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NAS linked to poor and deteriorating school performance
A neonatal diagnostic code of neonatal abstinence syndrome (NAS) is strongly associated with poor and deteriorating school performance, according to Ju Lee Oei, MD, of the University of New South Wales, Sydney, and her associates.
In a study of 604,829 children born in 2000-2006 in New South Wales, linkage rates were similar between matched controls (77.6% of 4,330) and other NSW children (77.4% of 598,265; P = .83) but were significantly lower in children with NAS (75.6% of 2,234; P = .03). The controls were matched for gender,gestation, and socioeconomic status.
The children with NAS had significantly lower scores than the controls and other NSW children in every grade and every domain of testing (reading, writing, numeracy, spelling, and grammar/punctuation). By grade 7, 38% of children with NAS did not meet National Minimum Standard (NMS) in one or more domains (versus 18.4% of controls and 14.5% of other NSW children). The mean serial composite scores also were lower in children with NAS from grades 3 to 7, compared with the other two groups; the difference was progressive, the investigators said. And by grade 7, the scores for children with NAS were lower than other children’s scores in grade 5.
It was noted that children with NAS, indigenous status (adjusted odds ratio, 1.7), male gender (aOR, 1.3), and having a primary parent without a grade 9 education (aOR, 1.3) increased the risk of failure to meet NMS. Overall, NAS (aOR, 2.5), indigenous status (aOR, 2.2), male gender (aOR, 1.3), and prematurity (less than 37 weeks’ gestation [aOR, 1.2]) increased the risk of failure to meet NMS.
“To date these are the only data demonstrating long-term school outcomes for children with a history of NAS. Similar data for children born from the current opioid epidemic gripping much of the Northern Hemisphere, assuming linkage is possible, will be available only in 7-10 years,” researchers concluded. “Although this study was conducted in Australia, the high risk of poor academic performance in this vulnerable group of children is applicable to all countries, and strategies to address this risk and prevent poor adult outcomes and intergenerational vulnerability must be urgently addressed.”
Read the full study in Pediatrics (doi: 10.1542/peds.2016-2651).
A neonatal diagnostic code of neonatal abstinence syndrome (NAS) is strongly associated with poor and deteriorating school performance, according to Ju Lee Oei, MD, of the University of New South Wales, Sydney, and her associates.
In a study of 604,829 children born in 2000-2006 in New South Wales, linkage rates were similar between matched controls (77.6% of 4,330) and other NSW children (77.4% of 598,265; P = .83) but were significantly lower in children with NAS (75.6% of 2,234; P = .03). The controls were matched for gender,gestation, and socioeconomic status.
The children with NAS had significantly lower scores than the controls and other NSW children in every grade and every domain of testing (reading, writing, numeracy, spelling, and grammar/punctuation). By grade 7, 38% of children with NAS did not meet National Minimum Standard (NMS) in one or more domains (versus 18.4% of controls and 14.5% of other NSW children). The mean serial composite scores also were lower in children with NAS from grades 3 to 7, compared with the other two groups; the difference was progressive, the investigators said. And by grade 7, the scores for children with NAS were lower than other children’s scores in grade 5.
It was noted that children with NAS, indigenous status (adjusted odds ratio, 1.7), male gender (aOR, 1.3), and having a primary parent without a grade 9 education (aOR, 1.3) increased the risk of failure to meet NMS. Overall, NAS (aOR, 2.5), indigenous status (aOR, 2.2), male gender (aOR, 1.3), and prematurity (less than 37 weeks’ gestation [aOR, 1.2]) increased the risk of failure to meet NMS.
“To date these are the only data demonstrating long-term school outcomes for children with a history of NAS. Similar data for children born from the current opioid epidemic gripping much of the Northern Hemisphere, assuming linkage is possible, will be available only in 7-10 years,” researchers concluded. “Although this study was conducted in Australia, the high risk of poor academic performance in this vulnerable group of children is applicable to all countries, and strategies to address this risk and prevent poor adult outcomes and intergenerational vulnerability must be urgently addressed.”
Read the full study in Pediatrics (doi: 10.1542/peds.2016-2651).
A neonatal diagnostic code of neonatal abstinence syndrome (NAS) is strongly associated with poor and deteriorating school performance, according to Ju Lee Oei, MD, of the University of New South Wales, Sydney, and her associates.
In a study of 604,829 children born in 2000-2006 in New South Wales, linkage rates were similar between matched controls (77.6% of 4,330) and other NSW children (77.4% of 598,265; P = .83) but were significantly lower in children with NAS (75.6% of 2,234; P = .03). The controls were matched for gender,gestation, and socioeconomic status.
The children with NAS had significantly lower scores than the controls and other NSW children in every grade and every domain of testing (reading, writing, numeracy, spelling, and grammar/punctuation). By grade 7, 38% of children with NAS did not meet National Minimum Standard (NMS) in one or more domains (versus 18.4% of controls and 14.5% of other NSW children). The mean serial composite scores also were lower in children with NAS from grades 3 to 7, compared with the other two groups; the difference was progressive, the investigators said. And by grade 7, the scores for children with NAS were lower than other children’s scores in grade 5.
It was noted that children with NAS, indigenous status (adjusted odds ratio, 1.7), male gender (aOR, 1.3), and having a primary parent without a grade 9 education (aOR, 1.3) increased the risk of failure to meet NMS. Overall, NAS (aOR, 2.5), indigenous status (aOR, 2.2), male gender (aOR, 1.3), and prematurity (less than 37 weeks’ gestation [aOR, 1.2]) increased the risk of failure to meet NMS.
“To date these are the only data demonstrating long-term school outcomes for children with a history of NAS. Similar data for children born from the current opioid epidemic gripping much of the Northern Hemisphere, assuming linkage is possible, will be available only in 7-10 years,” researchers concluded. “Although this study was conducted in Australia, the high risk of poor academic performance in this vulnerable group of children is applicable to all countries, and strategies to address this risk and prevent poor adult outcomes and intergenerational vulnerability must be urgently addressed.”
Read the full study in Pediatrics (doi: 10.1542/peds.2016-2651).
FROM PEDIATRICS
First-trimester blood glucose predicts congenital heart disease risk
NEW ORLEANS – A single, random, first-trimester maternal plasma glucose measurement is superior to an oral glucose tolerance test later in pregnancy as a predictor of congenital heart disease in newborns, Emmi Helle, MD, reported at the American Heart Association scientific sessions.
This finding from a large retrospective study, if confirmed in a prospective data set, is likely to be practice changing. At present, a 1-hour oral glucose tolerance test in the second or third trimester is considered the best means of identifying pregnant women who ought to undergo fetal echocardiography for prenatal diagnosis of congenital heart disease, noted Dr. Helle of Stanford (Calif.) University.
An elevated random plasma glucose value in the first trimester was broadly predictive of increased risk for a variety of congenital heart anomalies, not just, for example, cyanotic conditions.
Fetal heart development is completed during the first trimester, Dr. Helle observed.
Her study received a warm reception. Michael A. Portman, MD, singled it out in his final-day wrap-up of the meeting’s highlights in the field of congenital heart disease.
Several studies have demonstrated that prenatal diagnosis of congenital heart disease results in improved surgical outcomes in newborns. The question is, how to get the right women – those at increased risk – to diagnostic fetal echocardiography. Guidelines suggest but don’t mandate on the basis of weak evidence that an oral glucose tolerance test performed in the second or early third trimester may be a useful means of screening mothers for fetal imaging. Dr. Helle’s study points to a better way.
“Hopefully we can change our guidelines and make them more scientific for identification of mothers who should undergo fetal echocardiography,” said Dr. Portman, professor of pediatrics at the University of Washington, Seattle, and director of pediatric cardiovascular research at Seattle Children’s Hospital.
Dr. Helle and Dr. Portman reported having no relevant financial interests.
NEW ORLEANS – A single, random, first-trimester maternal plasma glucose measurement is superior to an oral glucose tolerance test later in pregnancy as a predictor of congenital heart disease in newborns, Emmi Helle, MD, reported at the American Heart Association scientific sessions.
This finding from a large retrospective study, if confirmed in a prospective data set, is likely to be practice changing. At present, a 1-hour oral glucose tolerance test in the second or third trimester is considered the best means of identifying pregnant women who ought to undergo fetal echocardiography for prenatal diagnosis of congenital heart disease, noted Dr. Helle of Stanford (Calif.) University.
An elevated random plasma glucose value in the first trimester was broadly predictive of increased risk for a variety of congenital heart anomalies, not just, for example, cyanotic conditions.
Fetal heart development is completed during the first trimester, Dr. Helle observed.
Her study received a warm reception. Michael A. Portman, MD, singled it out in his final-day wrap-up of the meeting’s highlights in the field of congenital heart disease.
Several studies have demonstrated that prenatal diagnosis of congenital heart disease results in improved surgical outcomes in newborns. The question is, how to get the right women – those at increased risk – to diagnostic fetal echocardiography. Guidelines suggest but don’t mandate on the basis of weak evidence that an oral glucose tolerance test performed in the second or early third trimester may be a useful means of screening mothers for fetal imaging. Dr. Helle’s study points to a better way.
“Hopefully we can change our guidelines and make them more scientific for identification of mothers who should undergo fetal echocardiography,” said Dr. Portman, professor of pediatrics at the University of Washington, Seattle, and director of pediatric cardiovascular research at Seattle Children’s Hospital.
Dr. Helle and Dr. Portman reported having no relevant financial interests.
NEW ORLEANS – A single, random, first-trimester maternal plasma glucose measurement is superior to an oral glucose tolerance test later in pregnancy as a predictor of congenital heart disease in newborns, Emmi Helle, MD, reported at the American Heart Association scientific sessions.
This finding from a large retrospective study, if confirmed in a prospective data set, is likely to be practice changing. At present, a 1-hour oral glucose tolerance test in the second or third trimester is considered the best means of identifying pregnant women who ought to undergo fetal echocardiography for prenatal diagnosis of congenital heart disease, noted Dr. Helle of Stanford (Calif.) University.
An elevated random plasma glucose value in the first trimester was broadly predictive of increased risk for a variety of congenital heart anomalies, not just, for example, cyanotic conditions.
Fetal heart development is completed during the first trimester, Dr. Helle observed.
Her study received a warm reception. Michael A. Portman, MD, singled it out in his final-day wrap-up of the meeting’s highlights in the field of congenital heart disease.
Several studies have demonstrated that prenatal diagnosis of congenital heart disease results in improved surgical outcomes in newborns. The question is, how to get the right women – those at increased risk – to diagnostic fetal echocardiography. Guidelines suggest but don’t mandate on the basis of weak evidence that an oral glucose tolerance test performed in the second or early third trimester may be a useful means of screening mothers for fetal imaging. Dr. Helle’s study points to a better way.
“Hopefully we can change our guidelines and make them more scientific for identification of mothers who should undergo fetal echocardiography,” said Dr. Portman, professor of pediatrics at the University of Washington, Seattle, and director of pediatric cardiovascular research at Seattle Children’s Hospital.
Dr. Helle and Dr. Portman reported having no relevant financial interests.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point:
Major finding: For every 10-mg/dL increase in maternal plasma glucose on a random first-trimester measurement, the risk of giving birth to a baby with congenital heart disease rose by 8%.
Data source: A retrospective study of 19,197 pregnancies, 811 of which resulted in congenital heart disease in the offspring.
Disclosures: The presenter reported having no financial conflicts of interest regarding the study.
Which maternal beta-blockers boost SGA risk?
NEW ORLEANS – The use of labetalol or atenolol in pregnancy is associated with significantly increased risk of having a small-for-gestational-age (SGA) baby; metoprolol and propranolol are not.
And none of these four beta-blockers are associated with increased risk of congenital cardiac anomalies, Angie Ng, MD, reported at the American Heart Association scientific sessions.
Overall, the average birth weight for babies whose mothers were on a beta-blocker was 2,996 g, significantly less than the 3,353 g in 374,391 controls who weren’t exposed to beta-blockers during pregnancy. But beta-blockers are not a monolithic class of drugs; their pharmacokinetics and physical properties differ. And so did their associated incidence of SGA, according to Dr. Ng of Kaiser Permanente Los Angeles.
The rate of SGA below the 10th percentile was 17.6% in the 3,357 women on labetalol during pregnancy and the same in the 638 women on atenolol. In contrast, the SGA rates in women on metoprolol or propranolol – 10.8% and 10.3%, respectively – weren’t significantly different from the 8.7% incidence in controls.
To deal with the possibility of confounding by indication, Dr. Ng and her coinvestigators performed a multivariate analysis adjusted for maternal age, white race, body mass index, gestational age, diabetes, hypertension, arrhythmias, dyslipidemia, and renal insufficiency. The resultant adjusted risk of having an SGA baby was 2.9-fold greater in women on labetalol and 2.4-fold greater in those on atenolol than in controls. Women on the other two beta-blockers faced no increased risk.
The incidence of congenital cardiac anomalies was 5.1% in women exposed to beta-blockers in pregnancy and 1.9% in controls who weren’t. The most commonly diagnosed anomalies – patent ductus arteriosus, atrial septal defect, and ventricular septal defect – were two- to threefold more frequent in the setting of maternal beta-blocker exposure. However, in a multivariate analysis the use of any beta-blocker was no longer associated with significantly elevated risk of congenital cardiac anomalies.
“This suggests that the initial association we see in the unadjusted analysis is likely due to confounders and not due to the beta-blocker exposure,” Dr. Ng said.
Labetalol and atenolol were prescribed during pregnancy most often for hypertension, while metoprolol and propranolol were typically prescribed to control arrhythmias.
Previous reports by other investigators have yielded conflicting results as to whether maternal beta-blocker therapy is associated with increased risk of SGA. A major limitation of those studies was that they examined beta-blockers as a class rather than assessing the impact of specific agents, according to Dr. Ng.
She reported having no financial conflicts of interest regarding her study, which was conducted free of commercial support.
NEW ORLEANS – The use of labetalol or atenolol in pregnancy is associated with significantly increased risk of having a small-for-gestational-age (SGA) baby; metoprolol and propranolol are not.
And none of these four beta-blockers are associated with increased risk of congenital cardiac anomalies, Angie Ng, MD, reported at the American Heart Association scientific sessions.
Overall, the average birth weight for babies whose mothers were on a beta-blocker was 2,996 g, significantly less than the 3,353 g in 374,391 controls who weren’t exposed to beta-blockers during pregnancy. But beta-blockers are not a monolithic class of drugs; their pharmacokinetics and physical properties differ. And so did their associated incidence of SGA, according to Dr. Ng of Kaiser Permanente Los Angeles.
The rate of SGA below the 10th percentile was 17.6% in the 3,357 women on labetalol during pregnancy and the same in the 638 women on atenolol. In contrast, the SGA rates in women on metoprolol or propranolol – 10.8% and 10.3%, respectively – weren’t significantly different from the 8.7% incidence in controls.
To deal with the possibility of confounding by indication, Dr. Ng and her coinvestigators performed a multivariate analysis adjusted for maternal age, white race, body mass index, gestational age, diabetes, hypertension, arrhythmias, dyslipidemia, and renal insufficiency. The resultant adjusted risk of having an SGA baby was 2.9-fold greater in women on labetalol and 2.4-fold greater in those on atenolol than in controls. Women on the other two beta-blockers faced no increased risk.
The incidence of congenital cardiac anomalies was 5.1% in women exposed to beta-blockers in pregnancy and 1.9% in controls who weren’t. The most commonly diagnosed anomalies – patent ductus arteriosus, atrial septal defect, and ventricular septal defect – were two- to threefold more frequent in the setting of maternal beta-blocker exposure. However, in a multivariate analysis the use of any beta-blocker was no longer associated with significantly elevated risk of congenital cardiac anomalies.
“This suggests that the initial association we see in the unadjusted analysis is likely due to confounders and not due to the beta-blocker exposure,” Dr. Ng said.
Labetalol and atenolol were prescribed during pregnancy most often for hypertension, while metoprolol and propranolol were typically prescribed to control arrhythmias.
Previous reports by other investigators have yielded conflicting results as to whether maternal beta-blocker therapy is associated with increased risk of SGA. A major limitation of those studies was that they examined beta-blockers as a class rather than assessing the impact of specific agents, according to Dr. Ng.
She reported having no financial conflicts of interest regarding her study, which was conducted free of commercial support.
NEW ORLEANS – The use of labetalol or atenolol in pregnancy is associated with significantly increased risk of having a small-for-gestational-age (SGA) baby; metoprolol and propranolol are not.
And none of these four beta-blockers are associated with increased risk of congenital cardiac anomalies, Angie Ng, MD, reported at the American Heart Association scientific sessions.
Overall, the average birth weight for babies whose mothers were on a beta-blocker was 2,996 g, significantly less than the 3,353 g in 374,391 controls who weren’t exposed to beta-blockers during pregnancy. But beta-blockers are not a monolithic class of drugs; their pharmacokinetics and physical properties differ. And so did their associated incidence of SGA, according to Dr. Ng of Kaiser Permanente Los Angeles.
The rate of SGA below the 10th percentile was 17.6% in the 3,357 women on labetalol during pregnancy and the same in the 638 women on atenolol. In contrast, the SGA rates in women on metoprolol or propranolol – 10.8% and 10.3%, respectively – weren’t significantly different from the 8.7% incidence in controls.
To deal with the possibility of confounding by indication, Dr. Ng and her coinvestigators performed a multivariate analysis adjusted for maternal age, white race, body mass index, gestational age, diabetes, hypertension, arrhythmias, dyslipidemia, and renal insufficiency. The resultant adjusted risk of having an SGA baby was 2.9-fold greater in women on labetalol and 2.4-fold greater in those on atenolol than in controls. Women on the other two beta-blockers faced no increased risk.
The incidence of congenital cardiac anomalies was 5.1% in women exposed to beta-blockers in pregnancy and 1.9% in controls who weren’t. The most commonly diagnosed anomalies – patent ductus arteriosus, atrial septal defect, and ventricular septal defect – were two- to threefold more frequent in the setting of maternal beta-blocker exposure. However, in a multivariate analysis the use of any beta-blocker was no longer associated with significantly elevated risk of congenital cardiac anomalies.
“This suggests that the initial association we see in the unadjusted analysis is likely due to confounders and not due to the beta-blocker exposure,” Dr. Ng said.
Labetalol and atenolol were prescribed during pregnancy most often for hypertension, while metoprolol and propranolol were typically prescribed to control arrhythmias.
Previous reports by other investigators have yielded conflicting results as to whether maternal beta-blocker therapy is associated with increased risk of SGA. A major limitation of those studies was that they examined beta-blockers as a class rather than assessing the impact of specific agents, according to Dr. Ng.
She reported having no financial conflicts of interest regarding her study, which was conducted free of commercial support.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point:
Major finding: Women on labetalol or atenolol during pregnancy had a 17.6% incidence of small-for-gestational-age babies, a rate more than twice that in women not exposed to a beta-blocker during pregnancy.
Data source: This was a retrospective study of fetal outcomes in nearly 380,000 pregnant women, 4,847 of whom were on beta-blocker therapy during their pregnancy.
Disclosures: The presenter reported having no financial conflicts of interest regarding her study, which was conducted free of commercial support.
Prenatal exposure to TNF inhibitors does not increase infections in newborns
WASHINGTON – Prenatal exposure to tumor necrosis factor–inhibiting drugs does not significantly increase the risk of a serious antenatal infection in infants born to women taking the drugs for rheumatoid arthritis, according to a large database study.
Researchers from McGill University, Montreal, and the University of Alabama at Birmingham who conducted the study did find a higher rate of serious infections among infants born to users of a tumor necrosis factor inhibitor (TNFi), especially among those exposed to infliximab, but after adjustment for maternal age and other antirheumatic drugs, the risk was not statistically significant.
Infliximab is unique among the TNFi drugs in that it concentrates in cord blood, reaching levels that can exceed 150% of the maternal blood level, Dr. Vinet noted. Adalimumab concentrates similarly, although the current study did not find any significantly increased infection risk associated with that medication.
Dr. Vinet and her colleagues analyzed drug exposure in 2,455 infants born to mothers with rheumatoid arthritis (RA), who were included in the PregnAncies in RA mothers and Outcomes in offspring in the United States cohort (PAROUS) registry. This cohort is drawn from data in the national MarketScan commercial database. The infants were age- and gender-matched with more than 11,000 matched controls born to women without RA, and with no prenatal TNFi exposure. Among these drugs, she looked for exposure to adalimumab, certolizumab pegol, etanercept, golimumab, and infliximab, as well as corticosteroids and other biologic and nonbiologic disease-modifying antirheumatic drugs (DMARDs).
Two exposures were considered: drugs taken during pregnancy and drugs taken before conception but not during pregnancy. These were compared with infants of mothers with RA who didn’t take TNFi drugs, and to the control infants. Serious infections were those that required a hospitalization during the first 12 months of life; only the index incident was counted.
Among the RA cohort, 290 (12%) were exposed to a TNFi during pregnancy and 109 (4%) were born to women who had taken a TNFi before conception. The remainder of the cohort was unexposed to those medications.
The mean maternal age was 32 years and similar in all RA categories and controls.
Corticosteroid use was common in women with RA, whether they took a TNFi during pregnancy (55%), before pregnancy (44%), or not at all (26%). Nonbiologic DMARDs were given to 19% of the TNFi cohort during pregnancy and 16% before pregnancy, as well as to 15% of those who didn’t take a TNFi.
The rate of serious neonatal infection was 2% among both infants born to RA mothers who didn’t take a TNFi and those born to RA mothers who took a TNFi before conception. Control infants born to women without RA had a serious infection rate of 0.2%.
Among infants exposed to a TNFi during pregnancy, the serious infection rate was 3%; it was also 3% among those exposed only in the third trimester.
A multivariate analysis that controlled for maternal age, prepregnancy diabetes, gestational diabetes, preterm birth, and exposure to the other drug categories determined that TNFi drugs did not significantly increase the risk of a serious infection in neonates with gestational exposure (odds ratio, 1.4) or whose mothers took the drugs before conception (OR, 0.9), compared with controls. The findings were similar when the analysis was restricted to TNFi exposure in the third trimester only.
When Dr. Vinet examined each drug independently, she found numerical differences in infection rates: golimumab and certolizumab pegol, 0%; adalimumab, 2.4%; etanercept 2.7%; and infliximab, 8.3%.
Because of the relatively small number of events, this portion of the regression analysis could not control for preterm birth and gestational diabetes. But after adjusting for maternal age and in utero corticosteroid exposure, Dr. Vinet found no significant associations with serious neonatal infection and any of the TNFi drugs, including infliximab (OR, 3.5; 95% CI, 0.8-15.0).
She and her colleagues had no financial disclosures.
[email protected]
On Twitter @alz_gal
WASHINGTON – Prenatal exposure to tumor necrosis factor–inhibiting drugs does not significantly increase the risk of a serious antenatal infection in infants born to women taking the drugs for rheumatoid arthritis, according to a large database study.
Researchers from McGill University, Montreal, and the University of Alabama at Birmingham who conducted the study did find a higher rate of serious infections among infants born to users of a tumor necrosis factor inhibitor (TNFi), especially among those exposed to infliximab, but after adjustment for maternal age and other antirheumatic drugs, the risk was not statistically significant.
Infliximab is unique among the TNFi drugs in that it concentrates in cord blood, reaching levels that can exceed 150% of the maternal blood level, Dr. Vinet noted. Adalimumab concentrates similarly, although the current study did not find any significantly increased infection risk associated with that medication.
Dr. Vinet and her colleagues analyzed drug exposure in 2,455 infants born to mothers with rheumatoid arthritis (RA), who were included in the PregnAncies in RA mothers and Outcomes in offspring in the United States cohort (PAROUS) registry. This cohort is drawn from data in the national MarketScan commercial database. The infants were age- and gender-matched with more than 11,000 matched controls born to women without RA, and with no prenatal TNFi exposure. Among these drugs, she looked for exposure to adalimumab, certolizumab pegol, etanercept, golimumab, and infliximab, as well as corticosteroids and other biologic and nonbiologic disease-modifying antirheumatic drugs (DMARDs).
Two exposures were considered: drugs taken during pregnancy and drugs taken before conception but not during pregnancy. These were compared with infants of mothers with RA who didn’t take TNFi drugs, and to the control infants. Serious infections were those that required a hospitalization during the first 12 months of life; only the index incident was counted.
Among the RA cohort, 290 (12%) were exposed to a TNFi during pregnancy and 109 (4%) were born to women who had taken a TNFi before conception. The remainder of the cohort was unexposed to those medications.
The mean maternal age was 32 years and similar in all RA categories and controls.
Corticosteroid use was common in women with RA, whether they took a TNFi during pregnancy (55%), before pregnancy (44%), or not at all (26%). Nonbiologic DMARDs were given to 19% of the TNFi cohort during pregnancy and 16% before pregnancy, as well as to 15% of those who didn’t take a TNFi.
The rate of serious neonatal infection was 2% among both infants born to RA mothers who didn’t take a TNFi and those born to RA mothers who took a TNFi before conception. Control infants born to women without RA had a serious infection rate of 0.2%.
Among infants exposed to a TNFi during pregnancy, the serious infection rate was 3%; it was also 3% among those exposed only in the third trimester.
A multivariate analysis that controlled for maternal age, prepregnancy diabetes, gestational diabetes, preterm birth, and exposure to the other drug categories determined that TNFi drugs did not significantly increase the risk of a serious infection in neonates with gestational exposure (odds ratio, 1.4) or whose mothers took the drugs before conception (OR, 0.9), compared with controls. The findings were similar when the analysis was restricted to TNFi exposure in the third trimester only.
When Dr. Vinet examined each drug independently, she found numerical differences in infection rates: golimumab and certolizumab pegol, 0%; adalimumab, 2.4%; etanercept 2.7%; and infliximab, 8.3%.
Because of the relatively small number of events, this portion of the regression analysis could not control for preterm birth and gestational diabetes. But after adjusting for maternal age and in utero corticosteroid exposure, Dr. Vinet found no significant associations with serious neonatal infection and any of the TNFi drugs, including infliximab (OR, 3.5; 95% CI, 0.8-15.0).
She and her colleagues had no financial disclosures.
[email protected]
On Twitter @alz_gal
WASHINGTON – Prenatal exposure to tumor necrosis factor–inhibiting drugs does not significantly increase the risk of a serious antenatal infection in infants born to women taking the drugs for rheumatoid arthritis, according to a large database study.
Researchers from McGill University, Montreal, and the University of Alabama at Birmingham who conducted the study did find a higher rate of serious infections among infants born to users of a tumor necrosis factor inhibitor (TNFi), especially among those exposed to infliximab, but after adjustment for maternal age and other antirheumatic drugs, the risk was not statistically significant.
Infliximab is unique among the TNFi drugs in that it concentrates in cord blood, reaching levels that can exceed 150% of the maternal blood level, Dr. Vinet noted. Adalimumab concentrates similarly, although the current study did not find any significantly increased infection risk associated with that medication.
Dr. Vinet and her colleagues analyzed drug exposure in 2,455 infants born to mothers with rheumatoid arthritis (RA), who were included in the PregnAncies in RA mothers and Outcomes in offspring in the United States cohort (PAROUS) registry. This cohort is drawn from data in the national MarketScan commercial database. The infants were age- and gender-matched with more than 11,000 matched controls born to women without RA, and with no prenatal TNFi exposure. Among these drugs, she looked for exposure to adalimumab, certolizumab pegol, etanercept, golimumab, and infliximab, as well as corticosteroids and other biologic and nonbiologic disease-modifying antirheumatic drugs (DMARDs).
Two exposures were considered: drugs taken during pregnancy and drugs taken before conception but not during pregnancy. These were compared with infants of mothers with RA who didn’t take TNFi drugs, and to the control infants. Serious infections were those that required a hospitalization during the first 12 months of life; only the index incident was counted.
Among the RA cohort, 290 (12%) were exposed to a TNFi during pregnancy and 109 (4%) were born to women who had taken a TNFi before conception. The remainder of the cohort was unexposed to those medications.
The mean maternal age was 32 years and similar in all RA categories and controls.
Corticosteroid use was common in women with RA, whether they took a TNFi during pregnancy (55%), before pregnancy (44%), or not at all (26%). Nonbiologic DMARDs were given to 19% of the TNFi cohort during pregnancy and 16% before pregnancy, as well as to 15% of those who didn’t take a TNFi.
The rate of serious neonatal infection was 2% among both infants born to RA mothers who didn’t take a TNFi and those born to RA mothers who took a TNFi before conception. Control infants born to women without RA had a serious infection rate of 0.2%.
Among infants exposed to a TNFi during pregnancy, the serious infection rate was 3%; it was also 3% among those exposed only in the third trimester.
A multivariate analysis that controlled for maternal age, prepregnancy diabetes, gestational diabetes, preterm birth, and exposure to the other drug categories determined that TNFi drugs did not significantly increase the risk of a serious infection in neonates with gestational exposure (odds ratio, 1.4) or whose mothers took the drugs before conception (OR, 0.9), compared with controls. The findings were similar when the analysis was restricted to TNFi exposure in the third trimester only.
When Dr. Vinet examined each drug independently, she found numerical differences in infection rates: golimumab and certolizumab pegol, 0%; adalimumab, 2.4%; etanercept 2.7%; and infliximab, 8.3%.
Because of the relatively small number of events, this portion of the regression analysis could not control for preterm birth and gestational diabetes. But after adjusting for maternal age and in utero corticosteroid exposure, Dr. Vinet found no significant associations with serious neonatal infection and any of the TNFi drugs, including infliximab (OR, 3.5; 95% CI, 0.8-15.0).
She and her colleagues had no financial disclosures.
[email protected]
On Twitter @alz_gal
AT THE ACR ANNUAL MEETING
Key clinical point:
Major finding: The rates of serious neonatal infection were 2% among infants born to RA mothers without exposure to TNFi drugs and 3% among those exposed to the drugs during gestation.
Data source: The case-control study comprised 2,455 cases and more than 11,000 controls.
Disclosures: Dr. Vinet and her colleagues had no financial disclosures.
RSV is top cause of severe respiratory disease in preterm infants
Respiratory syncytial virus is the number one virus causing severe lower respiratory disease in preterm infants, while those of younger age and those exposed to young children are at greatest risk, Eric A. F. Simões, MD, of the University of Colorado at Denver, Aurora, and his coauthors reported in the Nov. 29 edition of PLOS ONE.
“These data demonstrate that higher risk for 32 to 35 wGA [weeks gestational age] infants can be easily identified by age or birth month and significant exposure to other young children,” they wrote. “These infants would benefit from targeted efforts to prevent severe RSV disease.”
The overall rates of lower respiratory infections per 100 infant-seasons – a season being 5 months of observation from November 1 to March 31 in 2009-2010 or 2010-2011 – were 13.7 for respiratory syncytial virus (RSV), 2.9 for adenovirus, 1.7 for parainfluenza virus type 2, 1.3 for human metapneumovirus, and 0.3 for parainfluenza virus type 2 (PLoS One. 2016 Nov 29. doi: 10.1371/journal.pone.0166226).
Infants who had been exposed to young children, either through attending day care or living with non–multiple birth preschool-age siblings, had a twofold higher risk of RSV and human metapneumovirus, and a 3.3-fold greater risk of adenovirus.
The youngest infants showed the highest rate of hospitalizations with RSV: the incidence ranged from 8.2 per 100 infant season in those aged less than 1 month to 2.3 per 100 infant seasons in those aged 10 months of age. Similarly, the incidence of admission to ICU was significantly higher among younger infants.
Infants born in May, before the RSV season, had a much lower incidence of hospitalization, compared with those born in the height of RSV season in February. ICU admission rates also were higher among those born in February, compared with those born in May.
The highest overall rates of hospitalization with RSV – 19 per 100 infant-seasons – were among those born in February, and also those who were exposed to other young children.
“The current results are unique in that they provide continuous age-based risk models for outpatient and inpatient disease for infants with and without young child exposure,” wrote Dr. Simões and his coauthors.
They argued that their findings refute earlier suggestions that the rate of RSV infection in preterm infants is similar to the rate in term infants, and suggested that the limitations of their study may have even underestimated the incidence in preterm babies.
The study was supported by AstraZeneca, parent company of MedImmune. Two authors declared grant support and research funding from AstraZeneca, one author was a former employee of AstraZeneca, one author was a former employee of MedImmune and now contractor to AstraZeneca. One author was a current employee of AstraZeneca and holds stock options. Two authors also declared funding and consultancies with AbbVie.
Respiratory syncytial virus is the number one virus causing severe lower respiratory disease in preterm infants, while those of younger age and those exposed to young children are at greatest risk, Eric A. F. Simões, MD, of the University of Colorado at Denver, Aurora, and his coauthors reported in the Nov. 29 edition of PLOS ONE.
“These data demonstrate that higher risk for 32 to 35 wGA [weeks gestational age] infants can be easily identified by age or birth month and significant exposure to other young children,” they wrote. “These infants would benefit from targeted efforts to prevent severe RSV disease.”
The overall rates of lower respiratory infections per 100 infant-seasons – a season being 5 months of observation from November 1 to March 31 in 2009-2010 or 2010-2011 – were 13.7 for respiratory syncytial virus (RSV), 2.9 for adenovirus, 1.7 for parainfluenza virus type 2, 1.3 for human metapneumovirus, and 0.3 for parainfluenza virus type 2 (PLoS One. 2016 Nov 29. doi: 10.1371/journal.pone.0166226).
Infants who had been exposed to young children, either through attending day care or living with non–multiple birth preschool-age siblings, had a twofold higher risk of RSV and human metapneumovirus, and a 3.3-fold greater risk of adenovirus.
The youngest infants showed the highest rate of hospitalizations with RSV: the incidence ranged from 8.2 per 100 infant season in those aged less than 1 month to 2.3 per 100 infant seasons in those aged 10 months of age. Similarly, the incidence of admission to ICU was significantly higher among younger infants.
Infants born in May, before the RSV season, had a much lower incidence of hospitalization, compared with those born in the height of RSV season in February. ICU admission rates also were higher among those born in February, compared with those born in May.
The highest overall rates of hospitalization with RSV – 19 per 100 infant-seasons – were among those born in February, and also those who were exposed to other young children.
“The current results are unique in that they provide continuous age-based risk models for outpatient and inpatient disease for infants with and without young child exposure,” wrote Dr. Simões and his coauthors.
They argued that their findings refute earlier suggestions that the rate of RSV infection in preterm infants is similar to the rate in term infants, and suggested that the limitations of their study may have even underestimated the incidence in preterm babies.
The study was supported by AstraZeneca, parent company of MedImmune. Two authors declared grant support and research funding from AstraZeneca, one author was a former employee of AstraZeneca, one author was a former employee of MedImmune and now contractor to AstraZeneca. One author was a current employee of AstraZeneca and holds stock options. Two authors also declared funding and consultancies with AbbVie.
Respiratory syncytial virus is the number one virus causing severe lower respiratory disease in preterm infants, while those of younger age and those exposed to young children are at greatest risk, Eric A. F. Simões, MD, of the University of Colorado at Denver, Aurora, and his coauthors reported in the Nov. 29 edition of PLOS ONE.
“These data demonstrate that higher risk for 32 to 35 wGA [weeks gestational age] infants can be easily identified by age or birth month and significant exposure to other young children,” they wrote. “These infants would benefit from targeted efforts to prevent severe RSV disease.”
The overall rates of lower respiratory infections per 100 infant-seasons – a season being 5 months of observation from November 1 to March 31 in 2009-2010 or 2010-2011 – were 13.7 for respiratory syncytial virus (RSV), 2.9 for adenovirus, 1.7 for parainfluenza virus type 2, 1.3 for human metapneumovirus, and 0.3 for parainfluenza virus type 2 (PLoS One. 2016 Nov 29. doi: 10.1371/journal.pone.0166226).
Infants who had been exposed to young children, either through attending day care or living with non–multiple birth preschool-age siblings, had a twofold higher risk of RSV and human metapneumovirus, and a 3.3-fold greater risk of adenovirus.
The youngest infants showed the highest rate of hospitalizations with RSV: the incidence ranged from 8.2 per 100 infant season in those aged less than 1 month to 2.3 per 100 infant seasons in those aged 10 months of age. Similarly, the incidence of admission to ICU was significantly higher among younger infants.
Infants born in May, before the RSV season, had a much lower incidence of hospitalization, compared with those born in the height of RSV season in February. ICU admission rates also were higher among those born in February, compared with those born in May.
The highest overall rates of hospitalization with RSV – 19 per 100 infant-seasons – were among those born in February, and also those who were exposed to other young children.
“The current results are unique in that they provide continuous age-based risk models for outpatient and inpatient disease for infants with and without young child exposure,” wrote Dr. Simões and his coauthors.
They argued that their findings refute earlier suggestions that the rate of RSV infection in preterm infants is similar to the rate in term infants, and suggested that the limitations of their study may have even underestimated the incidence in preterm babies.
The study was supported by AstraZeneca, parent company of MedImmune. Two authors declared grant support and research funding from AstraZeneca, one author was a former employee of AstraZeneca, one author was a former employee of MedImmune and now contractor to AstraZeneca. One author was a current employee of AstraZeneca and holds stock options. Two authors also declared funding and consultancies with AbbVie.
FROM PLOS ONE
Key clinical point: Respiratory syncytial virus is the leading viral cause of severe lower respiratory disease in preterm infants, with those of younger age and those exposed to young children at greatest risk.
Major finding: The rates of lower respiratory infections per 100 infant-seasons were 13.7 for RSV, 2.9 for adenovirus, 1.7 for parainfluenza virus type 2, and 1.3 for human metapneumovirus.
Data source: The prospective RSV Respiratory Events Among Preterm Infants Outcomes and Risk Tracking (REPORT) study, in 1,642 preterm infants with medically attended acute respiratory illness.
Disclosures: The study was supported by AstraZeneca, parent company of MedImmune. Two authors declared grant support and research funding from AstraZeneca, one author was a former employee of AstraZeneca, and one author was a former employee of MedImmune and now contractor to AstraZeneca. One author was a current employee of AstraZeneca and holds stock options. Two authors also declared funding and consultancies with AbbVie.
Prenatal exposure to hydroxychloroquine cuts risk of neonatal cutaneous lupus
WASHINGTON – Prenatal hydroxychloroquine reduces the risk of cutaneous neonatal lupus by 60% among the infants of women with a systemic autoimmune rheumatic disease.
The medication easily passes the placental barrier and confers significant protection to neonates born to women who have anti-Ro and anti-La antibodies, Julie Barsalou, MD, said at the annual meeting of the American College of Rheumatology.
Toll-like receptors 7 and 9 have been implicated in the initiation and maintenance of interface dermatitis, and hydroxychloroquine inhibits these receptors. In mouse studies, the drug has led to improvement of this type of dermatitis. Hydroxychloroquine also works well in treating subacute cutaneous lupus, she said, and because it can travel across the placenta, it could be an effective means of preventing this disorder in at-risk neonates.
To examine any potential benefit, Dr. Barsalou looked at three pediatric lupus databases: the SickKids NLE database from Toronto, the U.S. Research Registry for Neonatal Lupus, and the French Registry for Neonatal Lupus.
These registries include infants born to mothers with anti-Ro and/or anti-La antibodies, and a diagnosis of lupus, dermatomyositis, Sjögren’s syndrome, juvenile idiopathic arthritis, or rheumatic arthritis. No infants with cardiac neonatal lupus were included in the study.
In addition to hydroxychloroquine, Dr. Barsalou examined the use of prenatal azathioprine, nonfluorinated and fluorinated steroids, and intravenous immunoglobulin.
The cohort comprised 545 neonates born to 535 mothers. Among these, 112 developed cNLE. The remaining 433 infants were used as controls.
Mothers of both cases and controls were a mean age of 31 years. Among cases, the most common diagnosis was Sjögren’s syndrome (53%), followed by systemic lupus erythematosus (46%). Among controls, the most common maternal diagnosis was SLE (62%), followed by Sjögren’s (31%).
All mothers of cases were positive for anti-Ro antibodies; 72% were positive for anti-La antibodies. Among mothers of controls, 99% had anti-Ro antibodies and 48% had anti-La antibodies.
Mothers of cases took hydroxychloroquine (17%), fluorinated steroids (6%), and nonfluorinated steroids with or without azathioprine (28%). Mothers of controls took hydroxychloroquine (34%), fluorinated steroids (4%), and nonfluorinated steroids with or without azathioprine (44%),
There were significantly more female than male infants in the case group (65%). The median age at rash onset was 6 weeks.
Dr. Barsalou performed several multivariate analyses on the entire cohort, as well as two subgroup analyses: one on infants who developed the cNLE rash within the first 4 weeks of life and one on only the infants of mothers with SLE.
In the primary analysis, maternal anti-Ro and anti-La antibodies more than doubled the risk of an infant developing cNLE (odds ratio, 2.5). The use of hydroxychloroquine decreased this risk by 60% (OR, 0.4). Being a female infant increased the risk by 70% (OR, 1.7).
In the group of infants with early-onset rash, maternal anti-La antibodies more than tripled the risk (OR, 3.5), while the use of hydroxychloroquine decreased the risk by 80% (OR, 0.2).
Among the infants born to women with SLE, concomitant secondary Sjögren’s syndrome increased the risk of cNLE by more than threefold (OR, 3.5). Anti-La antibodies more than doubled the risk (OR, 2.5), and the use of hydroxychloroquine decreased it by 60% (OR, 0.4).
“This is the first study to address the prevention of cutaneous neonatal lupus,” Dr. Barsalou said. “We found that prenatal exposure to hydroxychloroquine is likely protective.”
She had no financial disclosures.
[email protected]
On Twitter @alz_gal
WASHINGTON – Prenatal hydroxychloroquine reduces the risk of cutaneous neonatal lupus by 60% among the infants of women with a systemic autoimmune rheumatic disease.
The medication easily passes the placental barrier and confers significant protection to neonates born to women who have anti-Ro and anti-La antibodies, Julie Barsalou, MD, said at the annual meeting of the American College of Rheumatology.
Toll-like receptors 7 and 9 have been implicated in the initiation and maintenance of interface dermatitis, and hydroxychloroquine inhibits these receptors. In mouse studies, the drug has led to improvement of this type of dermatitis. Hydroxychloroquine also works well in treating subacute cutaneous lupus, she said, and because it can travel across the placenta, it could be an effective means of preventing this disorder in at-risk neonates.
To examine any potential benefit, Dr. Barsalou looked at three pediatric lupus databases: the SickKids NLE database from Toronto, the U.S. Research Registry for Neonatal Lupus, and the French Registry for Neonatal Lupus.
These registries include infants born to mothers with anti-Ro and/or anti-La antibodies, and a diagnosis of lupus, dermatomyositis, Sjögren’s syndrome, juvenile idiopathic arthritis, or rheumatic arthritis. No infants with cardiac neonatal lupus were included in the study.
In addition to hydroxychloroquine, Dr. Barsalou examined the use of prenatal azathioprine, nonfluorinated and fluorinated steroids, and intravenous immunoglobulin.
The cohort comprised 545 neonates born to 535 mothers. Among these, 112 developed cNLE. The remaining 433 infants were used as controls.
Mothers of both cases and controls were a mean age of 31 years. Among cases, the most common diagnosis was Sjögren’s syndrome (53%), followed by systemic lupus erythematosus (46%). Among controls, the most common maternal diagnosis was SLE (62%), followed by Sjögren’s (31%).
All mothers of cases were positive for anti-Ro antibodies; 72% were positive for anti-La antibodies. Among mothers of controls, 99% had anti-Ro antibodies and 48% had anti-La antibodies.
Mothers of cases took hydroxychloroquine (17%), fluorinated steroids (6%), and nonfluorinated steroids with or without azathioprine (28%). Mothers of controls took hydroxychloroquine (34%), fluorinated steroids (4%), and nonfluorinated steroids with or without azathioprine (44%),
There were significantly more female than male infants in the case group (65%). The median age at rash onset was 6 weeks.
Dr. Barsalou performed several multivariate analyses on the entire cohort, as well as two subgroup analyses: one on infants who developed the cNLE rash within the first 4 weeks of life and one on only the infants of mothers with SLE.
In the primary analysis, maternal anti-Ro and anti-La antibodies more than doubled the risk of an infant developing cNLE (odds ratio, 2.5). The use of hydroxychloroquine decreased this risk by 60% (OR, 0.4). Being a female infant increased the risk by 70% (OR, 1.7).
In the group of infants with early-onset rash, maternal anti-La antibodies more than tripled the risk (OR, 3.5), while the use of hydroxychloroquine decreased the risk by 80% (OR, 0.2).
Among the infants born to women with SLE, concomitant secondary Sjögren’s syndrome increased the risk of cNLE by more than threefold (OR, 3.5). Anti-La antibodies more than doubled the risk (OR, 2.5), and the use of hydroxychloroquine decreased it by 60% (OR, 0.4).
“This is the first study to address the prevention of cutaneous neonatal lupus,” Dr. Barsalou said. “We found that prenatal exposure to hydroxychloroquine is likely protective.”
She had no financial disclosures.
[email protected]
On Twitter @alz_gal
WASHINGTON – Prenatal hydroxychloroquine reduces the risk of cutaneous neonatal lupus by 60% among the infants of women with a systemic autoimmune rheumatic disease.
The medication easily passes the placental barrier and confers significant protection to neonates born to women who have anti-Ro and anti-La antibodies, Julie Barsalou, MD, said at the annual meeting of the American College of Rheumatology.
Toll-like receptors 7 and 9 have been implicated in the initiation and maintenance of interface dermatitis, and hydroxychloroquine inhibits these receptors. In mouse studies, the drug has led to improvement of this type of dermatitis. Hydroxychloroquine also works well in treating subacute cutaneous lupus, she said, and because it can travel across the placenta, it could be an effective means of preventing this disorder in at-risk neonates.
To examine any potential benefit, Dr. Barsalou looked at three pediatric lupus databases: the SickKids NLE database from Toronto, the U.S. Research Registry for Neonatal Lupus, and the French Registry for Neonatal Lupus.
These registries include infants born to mothers with anti-Ro and/or anti-La antibodies, and a diagnosis of lupus, dermatomyositis, Sjögren’s syndrome, juvenile idiopathic arthritis, or rheumatic arthritis. No infants with cardiac neonatal lupus were included in the study.
In addition to hydroxychloroquine, Dr. Barsalou examined the use of prenatal azathioprine, nonfluorinated and fluorinated steroids, and intravenous immunoglobulin.
The cohort comprised 545 neonates born to 535 mothers. Among these, 112 developed cNLE. The remaining 433 infants were used as controls.
Mothers of both cases and controls were a mean age of 31 years. Among cases, the most common diagnosis was Sjögren’s syndrome (53%), followed by systemic lupus erythematosus (46%). Among controls, the most common maternal diagnosis was SLE (62%), followed by Sjögren’s (31%).
All mothers of cases were positive for anti-Ro antibodies; 72% were positive for anti-La antibodies. Among mothers of controls, 99% had anti-Ro antibodies and 48% had anti-La antibodies.
Mothers of cases took hydroxychloroquine (17%), fluorinated steroids (6%), and nonfluorinated steroids with or without azathioprine (28%). Mothers of controls took hydroxychloroquine (34%), fluorinated steroids (4%), and nonfluorinated steroids with or without azathioprine (44%),
There were significantly more female than male infants in the case group (65%). The median age at rash onset was 6 weeks.
Dr. Barsalou performed several multivariate analyses on the entire cohort, as well as two subgroup analyses: one on infants who developed the cNLE rash within the first 4 weeks of life and one on only the infants of mothers with SLE.
In the primary analysis, maternal anti-Ro and anti-La antibodies more than doubled the risk of an infant developing cNLE (odds ratio, 2.5). The use of hydroxychloroquine decreased this risk by 60% (OR, 0.4). Being a female infant increased the risk by 70% (OR, 1.7).
In the group of infants with early-onset rash, maternal anti-La antibodies more than tripled the risk (OR, 3.5), while the use of hydroxychloroquine decreased the risk by 80% (OR, 0.2).
Among the infants born to women with SLE, concomitant secondary Sjögren’s syndrome increased the risk of cNLE by more than threefold (OR, 3.5). Anti-La antibodies more than doubled the risk (OR, 2.5), and the use of hydroxychloroquine decreased it by 60% (OR, 0.4).
“This is the first study to address the prevention of cutaneous neonatal lupus,” Dr. Barsalou said. “We found that prenatal exposure to hydroxychloroquine is likely protective.”
She had no financial disclosures.
[email protected]
On Twitter @alz_gal
AT THE ACR ANNUAL MEETING
Key clinical point:
Major finding: The drug was associated with a 60% decreased risk of developing the disorder.
Data source: The case-control study involved 545 infants.
Disclosures: Dr. Barsalou had no financial disclosures.
Many premature infants receive reflux medication after NICU discharge
Three-quarters of premature infants who receive gastroesophageal reflux medications get those drugs after being discharged from neonatal intensive care units, despite questions about the safety and efficacy of the medications in premature infants.
In a retrospective study of 2,217 premature infants treated within the Children’s Hospital of Philadelphia primary care network from 2005 to 2009, 812 were treated with gastroesophageal reflux (GER) medications. Of this group, 77% were started on GER medication after neonatal intensive care unit (NICU) discharge, according to Jo Ann D’Agostino, DNP, CRNP, and her associates (Pediatrics. 2016 Nov 23. doi: 10.1542/peds.2016-1977).
Histamine-2 receptor antagonists were the most commonly prescribed GER medication, received by 90% of infants. Proton pump inhibitors were prescribed to 37% of infants, 22% received prokinetics, and 2% received cholinergics. During the first year of life, 40% of treated infants received multiple GER medications, with 73% of these infants receiving at least two medications simultaneously.
Risk factors associated with the use of multiple GER medications include a gestation period less than 32 weeks, feeding difficulty, tube feeding, a need for supplemental oxygen, and asthma.
“Because premature infants are a medically fragile group, the need for 1 acid suppression medication, let alone 2 or more in combination, should be given careful consideration. The potential impact of acid suppression on community-acquired illnesses has yet to be explored for this vulnerable population,” said Dr. D’Agostino of the department of pediatrics at the Children’s Hospital of Philadelphia, and her coauthors.
Infants who received GER treatment after NICU discharge were started on medication at a mean chronological age of 95 days and received medication for a mean of 294 days. Infants who started GER treatment while in the NICU received medication for a mean of 375 days.
A total of 743 infants were started on GER medications before the age of 6 months, and of this group, 43% were still being treated at the age of 1 year. Extended medication usage was associated with a gestational age under 32 weeks, chronic lung disease, airway malacia, and reactive airways disease.
A gestation period of less than 32 weeks was associated with a 31% increase in GER medication duration, compared with infants with a gestation period of 34-35 weeks, and a gestation period of less than 28 weeks was associated with a 50% increase in medication duration.
“Physiologic reflux symptoms are reported to peak at 4 months of age. Feeding issues are also common for premature infants. Whether this combination of issues is influencing the decision to start treatment, as opposed to actual GER disease, is an important distinction for providers to consider before starting medication,” Dr. D’Agostino and her associates noted.
“With uncertain evidence of efficacy, the rationale for using these medications in this high-risk population should be carefully evaluated,” they concluded.
The study was funded by the National Institutes of Health. The authors had no relevant financial disclosures.
“Medications are frequently used to treat gastroesophageal reflux in premature infants,” wrote P. Brian Smith, MD, but “a number of these medications have been associated with significant harm” and the “short- or long-term benefits of GER medications in this population are undocumented.”
Histamine-2 receptor blockers, the most common GER medications, induce alterations to the fecal microbiota of premature infants by lowering microbial diversity and promoting overgrowth of Proteobacteria. “These alterations weaken the gastrointestinal tract’s protective barrier and render very low birth weight infants, already predisposed to [necrotizing enterocolitis] and other infections, even more vulnerable,” he noted.
“Infants receiving antacid therapy are also at increased risk of bacteremia, lower respiratory tract infections, aspiration pneumonia, and death,” he added.
“Pediatrics has a long history of widespread use of medications for which the risks did not outweigh the benefits. All drugs should be shown to be both safe and effective before use. [This study] has documented widespread, long-term use of medications that are likely neither,” he said.
Dr. Smith is with Duke University Medical Center, Durham, N.C. These comments are taken from an accompanying editorial (Pediatrics. 2016 Nov 23. doi: 10.1542/peds.2016-2849). Dr. Smith is a consultant for Astellas Pharma and Abbvie and receives grant support from Cempra Pharmaceuticals and Shionogi. Dr Smith receives salary support from the National Institutes of Health and the U.S. Food and Drug Administration.
“Medications are frequently used to treat gastroesophageal reflux in premature infants,” wrote P. Brian Smith, MD, but “a number of these medications have been associated with significant harm” and the “short- or long-term benefits of GER medications in this population are undocumented.”
Histamine-2 receptor blockers, the most common GER medications, induce alterations to the fecal microbiota of premature infants by lowering microbial diversity and promoting overgrowth of Proteobacteria. “These alterations weaken the gastrointestinal tract’s protective barrier and render very low birth weight infants, already predisposed to [necrotizing enterocolitis] and other infections, even more vulnerable,” he noted.
“Infants receiving antacid therapy are also at increased risk of bacteremia, lower respiratory tract infections, aspiration pneumonia, and death,” he added.
“Pediatrics has a long history of widespread use of medications for which the risks did not outweigh the benefits. All drugs should be shown to be both safe and effective before use. [This study] has documented widespread, long-term use of medications that are likely neither,” he said.
Dr. Smith is with Duke University Medical Center, Durham, N.C. These comments are taken from an accompanying editorial (Pediatrics. 2016 Nov 23. doi: 10.1542/peds.2016-2849). Dr. Smith is a consultant for Astellas Pharma and Abbvie and receives grant support from Cempra Pharmaceuticals and Shionogi. Dr Smith receives salary support from the National Institutes of Health and the U.S. Food and Drug Administration.
“Medications are frequently used to treat gastroesophageal reflux in premature infants,” wrote P. Brian Smith, MD, but “a number of these medications have been associated with significant harm” and the “short- or long-term benefits of GER medications in this population are undocumented.”
Histamine-2 receptor blockers, the most common GER medications, induce alterations to the fecal microbiota of premature infants by lowering microbial diversity and promoting overgrowth of Proteobacteria. “These alterations weaken the gastrointestinal tract’s protective barrier and render very low birth weight infants, already predisposed to [necrotizing enterocolitis] and other infections, even more vulnerable,” he noted.
“Infants receiving antacid therapy are also at increased risk of bacteremia, lower respiratory tract infections, aspiration pneumonia, and death,” he added.
“Pediatrics has a long history of widespread use of medications for which the risks did not outweigh the benefits. All drugs should be shown to be both safe and effective before use. [This study] has documented widespread, long-term use of medications that are likely neither,” he said.
Dr. Smith is with Duke University Medical Center, Durham, N.C. These comments are taken from an accompanying editorial (Pediatrics. 2016 Nov 23. doi: 10.1542/peds.2016-2849). Dr. Smith is a consultant for Astellas Pharma and Abbvie and receives grant support from Cempra Pharmaceuticals and Shionogi. Dr Smith receives salary support from the National Institutes of Health and the U.S. Food and Drug Administration.
Three-quarters of premature infants who receive gastroesophageal reflux medications get those drugs after being discharged from neonatal intensive care units, despite questions about the safety and efficacy of the medications in premature infants.
In a retrospective study of 2,217 premature infants treated within the Children’s Hospital of Philadelphia primary care network from 2005 to 2009, 812 were treated with gastroesophageal reflux (GER) medications. Of this group, 77% were started on GER medication after neonatal intensive care unit (NICU) discharge, according to Jo Ann D’Agostino, DNP, CRNP, and her associates (Pediatrics. 2016 Nov 23. doi: 10.1542/peds.2016-1977).
Histamine-2 receptor antagonists were the most commonly prescribed GER medication, received by 90% of infants. Proton pump inhibitors were prescribed to 37% of infants, 22% received prokinetics, and 2% received cholinergics. During the first year of life, 40% of treated infants received multiple GER medications, with 73% of these infants receiving at least two medications simultaneously.
Risk factors associated with the use of multiple GER medications include a gestation period less than 32 weeks, feeding difficulty, tube feeding, a need for supplemental oxygen, and asthma.
“Because premature infants are a medically fragile group, the need for 1 acid suppression medication, let alone 2 or more in combination, should be given careful consideration. The potential impact of acid suppression on community-acquired illnesses has yet to be explored for this vulnerable population,” said Dr. D’Agostino of the department of pediatrics at the Children’s Hospital of Philadelphia, and her coauthors.
Infants who received GER treatment after NICU discharge were started on medication at a mean chronological age of 95 days and received medication for a mean of 294 days. Infants who started GER treatment while in the NICU received medication for a mean of 375 days.
A total of 743 infants were started on GER medications before the age of 6 months, and of this group, 43% were still being treated at the age of 1 year. Extended medication usage was associated with a gestational age under 32 weeks, chronic lung disease, airway malacia, and reactive airways disease.
A gestation period of less than 32 weeks was associated with a 31% increase in GER medication duration, compared with infants with a gestation period of 34-35 weeks, and a gestation period of less than 28 weeks was associated with a 50% increase in medication duration.
“Physiologic reflux symptoms are reported to peak at 4 months of age. Feeding issues are also common for premature infants. Whether this combination of issues is influencing the decision to start treatment, as opposed to actual GER disease, is an important distinction for providers to consider before starting medication,” Dr. D’Agostino and her associates noted.
“With uncertain evidence of efficacy, the rationale for using these medications in this high-risk population should be carefully evaluated,” they concluded.
The study was funded by the National Institutes of Health. The authors had no relevant financial disclosures.
Three-quarters of premature infants who receive gastroesophageal reflux medications get those drugs after being discharged from neonatal intensive care units, despite questions about the safety and efficacy of the medications in premature infants.
In a retrospective study of 2,217 premature infants treated within the Children’s Hospital of Philadelphia primary care network from 2005 to 2009, 812 were treated with gastroesophageal reflux (GER) medications. Of this group, 77% were started on GER medication after neonatal intensive care unit (NICU) discharge, according to Jo Ann D’Agostino, DNP, CRNP, and her associates (Pediatrics. 2016 Nov 23. doi: 10.1542/peds.2016-1977).
Histamine-2 receptor antagonists were the most commonly prescribed GER medication, received by 90% of infants. Proton pump inhibitors were prescribed to 37% of infants, 22% received prokinetics, and 2% received cholinergics. During the first year of life, 40% of treated infants received multiple GER medications, with 73% of these infants receiving at least two medications simultaneously.
Risk factors associated with the use of multiple GER medications include a gestation period less than 32 weeks, feeding difficulty, tube feeding, a need for supplemental oxygen, and asthma.
“Because premature infants are a medically fragile group, the need for 1 acid suppression medication, let alone 2 or more in combination, should be given careful consideration. The potential impact of acid suppression on community-acquired illnesses has yet to be explored for this vulnerable population,” said Dr. D’Agostino of the department of pediatrics at the Children’s Hospital of Philadelphia, and her coauthors.
Infants who received GER treatment after NICU discharge were started on medication at a mean chronological age of 95 days and received medication for a mean of 294 days. Infants who started GER treatment while in the NICU received medication for a mean of 375 days.
A total of 743 infants were started on GER medications before the age of 6 months, and of this group, 43% were still being treated at the age of 1 year. Extended medication usage was associated with a gestational age under 32 weeks, chronic lung disease, airway malacia, and reactive airways disease.
A gestation period of less than 32 weeks was associated with a 31% increase in GER medication duration, compared with infants with a gestation period of 34-35 weeks, and a gestation period of less than 28 weeks was associated with a 50% increase in medication duration.
“Physiologic reflux symptoms are reported to peak at 4 months of age. Feeding issues are also common for premature infants. Whether this combination of issues is influencing the decision to start treatment, as opposed to actual GER disease, is an important distinction for providers to consider before starting medication,” Dr. D’Agostino and her associates noted.
“With uncertain evidence of efficacy, the rationale for using these medications in this high-risk population should be carefully evaluated,” they concluded.
The study was funded by the National Institutes of Health. The authors had no relevant financial disclosures.
FROM PEDIATRICS
Key clinical point:
Major finding: 37% of infants in the study received GER medication, with 77% of prescriptions occurring after NICU discharge.
Data source: Retrospective study of 2,217 preterm infants in the primary care network of the Children’s Hospital of Philadelphia.
Disclosures: The study was funded by the National Institutes of Health. The authors have no relevant financial disclosures.
Infants with congenital Zika born without microcephaly still can still develop it
Infants born with laboratory-confirmed congenital Zika virus but who show no signs of microcephaly at birth may still experience a reduction in cranial size as they grow older, according to the Centers for Disease Control and Prevention’s latest Morbidity and Mortality Weekly Report.
“These findings demonstrate the importance of early neuroimaging for infants exposed to Zika virus prenatally and the need for comprehensive medical and developmental follow-up,” wrote Vanessa van der Linden, MD, of the Association for Assistance of Disabled Children in Recife, Brazil, and her coauthors.
Dr. van der Linden and her coinvestigators examined 13 infants, all of whom were born in Brazil between October 2015 and January 2016, who had confirmed brain abnormalities at birth despite having a normal head size. These abnormalities included ventriculomegaly, subcortical calcifications, cortical malformations, and decreased brain volume. Investigators defined microcephaly as being “head circumference (HC) [that’s] more than 2 [standard deviations] below the mean for gestational age and sex.”
Nine of the infants were male, four were female. Eleven of the infants were born within 37-41 weeks’ of gestation. The remaining two were born at 35-36 weeks’ of gestation, considered “preterm” by the investigators. All infants tested positive for Zika via immunoglobulin M testing of cerebrospinal fluid, serum, or both. Only six of the mothers reported having a rash while pregnant; four reported experiencing it during the first trimester, while the other two said it occurred in the second.
All 13 infants showed a decrease in HC to what was defined as microcephaly within 1 year of birth (October 2016). Neuroimaging showed that all but one had decreased brain volume, all had malformations of cortical development, four had cerebellum or brain-stem hypoplasia, ten had ventriculomegaly, and three had increased extra-axial CSF space.
“More than 60% of infants in this series had epilepsy (likely related to the cortical malformations), and all had significant motor disabilities consistent with mixed cerebral palsy,” the authors noted, adding that the “pathogenesis of postnatal microcephaly from congenital Zika virus infections is [still] not known.”
Infants born with laboratory-confirmed congenital Zika virus but who show no signs of microcephaly at birth may still experience a reduction in cranial size as they grow older, according to the Centers for Disease Control and Prevention’s latest Morbidity and Mortality Weekly Report.
“These findings demonstrate the importance of early neuroimaging for infants exposed to Zika virus prenatally and the need for comprehensive medical and developmental follow-up,” wrote Vanessa van der Linden, MD, of the Association for Assistance of Disabled Children in Recife, Brazil, and her coauthors.
Dr. van der Linden and her coinvestigators examined 13 infants, all of whom were born in Brazil between October 2015 and January 2016, who had confirmed brain abnormalities at birth despite having a normal head size. These abnormalities included ventriculomegaly, subcortical calcifications, cortical malformations, and decreased brain volume. Investigators defined microcephaly as being “head circumference (HC) [that’s] more than 2 [standard deviations] below the mean for gestational age and sex.”
Nine of the infants were male, four were female. Eleven of the infants were born within 37-41 weeks’ of gestation. The remaining two were born at 35-36 weeks’ of gestation, considered “preterm” by the investigators. All infants tested positive for Zika via immunoglobulin M testing of cerebrospinal fluid, serum, or both. Only six of the mothers reported having a rash while pregnant; four reported experiencing it during the first trimester, while the other two said it occurred in the second.
All 13 infants showed a decrease in HC to what was defined as microcephaly within 1 year of birth (October 2016). Neuroimaging showed that all but one had decreased brain volume, all had malformations of cortical development, four had cerebellum or brain-stem hypoplasia, ten had ventriculomegaly, and three had increased extra-axial CSF space.
“More than 60% of infants in this series had epilepsy (likely related to the cortical malformations), and all had significant motor disabilities consistent with mixed cerebral palsy,” the authors noted, adding that the “pathogenesis of postnatal microcephaly from congenital Zika virus infections is [still] not known.”
Infants born with laboratory-confirmed congenital Zika virus but who show no signs of microcephaly at birth may still experience a reduction in cranial size as they grow older, according to the Centers for Disease Control and Prevention’s latest Morbidity and Mortality Weekly Report.
“These findings demonstrate the importance of early neuroimaging for infants exposed to Zika virus prenatally and the need for comprehensive medical and developmental follow-up,” wrote Vanessa van der Linden, MD, of the Association for Assistance of Disabled Children in Recife, Brazil, and her coauthors.
Dr. van der Linden and her coinvestigators examined 13 infants, all of whom were born in Brazil between October 2015 and January 2016, who had confirmed brain abnormalities at birth despite having a normal head size. These abnormalities included ventriculomegaly, subcortical calcifications, cortical malformations, and decreased brain volume. Investigators defined microcephaly as being “head circumference (HC) [that’s] more than 2 [standard deviations] below the mean for gestational age and sex.”
Nine of the infants were male, four were female. Eleven of the infants were born within 37-41 weeks’ of gestation. The remaining two were born at 35-36 weeks’ of gestation, considered “preterm” by the investigators. All infants tested positive for Zika via immunoglobulin M testing of cerebrospinal fluid, serum, or both. Only six of the mothers reported having a rash while pregnant; four reported experiencing it during the first trimester, while the other two said it occurred in the second.
All 13 infants showed a decrease in HC to what was defined as microcephaly within 1 year of birth (October 2016). Neuroimaging showed that all but one had decreased brain volume, all had malformations of cortical development, four had cerebellum or brain-stem hypoplasia, ten had ventriculomegaly, and three had increased extra-axial CSF space.
“More than 60% of infants in this series had epilepsy (likely related to the cortical malformations), and all had significant motor disabilities consistent with mixed cerebral palsy,” the authors noted, adding that the “pathogenesis of postnatal microcephaly from congenital Zika virus infections is [still] not known.”
FROM THE MMWR
Wide spectrum of feeding problems poses challenge for clinicians
SAN FRANCISCO – Clinicians are likely to encounter diverse feeding problems in daily practice that will challenge their diagnostic and treatment acumen, Dr. Irene Chatoor told attendees of the annual meeting of the American Academy of Pediatrics.
These problems run the gamut from the most prevalent but least serious picky eating, to the least prevalent but most serious feeding disorders, she noted. Correspondingly, management will range from simple reassurance of parents to more intensive behavioral and medical interventions.
Assessment
“When you assess a feeding problem, you have to look at both the mother and father, and the child,” she advised. The parents are evaluated for their feeding style, while the child is evaluated for three feeding problems: limited appetite, selective intake, and fear of feeding (Pediatrics. 2015;135[2]:344-53).
Clinicians must be alert for organic red flags, such as dysphagia, aspiration, and vomiting, and for behavioral red flags, such as food fixation, abrupt cessation of feeding after a trigger event, and anticipatory gagging. An overarching red flag is failure to thrive.
Sometimes, a child will have both an organic condition and a behavioral feeding disorder at the same time. “It’s very important that you don’t think one excludes the other,” she cautioned.
Diagnosis
“To delineate milder feeding difficulties from feeding disorders, there must be some form of impairment caused by the feeding problem,” Dr. Chatoor commented. “Why is this important? For two reasons. One is for the insurance companies, because they don’t pay unless there is a disorder. And then there is research: you cannot do research unless you clearly define what you are studying.”
Children are considered to have impairment if they have weight loss or growth faltering, considerable nutritional deficiency, or a marked interference with psychosocial functioning.
“When we diagnose feeding problems, it is best done with a multidisciplinary team,” Dr. Chatoor maintained. “I have learned many years ago that I’m not effective in helping parents deal with the feeding disorder if they are still in the back of their mind worried that the child has something organically wrong and that’s why the child does not want to eat.”
Accordingly, various team members perform a medical examination, a nutritional assessment, an oral motor and sensory evaluation, and a psychiatric or psychological assessment to identify the root cause or causes of the problem.
When it comes to behavioral etiologies, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) now groups all feeding and eating disorders together in one section, reflecting the fact that disorders starting early in life can and often do track into adolescence and adulthood, according to Dr. Chatoor.
The manual also features a new diagnosis, avoidant/restrictive food intake disorder (ARFID). Key criteria include the presence of an eating or feeding disturbance that cannot be better explained by lack of available food, culturally sanctioned practices, or a concurrent medical condition or another mental disorder.
The child must have a persistent failure to meet appropriate nutritional and/or energy needs, associated with any of four findings: significant weight loss or failure to achieve expected weight gain or growth, significant nutritional deficiencies, dependence on enteral feeding or oral nutritional supplements, and marked interference with psychosocial functioning.
“You need to have at least one but often you have a combination of nutritional and emotional impairment in the same child,” she commented.
ARFID and its treatment
There are three subtypes of ARFID having different features, treatments, and prognosis, although they all share in common food refusal, according to Dr. Chatoor.
The first subtype – apparent lack of interest in eating or food – emerges by 3 years of age, most often during the transition to self-feeding between 9 and 18 months. Affected children refuse to eat an adequate amount of food for at least 1 month, rarely communicate hunger, lack interest in food, and prefer to play or talk. They typically present with growth deficiency.
“If you have a child who refuses to eat, it generates anxiety in the mother. The mother does things she would not normally do with the child who is eating well. She starts to distract, to cajole, to sometimes even force-feed the child,” Dr. Chatoor explained. “And the more she engages in these behaviors, the more resistant the child becomes. So they become trapped in this vicious cycle.”
Treatment is aimed at removing this conflict with three approaches: explaining to parents the infant’s special temperament (notably, high arousal and difficulty turning off excitement); addressing their background, including any eating issues of their own, and difficulty with setting limits; and providing specific feeding guidelines and a time-out procedure.
The guidelines stress regular feeding, withholding of all snacks, keeping the child at the table for 20 to 30 minutes, and not using any distractions or pressure. Also, importantly, the parents should have dinner with their child. “I always tell the parents what is good for the child is good for you. It’s good for your whole family,” she said. “If they have other children, these rules apply to everybody. Young children learn to eat by watching their parents eating.”
With early and consistent use of these interventions, about two-thirds of children outgrow this eating/feeding disturbance by mid-childhood, according to Dr. Chatoor.
Children with the second subtype of ARFID – avoidance based on the sensory characteristics of food – consistently refuse to eat certain foods having specific tastes, textures, temperatures, smells, and/or appearances. Onset occurs during the toddler years, when a new or different food is introduced.
“Not only do they refuse the same foods that were aversive, but they also generalize it. So these children are afraid to try other foods and they may end up limiting food groups – they don’t eat any vegetables and some of them don’t eat any meats,” she explained. “They are a challenge because this always causes a nutritional deficiency and they also have problems socially as they get older.”
Treatment varies by age, with gradual desensitization for infants and parent modeling of eating new foods for toddlers. A multifaceted approach is used for preschoolers, combining modeling, giving foods attractive shapes and names, having the child participate in food preparation, and using focused play therapy, such as feeding dolls who are “brave” and try new foods.
Clinicians can explain to affected school-aged children that they are “supertasters,” having more taste buds and therefore experiencing food more intensely, and that they can help their taste buds not react so strongly by starting to eat small amounts of new foods and gradually increasing over time. Parents can let the child make a list of 10 foods they would like to eat, and award them points for “courage” for every bite of a new food they try.
Prognosis of this type of ARFID varies, according to Dr. Chatoor. “Through gradual exposure, young children can expand the variety of foods they eat,” she elaborated. However, “some children become very rigid and brand sensitive in regard to the food they are willing to eat and begin to experience social problems during mid-childhood and adolescence. Some children grow up eating a limited diet, but finding ways to compensate nutritionally and socially.”
Children with the third subtype of ARFID – concern about aversive consequences of eating – have an acute onset of consistent food refusal at any age, from infancy onward, after experiencing a traumatic event or repeated traumatic insults to the oropharynx or gastrointestinal tract that trigger distress in the child. These children often have comorbidities such as gastroesophageal reflux, eosinophilic gastroenteritis, or anxiety disorder.
“Treatment involves gradual desensitization to feared objects: the highchair, bib, bottle, or spoon,” Dr. Chatoor explained. “It also involves training of the mother in behavioral techniques to feed the child in spite of the child’s fear and distress.”
Any underlying medical condition causing pain or distress should be treated. Additional measures may include, for example, use of a graduated approach, starting with liquids and progressing to purees, if the child fears solid foods, and prescribing anxiolytic medication in cases of severe anxiety.
Dr. Chatoor disclosed that she has lectured internationally at conferences on feeding disorders that were organized by Abbott Nutrition International and that the company provided a research grant for a study on feeding.
SAN FRANCISCO – Clinicians are likely to encounter diverse feeding problems in daily practice that will challenge their diagnostic and treatment acumen, Dr. Irene Chatoor told attendees of the annual meeting of the American Academy of Pediatrics.
These problems run the gamut from the most prevalent but least serious picky eating, to the least prevalent but most serious feeding disorders, she noted. Correspondingly, management will range from simple reassurance of parents to more intensive behavioral and medical interventions.
Assessment
“When you assess a feeding problem, you have to look at both the mother and father, and the child,” she advised. The parents are evaluated for their feeding style, while the child is evaluated for three feeding problems: limited appetite, selective intake, and fear of feeding (Pediatrics. 2015;135[2]:344-53).
Clinicians must be alert for organic red flags, such as dysphagia, aspiration, and vomiting, and for behavioral red flags, such as food fixation, abrupt cessation of feeding after a trigger event, and anticipatory gagging. An overarching red flag is failure to thrive.
Sometimes, a child will have both an organic condition and a behavioral feeding disorder at the same time. “It’s very important that you don’t think one excludes the other,” she cautioned.
Diagnosis
“To delineate milder feeding difficulties from feeding disorders, there must be some form of impairment caused by the feeding problem,” Dr. Chatoor commented. “Why is this important? For two reasons. One is for the insurance companies, because they don’t pay unless there is a disorder. And then there is research: you cannot do research unless you clearly define what you are studying.”
Children are considered to have impairment if they have weight loss or growth faltering, considerable nutritional deficiency, or a marked interference with psychosocial functioning.
“When we diagnose feeding problems, it is best done with a multidisciplinary team,” Dr. Chatoor maintained. “I have learned many years ago that I’m not effective in helping parents deal with the feeding disorder if they are still in the back of their mind worried that the child has something organically wrong and that’s why the child does not want to eat.”
Accordingly, various team members perform a medical examination, a nutritional assessment, an oral motor and sensory evaluation, and a psychiatric or psychological assessment to identify the root cause or causes of the problem.
When it comes to behavioral etiologies, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) now groups all feeding and eating disorders together in one section, reflecting the fact that disorders starting early in life can and often do track into adolescence and adulthood, according to Dr. Chatoor.
The manual also features a new diagnosis, avoidant/restrictive food intake disorder (ARFID). Key criteria include the presence of an eating or feeding disturbance that cannot be better explained by lack of available food, culturally sanctioned practices, or a concurrent medical condition or another mental disorder.
The child must have a persistent failure to meet appropriate nutritional and/or energy needs, associated with any of four findings: significant weight loss or failure to achieve expected weight gain or growth, significant nutritional deficiencies, dependence on enteral feeding or oral nutritional supplements, and marked interference with psychosocial functioning.
“You need to have at least one but often you have a combination of nutritional and emotional impairment in the same child,” she commented.
ARFID and its treatment
There are three subtypes of ARFID having different features, treatments, and prognosis, although they all share in common food refusal, according to Dr. Chatoor.
The first subtype – apparent lack of interest in eating or food – emerges by 3 years of age, most often during the transition to self-feeding between 9 and 18 months. Affected children refuse to eat an adequate amount of food for at least 1 month, rarely communicate hunger, lack interest in food, and prefer to play or talk. They typically present with growth deficiency.
“If you have a child who refuses to eat, it generates anxiety in the mother. The mother does things she would not normally do with the child who is eating well. She starts to distract, to cajole, to sometimes even force-feed the child,” Dr. Chatoor explained. “And the more she engages in these behaviors, the more resistant the child becomes. So they become trapped in this vicious cycle.”
Treatment is aimed at removing this conflict with three approaches: explaining to parents the infant’s special temperament (notably, high arousal and difficulty turning off excitement); addressing their background, including any eating issues of their own, and difficulty with setting limits; and providing specific feeding guidelines and a time-out procedure.
The guidelines stress regular feeding, withholding of all snacks, keeping the child at the table for 20 to 30 minutes, and not using any distractions or pressure. Also, importantly, the parents should have dinner with their child. “I always tell the parents what is good for the child is good for you. It’s good for your whole family,” she said. “If they have other children, these rules apply to everybody. Young children learn to eat by watching their parents eating.”
With early and consistent use of these interventions, about two-thirds of children outgrow this eating/feeding disturbance by mid-childhood, according to Dr. Chatoor.
Children with the second subtype of ARFID – avoidance based on the sensory characteristics of food – consistently refuse to eat certain foods having specific tastes, textures, temperatures, smells, and/or appearances. Onset occurs during the toddler years, when a new or different food is introduced.
“Not only do they refuse the same foods that were aversive, but they also generalize it. So these children are afraid to try other foods and they may end up limiting food groups – they don’t eat any vegetables and some of them don’t eat any meats,” she explained. “They are a challenge because this always causes a nutritional deficiency and they also have problems socially as they get older.”
Treatment varies by age, with gradual desensitization for infants and parent modeling of eating new foods for toddlers. A multifaceted approach is used for preschoolers, combining modeling, giving foods attractive shapes and names, having the child participate in food preparation, and using focused play therapy, such as feeding dolls who are “brave” and try new foods.
Clinicians can explain to affected school-aged children that they are “supertasters,” having more taste buds and therefore experiencing food more intensely, and that they can help their taste buds not react so strongly by starting to eat small amounts of new foods and gradually increasing over time. Parents can let the child make a list of 10 foods they would like to eat, and award them points for “courage” for every bite of a new food they try.
Prognosis of this type of ARFID varies, according to Dr. Chatoor. “Through gradual exposure, young children can expand the variety of foods they eat,” she elaborated. However, “some children become very rigid and brand sensitive in regard to the food they are willing to eat and begin to experience social problems during mid-childhood and adolescence. Some children grow up eating a limited diet, but finding ways to compensate nutritionally and socially.”
Children with the third subtype of ARFID – concern about aversive consequences of eating – have an acute onset of consistent food refusal at any age, from infancy onward, after experiencing a traumatic event or repeated traumatic insults to the oropharynx or gastrointestinal tract that trigger distress in the child. These children often have comorbidities such as gastroesophageal reflux, eosinophilic gastroenteritis, or anxiety disorder.
“Treatment involves gradual desensitization to feared objects: the highchair, bib, bottle, or spoon,” Dr. Chatoor explained. “It also involves training of the mother in behavioral techniques to feed the child in spite of the child’s fear and distress.”
Any underlying medical condition causing pain or distress should be treated. Additional measures may include, for example, use of a graduated approach, starting with liquids and progressing to purees, if the child fears solid foods, and prescribing anxiolytic medication in cases of severe anxiety.
Dr. Chatoor disclosed that she has lectured internationally at conferences on feeding disorders that were organized by Abbott Nutrition International and that the company provided a research grant for a study on feeding.
SAN FRANCISCO – Clinicians are likely to encounter diverse feeding problems in daily practice that will challenge their diagnostic and treatment acumen, Dr. Irene Chatoor told attendees of the annual meeting of the American Academy of Pediatrics.
These problems run the gamut from the most prevalent but least serious picky eating, to the least prevalent but most serious feeding disorders, she noted. Correspondingly, management will range from simple reassurance of parents to more intensive behavioral and medical interventions.
Assessment
“When you assess a feeding problem, you have to look at both the mother and father, and the child,” she advised. The parents are evaluated for their feeding style, while the child is evaluated for three feeding problems: limited appetite, selective intake, and fear of feeding (Pediatrics. 2015;135[2]:344-53).
Clinicians must be alert for organic red flags, such as dysphagia, aspiration, and vomiting, and for behavioral red flags, such as food fixation, abrupt cessation of feeding after a trigger event, and anticipatory gagging. An overarching red flag is failure to thrive.
Sometimes, a child will have both an organic condition and a behavioral feeding disorder at the same time. “It’s very important that you don’t think one excludes the other,” she cautioned.
Diagnosis
“To delineate milder feeding difficulties from feeding disorders, there must be some form of impairment caused by the feeding problem,” Dr. Chatoor commented. “Why is this important? For two reasons. One is for the insurance companies, because they don’t pay unless there is a disorder. And then there is research: you cannot do research unless you clearly define what you are studying.”
Children are considered to have impairment if they have weight loss or growth faltering, considerable nutritional deficiency, or a marked interference with psychosocial functioning.
“When we diagnose feeding problems, it is best done with a multidisciplinary team,” Dr. Chatoor maintained. “I have learned many years ago that I’m not effective in helping parents deal with the feeding disorder if they are still in the back of their mind worried that the child has something organically wrong and that’s why the child does not want to eat.”
Accordingly, various team members perform a medical examination, a nutritional assessment, an oral motor and sensory evaluation, and a psychiatric or psychological assessment to identify the root cause or causes of the problem.
When it comes to behavioral etiologies, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) now groups all feeding and eating disorders together in one section, reflecting the fact that disorders starting early in life can and often do track into adolescence and adulthood, according to Dr. Chatoor.
The manual also features a new diagnosis, avoidant/restrictive food intake disorder (ARFID). Key criteria include the presence of an eating or feeding disturbance that cannot be better explained by lack of available food, culturally sanctioned practices, or a concurrent medical condition or another mental disorder.
The child must have a persistent failure to meet appropriate nutritional and/or energy needs, associated with any of four findings: significant weight loss or failure to achieve expected weight gain or growth, significant nutritional deficiencies, dependence on enteral feeding or oral nutritional supplements, and marked interference with psychosocial functioning.
“You need to have at least one but often you have a combination of nutritional and emotional impairment in the same child,” she commented.
ARFID and its treatment
There are three subtypes of ARFID having different features, treatments, and prognosis, although they all share in common food refusal, according to Dr. Chatoor.
The first subtype – apparent lack of interest in eating or food – emerges by 3 years of age, most often during the transition to self-feeding between 9 and 18 months. Affected children refuse to eat an adequate amount of food for at least 1 month, rarely communicate hunger, lack interest in food, and prefer to play or talk. They typically present with growth deficiency.
“If you have a child who refuses to eat, it generates anxiety in the mother. The mother does things she would not normally do with the child who is eating well. She starts to distract, to cajole, to sometimes even force-feed the child,” Dr. Chatoor explained. “And the more she engages in these behaviors, the more resistant the child becomes. So they become trapped in this vicious cycle.”
Treatment is aimed at removing this conflict with three approaches: explaining to parents the infant’s special temperament (notably, high arousal and difficulty turning off excitement); addressing their background, including any eating issues of their own, and difficulty with setting limits; and providing specific feeding guidelines and a time-out procedure.
The guidelines stress regular feeding, withholding of all snacks, keeping the child at the table for 20 to 30 minutes, and not using any distractions or pressure. Also, importantly, the parents should have dinner with their child. “I always tell the parents what is good for the child is good for you. It’s good for your whole family,” she said. “If they have other children, these rules apply to everybody. Young children learn to eat by watching their parents eating.”
With early and consistent use of these interventions, about two-thirds of children outgrow this eating/feeding disturbance by mid-childhood, according to Dr. Chatoor.
Children with the second subtype of ARFID – avoidance based on the sensory characteristics of food – consistently refuse to eat certain foods having specific tastes, textures, temperatures, smells, and/or appearances. Onset occurs during the toddler years, when a new or different food is introduced.
“Not only do they refuse the same foods that were aversive, but they also generalize it. So these children are afraid to try other foods and they may end up limiting food groups – they don’t eat any vegetables and some of them don’t eat any meats,” she explained. “They are a challenge because this always causes a nutritional deficiency and they also have problems socially as they get older.”
Treatment varies by age, with gradual desensitization for infants and parent modeling of eating new foods for toddlers. A multifaceted approach is used for preschoolers, combining modeling, giving foods attractive shapes and names, having the child participate in food preparation, and using focused play therapy, such as feeding dolls who are “brave” and try new foods.
Clinicians can explain to affected school-aged children that they are “supertasters,” having more taste buds and therefore experiencing food more intensely, and that they can help their taste buds not react so strongly by starting to eat small amounts of new foods and gradually increasing over time. Parents can let the child make a list of 10 foods they would like to eat, and award them points for “courage” for every bite of a new food they try.
Prognosis of this type of ARFID varies, according to Dr. Chatoor. “Through gradual exposure, young children can expand the variety of foods they eat,” she elaborated. However, “some children become very rigid and brand sensitive in regard to the food they are willing to eat and begin to experience social problems during mid-childhood and adolescence. Some children grow up eating a limited diet, but finding ways to compensate nutritionally and socially.”
Children with the third subtype of ARFID – concern about aversive consequences of eating – have an acute onset of consistent food refusal at any age, from infancy onward, after experiencing a traumatic event or repeated traumatic insults to the oropharynx or gastrointestinal tract that trigger distress in the child. These children often have comorbidities such as gastroesophageal reflux, eosinophilic gastroenteritis, or anxiety disorder.
“Treatment involves gradual desensitization to feared objects: the highchair, bib, bottle, or spoon,” Dr. Chatoor explained. “It also involves training of the mother in behavioral techniques to feed the child in spite of the child’s fear and distress.”
Any underlying medical condition causing pain or distress should be treated. Additional measures may include, for example, use of a graduated approach, starting with liquids and progressing to purees, if the child fears solid foods, and prescribing anxiolytic medication in cases of severe anxiety.
Dr. Chatoor disclosed that she has lectured internationally at conferences on feeding disorders that were organized by Abbott Nutrition International and that the company provided a research grant for a study on feeding.
EXPERT ANALYSIS FROM AAP 16
Roommates
The American Academy of Pediatrics has recently released a new policy for parents on safe sleep practices that in addition to the previous warnings about bed sharing and positioning includes the recommendation that an infant sleep in the same room as her parent for at least the first 6 months (Pediatrics. 2016 Oct;138[5]:e20162938). Apparently what prompted this new set of recommendations is the observation that deaths from sudden unexpected infant deaths (SUIDS) and sudden infant deaths (SIDS) has plateaued since the dramatic decline we witnessed in the 1990s following the Back-to-Sleep campaign.
Although the policy statement refers to “new research” that has become available since the last policy statement was released in 2011, I have had trouble finding convincing evidence in the references I reviewed to support the room sharing recommendation. In some studies, room sharing was the cultural norm, making it difficult to establish a control group. In one of the most frequently cited papers from New Zealand, the authors could not sort out the effects of prone sleeping and sleeping alone, and wonder whether both factors may be affecting risk “through a common mechanism” (Lancet. 1996 Jan 6;347[8993]:7-12).
For some, parents attempting to follow this recommendation may not be without its negative consequences. Sleeping like a baby is not the same as sleeping quietly. Infants often breathe in a pattern that includes long, anxiety-provoking pauses. The implication of this policy recommendation is that parents can prevent crib death by being more vigilant at night. Do we have enough evidence that this is indeed the case?
Most parents are already anxious, and none of them are getting enough sleep. I can envision that trying to follow this recommendation could aggravate both conditions for some parents. Sleep-deprived parents often are not as capable parents as they could be. And they certainly aren’t as happy as they could be. Postpartum depression compounded by sleep deprivation continues to be an underreported and inadequately managed condition that can have negative effects for the health of the child.
For some parents, room sharing is something they gravitate toward naturally, and it can help them deal with the anxiety of new parenthood. They may sleep better with their infant close by. But for others, the better solution to their own sleep deprivation lies in sleep training, a strategy that is very difficult, if not impossible, for parents who are sharing their bedroom with their infant.
As the authors of one of the most frequently quoted papers that supports room sharing have written, “the traditional habit of labeling one sleep arrangement as being superior to another without awareness of the family context is not only wrong but potentially harmful” (Paediatric Resp Review. 2005, Jun;6[2]:134-52).
I think the academy has gone too far or at least moved prematurely with its room sharing recommendation. For some families, room sharing is a better arrangement, for others it is not. It may well be that the plateau in crib deaths is telling us that we have reached the limits of our abilities to effect any further decline with our recommendations about sleep environments. But more research needs to be done.
On a more positive note, the new recommendation may force parents to reevaluate their habit of having a television in their bedroom. Will it be baby or TV in the bedroom? Unfortunately, I fear too many will opt to have both.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
The American Academy of Pediatrics has recently released a new policy for parents on safe sleep practices that in addition to the previous warnings about bed sharing and positioning includes the recommendation that an infant sleep in the same room as her parent for at least the first 6 months (Pediatrics. 2016 Oct;138[5]:e20162938). Apparently what prompted this new set of recommendations is the observation that deaths from sudden unexpected infant deaths (SUIDS) and sudden infant deaths (SIDS) has plateaued since the dramatic decline we witnessed in the 1990s following the Back-to-Sleep campaign.
Although the policy statement refers to “new research” that has become available since the last policy statement was released in 2011, I have had trouble finding convincing evidence in the references I reviewed to support the room sharing recommendation. In some studies, room sharing was the cultural norm, making it difficult to establish a control group. In one of the most frequently cited papers from New Zealand, the authors could not sort out the effects of prone sleeping and sleeping alone, and wonder whether both factors may be affecting risk “through a common mechanism” (Lancet. 1996 Jan 6;347[8993]:7-12).
For some, parents attempting to follow this recommendation may not be without its negative consequences. Sleeping like a baby is not the same as sleeping quietly. Infants often breathe in a pattern that includes long, anxiety-provoking pauses. The implication of this policy recommendation is that parents can prevent crib death by being more vigilant at night. Do we have enough evidence that this is indeed the case?
Most parents are already anxious, and none of them are getting enough sleep. I can envision that trying to follow this recommendation could aggravate both conditions for some parents. Sleep-deprived parents often are not as capable parents as they could be. And they certainly aren’t as happy as they could be. Postpartum depression compounded by sleep deprivation continues to be an underreported and inadequately managed condition that can have negative effects for the health of the child.
For some parents, room sharing is something they gravitate toward naturally, and it can help them deal with the anxiety of new parenthood. They may sleep better with their infant close by. But for others, the better solution to their own sleep deprivation lies in sleep training, a strategy that is very difficult, if not impossible, for parents who are sharing their bedroom with their infant.
As the authors of one of the most frequently quoted papers that supports room sharing have written, “the traditional habit of labeling one sleep arrangement as being superior to another without awareness of the family context is not only wrong but potentially harmful” (Paediatric Resp Review. 2005, Jun;6[2]:134-52).
I think the academy has gone too far or at least moved prematurely with its room sharing recommendation. For some families, room sharing is a better arrangement, for others it is not. It may well be that the plateau in crib deaths is telling us that we have reached the limits of our abilities to effect any further decline with our recommendations about sleep environments. But more research needs to be done.
On a more positive note, the new recommendation may force parents to reevaluate their habit of having a television in their bedroom. Will it be baby or TV in the bedroom? Unfortunately, I fear too many will opt to have both.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
The American Academy of Pediatrics has recently released a new policy for parents on safe sleep practices that in addition to the previous warnings about bed sharing and positioning includes the recommendation that an infant sleep in the same room as her parent for at least the first 6 months (Pediatrics. 2016 Oct;138[5]:e20162938). Apparently what prompted this new set of recommendations is the observation that deaths from sudden unexpected infant deaths (SUIDS) and sudden infant deaths (SIDS) has plateaued since the dramatic decline we witnessed in the 1990s following the Back-to-Sleep campaign.
Although the policy statement refers to “new research” that has become available since the last policy statement was released in 2011, I have had trouble finding convincing evidence in the references I reviewed to support the room sharing recommendation. In some studies, room sharing was the cultural norm, making it difficult to establish a control group. In one of the most frequently cited papers from New Zealand, the authors could not sort out the effects of prone sleeping and sleeping alone, and wonder whether both factors may be affecting risk “through a common mechanism” (Lancet. 1996 Jan 6;347[8993]:7-12).
For some, parents attempting to follow this recommendation may not be without its negative consequences. Sleeping like a baby is not the same as sleeping quietly. Infants often breathe in a pattern that includes long, anxiety-provoking pauses. The implication of this policy recommendation is that parents can prevent crib death by being more vigilant at night. Do we have enough evidence that this is indeed the case?
Most parents are already anxious, and none of them are getting enough sleep. I can envision that trying to follow this recommendation could aggravate both conditions for some parents. Sleep-deprived parents often are not as capable parents as they could be. And they certainly aren’t as happy as they could be. Postpartum depression compounded by sleep deprivation continues to be an underreported and inadequately managed condition that can have negative effects for the health of the child.
For some parents, room sharing is something they gravitate toward naturally, and it can help them deal with the anxiety of new parenthood. They may sleep better with their infant close by. But for others, the better solution to their own sleep deprivation lies in sleep training, a strategy that is very difficult, if not impossible, for parents who are sharing their bedroom with their infant.
As the authors of one of the most frequently quoted papers that supports room sharing have written, “the traditional habit of labeling one sleep arrangement as being superior to another without awareness of the family context is not only wrong but potentially harmful” (Paediatric Resp Review. 2005, Jun;6[2]:134-52).
I think the academy has gone too far or at least moved prematurely with its room sharing recommendation. For some families, room sharing is a better arrangement, for others it is not. It may well be that the plateau in crib deaths is telling us that we have reached the limits of our abilities to effect any further decline with our recommendations about sleep environments. But more research needs to be done.
On a more positive note, the new recommendation may force parents to reevaluate their habit of having a television in their bedroom. Will it be baby or TV in the bedroom? Unfortunately, I fear too many will opt to have both.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].