title: Hypoproteinemia in severe childhood atopic dermatitis: a serious complication.
abstract: As a complication of atopic dermatitis (AD), the incidence of hypoproteinemia is increasing among infants with severe AD in Japan. It can be a life-threatening condition owing to hypovolemic shock as a result of hypoproteinemia and vascular infarction as a result of thrombocythemia. However, the pathophysiology of this condition remains unclear. The objectives of the present study were two-fold. The first objective was to determine the main route of protein loss, i.e. through the damaged skin or the gastrointestinal tract, or as a result of insufficient food intake. The second objective was to identify whether allergy or infection was the cause of severe skin inflammation. Fifteen patients with AD were enrolled who had serum protein levels of 3.2-5.8 g/dl. Specific immunoglobulin E (IgE) and skin test to allergens, stool eosinophils, alpha1-antitrypsin clearance, skin Staphylococcus aureus colonization and superantigens (SAgs) produced by the organism, serum SAg-specific IgE antibodies, serum interleukin (IL)-5, IL-6, IL-12, and interferon-gamma (IFN-gamma) were evaluated. Prominent serous skin discharge was seen in all of the patients and was found to have almost the same protein concentration as serum. Marked thrombocytosis, with a maximum of 1,060 x 103/ml, was seen. Skin culture revealed S. aureus colonization in all patients. SAg-producing S. aureus were found in 84.6% of the patients. The concentration of serum IL-5 was significantly increased and correlated well with the blood eosinophil count. Hence, the main route of protein loss was believed to be through damaged skin. The cause of severe inflammation was thought to be a combination of allergic inflammation and skin colonization by SAg-producing S. aureus. Serum cytokines showed a T helper 2 (Th2) T-cell-mediated pattern. To prevent hypovolemic shock, vascular occlusion, and growth retardation, it is of vital importance to diagnose hypoproteinemia at an early stage and start appropriate therapy.
authors.affiliation: Department of Allergy, National Children's Hospital, Taishido, Setagayaku, Tokyo, Japan.
authors.forename: Ichiro
authors.initials: I
authors.lastname: Nomura
authors.forename: Toshio
authors.initials: T
authors.lastname: Katsunuma
authors.forename: Morimitsu
authors.initials: M
authors.lastname: Tomikawa
authors.forename: Atsushi
authors.initials: A
authors.lastname: Shibata
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Kawahara
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Ohya
authors.forename: Jun
authors.initials: J
authors.lastname: Abe
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Saito
authors.forename: Akira
authors.initials: A
authors.lastname: Akasawa
mesh_terms: D000293:Adolescent; D017677:Age Distribution; D000704:Analysis of Variance; D001772:Blood Cell Count; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D004064:Digestive System / Q000276:immunology; D005260:Female; D006801:Humans; D007019:Hypoproteinemia / Q000097:blood / Q000150:complications* / Q000276:immunology*; D007223:Infant; D007564:Japan; D008297:Male