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Hypoproteinemia in severe childhood atopic dermatitis: a serious complication
Ichiro Nomura1, Toshio Katsunuma, Morimitsu Tomikawa
1Department of Allergy, National Children's Hospital, Taishido, Setagayaku, Tokyo, Japan.
Insights
Infants with severe atopic dermatitis (AD) can lose protein through skin discharge, leading to hypoproteinemia. Staphylococcus aureus colonization contributes to severe inflammation and protein loss in these patients.
Area of Science:
- Pediatric Dermatology
- Immunology
- Biochemistry
Background:
- Hypoproteinemia is an increasing complication in infants with severe atopic dermatitis (AD) in Japan.
- This condition can be life-threatening due to hypovolemic shock and vascular infarction.
- The exact pathophysiology of hypoproteinemia in severe AD remains unclear.
Purpose of the Study:
- To determine the primary route of protein loss in infants with severe AD (skin, gastrointestinal, or insufficient intake).
- To identify whether allergic reactions or infection cause severe skin inflammation in these patients.
Main Methods:
- Fifteen infants with severe AD and hypoproteinemia were studied.
- Evaluated serum protein levels, specific IgE, skin tests, stool eosinophils, alpha1-antitrypsin clearance, Staphylococcus aureus colonization, superantigens (SAgs), and serum cytokines (IL-5, IL-6, IL-12, IFN-gamma).
Main Results:
- All patients exhibited prominent serous skin discharge with protein concentration similar to serum.
- Marked thrombocytosis was observed in patients.
- Staphylococcus aureus colonization was present in all patients, with 84.6% producing SAgs.
- Significantly increased serum IL-5 correlated with blood eosinophil counts, indicating a T helper 2 (Th2) pattern.
Conclusions:
- The main route of protein loss in severe AD is through damaged skin.
- Severe skin inflammation is caused by a combination of allergic reactions and S. aureus colonization.
- Early diagnosis and treatment of hypoproteinemia are crucial to prevent severe complications.
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.