Journal
ACTA DERMATOVENEROLOGICA CROATICA
Volume 30, Issue 2, Pages 106-109Publisher
CROATION DERMATOVENEROLOGICAL SOC
Keywords
atopic dermatitis; corticosteroids; eosinophilia; inflammation; hyper-sensitivity
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This study reports the clinical case of an infant with extremely severe atopic dermatitis. The patient experienced protein loss, electrolyte imbalance, and immune deficiency as serious complications. The main mechanism of protein loss is attributed to damaged skin and eosinophilic inflammation of the small intestine.
Protein loss is often the result of kidney or intestinal disease (protein -losing enteropathy) and can cause a number of serious, potentially life-threatening complications such as hypotension, thrombocytosis, electrolyte imbalance, and cer-ebellar ischemia. Recent research suggests an association between extremely severe atopic dermatitis (AD) and allergic enteropathy. An exclusively breastfed 6-month -old infant was admitted to our institution due to failure to thrive, electrolyte imbal-ance, and severe AD (SCORing Atopic Dermatitis; SCORAD 40). On admission, the infant was in poor general condition, dehydrated, malnourished (bodyweight 4870 g,-3.98 z-score), with exudative erythematous morphs scattered throughout the body. Initial laboratory results showed microcytic hypochromic anemia, hypoal-buminemia, hypogammaglobinemia, thrombocytosis, hyponatremia, high values of total immunoglobulin E (IgE), and eosinophilia. Polysensitization to a number of nutritional and inhalation allergens was demonstrated, and an exclusive amino ac-id-based formula has been introduced into the diet. During the hospital course, the patient developed superficial thrombophlebitis and methicillin-resistant Staphylo-coccus aureus (MRSA) bacteremia. Eosinophilia was found in a small intestine biopsy sample. Due to severe hypogammaglobulinemia, skin infections, and bacteremia, the differential diagnosis included primary immune deficiency (STAT3 deficiency, DOCK8 deficiency, PGM3 deficiency, IPEX), but all available immunological tests were unremarkable. Exclusive amino acid-based formula diet was continued in the infant, with topical corticosteroids under wet-dressing therapy and intravenous im-munoglobulin replacement therapy. With the gradual improvement of the general condition, the introduction of solid foods was started according to the findings of allergy testing. At 17 months of age, the patient gained weight and his skin status has been improving, although frequent use of topical corticosteroids was necessary. There were no infections, no anemia or thrombocytosis, and albumin and immuno-globulin supplementation were no longer required. The main mechanism of protein loss in infants with extremely severe atopic dermatitis is probably due to damaged skin, and partially due to the eosinophilic inflammation of the small intestine. Immu-noglobulin loss, potentiated by physiological or transient hypogammaglobulinemia in infants, poses a very high risk for severe, potentially life-threatening infections.
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