ABSTRACT
OBJECTIVE: To determine whether probiotic lactobacilli may alleviate small intestinal inflammation and strengthen the intestinal barrier function in children with atopic dermatitis. STUDY DESIGN: In a double-blinded, placebo-controlled, cross-over study, probiotic lactobacilli (Lactobacillus rhamnosus 19070-2 and L reuteri DSM 12246) were administered for 6 weeks to 41 children with moderate and severe atopic dermatitis. Gastrointestinal symptoms were registered before and during treatment and small intestinal permeability was measured by the lactulose-mannitol test. RESULTS: During Lactobacillus supplementation, there was a significant decrease in the frequency of gastrointestinal symptoms (39% during the placebo period versus 10% during active treatment, P=.002). There was a positive association between the lactulose to mannitol ratio and the severity of the eczema (r=0.61, P=.02 after placebo and r=0.53, P=.05 after active treatment). After probiotic treatment, the lactulose to mannitol ratio was lower (0.073) than after placebo (0.110, P=.001). CONCLUSIONS: Impairment of the intestinal mucosal barrier appears to be involved in the pathogenesis of atopic dermatitis. The study suggests that probiotic supplementation may stabilize the intestinal barrier function and decrease gastrointestinal symptoms in children with atopic dermatitis.
Subject(s)
Dermatitis, Atopic/metabolism , Gastrointestinal Diseases/therapy , Intestine, Small/metabolism , Lactobacillus , Probiotics/therapeutic use , Adolescent , Child , Child, Preschool , Cross-Over Studies , Dermatitis, Atopic/complications , Double-Blind Method , Gastrointestinal Diseases/etiology , Humans , Infant , Intestinal Absorption , PermeabilityABSTRACT
We describe four members in a family of 8 individuals over 3 generations with the autosomal dominant inherited periodic fever syndrome tumor necrosis factor receptor-associated periodic syndrome (TRAPS). The patients had recurrent episodes of fever, abdominal pain, arthritis, and rash. We examined the gene coding for the tumor necrosis factor receptor TNFRSF1A in all first-degree family members. In all 4 symptomatic members of the family, a hitherto undescribed mutation C98Y (380G-->A) in the TNFRSF1A gene was identified. In contrast, this mutation was not found in the 4 family members reported to be healthy nor in 50 normal control patients. The youngest member of the family, a 2-year-old boy, was treated successfully with etanercept.