Faculty Bibliography

OBJECTIVE: Given the prevalence of mental health (MH) conditions (MHC) in children, pediatricians should initiate treatment alone or in collaboration with a specialist for children with MHC. However, the majority of pediatricians do not manage or comanage common MHC even with an on-site MH provider. We examined which physician, practice, and training characteristics are associated with pediatricians' comanaging at least half of their patients with MHC. METHODS: We analyzed responses of general pediatricians (n = 305) from the American Academy of Pediatrics 2013 Periodic Survey. Practice characteristics include presence of an on-site MH provider and perceived access to services. Independent variables included sociodemographics, training experiences, and interest in further training. The outcome was comanagement of >/=50% of patients with MHC. Weighted univariate, bivariate, and multivariable analyses were performed. RESULTS: Of the pediatricians who reported comanaging >/=50% of their patients with MHC, logistic regression analysis showed that pediatricians who completed >/=4 weeks of developmental behavioral pediatrics training had 1.8 increased odds (95% confidence interval 1.06, 3.08, P = .03) of comanagement, those very interested in further education in managing/treating MHC had 2.75 increased odds (95% confidence interval 1.63, 3.08, P < .001), and those with more training in MH treatment with medications had 1.4 increased odds (95% confidence interval 1.12, 1.75, P = .004) of comanaging children with MHC. CONCLUSIONS: Specific educational experiences and interest in further education in managing or treating MHC were significantly associated with comanaging >/=50% of patients, suggesting that enhanced MH training among pediatricians could increase the comanagement of children with MHC.

PURPOSE OF REVIEW: Post-traumatic headache (PTH) is a common headache type after traumatic brain injury (TBI). There are no FDA approved medications for PTH, and it is unknown how medications can affect the brain's ability to recover from TBI. Thus, we sought to examine the biopsychosocial factors that influence PTH and the non-pharmacologic treatments studied for headache treatment. We also sought to determine if there is literature examining whether the non-pharmacologic treatments influence the biopsychosocial factors. The non-pharmacologic treatments assessed included cognitive behavioral therapy (CBT), biofeedback, progressive muscle relaxation therapy (PMR), acupuncture, and physical therapy (PT). RECENT FINDINGS: Factors associated with prognosis in PTH may include the following: severity of TBI, stress, post-traumatic stress disorder, other psychiatric comorbidities, sociocultural and psychosocial factors, litigation, base rate misattribution, expectation as etiology, and chronic pain. There are few high quality studies on the non-pharmacologic treatments for PTH. Thermal and EMG biofeedback appear to have been examined the most followed by CBT. Studies did not have secondary outcomes examining the psychosocial factors related to PTH. Most of the behavioral studies involved a multi-modality intervention limiting the ability to assess the individual non-pharmacologic interventions we sought to study. There were very few randomized clinical trials evaluating the efficacy of non-pharmacologic interventions. Therefore, future research, which considers the noted biopsychosocial factors, is needed in the field to determine if these interventions reduce PTH.

The current study examines the longitudinal patterns of both cigarette smoking and depressive symptoms as predictors of generalized anxiety disorder (GAD) using data from the Harlem Longitudinal Development Study. There were 674 African American (53%) and Puerto Rican (47%) participants. Among the 674 participants, 60% were females. In the logistic regression analyses, the indicator variables of membership in each of the joint trajectories of cigarette smoking and depressive symptoms from the mid 20s to the mid 30s were used as the independent variables, and the diagnosis of GAD in the mid 30s was used as the dependent variable. The high cigarette smoking with high depressive symptoms group and the low cigarette smoking with high depressive symptoms group were associated with an increased likelihood of having GAD as compared to the no cigarette smoking with low depressive symptoms group. The findings shed light on the prevention and treatment of GAD.

Idiopathic granulomatous mastitis (IGM) is a chronic inflammatory disease characterized by tender, erythematous, indurated breast plaques with associated edema, drainage, and scar formation.1 IGM is often mistaken for breast carcinoma or infectious mastitis.1,2 Histopathology readily distinguishes IGM from breast carcinoma, as the primary finding in IGM is granulomas centered around mammary lobules.3 Nevertheless, differentiating IGM from bacterial mastitis and other mimickers, such as atypical mycobacterial infections or sarcoidosis, can be more difficult.4 Herein, we report the largest case series of concurrent IGM and erythema nodosum (EN)

OBJECTIVES: We examined whether the cut-point 10 for the Patient Health Questionnaire-9 (PHQ9) depression screen used in primary care populations is equally valid for Mexicans (M), Ecuadorians (E), Puerto Ricans (PR) and non-Hispanic whites (W) from inner-city hospital-based primary care clinics; and whether stressful life events elevate scores and the probability of major depressive disorder (MDD). METHODS: Over 18-months, a sample of persons from hospital clinics with a positive initial PHQ2 and a subsequent PHQ9 were administered a stressful life event questionnaire and a Structured Clinical Interview to establish an MDD diagnosis, with oversampling of those between 8 and 12: (n=261: 75 E, 71 M, 51 PR, 64 W). For analysis, the sample was weighted using chart review (n=368) to represent a typical clinic population. Receiver Operating Characteristics analysis selected cut-points maximizing sensitivity (Sn) plus specificity (Sp). RESULTS: The optimal cut-point for all groups was 13 with the corresponding Sn and Sp estimates for E=(Sn 73%, Sp 71%), M=(76%, 81%), PR=(81%, 63%) and W=(80%, 74%). Stressful life events impacted screen scores and MDD diagnosis. CONCLUSIONS: Elevating the PHQ9 cut-point for inner-city Latinos as well as whites is suggested to avoid high false positive rates leading to improper treatment with clinical and economic consequences.

BACKGROUND: Many hospitalized patients have at least 1 chronic disease that is not optimally controlled. The purpose of this study was to explore inpatient provider attitudes about chronic disease management and, in particular, barriers and facilitators of chronic disease management in the hospital. METHODS: We conducted a qualitative study of semi-structured interviews of 31 inpatient providers from an academic medical center. We interviewed attending physicians, resident physicians, physician assistants, and nurse practitioners from various specialties about attitudes, experiences with, and barriers and facilitators towards chronic disease management in the hospital. Qualitative data were analyzed using constant comparative analysis. RESULTS: Providers perceived that hospitalizations offer an opportunity to improve chronic disease management, as patients are evaluated by a new care team and observed in a controlled environment. Providers perceived clinical benefits to in-hospital chronic care, including improvements in readmission and length of stay, but expressed concerns for risks related to adverse events and distraction from the acute problem. Barriers included provider lack of comfort with managing chronic diseases, poor communication between inpatient and outpatient providers, and hospital-system focus on patient discharge. A strong relationship with the outpatient provider and involvement of specialists were facilitators of inpatient chronic disease management. CONCLUSIONS: Providers perceived benefits to in-hospital chronic disease management for both processes of care and clinical outcomes. Efforts to increase inpatient chronic disease management will need to overcome barriers in multiple domains. Journal of Hospital Medicine 2017;12:162-167.

BACKGROUND: Previous studies identified associations between maternal obesity and childhood neurodevelopment, but few examined paternal obesity despite potentially distinct genetic/epigenetic effects related to developmental programming. METHODS: Upstate KIDS (2008-2010) recruited mothers from New York State (excluding New York City) at approximately 4 months postpartum. Parents completed the Ages and Stages Questionnaire (ASQ) when their children were 4, 8, 12, 18, 24, 30, and 36 months of age corrected for gestation. The ASQ is validated to screen for delays in 5 developmental domains (ie, fine motor, gross motor, communication, personal-social functioning, and problem-solving ability). Analyses included 3759 singletons and 1062 nonrelated twins with >/=1 ASQs returned. Adjusted odds ratios (aORs) and 95% confidence intervals were estimated by using generalized linear mixed models accounting for maternal covariates (ie, age, race, education, insurance, marital status, parity, and pregnancy smoking). RESULTS: Compared with normal/underweight mothers (BMI <25), children of obese mothers (26% with BMI >/=30) had increased odds of failing the fine motor domain (aOR 1.67; confidence interval 1.12-2.47). The association remained after additional adjustment for paternal BMI (1.67; 1.11-2.52). Paternal obesity (29%) was associated with increased risk of failing the personal-social domain (1.75; 1.13-2.71), albeit attenuated after adjustment for maternal obesity (aOR 1.71; 1.08-2.70). Children whose parents both had BMI >/=35 were likely to additionally fail the problem-solving domain (2.93; 1.09-7.85). CONCLUSIONS: Findings suggest that maternal and paternal obesity are each associated with specific delays in early childhood development, emphasizing the importance of family information when screening child development.

In a longitudinal population-based study of 2,905 children, we investigated if infants' neuromotor development was associated with autistic traits in childhood. Overall motor development and muscle tone were examined by trained research assistants with an adapted version of Touwen's Neurodevelopmental Examination between ages 2 and 5 months. Tone was assessed in several positions and items were scored as normal, low, or high tone. Parents rated their children's autistic traits with the Social Responsiveness Scale (SRS) and the Pervasive Developmental Problems (PDP) subscale of the Child Behavior Checklist at 6 years. We defined clinical PDP if scores were >98th percentile of the norm population. Diagnosis of autism spectrum disorder (ASD) was clinically confirmed in 30 children. We observed a modest association between overall neuromotor development in infants and autistic traits. Low muscle tone in infancy predicted autistic traits measured by SRS (adjusted beta = 0.05, 95% CI for B: 0.00-0.02, P = 0.01), and PDP (adjusted beta = 0.08, 95% CI for B: 0.04-0.10, P < 0.001). Similar results emerged for the association of low muscle tone and clinical PDP (adjusted OR = 1.36, 95% CI: 1.08-1.72, P = 0.01) at age 6 years. Results remained unchanged if adjusted for child intelligence. There was no association between high muscle tone and SRS or PDP. Exclusion of children with ASD diagnosis did not change the association. This large study showed a prospective association of infant muscle tone with autistic traits in childhood. Our findings suggest that early detection of low muscle tone might be a gateway to improve early diagnosis of ASD. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.

INTRODUCTION: Prenatal smoking exposure may lead to permanent changes in neonatal inflammation and immune response that have lifelong implications, including increased risks for atopy and respiratory disorders. METHODS: The effect of maternal smoking on neonatal biomarkers of inflammation and immune response was assessed among 3459 singletons and twins in the Upstate KIDS Study. The following inflammatory biomarkers were measured using newborn dried blood spots (DBSs): interleukin (IL)-1alpha, IL-1 receptor antagonist, IL-6, IL-8, C-reactive protein, and tumor necrosis factor alpha. Immunoglobulins (IgE, IgA, IgM, and IgG subclasses) were also assessed. We used generalized estimating equations to calculate mean differences (beta) in biomarker levels by timing of pregnancy smoking, cigarette load, and secondhand smoke exposure after adjusting for sociodemographic and lifestyle factors including maternal body mass index. RESULTS: Of the 344 (12%) women reporting smoking during pregnancy, about 40% continued throughout pregnancy and 13% reported smoking more than 1 pack per day. After covariate adjustment and Bonferroni correction for multiple comparisons, maternal smoking throughout pregnancy remained significantly associated with increased levels of IL-8 (beta = 0.20, 95% confidence interval: 0.07, 0.32; p < .003). No significant associations were found with cigarette load or secondhand smoke exposure. Higher IgG3 levels were also associated with maternal smoking throughout pregnancy, although the association became nominally significant after adjustment for covariates (beta = 0.09; 95% confidence interval: 0.0007, 0.17; p < .05). CONCLUSIONS: Maternal smoking throughout pregnancy was independently associated with increased IL-8 levels in newborns. Importantly, neonates of women who stopped smoking anytime in pregnancy did not have increased IL-8 levels. IMPLICATIONS: This study evaluated a range of inflammatory biomarkers and immunoglobulins in association with maternal smoking and timing/duration of smoking along with secondhand smoke exposure. By using DBSs, we present data from a large cohort of children born in Upstate New York. Our findings suggest that early differences in immunoregulation of neonates exposed to maternal smoking for full duration in utero may already be detected at birth.

BACKGROUND/OBJECTIVES: Maternal obesity may influence neonatal and childhood morbidities through increased inflammation and/or altered immune response. Less is known about paternal obesity. We hypothesized that excessive parental weight contributes to elevated inflammation and altered immunoglobulin (Ig) profiles in neonates. SUBJECTS/METHODS: In the Upstate KIDS Study maternal pre-pregnancy body mass index (BMI) was obtained from vital records and paternal BMI from maternal report. Biomarkers were measured from newborn dried blood spots (DBS) among neonates whose parents provided consent. Inflammatory scores were calculated by assigning one point for each of five pro-inflammatory biomarkers above the median and one point for an anti-inflammatory cytokine below the median. Linear regression models and generalized estimating equations were used to estimate mean differences (beta) and 95% confidence intervals (CI) in the inflammatory score and Ig levels by parental overweight/obesity status compared with normal weight. RESULTS: Among 2974 pregnancies, 51% were complicated by excessive maternal weight (BMI>25), 73% by excessive paternal weight and 28% by excessive gestational weight gain. Maternal BMI categories of overweight (BMI 25.0-29.9) and obese class II/III (BMI>/=35) were associated with increased neonatal inflammation scores (beta=0.12, 95% CI: 0.02, 0.21; P=0.02 and beta=0.13, CI: -0.002, 0.26; P=0.05, respectively) but no increase was observed in the obese class I group (BMI 30-34.9). Mothers with class I and class II/III obesity had newborns with increased IgM levels (beta=0.11, CI: 0.04, 0.17; P=0.001 and beta=0.12, CI: 0.05, 0.19); P<0.001, respectively). Paternal groups of overweight, obese class I and obese class II/III had decreased neonatal IgM levels (beta=-0.08, CI: -0.13,-0.03, P=0.001; beta=-0.07, CI: -0.13, -0.01, P=0.029 and beta=-0.11, CI:-0.19,-0.04, P=0.003, respectively). CONCLUSIONS: Excessive maternal weight was generally associated with increased inflammation and IgM supporting previous observations of maternal obesity and immune dysregulation in offspring. The role of paternal obesity requires further study.