Article

Gender differences in presentation and course of disease in pediatric patients with Crohn disease

Department of Pediatrics, The Children's Hospital of Philadelphia, Filadelfia, Pennsylvania, United States
PEDIATRICS (Impact Factor: 5.47). 01/2008; 120(6):e1418-25. DOI: 10.1542/peds.2007-0905
Source: PubMed

ABSTRACT

The objective of this study was to determine gender differences in pediatric patients with Crohn disease.
We conducted a retrospective cohort study of 989 consecutive pediatric patients (566 boys, 423 girls) who had Crohn disease (aged 0 to 17 years at diagnosis) by using the Pediatric IBD Consortium Registry. Uniform data were analyzed to compare the presentation and course of disease according to gender.
Median follow-up time was 2.8 years. Mean +/- SD age at diagnosis of inflammatory bowel disease (11.5 +/- 3.8 years) did not differ by gender. Compared with boys, girls had a higher prevalence of mouth sores at symptom onset and a higher prevalence of hypoalbuminemia at the time of diagnosis. Location of disease did not differ by gender. A higher proportion of girls had abnormal anti-outer membrane porin of Escherichia coli levels compared with boys. Girls were at increased risk for erythema nodosum/pyoderma gangrenosum and decreased risk for growth failure compared with boys.
Girls appear to have an overall more severe course of disease; however, boys are at increased risk for developing growth failure. Disease course and the impact of disease severity on growth according to gender in pediatric Crohn disease require prospective study.

Download full-text

Full-text

Available from: Benjamin D Gold, Apr 20, 2015
  • Source
    • "Another limitation to our study is that we only used male mice to avoid the confounding effects of high levels of estrogens in female mice. Female pediatric patients with CD experience more severe disease course (Gupta et al., 2007 "
    [Show abstract] [Hide abstract]
    ABSTRACT: Crohn's disease (CD) is associated with increased psychiatric co-morbidities. Nitric oxide (NO) is implicated in inflammation and tissue injury in CD, and it may also play a central role in pathogenesis of the accompanying behavioral despair. This study investigated the role of the NO pathway in behavioral despair associated with a mouse model of CD. Colitis was induced by intrarectal (i.r.) injection of 2, 4, 6-trinitrobenzenesulfonic acid (10mg TNBS in 50% ethanol). Forced swimming test (FST), pharmacological studies and tissues collection were performed 72hours following TNBS administration. To address a possible inflammatory origin for the behavioral despair following colitis induction, tumor necrosis factor-alpha (TNF-α) level was measured in both the hippocampal and colonic tissue samples. In parallel, hippocampal inducible nitric oxide synthase (iNOS) and nitrite level were evaluated. Pharmacological studies targeting the NO pathway was performed 30-60 mins before behavioral test. Colitis was confirmed by increased colonic TNF-α level and microscopic score. Colitic mice demonstrated a significantly higher immobility time in the FST associated to a significant increase of hippocampal TNF-α, iNOS expression and nitrite content. Acute NOS inhibition using either Nω-nitro-L-arginine methyl ester (a non-specific NOS inhibitor) or aminoguanidine hydrochloride (a specific iNOS inhibitor) decreased the immobility time in colitic groups. Moreover, acute treatment with both NOS inhibitors decreased the TNF-α level and nitrite content in the hippocampal samples. This study suggests that the NO pathway may be involved in the behavioral effects in the mouse TNBS model of CD. These findings endow new insights into the gut-brain communication during the development of colonic inflammation, which may ultimately lead to improved therapeutic strategies to combat behavior changes associated with gastrointestinal disorders. Copyright © 2015. Published by Elsevier Inc.
    Full-text · Article · Aug 2015 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
  • Source
    • "Another limitation to our study is that we only used male mice to avoid the confounding effects of high levels of estrogens in female mice. Female pediatric patients with CD experience more severe disease course (Gupta et al., 2007). Consistently, Alex et al. observed elevations in IL-6 and IL-12 in the females relative to males, in chronic dextran sulfate sodium (DSS) and TNBS colitis groups respectively. "

    Full-text · Article · Apr 2015 · Gastroenterology
  • Source
    • "Men develop autoimmune hepatitis at a younger age and have high relapse rates, but also have better prognosis than women (Al-Chalabi et al., 2008). By contrast, the clinical course in CD is more severe in girls (Gupta et al., 2007), whereas in diseases like RA, gender does not necessarily predict outcome (Courvoisier et al., 2008). In MS, disease severity, measured as disability progression , appears to be greater in males (Runmarker and Andersen, 1993; Weinshenker et al., 1991). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Autoimmune diseases are a range of diseases in which the immune response to self-antigens results in damage or dysfunction of tissues. Autoimmune diseases can be systemic or can affect specific organs or body systems. For most autoimmune diseases there is a clear sex difference in prevalence, whereby females are generally more frequently affected than males. In this review, we consider gender differences in systemic and organ-specific autoimmune diseases, and we summarize human data that outlines the prevalence of common autoimmune diseases specific to adult males and females in countries commonly surveyed. We discuss possible mechanisms for sex specific differences including gender differences in immune response and organ vulnerability, reproductive capacity including pregnancy, sex hormones, genetic predisposition, parental inheritance, and epigenetics. Evidence demonstrates that gender has a significant influence on the development of autoimmune disease. Thus, considerations of gender should be at the forefront of all studies that attempt to define mechanisms that underpin autoimmune disease.
    Full-text · Article · Apr 2014 · Frontiers in Neuroendocrinology
Show more