were positive, and compared these with an equal number of controls flagged through the same screening program as likely to have OSA, but who had never received a diagnosis in a sleep clinic or treatment with auto-adjusting positive airway pressure (APAP). All cases received auto-adjusting positive airway pressure (APAP) treatment. The investigators then looked at insurance costs for diagnosed drivers, compared with screen-positive controls before and after the polysomnogram date, over an 18-month period.

Most of the diagnosed cases in the cohort (n = 932) were deemed compliant with treatment. For every pair of subjects and controls, the researchers looked at per-member insurance costs over 18 months, though not all drivers were observed for a full period of 18 months, mostly because of turnover. Dr. Burks and colleagues found that non-OSA related medical claim costs savings after diagnosis and treatment of every 100 screen-positive controls was $153,042 (95% confidence interval, –$5,352, $330,525, P = .06.) Subjects adhering to treatment with APAP saw mean non-OSA related savings of $441 per member per month (95% CI, –$861, –$21, P = .035).

“Taken together, this is substantial evidence that OSA treatment is associated with savings in non-OSA–program medical insurance claim costs,” the authors wrote, adding that such savings could be expected to help offset expenses related to mandatory OSA programs. The authors acknowledged as a limitation of their study that it did not capture costs of pharmaceutical treatment or those of the OSA program itself. Nor did the findings capture “the value of injuries, lost work time, or disability days associated with untreated OSA, nor the savings from avoided preventable crashes.”

The study received funding from Harvard University and the National Surface Transportation Safety Center for Excellence. Two coauthors disclosed funding from pharmaceutical and device manufacturers and hold patents on sleep therapies. Another coauthor disclosed being an expert witness in trucking-related cases and one received funds from the study’s sponsor, a trucking safety research group.

SOURCE: Burks SV et al. Sleep 2019 Oct 24. doi: 10.1093/sleep/zsz262.

Diagnosis and treatment for obstructive sleep apnea resulted in medical cost savings in a group of U.S. truck drivers.

welcomia/Getty Images

“Among the 1.87 million U.S. commercial drivers estimated by the Bureau of Labor Statistics to be operating non–farm-based heavy trucks (gross weight at least 26,000 pounds), 17%-28%, or 318,00 to 524,000, are expected to have at least mild [obstructive sleep apnea] based on prevalence studies on commercial drivers,” wrote Stephen V. Burks, PhD, of the University of Minnesota, Morris, and colleagues.

“If the larger population of the 4.0 million drivers estimated by the Federal Motor Carrier Safety Administration to be using commercial driver’s licenses in interstate and intrastate transportation is considered, 0.68 to 1.1 million drivers may have OSA. The majority of these drivers are thought to be undiagnosed and untreated. There is thus considerable scope for healthcare cost savings through treatment of OSA among commercial drivers,” they noted.

The study was published in Sleep.

In 2017, after industry complaints about costs, the federal government withdrew its proposal to mandate testing truckers for OSA. Yet some commercial fleets do require testing, and a new study looking at retrospective data from a large fleet’s health insurance program shows that drivers diagnosed and treated for OSA saw medical cost savings, compared with those considered likely to have OSA who had neither diagnosis nor treatment.

Dr. Burks and his colleagues looked at records for 1,516 drivers tested for OSA, of whom 1,224 were positive, and compared these with an equal number of controls flagged through the same screening program as likely to have OSA, but who had never received a diagnosis in a sleep clinic or treatment with auto-adjusting positive airway pressure (APAP). All cases received auto-adjusting positive airway pressure (APAP) treatment. The investigators then looked at insurance costs for diagnosed drivers, compared with screen-positive controls before and after the polysomnogram date, over an 18-month period.

Most of the diagnosed cases in the cohort (n = 932) were deemed compliant with treatment. For every pair of subjects and controls, the researchers looked at per-member insurance costs over 18 months, though not all drivers were observed for a full period of 18 months, mostly because of turnover. Dr. Burks and colleagues found that non-OSA related medical claim costs savings after diagnosis and treatment of every 100 screen-positive controls was $153,042 (95% confidence interval, –$5,352, $330,525, P = .06.) Subjects adhering to treatment with APAP saw mean non-OSA related savings of $441 per member per month (95% CI, –$861, –$21, P = .035).

“Taken together, this is substantial evidence that OSA treatment is associated with savings in non-OSA–program medical insurance claim costs,” the authors wrote, adding that such savings could be expected to help offset expenses related to mandatory OSA programs. The authors acknowledged as a limitation of their study that it did not capture costs of pharmaceutical treatment or those of the OSA program itself. Nor did the findings capture “the value of injuries, lost work time, or disability days associated with untreated OSA, nor the savings from avoided preventable crashes.”

The study received funding from Harvard University and the National Surface Transportation Safety Center for Excellence. Two coauthors disclosed funding from pharmaceutical and device manufacturers and hold patents on sleep therapies. Another coauthor disclosed being an expert witness in trucking-related cases and one received funds from the study’s sponsor, a trucking safety research group.

SOURCE: Burks SV et al. Sleep 2019 Oct 24. doi: 10.1093/sleep/zsz262.

Diagnosis and treatment for obstructive sleep apnea resulted in medical cost savings in a group of U.S. truck drivers.

welcomia/Getty Images

“Among the 1.87 million U.S. commercial drivers estimated by the Bureau of Labor Statistics to be operating non–farm-based heavy trucks (gross weight at least 26,000 pounds), 17%-28%, or 318,00 to 524,000, are expected to have at least mild [obstructive sleep apnea] based on prevalence studies on commercial drivers,” wrote Stephen V. Burks, PhD, of the University of Minnesota, Morris, and colleagues.

“If the larger population of the 4.0 million drivers estimated by the Federal Motor Carrier Safety Administration to be using commercial driver’s licenses in interstate and intrastate transportation is considered, 0.68 to 1.1 million drivers may have OSA. The majority of these drivers are thought to be undiagnosed and untreated. There is thus considerable scope for healthcare cost savings through treatment of OSA among commercial drivers,” they noted.

The study was published in Sleep.

In 2017, after industry complaints about costs, the federal government withdrew its proposal to mandate testing truckers for OSA. Yet some commercial fleets do require testing, and a new study looking at retrospective data from a large fleet’s health insurance program shows that drivers diagnosed and treated for OSA saw medical cost savings, compared with those considered likely to have OSA who had neither diagnosis nor treatment.

Dr. Burks and his colleagues looked at records for 1,516 drivers tested for OSA, of whom 1,224 were positive, and compared these with an equal number of controls flagged through the same screening program as likely to have OSA, but who had never received a diagnosis in a sleep clinic or treatment with auto-adjusting positive airway pressure (APAP). All cases received auto-adjusting positive airway pressure (APAP) treatment. The investigators then looked at insurance costs for diagnosed drivers, compared with screen-positive controls before and after the polysomnogram date, over an 18-month period.

Most of the diagnosed cases in the cohort (n = 932) were deemed compliant with treatment. For every pair of subjects and controls, the researchers looked at per-member insurance costs over 18 months, though not all drivers were observed for a full period of 18 months, mostly because of turnover. Dr. Burks and colleagues found that non-OSA related medical claim costs savings after diagnosis and treatment of every 100 screen-positive controls was $153,042 (95% confidence interval, –$5,352, $330,525, P = .06.) Subjects adhering to treatment with APAP saw mean non-OSA related savings of $441 per member per month (95% CI, –$861, –$21, P = .035).

“Taken together, this is substantial evidence that OSA treatment is associated with savings in non-OSA–program medical insurance claim costs,” the authors wrote, adding that such savings could be expected to help offset expenses related to mandatory OSA programs. The authors acknowledged as a limitation of their study that it did not capture costs of pharmaceutical treatment or those of the OSA program itself. Nor did the findings capture “the value of injuries, lost work time, or disability days associated with untreated OSA, nor the savings from avoided preventable crashes.”

The study received funding from Harvard University and the National Surface Transportation Safety Center for Excellence. Two coauthors disclosed funding from pharmaceutical and device manufacturers and hold patents on sleep therapies. Another coauthor disclosed being an expert witness in trucking-related cases and one received funds from the study’s sponsor, a trucking safety research group.

SOURCE: Burks SV et al. Sleep 2019 Oct 24. doi: 10.1093/sleep/zsz262.

Adolescents diagnosed with insomnia have a high prevalence of concurrent mental health disorders and should be screened for them, according to new research.

Monkey Business Images Ltd/Thinkstock

For a study published in the Journal of Clinical Sleep Medicine, Tori R. Van Dyk, PhD, of Loma Linda (Calif.) University, and colleagues, enrolled 376 adolescents aged 11-18 years (mean age 14.5, 55% female) diagnosed with primary insomnia and referred to a sleep clinic. Subjects were evaluated using two validated questionnaires used to measure sleep disorders in adolescents, while caregivers reported and mental health diagnoses and symptoms using a standard behavioral checklist for adolescents.

Dr. Van Dyk and colleagues found that 75% of subjects had at least one or more parent-reported mental health diagnosis, most commonly anxiety, mood disorders, and ADHD. Some 64% had a clinical elevation of mental health symptoms on evaluation, most commonly affective disorders, with 40% of the cohort having two or more elevations. Specific mental health symptoms were seen linked with particular sleep symptoms. A greater burden of ADHD symptoms, for example, was significantly associated with more difficulties falling asleep, maintaining sleep, and reinitiating sleep after waking at night.

A total of 15% of subjects were reported by caregivers to engage in deliberate self-harming behaviors or talking about or attempting suicide – a higher rate than in the general adolescent population. “Because youth presenting for insomnia treatment may be even more likely to engage in self-harm behavior or to be suicidal, particular attention should be paid to directly assessing for these high-risk behaviors within the context of behavioral sleep medicine evaluations,” Dr. Van Dyk and colleagues wrote in their analysis.

Although mental health symptoms have been linked to sleep problems in other studies of children and adults, “associations identified in younger youths and/or adults should not be assumed to hold true among adolescents,” the researchers wrote, adding that adolescence “is a distinctive developmental period characterized by increases in both psychopathology and sleep problems, changing biology, increasing independence, and unique social and societal demands.” The investigators noted that because pediatric sleep specialists are relatively rare, the management of adolescent sleep problems and related mental health symptoms is likely to fall on primary care and other providers who “would benefit in recognizing the relationship between sleep problems and mental health symptoms in this population.”

Dr. Van Dyk and colleagues noted among the weaknesses of their study its cross-sectional design, use of parent-reported mental health symptoms only, lack of information on medication use or mental health treatment, and the potential for selection bias toward more severe cases.

The authors disclosed no outside funding or conflicts of interest related to their study.

SOURCE: Van Dyk TR et al. J Clin Sleep Med. 2019 Sep 6. doi: 10.5664/jcsm.7970.

Adolescents diagnosed with insomnia have a high prevalence of concurrent mental health disorders and should be screened for them, according to new research.

Monkey Business Images Ltd/Thinkstock

For a study published in the Journal of Clinical Sleep Medicine, Tori R. Van Dyk, PhD, of Loma Linda (Calif.) University, and colleagues, enrolled 376 adolescents aged 11-18 years (mean age 14.5, 55% female) diagnosed with primary insomnia and referred to a sleep clinic. Subjects were evaluated using two validated questionnaires used to measure sleep disorders in adolescents, while caregivers reported and mental health diagnoses and symptoms using a standard behavioral checklist for adolescents.

Dr. Van Dyk and colleagues found that 75% of subjects had at least one or more parent-reported mental health diagnosis, most commonly anxiety, mood disorders, and ADHD. Some 64% had a clinical elevation of mental health symptoms on evaluation, most commonly affective disorders, with 40% of the cohort having two or more elevations. Specific mental health symptoms were seen linked with particular sleep symptoms. A greater burden of ADHD symptoms, for example, was significantly associated with more difficulties falling asleep, maintaining sleep, and reinitiating sleep after waking at night.

A total of 15% of subjects were reported by caregivers to engage in deliberate self-harming behaviors or talking about or attempting suicide – a higher rate than in the general adolescent population. “Because youth presenting for insomnia treatment may be even more likely to engage in self-harm behavior or to be suicidal, particular attention should be paid to directly assessing for these high-risk behaviors within the context of behavioral sleep medicine evaluations,” Dr. Van Dyk and colleagues wrote in their analysis.

Although mental health symptoms have been linked to sleep problems in other studies of children and adults, “associations identified in younger youths and/or adults should not be assumed to hold true among adolescents,” the researchers wrote, adding that adolescence “is a distinctive developmental period characterized by increases in both psychopathology and sleep problems, changing biology, increasing independence, and unique social and societal demands.” The investigators noted that because pediatric sleep specialists are relatively rare, the management of adolescent sleep problems and related mental health symptoms is likely to fall on primary care and other providers who “would benefit in recognizing the relationship between sleep problems and mental health symptoms in this population.”

Dr. Van Dyk and colleagues noted among the weaknesses of their study its cross-sectional design, use of parent-reported mental health symptoms only, lack of information on medication use or mental health treatment, and the potential for selection bias toward more severe cases.

The authors disclosed no outside funding or conflicts of interest related to their study.

SOURCE: Van Dyk TR et al. J Clin Sleep Med. 2019 Sep 6. doi: 10.5664/jcsm.7970.

Adolescents diagnosed with insomnia have a high prevalence of concurrent mental health disorders and should be screened for them, according to new research.

Monkey Business Images Ltd/Thinkstock

For a study published in the Journal of Clinical Sleep Medicine, Tori R. Van Dyk, PhD, of Loma Linda (Calif.) University, and colleagues, enrolled 376 adolescents aged 11-18 years (mean age 14.5, 55% female) diagnosed with primary insomnia and referred to a sleep clinic. Subjects were evaluated using two validated questionnaires used to measure sleep disorders in adolescents, while caregivers reported and mental health diagnoses and symptoms using a standard behavioral checklist for adolescents.

Dr. Van Dyk and colleagues found that 75% of subjects had at least one or more parent-reported mental health diagnosis, most commonly anxiety, mood disorders, and ADHD. Some 64% had a clinical elevation of mental health symptoms on evaluation, most commonly affective disorders, with 40% of the cohort having two or more elevations. Specific mental health symptoms were seen linked with particular sleep symptoms. A greater burden of ADHD symptoms, for example, was significantly associated with more difficulties falling asleep, maintaining sleep, and reinitiating sleep after waking at night.

A total of 15% of subjects were reported by caregivers to engage in deliberate self-harming behaviors or talking about or attempting suicide – a higher rate than in the general adolescent population. “Because youth presenting for insomnia treatment may be even more likely to engage in self-harm behavior or to be suicidal, particular attention should be paid to directly assessing for these high-risk behaviors within the context of behavioral sleep medicine evaluations,” Dr. Van Dyk and colleagues wrote in their analysis.

Although mental health symptoms have been linked to sleep problems in other studies of children and adults, “associations identified in younger youths and/or adults should not be assumed to hold true among adolescents,” the researchers wrote, adding that adolescence “is a distinctive developmental period characterized by increases in both psychopathology and sleep problems, changing biology, increasing independence, and unique social and societal demands.” The investigators noted that because pediatric sleep specialists are relatively rare, the management of adolescent sleep problems and related mental health symptoms is likely to fall on primary care and other providers who “would benefit in recognizing the relationship between sleep problems and mental health symptoms in this population.”

Dr. Van Dyk and colleagues noted among the weaknesses of their study its cross-sectional design, use of parent-reported mental health symptoms only, lack of information on medication use or mental health treatment, and the potential for selection bias toward more severe cases.

The authors disclosed no outside funding or conflicts of interest related to their study.

SOURCE: Van Dyk TR et al. J Clin Sleep Med. 2019 Sep 6. doi: 10.5664/jcsm.7970.

A diet low in fermentable carbohydrates can reduce gut symptoms related to inflammatory bowel disease (IBD), according to a study by U.K. researchers.

Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) occur in a number of common foods, including certain fruits, vegetables, and dairy products. They can draw increased water to the gut, and through microbial fermentation increase hydrogen in the colon.

While previous research has shown that a low-FODMAP diet can relieve gut symptoms such as swelling and flatulence in people with irritable bowel syndrome, the diet has been little studied in IBD patients, for whom gut symptoms often persist even in the absence of gastrointestinal inflammation. In a study published in Gastroenterology, Selina Cox, MD, of King’s College, London, and colleagues randomized 52 people with ulcerative colitis or Crohn’s disease with persistent gut symptoms but without active inflammation to 4 weeks on a low-FODMAP diet (n = 27) or a control diet comprising sham dietary advice (n = 25). Investigators were not blinded to treatment allocation.

At 4 weeks, Dr. Cox and her colleagues reported more patients on the low-FODMAP diet reported “adequate” relief of gut symptoms (52% vs. 16%, P = .007), and saw slight improvements in health-related quality of life scores, compared with the control group. Patient-reported flatulence and bloating were significantly lower in the treatment group, while few other symptom-specific differences were seen between groups.

Stool samples collected at baseline and at the study’s endpoint showed significantly reduced abundance of three types of gut bacteria thought to have a role in immune response – Bifidobacterium adolescentis, B longum, and Faecalibacterium prausnitzii – compared with control subjects. But there were no significant between-group differences in bacterial diversity or in biomarkers of inflammation.

“A major strength of this trial is that low-FODMAP dietary advice was compared to sham dietary advice, providing the first placebo-controlled evidence of effectiveness in IBD,” the researchers wrote in their analysis. Weaknesses of the study include its single-blinded design and inability to control for nutritional alterations related to the low-FODMAP diet.

Ms. Cox and her colleagues recommended a 4-week low-FODMAP diet along with “expert advice and intensive follow-up” for the management of gut symptoms in IBD, but cautioned that longer-term use may not be appropriate.

The study was funded by the U.S.-based Kenneth Rainin Foundation. Two of Dr. Cox’s coauthors declared financial conflicts of interest from a patent on a mobile application to support the low-FODMAP diet; the study’s corresponding author, Kevin Whelan, PhD, additionally reported receiving fees or research support from food and nutrition firms.

SOURCE: Cox S et al. Gastroenterology 2019. doi: 10.1053/j.gastro.2019.09.024.

AGA’s patient education can help your patients better understand the low-FODMAP diet. Learn more at https://www.gastro.org/practice-guidance/gi-patient-center/topic/low-fodmap-diet.

A diet low in fermentable carbohydrates can reduce gut symptoms related to inflammatory bowel disease (IBD), according to a study by U.K. researchers.

Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) occur in a number of common foods, including certain fruits, vegetables, and dairy products. They can draw increased water to the gut, and through microbial fermentation increase hydrogen in the colon.

While previous research has shown that a low-FODMAP diet can relieve gut symptoms such as swelling and flatulence in people with irritable bowel syndrome, the diet has been little studied in IBD patients, for whom gut symptoms often persist even in the absence of gastrointestinal inflammation. In a study published in Gastroenterology, Selina Cox, MD, of King’s College, London, and colleagues randomized 52 people with ulcerative colitis or Crohn’s disease with persistent gut symptoms but without active inflammation to 4 weeks on a low-FODMAP diet (n = 27) or a control diet comprising sham dietary advice (n = 25). Investigators were not blinded to treatment allocation.

At 4 weeks, Dr. Cox and her colleagues reported more patients on the low-FODMAP diet reported “adequate” relief of gut symptoms (52% vs. 16%, P = .007), and saw slight improvements in health-related quality of life scores, compared with the control group. Patient-reported flatulence and bloating were significantly lower in the treatment group, while few other symptom-specific differences were seen between groups.

Stool samples collected at baseline and at the study’s endpoint showed significantly reduced abundance of three types of gut bacteria thought to have a role in immune response – Bifidobacterium adolescentis, B longum, and Faecalibacterium prausnitzii – compared with control subjects. But there were no significant between-group differences in bacterial diversity or in biomarkers of inflammation.

“A major strength of this trial is that low-FODMAP dietary advice was compared to sham dietary advice, providing the first placebo-controlled evidence of effectiveness in IBD,” the researchers wrote in their analysis. Weaknesses of the study include its single-blinded design and inability to control for nutritional alterations related to the low-FODMAP diet.

Ms. Cox and her colleagues recommended a 4-week low-FODMAP diet along with “expert advice and intensive follow-up” for the management of gut symptoms in IBD, but cautioned that longer-term use may not be appropriate.

The study was funded by the U.S.-based Kenneth Rainin Foundation. Two of Dr. Cox’s coauthors declared financial conflicts of interest from a patent on a mobile application to support the low-FODMAP diet; the study’s corresponding author, Kevin Whelan, PhD, additionally reported receiving fees or research support from food and nutrition firms.

SOURCE: Cox S et al. Gastroenterology 2019. doi: 10.1053/j.gastro.2019.09.024.

AGA’s patient education can help your patients better understand the low-FODMAP diet. Learn more at https://www.gastro.org/practice-guidance/gi-patient-center/topic/low-fodmap-diet.

A diet low in fermentable carbohydrates can reduce gut symptoms related to inflammatory bowel disease (IBD), according to a study by U.K. researchers.

Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) occur in a number of common foods, including certain fruits, vegetables, and dairy products. They can draw increased water to the gut, and through microbial fermentation increase hydrogen in the colon.

While previous research has shown that a low-FODMAP diet can relieve gut symptoms such as swelling and flatulence in people with irritable bowel syndrome, the diet has been little studied in IBD patients, for whom gut symptoms often persist even in the absence of gastrointestinal inflammation. In a study published in Gastroenterology, Selina Cox, MD, of King’s College, London, and colleagues randomized 52 people with ulcerative colitis or Crohn’s disease with persistent gut symptoms but without active inflammation to 4 weeks on a low-FODMAP diet (n = 27) or a control diet comprising sham dietary advice (n = 25). Investigators were not blinded to treatment allocation.

At 4 weeks, Dr. Cox and her colleagues reported more patients on the low-FODMAP diet reported “adequate” relief of gut symptoms (52% vs. 16%, P = .007), and saw slight improvements in health-related quality of life scores, compared with the control group. Patient-reported flatulence and bloating were significantly lower in the treatment group, while few other symptom-specific differences were seen between groups.

Stool samples collected at baseline and at the study’s endpoint showed significantly reduced abundance of three types of gut bacteria thought to have a role in immune response – Bifidobacterium adolescentis, B longum, and Faecalibacterium prausnitzii – compared with control subjects. But there were no significant between-group differences in bacterial diversity or in biomarkers of inflammation.

“A major strength of this trial is that low-FODMAP dietary advice was compared to sham dietary advice, providing the first placebo-controlled evidence of effectiveness in IBD,” the researchers wrote in their analysis. Weaknesses of the study include its single-blinded design and inability to control for nutritional alterations related to the low-FODMAP diet.

Ms. Cox and her colleagues recommended a 4-week low-FODMAP diet along with “expert advice and intensive follow-up” for the management of gut symptoms in IBD, but cautioned that longer-term use may not be appropriate.

The study was funded by the U.S.-based Kenneth Rainin Foundation. Two of Dr. Cox’s coauthors declared financial conflicts of interest from a patent on a mobile application to support the low-FODMAP diet; the study’s corresponding author, Kevin Whelan, PhD, additionally reported receiving fees or research support from food and nutrition firms.

SOURCE: Cox S et al. Gastroenterology 2019. doi: 10.1053/j.gastro.2019.09.024.

AGA’s patient education can help your patients better understand the low-FODMAP diet. Learn more at https://www.gastro.org/practice-guidance/gi-patient-center/topic/low-fodmap-diet.

A diet low in fermentable carbohydrates can reduce gut symptoms related to inflammatory bowel disease (IBD), according to a study by U.K. researchers.

Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) occur in a number of common foods, including certain fruits, vegetables, and dairy products. They can draw increased water to the gut, and through microbial fermentation increase hydrogen in the colon.

While previous research has shown that a low-FODMAP diet can relieve gut symptoms such as swelling and flatulence in people with irritable bowel syndrome, the diet has been little studied in IBD patients, for whom gut symptoms often persist even in the absence of gastrointestinal inflammation. In a study published in Gastroenterology, Selina Cox, MD, of King’s College, London, and colleagues randomized 52 people with ulcerative colitis or Crohn’s disease with persistent gut symptoms but without active inflammation to 4 weeks on a low-FODMAP diet (n = 27) or a control diet comprising sham dietary advice (n = 25). Investigators were not blinded to treatment allocation.

At 4 weeks, Dr. Cox and her colleagues reported more patients on the low-FODMAP diet reported “adequate” relief of gut symptoms (52% vs. 16%, P = .007), and saw slight improvements in health-related quality of life scores, compared with the control group. Patient-reported flatulence and bloating were significantly lower in the treatment group, while few other symptom-specific differences were seen between groups.

Stool samples collected at baseline and at the study’s endpoint showed significantly reduced abundance of three types of gut bacteria thought to have a role in immune response – Bifidobacterium adolescentis, B longum, and Faecalibacterium prausnitzii – compared with control subjects. But there were no significant between-group differences in bacterial diversity or in biomarkers of inflammation.

“A major strength of this trial is that low-FODMAP dietary advice was compared to sham dietary advice, providing the first placebo-controlled evidence of effectiveness in IBD,” the researchers wrote in their analysis. Weaknesses of the study include its single-blinded design and inability to control for nutritional alterations related to the low-FODMAP diet.

Ms. Cox and her colleagues recommended a 4-week low-FODMAP diet along with “expert advice and intensive follow-up” for the management of gut symptoms in IBD, but cautioned that longer-term use may not be appropriate.

The study was funded by the U.S.-based Kenneth Rainin Foundation. Two of Dr. Cox’s coauthors declared financial conflicts of interest from a patent on a mobile application to support the low-FODMAP diet; the study’s corresponding author, Kevin Whelan, PhD, additionally reported receiving fees or research support from food and nutrition firms.

SOURCE: Cox S et al. Gastroenterology 2019. doi: 10.1053/j.gastro.2019.09.024.

A diet low in fermentable carbohydrates can reduce gut symptoms related to inflammatory bowel disease (IBD), according to a study by U.K. researchers.

Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) occur in a number of common foods, including certain fruits, vegetables, and dairy products. They can draw increased water to the gut, and through microbial fermentation increase hydrogen in the colon.

While previous research has shown that a low-FODMAP diet can relieve gut symptoms such as swelling and flatulence in people with irritable bowel syndrome, the diet has been little studied in IBD patients, for whom gut symptoms often persist even in the absence of gastrointestinal inflammation. In a study published in Gastroenterology, Selina Cox, MD, of King’s College, London, and colleagues randomized 52 people with ulcerative colitis or Crohn’s disease with persistent gut symptoms but without active inflammation to 4 weeks on a low-FODMAP diet (n = 27) or a control diet comprising sham dietary advice (n = 25). Investigators were not blinded to treatment allocation.

At 4 weeks, Dr. Cox and her colleagues reported more patients on the low-FODMAP diet reported “adequate” relief of gut symptoms (52% vs. 16%, P = .007), and saw slight improvements in health-related quality of life scores, compared with the control group. Patient-reported flatulence and bloating were significantly lower in the treatment group, while few other symptom-specific differences were seen between groups.

Stool samples collected at baseline and at the study’s endpoint showed significantly reduced abundance of three types of gut bacteria thought to have a role in immune response – Bifidobacterium adolescentis, B longum, and Faecalibacterium prausnitzii – compared with control subjects. But there were no significant between-group differences in bacterial diversity or in biomarkers of inflammation.

“A major strength of this trial is that low-FODMAP dietary advice was compared to sham dietary advice, providing the first placebo-controlled evidence of effectiveness in IBD,” the researchers wrote in their analysis. Weaknesses of the study include its single-blinded design and inability to control for nutritional alterations related to the low-FODMAP diet.

Ms. Cox and her colleagues recommended a 4-week low-FODMAP diet along with “expert advice and intensive follow-up” for the management of gut symptoms in IBD, but cautioned that longer-term use may not be appropriate.

The study was funded by the U.S.-based Kenneth Rainin Foundation. Two of Dr. Cox’s coauthors declared financial conflicts of interest from a patent on a mobile application to support the low-FODMAP diet; the study’s corresponding author, Kevin Whelan, PhD, additionally reported receiving fees or research support from food and nutrition firms.

SOURCE: Cox S et al. Gastroenterology 2019. doi: 10.1053/j.gastro.2019.09.024.

A diet low in fermentable carbohydrates can reduce gut symptoms related to inflammatory bowel disease (IBD), according to a study by U.K. researchers.

Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) occur in a number of common foods, including certain fruits, vegetables, and dairy products. They can draw increased water to the gut, and through microbial fermentation increase hydrogen in the colon.

While previous research has shown that a low-FODMAP diet can relieve gut symptoms such as swelling and flatulence in people with irritable bowel syndrome, the diet has been little studied in IBD patients, for whom gut symptoms often persist even in the absence of gastrointestinal inflammation. In a study published in Gastroenterology, Selina Cox, MD, of King’s College, London, and colleagues randomized 52 people with ulcerative colitis or Crohn’s disease with persistent gut symptoms but without active inflammation to 4 weeks on a low-FODMAP diet (n = 27) or a control diet comprising sham dietary advice (n = 25). Investigators were not blinded to treatment allocation.

At 4 weeks, Dr. Cox and her colleagues reported more patients on the low-FODMAP diet reported “adequate” relief of gut symptoms (52% vs. 16%, P = .007), and saw slight improvements in health-related quality of life scores, compared with the control group. Patient-reported flatulence and bloating were significantly lower in the treatment group, while few other symptom-specific differences were seen between groups.

Stool samples collected at baseline and at the study’s endpoint showed significantly reduced abundance of three types of gut bacteria thought to have a role in immune response – Bifidobacterium adolescentis, B longum, and Faecalibacterium prausnitzii – compared with control subjects. But there were no significant between-group differences in bacterial diversity or in biomarkers of inflammation.

“A major strength of this trial is that low-FODMAP dietary advice was compared to sham dietary advice, providing the first placebo-controlled evidence of effectiveness in IBD,” the researchers wrote in their analysis. Weaknesses of the study include its single-blinded design and inability to control for nutritional alterations related to the low-FODMAP diet.

Ms. Cox and her colleagues recommended a 4-week low-FODMAP diet along with “expert advice and intensive follow-up” for the management of gut symptoms in IBD, but cautioned that longer-term use may not be appropriate.

The study was funded by the U.S.-based Kenneth Rainin Foundation. Two of Dr. Cox’s coauthors declared financial conflicts of interest from a patent on a mobile application to support the low-FODMAP diet; the study’s corresponding author, Kevin Whelan, PhD, additionally reported receiving fees or research support from food and nutrition firms.

SOURCE: Cox S et al. Gastroenterology 2019. doi: 10.1053/j.gastro.2019.09.024.

The biologic drug anakinra appears to be effective in treating children with secondary hemophagocytic lymphohistiocytosis (sHLH)/macrophage activation syndrome (MAS), a dangerous “cytokine storm” that can emerge from infections, cancer, and rheumatic diseases.

Children with systematic juvenile idiopathic arthritis (sJIA) and sHLH/MAS are especially good candidates for treatment with the interleukin-1 receptor antagonist anakinra (Kineret), in whom its safety and benefits have been more widely explored than in pediatric patients with sHLH/MAS related to non-sJIA underlying conditions.

In a study published in Arthritis & Rheumatology, Esraa Eloseily, MD, and colleagues at the University of Alabama at Birmingham, looked at hospitalization records for 44 children (mean age, 10 years; n = 25 females) with sHLH/MAS. The children in the study had heterogeneous underlying conditions including leukemias, infections, and rheumatic diseases. About one-third of patients had no known rheumatic or autoimmune disorder.

Dr. Eloseily and colleagues found that early initiation of anakinra (within 5 days of hospitalization) was significantly associated with improved survival across the cohort, for which mortality was 27%. Thrombocytopenia (less than 100,000/mcL) and STXBP2 mutations were both seen significantly associated with mortality.

Patients with blood cancers – even those in remission at the time of treatment – did poorly. None of the three patients in the cohort with leukemia survived.

Importantly, no deaths were seen among the 13 patients with underlying SJIA who were treated with anakinra, suggesting particular benefit for this patient group.

“In addition to the 10% risk of developing overt MAS as part of sJIA, another 30%-40% of sJIA patients may have occult or subclinical MAS during a disease flare that can eventually lead to overt MAS,” Dr. Eloseily and colleagues wrote. “This association of MAS with sJIA suggested that anakinra would also be a valuable treatment for sJIA-MAS.”

The investigators acknowledged that their study was limited by its retrospective design and “nonuniform approach to therapy, lack of treatment controls, and variable follow-up period.” The authors also acknowledged the potential for selection bias favoring anakinra use in patients who are less severely ill.

In a comment accompanying Dr. Eloseily and colleagues’ study, Sarah Nikiforow, MD, PhD, of the Dana-Farber Cancer Institute in Boston, and Nancy Berliner, MD, of Brigham & Women’s Hospital in Boston, urged clinicians not to interpret the study results as supporting anakinra as “a carte blanche approach to hyperinflammatory syndromes.”

While the study supported the use of anakinra in sJIA with MAS or sHLH, “we posit that patients [with sHLH/MAS] in sepsis, cytokine release syndrome following chimeric antigen receptor T-cell therapy, and other hyperinflammatory syndromes still require individualized approaches to therapy,” Dr. Nikiforow and Dr. Berliner wrote, adding that, “in several studies and anecdotally in our institutional practice, cytotoxic chemotherapy was/is preferred over biologic agents in patients with evidence of more severe inflammatory activity.”

Outside sJIA, Dr. Nikiforow and Dr. Berliner wrote, “early anakinra therapy should be extended to treatment of other forms of sHLH with extreme caution. Specifically, the authors’ suggestion that cytotoxic therapy should be ‘considered’ only after anakinra therapy may be dangerous for some patients.”

Two of Dr. Eloseily’s coinvestigators reported financial and research support from Sobi, the manufacturer of anakinra. No other conflicts of interest were reported.

SOURCES: Eloseily E et al. Arthritis Rheumatol. 2019 Sep 12. doi: 10.1002/art.41103; Nikiforow S, Berliner N. Arthritis Rheumatol. 2019 Sep 16. doi: 10.1002/art.41106.

The biologic drug anakinra appears to be effective in treating children with secondary hemophagocytic lymphohistiocytosis (sHLH)/macrophage activation syndrome (MAS), a dangerous “cytokine storm” that can emerge from infections, cancer, and rheumatic diseases.

Children with systematic juvenile idiopathic arthritis (sJIA) and sHLH/MAS are especially good candidates for treatment with the interleukin-1 receptor antagonist anakinra (Kineret), in whom its safety and benefits have been more widely explored than in pediatric patients with sHLH/MAS related to non-sJIA underlying conditions.

In a study published in Arthritis & Rheumatology, Esraa Eloseily, MD, and colleagues at the University of Alabama at Birmingham, looked at hospitalization records for 44 children (mean age, 10 years; n = 25 females) with sHLH/MAS. The children in the study had heterogeneous underlying conditions including leukemias, infections, and rheumatic diseases. About one-third of patients had no known rheumatic or autoimmune disorder.

Dr. Eloseily and colleagues found that early initiation of anakinra (within 5 days of hospitalization) was significantly associated with improved survival across the cohort, for which mortality was 27%. Thrombocytopenia (less than 100,000/mcL) and STXBP2 mutations were both seen significantly associated with mortality.

Patients with blood cancers – even those in remission at the time of treatment – did poorly. None of the three patients in the cohort with leukemia survived.

Importantly, no deaths were seen among the 13 patients with underlying SJIA who were treated with anakinra, suggesting particular benefit for this patient group.

“In addition to the 10% risk of developing overt MAS as part of sJIA, another 30%-40% of sJIA patients may have occult or subclinical MAS during a disease flare that can eventually lead to overt MAS,” Dr. Eloseily and colleagues wrote. “This association of MAS with sJIA suggested that anakinra would also be a valuable treatment for sJIA-MAS.”

The investigators acknowledged that their study was limited by its retrospective design and “nonuniform approach to therapy, lack of treatment controls, and variable follow-up period.” The authors also acknowledged the potential for selection bias favoring anakinra use in patients who are less severely ill.

In a comment accompanying Dr. Eloseily and colleagues’ study, Sarah Nikiforow, MD, PhD, of the Dana-Farber Cancer Institute in Boston, and Nancy Berliner, MD, of Brigham & Women’s Hospital in Boston, urged clinicians not to interpret the study results as supporting anakinra as “a carte blanche approach to hyperinflammatory syndromes.”

While the study supported the use of anakinra in sJIA with MAS or sHLH, “we posit that patients [with sHLH/MAS] in sepsis, cytokine release syndrome following chimeric antigen receptor T-cell therapy, and other hyperinflammatory syndromes still require individualized approaches to therapy,” Dr. Nikiforow and Dr. Berliner wrote, adding that, “in several studies and anecdotally in our institutional practice, cytotoxic chemotherapy was/is preferred over biologic agents in patients with evidence of more severe inflammatory activity.”

Outside sJIA, Dr. Nikiforow and Dr. Berliner wrote, “early anakinra therapy should be extended to treatment of other forms of sHLH with extreme caution. Specifically, the authors’ suggestion that cytotoxic therapy should be ‘considered’ only after anakinra therapy may be dangerous for some patients.”

Two of Dr. Eloseily’s coinvestigators reported financial and research support from Sobi, the manufacturer of anakinra. No other conflicts of interest were reported.

SOURCES: Eloseily E et al. Arthritis Rheumatol. 2019 Sep 12. doi: 10.1002/art.41103; Nikiforow S, Berliner N. Arthritis Rheumatol. 2019 Sep 16. doi: 10.1002/art.41106.

The biologic drug anakinra appears to be effective in treating children with secondary hemophagocytic lymphohistiocytosis (sHLH)/macrophage activation syndrome (MAS), a dangerous “cytokine storm” that can emerge from infections, cancer, and rheumatic diseases.

Children with systematic juvenile idiopathic arthritis (sJIA) and sHLH/MAS are especially good candidates for treatment with the interleukin-1 receptor antagonist anakinra (Kineret), in whom its safety and benefits have been more widely explored than in pediatric patients with sHLH/MAS related to non-sJIA underlying conditions.

In a study published in Arthritis & Rheumatology, Esraa Eloseily, MD, and colleagues at the University of Alabama at Birmingham, looked at hospitalization records for 44 children (mean age, 10 years; n = 25 females) with sHLH/MAS. The children in the study had heterogeneous underlying conditions including leukemias, infections, and rheumatic diseases. About one-third of patients had no known rheumatic or autoimmune disorder.

Dr. Eloseily and colleagues found that early initiation of anakinra (within 5 days of hospitalization) was significantly associated with improved survival across the cohort, for which mortality was 27%. Thrombocytopenia (less than 100,000/mcL) and STXBP2 mutations were both seen significantly associated with mortality.

Patients with blood cancers – even those in remission at the time of treatment – did poorly. None of the three patients in the cohort with leukemia survived.

Importantly, no deaths were seen among the 13 patients with underlying SJIA who were treated with anakinra, suggesting particular benefit for this patient group.

“In addition to the 10% risk of developing overt MAS as part of sJIA, another 30%-40% of sJIA patients may have occult or subclinical MAS during a disease flare that can eventually lead to overt MAS,” Dr. Eloseily and colleagues wrote. “This association of MAS with sJIA suggested that anakinra would also be a valuable treatment for sJIA-MAS.”

The investigators acknowledged that their study was limited by its retrospective design and “nonuniform approach to therapy, lack of treatment controls, and variable follow-up period.” The authors also acknowledged the potential for selection bias favoring anakinra use in patients who are less severely ill.

In a comment accompanying Dr. Eloseily and colleagues’ study, Sarah Nikiforow, MD, PhD, of the Dana-Farber Cancer Institute in Boston, and Nancy Berliner, MD, of Brigham & Women’s Hospital in Boston, urged clinicians not to interpret the study results as supporting anakinra as “a carte blanche approach to hyperinflammatory syndromes.”

While the study supported the use of anakinra in sJIA with MAS or sHLH, “we posit that patients [with sHLH/MAS] in sepsis, cytokine release syndrome following chimeric antigen receptor T-cell therapy, and other hyperinflammatory syndromes still require individualized approaches to therapy,” Dr. Nikiforow and Dr. Berliner wrote, adding that, “in several studies and anecdotally in our institutional practice, cytotoxic chemotherapy was/is preferred over biologic agents in patients with evidence of more severe inflammatory activity.”

Outside sJIA, Dr. Nikiforow and Dr. Berliner wrote, “early anakinra therapy should be extended to treatment of other forms of sHLH with extreme caution. Specifically, the authors’ suggestion that cytotoxic therapy should be ‘considered’ only after anakinra therapy may be dangerous for some patients.”

Two of Dr. Eloseily’s coinvestigators reported financial and research support from Sobi, the manufacturer of anakinra. No other conflicts of interest were reported.

SOURCES: Eloseily E et al. Arthritis Rheumatol. 2019 Sep 12. doi: 10.1002/art.41103; Nikiforow S, Berliner N. Arthritis Rheumatol. 2019 Sep 16. doi: 10.1002/art.41106.

Hospitalizations for infective endocarditis associated with drug abuse doubled in the United States from 2002 to 2016, in a trend investigators call “alarming,” and link to a concurrent rise in opioid abuse.

Patients tend to be younger, poorer white males, according to findings published online in the Journal of the American Heart Association.

For their research, Amer N. Kadri, MD, of the Cleveland Clinic and colleagues looked at records for nearly a million hospitalizations for infective endocarditis (IE) in the National Inpatient Sample registry. All U.S. regions saw increases in drug abuse–linked cases of IE as a share of IE hospitalizations. Incidence of drug abuse–associated IC rose from 48 cases/100,000 population in 2002 to 79/100,000 in 2016. The Midwest saw the highest rate of change, with an annual percent increase of 4.9%.

While most IE hospitalizations in the study cohort were of white men (including 68% for drug-linked cases), the drug abuse–related cases were younger (median age, 38 vs. 70 years for nondrug-related IE), and more likely male (55.5% vs. 50%). About 45% of the drug-related cases were in people receiving Medicaid, and 42% were in the lowest quartile of median household income.

The drug abuse cases had fewer renal and cardiovascular comorbidities, compared with the nondrug cases, but were significantly more likely to present with HIV, hepatitis C, alcohol abuse, and liver disease. Inpatient mortality was lower among the drug-linked cases – 6% vs. 9% – but the drug cases saw significantly more cardiac or valve surgeries, longer hospital stays, and higher costs.

“Hospitalizations for IE have been increasing side by side with the opioid epidemic,” the investigators wrote in their analysis. “The opioid crisis has reached epidemic levels, and now drug overdoses have been the leading cause of injury-related death in the U.S. Heroin deaths had remained relatively low from 1999 until 2010 whereas it then increased threefold from 2010-2015.” The analysis showed a rise in drug abuse–associated IE “that corresponds to this general period.” The findings argue, the investigators said, for better treatment for opioid addiction after hospitalization and greater efforts to make drug rehabilitation available after discharge. The researchers described as a limitation of their study the use of billing codes that changed late in the study period, increasing detection of drug abuse cases after 2015. They reported no outside funding or conflicts of interest.
 

SOURCE: Kadri AN et al. J Am Heart Assoc. 2019 Sep 18.

Hospitalizations for infective endocarditis associated with drug abuse doubled in the United States from 2002 to 2016, in a trend investigators call “alarming,” and link to a concurrent rise in opioid abuse.

Patients tend to be younger, poorer white males, according to findings published online in the Journal of the American Heart Association.

For their research, Amer N. Kadri, MD, of the Cleveland Clinic and colleagues looked at records for nearly a million hospitalizations for infective endocarditis (IE) in the National Inpatient Sample registry. All U.S. regions saw increases in drug abuse–linked cases of IE as a share of IE hospitalizations. Incidence of drug abuse–associated IC rose from 48 cases/100,000 population in 2002 to 79/100,000 in 2016. The Midwest saw the highest rate of change, with an annual percent increase of 4.9%.

While most IE hospitalizations in the study cohort were of white men (including 68% for drug-linked cases), the drug abuse–related cases were younger (median age, 38 vs. 70 years for nondrug-related IE), and more likely male (55.5% vs. 50%). About 45% of the drug-related cases were in people receiving Medicaid, and 42% were in the lowest quartile of median household income.

The drug abuse cases had fewer renal and cardiovascular comorbidities, compared with the nondrug cases, but were significantly more likely to present with HIV, hepatitis C, alcohol abuse, and liver disease. Inpatient mortality was lower among the drug-linked cases – 6% vs. 9% – but the drug cases saw significantly more cardiac or valve surgeries, longer hospital stays, and higher costs.

“Hospitalizations for IE have been increasing side by side with the opioid epidemic,” the investigators wrote in their analysis. “The opioid crisis has reached epidemic levels, and now drug overdoses have been the leading cause of injury-related death in the U.S. Heroin deaths had remained relatively low from 1999 until 2010 whereas it then increased threefold from 2010-2015.” The analysis showed a rise in drug abuse–associated IE “that corresponds to this general period.” The findings argue, the investigators said, for better treatment for opioid addiction after hospitalization and greater efforts to make drug rehabilitation available after discharge. The researchers described as a limitation of their study the use of billing codes that changed late in the study period, increasing detection of drug abuse cases after 2015. They reported no outside funding or conflicts of interest.
 

SOURCE: Kadri AN et al. J Am Heart Assoc. 2019 Sep 18.

Hospitalizations for infective endocarditis associated with drug abuse doubled in the United States from 2002 to 2016, in a trend investigators call “alarming,” and link to a concurrent rise in opioid abuse.

Patients tend to be younger, poorer white males, according to findings published online in the Journal of the American Heart Association.

For their research, Amer N. Kadri, MD, of the Cleveland Clinic and colleagues looked at records for nearly a million hospitalizations for infective endocarditis (IE) in the National Inpatient Sample registry. All U.S. regions saw increases in drug abuse–linked cases of IE as a share of IE hospitalizations. Incidence of drug abuse–associated IC rose from 48 cases/100,000 population in 2002 to 79/100,000 in 2016. The Midwest saw the highest rate of change, with an annual percent increase of 4.9%.

While most IE hospitalizations in the study cohort were of white men (including 68% for drug-linked cases), the drug abuse–related cases were younger (median age, 38 vs. 70 years for nondrug-related IE), and more likely male (55.5% vs. 50%). About 45% of the drug-related cases were in people receiving Medicaid, and 42% were in the lowest quartile of median household income.

The drug abuse cases had fewer renal and cardiovascular comorbidities, compared with the nondrug cases, but were significantly more likely to present with HIV, hepatitis C, alcohol abuse, and liver disease. Inpatient mortality was lower among the drug-linked cases – 6% vs. 9% – but the drug cases saw significantly more cardiac or valve surgeries, longer hospital stays, and higher costs.

“Hospitalizations for IE have been increasing side by side with the opioid epidemic,” the investigators wrote in their analysis. “The opioid crisis has reached epidemic levels, and now drug overdoses have been the leading cause of injury-related death in the U.S. Heroin deaths had remained relatively low from 1999 until 2010 whereas it then increased threefold from 2010-2015.” The analysis showed a rise in drug abuse–associated IE “that corresponds to this general period.” The findings argue, the investigators said, for better treatment for opioid addiction after hospitalization and greater efforts to make drug rehabilitation available after discharge. The researchers described as a limitation of their study the use of billing codes that changed late in the study period, increasing detection of drug abuse cases after 2015. They reported no outside funding or conflicts of interest.
 

SOURCE: Kadri AN et al. J Am Heart Assoc. 2019 Sep 18.

A blood test for elevated carbon dioxide may be used in screening adults for obesity hypoventilation syndrome, according to new guidelines.

Obese adults with sleep-disordered breathing and increased blood carbon dioxide levels during the day are likely to have obesity hypoventilation syndrome (OHS), a result of shallow or slow breathing that can lead to respiratory failure, heart failure, pulmonary hypertension, and death. Pulmonologists and sleep specialists may be the first to see and diagnose patients with OHS in the outpatient setting, while other cases are diagnosed in the hospital when patients present with hypercapnic respiratory failure.

Screening for OHS usually involves measuring arterial blood gases, which is not standard practice in outpatient clinics. Patients often remain undiagnosed and untreated until late in the course of the disease, according to the American Thoracic Society, which in August published a new diagnosis and management guideline aiming to boost early diagnosis and reduce variability in treatment (Am J Respir Crit Care Med. 2019;200:3,e6–e24).

The guideline authors, led by Babak Mokhlesi, MD, of the University of Chicago, recommend a simpler screening method – measuring serum bicarbonate only – to rule out OHS in obese patients with nighttime breathing problems.

Serum bicarbonate should be measured in obese patients with sleep-disordered breathing and a low likelihood of OHS, Dr. Mokhlesi and colleagues recommend in the guideline. If serum bicarbonate is below 27 mmol/L, it is not necessary to conduct further testing as the patient is unlikely to have OHS.

In patients whose serum bicarbonate is higher than 27 mmol/L, or who are strongly suspected of having OHS at presentation because of severe obesity or other symptoms, arterial blood gases should be measured and a sleep study conducted. The guideline authors said that there is insufficient evidence to recommend that pulse oximetry be used in the diagnostic pathway for OHS.

First-line treatment for stable, ambulatory patients with OHS should be positive airway pressure during sleep, rather than noninvasive ventilation, Dr. Mokhlesi and colleagues concluded. For patients with comorbid obstructive sleep apnea – as many as 70% of OHS patients also have OSA – the first-line treatment should be continuous positive airway pressure (CPAP) at night, the guideline states.

Patients hospitalized with respiratory failure and suspected of having OHS should be discharged with noninvasive ventilation until diagnostic procedures can be performed, along with PAP titration in a sleep lab.

In patients initially treated with CPAP who remain symptomatic or whose blood carbon dioxide does not improve, noninvasive ventilation can be tried, the guidelines say. Finally, patients diagnosed with OHS should be guided to weight loss interventions with the aim of reducing body weight by 25%-30%. This can include referral for bariatric surgery in patients without contraindications.

Dr. Mokhlesi and colleagues acknowledged that all of the recommendations contained in the guideline are classed as “conditional,” based on the quality of evidence assessed.

The American Thoracic Society funded the study. Dr. Mokhlesi and 7 coauthors disclosed financial conflicts of interest, while an additional 13 coauthors had none. Disclosures can be found on the AJRCCM website.

SOURCE: Mokhlesi B et al. Am J Respir Crit Care Med. 2019;200:3,e6-e24

A blood test for elevated carbon dioxide may be used in screening adults for obesity hypoventilation syndrome, according to new guidelines.

Obese adults with sleep-disordered breathing and increased blood carbon dioxide levels during the day are likely to have obesity hypoventilation syndrome (OHS), a result of shallow or slow breathing that can lead to respiratory failure, heart failure, pulmonary hypertension, and death. Pulmonologists and sleep specialists may be the first to see and diagnose patients with OHS in the outpatient setting, while other cases are diagnosed in the hospital when patients present with hypercapnic respiratory failure.

Screening for OHS usually involves measuring arterial blood gases, which is not standard practice in outpatient clinics. Patients often remain undiagnosed and untreated until late in the course of the disease, according to the American Thoracic Society, which in August published a new diagnosis and management guideline aiming to boost early diagnosis and reduce variability in treatment (Am J Respir Crit Care Med. 2019;200:3,e6–e24).

The guideline authors, led by Babak Mokhlesi, MD, of the University of Chicago, recommend a simpler screening method – measuring serum bicarbonate only – to rule out OHS in obese patients with nighttime breathing problems.

Serum bicarbonate should be measured in obese patients with sleep-disordered breathing and a low likelihood of OHS, Dr. Mokhlesi and colleagues recommend in the guideline. If serum bicarbonate is below 27 mmol/L, it is not necessary to conduct further testing as the patient is unlikely to have OHS.

In patients whose serum bicarbonate is higher than 27 mmol/L, or who are strongly suspected of having OHS at presentation because of severe obesity or other symptoms, arterial blood gases should be measured and a sleep study conducted. The guideline authors said that there is insufficient evidence to recommend that pulse oximetry be used in the diagnostic pathway for OHS.

First-line treatment for stable, ambulatory patients with OHS should be positive airway pressure during sleep, rather than noninvasive ventilation, Dr. Mokhlesi and colleagues concluded. For patients with comorbid obstructive sleep apnea – as many as 70% of OHS patients also have OSA – the first-line treatment should be continuous positive airway pressure (CPAP) at night, the guideline states.

Patients hospitalized with respiratory failure and suspected of having OHS should be discharged with noninvasive ventilation until diagnostic procedures can be performed, along with PAP titration in a sleep lab.

In patients initially treated with CPAP who remain symptomatic or whose blood carbon dioxide does not improve, noninvasive ventilation can be tried, the guidelines say. Finally, patients diagnosed with OHS should be guided to weight loss interventions with the aim of reducing body weight by 25%-30%. This can include referral for bariatric surgery in patients without contraindications.

Dr. Mokhlesi and colleagues acknowledged that all of the recommendations contained in the guideline are classed as “conditional,” based on the quality of evidence assessed.

The American Thoracic Society funded the study. Dr. Mokhlesi and 7 coauthors disclosed financial conflicts of interest, while an additional 13 coauthors had none. Disclosures can be found on the AJRCCM website.

SOURCE: Mokhlesi B et al. Am J Respir Crit Care Med. 2019;200:3,e6-e24

A blood test for elevated carbon dioxide may be used in screening adults for obesity hypoventilation syndrome, according to new guidelines.

Obese adults with sleep-disordered breathing and increased blood carbon dioxide levels during the day are likely to have obesity hypoventilation syndrome (OHS), a result of shallow or slow breathing that can lead to respiratory failure, heart failure, pulmonary hypertension, and death. Pulmonologists and sleep specialists may be the first to see and diagnose patients with OHS in the outpatient setting, while other cases are diagnosed in the hospital when patients present with hypercapnic respiratory failure.

Screening for OHS usually involves measuring arterial blood gases, which is not standard practice in outpatient clinics. Patients often remain undiagnosed and untreated until late in the course of the disease, according to the American Thoracic Society, which in August published a new diagnosis and management guideline aiming to boost early diagnosis and reduce variability in treatment (Am J Respir Crit Care Med. 2019;200:3,e6–e24).

The guideline authors, led by Babak Mokhlesi, MD, of the University of Chicago, recommend a simpler screening method – measuring serum bicarbonate only – to rule out OHS in obese patients with nighttime breathing problems.

Serum bicarbonate should be measured in obese patients with sleep-disordered breathing and a low likelihood of OHS, Dr. Mokhlesi and colleagues recommend in the guideline. If serum bicarbonate is below 27 mmol/L, it is not necessary to conduct further testing as the patient is unlikely to have OHS.

In patients whose serum bicarbonate is higher than 27 mmol/L, or who are strongly suspected of having OHS at presentation because of severe obesity or other symptoms, arterial blood gases should be measured and a sleep study conducted. The guideline authors said that there is insufficient evidence to recommend that pulse oximetry be used in the diagnostic pathway for OHS.

First-line treatment for stable, ambulatory patients with OHS should be positive airway pressure during sleep, rather than noninvasive ventilation, Dr. Mokhlesi and colleagues concluded. For patients with comorbid obstructive sleep apnea – as many as 70% of OHS patients also have OSA – the first-line treatment should be continuous positive airway pressure (CPAP) at night, the guideline states.

Patients hospitalized with respiratory failure and suspected of having OHS should be discharged with noninvasive ventilation until diagnostic procedures can be performed, along with PAP titration in a sleep lab.

In patients initially treated with CPAP who remain symptomatic or whose blood carbon dioxide does not improve, noninvasive ventilation can be tried, the guidelines say. Finally, patients diagnosed with OHS should be guided to weight loss interventions with the aim of reducing body weight by 25%-30%. This can include referral for bariatric surgery in patients without contraindications.

Dr. Mokhlesi and colleagues acknowledged that all of the recommendations contained in the guideline are classed as “conditional,” based on the quality of evidence assessed.

The American Thoracic Society funded the study. Dr. Mokhlesi and 7 coauthors disclosed financial conflicts of interest, while an additional 13 coauthors had none. Disclosures can be found on the AJRCCM website.

SOURCE: Mokhlesi B et al. Am J Respir Crit Care Med. 2019;200:3,e6-e24

Type 2 diabetes is a risk factor for heart failure and a common comorbidity in heart failure patients. New results from a large cohort study in Asia show that, for people with heart failure, having diabetes is associated with changes to the structure of the heart, lower quality of life, more readmissions to hospital, and higher risk of death.

Jonathan Yap, MBBS, MPH, of the National Heart Centre in Singapore, and colleagues, looked at data from a cohort enrolling 6,167 heart failure patients in 11 Asian countries for the prospective ASIAN-HF (Asian Sudden

Cardiac Death in Heart Failure) registry. The researchers identified 5,028 patients with heart failure and reduced left ventricle ejection fraction (LVEF; 22% women), of whom 40% had type 2 diabetes. They also looked at 1,139 patients in the registry with heart failure and preserved LVEF (51% women), of whom 45% had type 2 disease. Controls without heart failure (n = 985; 9% with diabetes) from the SHOP (Singapore Heart Failure Outcomes and Phenotypes) study were included in the analysis, which was published August 21 in the Journal of the American Heart Association.

For both heart failure phenotypes, diabetes was associated with left ventricular hypertrophy, but there was no similar association in patients without diabetes. Dr. Yap and his colleagues reported differences in cardiac remodeling based on heart failure phenotype: The reduced LVEF patients had more eccentric hypertrophy, or dilation, of the left ventricular chamber, whereas the preserved LVEF patients had more concentric hypertrophy, or thickening, of the left ventricular wall.

The researchers also reported that patients with diabetes had lower health-related quality of life scores in both heart failure groups, compared with patients without diabetes, although those in the latter group with preserved LVEF did significantly worse on some quality of life measures. Patients with diabetes had more heart failure rehospitalizations (adjusted hazard ratio, 1.27; 95% confidence interval, 1.05-1.54; P = .014) and higher 1-year rates of a combined measure of all-cause mortality and hospitalization for heart failure (aHR, 1.22; 95% CI, 1.05-1.41; P = .011). No differences were seen between phenotypes for these outcomes.

Dr. Yap and colleagues noted that this was the first large, multinational study investigating diabetes and heart failure in Asia and that “no prior studies have concomitantly included both HF types or controls without HF from the same population.” They listed among the study’s limitations a lack of uniform screening for diabetes that may have resulted in under-identification of diabetics in the cohort.

The Singapore government, the Biomedical Research Council, Boston Scientific, and Bayer sponsored the study. One coauthor disclosed receiving pharmaceutical industry support.

Source: Yap J et al. J Am Heart Assoc. 2019 Aug. doi: 10.1161/JAHA.119.013114.

Type 2 diabetes is a risk factor for heart failure and a common comorbidity in heart failure patients. New results from a large cohort study in Asia show that, for people with heart failure, having diabetes is associated with changes to the structure of the heart, lower quality of life, more readmissions to hospital, and higher risk of death.

Jonathan Yap, MBBS, MPH, of the National Heart Centre in Singapore, and colleagues, looked at data from a cohort enrolling 6,167 heart failure patients in 11 Asian countries for the prospective ASIAN-HF (Asian Sudden

Cardiac Death in Heart Failure) registry. The researchers identified 5,028 patients with heart failure and reduced left ventricle ejection fraction (LVEF; 22% women), of whom 40% had type 2 diabetes. They also looked at 1,139 patients in the registry with heart failure and preserved LVEF (51% women), of whom 45% had type 2 disease. Controls without heart failure (n = 985; 9% with diabetes) from the SHOP (Singapore Heart Failure Outcomes and Phenotypes) study were included in the analysis, which was published August 21 in the Journal of the American Heart Association.

For both heart failure phenotypes, diabetes was associated with left ventricular hypertrophy, but there was no similar association in patients without diabetes. Dr. Yap and his colleagues reported differences in cardiac remodeling based on heart failure phenotype: The reduced LVEF patients had more eccentric hypertrophy, or dilation, of the left ventricular chamber, whereas the preserved LVEF patients had more concentric hypertrophy, or thickening, of the left ventricular wall.

The researchers also reported that patients with diabetes had lower health-related quality of life scores in both heart failure groups, compared with patients without diabetes, although those in the latter group with preserved LVEF did significantly worse on some quality of life measures. Patients with diabetes had more heart failure rehospitalizations (adjusted hazard ratio, 1.27; 95% confidence interval, 1.05-1.54; P = .014) and higher 1-year rates of a combined measure of all-cause mortality and hospitalization for heart failure (aHR, 1.22; 95% CI, 1.05-1.41; P = .011). No differences were seen between phenotypes for these outcomes.

Dr. Yap and colleagues noted that this was the first large, multinational study investigating diabetes and heart failure in Asia and that “no prior studies have concomitantly included both HF types or controls without HF from the same population.” They listed among the study’s limitations a lack of uniform screening for diabetes that may have resulted in under-identification of diabetics in the cohort.

The Singapore government, the Biomedical Research Council, Boston Scientific, and Bayer sponsored the study. One coauthor disclosed receiving pharmaceutical industry support.

Source: Yap J et al. J Am Heart Assoc. 2019 Aug. doi: 10.1161/JAHA.119.013114.

Type 2 diabetes is a risk factor for heart failure and a common comorbidity in heart failure patients. New results from a large cohort study in Asia show that, for people with heart failure, having diabetes is associated with changes to the structure of the heart, lower quality of life, more readmissions to hospital, and higher risk of death.

Jonathan Yap, MBBS, MPH, of the National Heart Centre in Singapore, and colleagues, looked at data from a cohort enrolling 6,167 heart failure patients in 11 Asian countries for the prospective ASIAN-HF (Asian Sudden

Cardiac Death in Heart Failure) registry. The researchers identified 5,028 patients with heart failure and reduced left ventricle ejection fraction (LVEF; 22% women), of whom 40% had type 2 diabetes. They also looked at 1,139 patients in the registry with heart failure and preserved LVEF (51% women), of whom 45% had type 2 disease. Controls without heart failure (n = 985; 9% with diabetes) from the SHOP (Singapore Heart Failure Outcomes and Phenotypes) study were included in the analysis, which was published August 21 in the Journal of the American Heart Association.

For both heart failure phenotypes, diabetes was associated with left ventricular hypertrophy, but there was no similar association in patients without diabetes. Dr. Yap and his colleagues reported differences in cardiac remodeling based on heart failure phenotype: The reduced LVEF patients had more eccentric hypertrophy, or dilation, of the left ventricular chamber, whereas the preserved LVEF patients had more concentric hypertrophy, or thickening, of the left ventricular wall.

The researchers also reported that patients with diabetes had lower health-related quality of life scores in both heart failure groups, compared with patients without diabetes, although those in the latter group with preserved LVEF did significantly worse on some quality of life measures. Patients with diabetes had more heart failure rehospitalizations (adjusted hazard ratio, 1.27; 95% confidence interval, 1.05-1.54; P = .014) and higher 1-year rates of a combined measure of all-cause mortality and hospitalization for heart failure (aHR, 1.22; 95% CI, 1.05-1.41; P = .011). No differences were seen between phenotypes for these outcomes.

Dr. Yap and colleagues noted that this was the first large, multinational study investigating diabetes and heart failure in Asia and that “no prior studies have concomitantly included both HF types or controls without HF from the same population.” They listed among the study’s limitations a lack of uniform screening for diabetes that may have resulted in under-identification of diabetics in the cohort.

The Singapore government, the Biomedical Research Council, Boston Scientific, and Bayer sponsored the study. One coauthor disclosed receiving pharmaceutical industry support.

Source: Yap J et al. J Am Heart Assoc. 2019 Aug. doi: 10.1161/JAHA.119.013114.

The progression, not just age of onset, of Huntington’s disease can be predicted by a measurable genetic factor, researchers have learned.

Huntington’s, an inherited neurodegenerative disease that affects motor function and cognition, is caused by an expansion of the CAG trinucleotide sequence on the huntingtin gene. Scientists have previously linked younger age at onset to a higher number of CAG repeats on the gene, but the association between these and the rate of progression after onset was poorly understood.

In research published online August 12 in JAMA Neurology, investigators linked the rate of progression – which, like age at onset, is highly variable in Huntington’s – to CAG repeat length. CAG repeat length was strongly associated with distinct patterns of brain damage, as well as clinical measures of cognitive and motor decline.

For their research, Douglas R. Langbehn, MD, PhD, of the University of Iowa, Iowa City, and colleagues used data from two longitudinal observational studies in gene carriers for Huntington’s and nonrelated controls. The researchers looked at data from 443 participants (56% female; mean age, 44.4 years) who were followed for a mean of 4 years, with more than 2,000 study visits across the multisite cohort. Neuropsychiatric testing and brain imaging were conducted annually, using composite scoring systems of the investigators’ design. These composite scores sought to be more sensitive by combining results from several validated clinical and imaging tests.

Age and speed of decline in total functional capacity tracked with more CAG repeats, the researchers found. For example, in people with 40 CAG repeats, the estimated mean age of initial motor-cognitive score change was 42.46 years; for those with 45 repeats, 26.65 years, and for people with 50 CAG repeats, 18.49 years. Higher repeats were seen significantly associated with accelerated, nonlinear decline on both clinical and brain-volume measures, except gray matter volume, according to principal component analyses conducted on the data.

“We derived a single summary measure capturing the motor-cognitive phenotype and showed that the accelerating progression of the phenotype with aging is highly CAG repeat length dependent (i.e., those with higher CAG decline earlier and faster). Contrary to some previous assertions, this CAG dependence continues well past the onset of clinical illness,” Dr. Langbehn and colleagues wrote in their analysis. “By characterizing these CAG repeat length–dependent disease trajectories, we provide insights into disease progression that may guide future therapeutic approaches and identify the most appropriate intervention ages to prevent clinical decline.”

Dr. Langbehn and colleagues acknowledged as a limitation of their study its likely exclusion of the sickest subjects because of the cohorts’ design. The CHDI Foundation funded the study. Of the 16 coauthors, 13 reported receiving funding from CHDI and/or from pharmaceutical manufacturers.

SOURCE: Langbehn et al. JAMA Neurol. 2019 Aug 12. doi: 10.1001/jamaneurol.2019.2328

The progression, not just age of onset, of Huntington’s disease can be predicted by a measurable genetic factor, researchers have learned.

Huntington’s, an inherited neurodegenerative disease that affects motor function and cognition, is caused by an expansion of the CAG trinucleotide sequence on the huntingtin gene. Scientists have previously linked younger age at onset to a higher number of CAG repeats on the gene, but the association between these and the rate of progression after onset was poorly understood.

In research published online August 12 in JAMA Neurology, investigators linked the rate of progression – which, like age at onset, is highly variable in Huntington’s – to CAG repeat length. CAG repeat length was strongly associated with distinct patterns of brain damage, as well as clinical measures of cognitive and motor decline.

For their research, Douglas R. Langbehn, MD, PhD, of the University of Iowa, Iowa City, and colleagues used data from two longitudinal observational studies in gene carriers for Huntington’s and nonrelated controls. The researchers looked at data from 443 participants (56% female; mean age, 44.4 years) who were followed for a mean of 4 years, with more than 2,000 study visits across the multisite cohort. Neuropsychiatric testing and brain imaging were conducted annually, using composite scoring systems of the investigators’ design. These composite scores sought to be more sensitive by combining results from several validated clinical and imaging tests.

Age and speed of decline in total functional capacity tracked with more CAG repeats, the researchers found. For example, in people with 40 CAG repeats, the estimated mean age of initial motor-cognitive score change was 42.46 years; for those with 45 repeats, 26.65 years, and for people with 50 CAG repeats, 18.49 years. Higher repeats were seen significantly associated with accelerated, nonlinear decline on both clinical and brain-volume measures, except gray matter volume, according to principal component analyses conducted on the data.

“We derived a single summary measure capturing the motor-cognitive phenotype and showed that the accelerating progression of the phenotype with aging is highly CAG repeat length dependent (i.e., those with higher CAG decline earlier and faster). Contrary to some previous assertions, this CAG dependence continues well past the onset of clinical illness,” Dr. Langbehn and colleagues wrote in their analysis. “By characterizing these CAG repeat length–dependent disease trajectories, we provide insights into disease progression that may guide future therapeutic approaches and identify the most appropriate intervention ages to prevent clinical decline.”

Dr. Langbehn and colleagues acknowledged as a limitation of their study its likely exclusion of the sickest subjects because of the cohorts’ design. The CHDI Foundation funded the study. Of the 16 coauthors, 13 reported receiving funding from CHDI and/or from pharmaceutical manufacturers.

SOURCE: Langbehn et al. JAMA Neurol. 2019 Aug 12. doi: 10.1001/jamaneurol.2019.2328

The progression, not just age of onset, of Huntington’s disease can be predicted by a measurable genetic factor, researchers have learned.

Huntington’s, an inherited neurodegenerative disease that affects motor function and cognition, is caused by an expansion of the CAG trinucleotide sequence on the huntingtin gene. Scientists have previously linked younger age at onset to a higher number of CAG repeats on the gene, but the association between these and the rate of progression after onset was poorly understood.

In research published online August 12 in JAMA Neurology, investigators linked the rate of progression – which, like age at onset, is highly variable in Huntington’s – to CAG repeat length. CAG repeat length was strongly associated with distinct patterns of brain damage, as well as clinical measures of cognitive and motor decline.

For their research, Douglas R. Langbehn, MD, PhD, of the University of Iowa, Iowa City, and colleagues used data from two longitudinal observational studies in gene carriers for Huntington’s and nonrelated controls. The researchers looked at data from 443 participants (56% female; mean age, 44.4 years) who were followed for a mean of 4 years, with more than 2,000 study visits across the multisite cohort. Neuropsychiatric testing and brain imaging were conducted annually, using composite scoring systems of the investigators’ design. These composite scores sought to be more sensitive by combining results from several validated clinical and imaging tests.

Age and speed of decline in total functional capacity tracked with more CAG repeats, the researchers found. For example, in people with 40 CAG repeats, the estimated mean age of initial motor-cognitive score change was 42.46 years; for those with 45 repeats, 26.65 years, and for people with 50 CAG repeats, 18.49 years. Higher repeats were seen significantly associated with accelerated, nonlinear decline on both clinical and brain-volume measures, except gray matter volume, according to principal component analyses conducted on the data.

“We derived a single summary measure capturing the motor-cognitive phenotype and showed that the accelerating progression of the phenotype with aging is highly CAG repeat length dependent (i.e., those with higher CAG decline earlier and faster). Contrary to some previous assertions, this CAG dependence continues well past the onset of clinical illness,” Dr. Langbehn and colleagues wrote in their analysis. “By characterizing these CAG repeat length–dependent disease trajectories, we provide insights into disease progression that may guide future therapeutic approaches and identify the most appropriate intervention ages to prevent clinical decline.”

Dr. Langbehn and colleagues acknowledged as a limitation of their study its likely exclusion of the sickest subjects because of the cohorts’ design. The CHDI Foundation funded the study. Of the 16 coauthors, 13 reported receiving funding from CHDI and/or from pharmaceutical manufacturers.

SOURCE: Langbehn et al. JAMA Neurol. 2019 Aug 12. doi: 10.1001/jamaneurol.2019.2328