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Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids
Author(s) -
Savvatianos S.,
Giavi S.,
Stefanaki E.,
Siragakis G.,
Manousakis E.,
Papadopoulos N. G.
Publication year - 2011
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2011.02566.x
Subject(s) - allergy , medicine , cow's milk allergy , anaphylaxis , milk allergy , food allergy , pediatrics , immunology
unblinded manner. Six to ten hours after consumption of kiwi she reproducibly developed an itchy rash consisting of confluent 3–5 mm purpuric macules and papules on the legs, lower trunk and forearms with consecutive bleeding in the central part of the lesions. Oral provocations with apple, banana and pineapple were negative. Western Blot analysis of a kiwi fruit extract with the patient’s serum showed IgG-, but no IgE-reactivity, corresponding to themajor kiwi fruit antigen Act c 1 (Fig. 1C). HE staining of a fresh lesion, that was taken soon after appearance, showed neutrophilic infiltration in and around cutaneous vessels with leucocytoclasia consistent with leucocytoclastic (allergic) vasculitis (Fig. 1D/E). In the light of the patient’s history, diagnostic findings and the reproducible induction of symptoms by oral provocation with kiwi, we diagnosed ‘kiwiinduced allergic leucocytoclastic vasculitis’. Elimination diet with avoidance of the consumption of kiwi lead to slow resolution of the purpuric lesions and hyperpigmentations over time. No recurrences of vasculitis were observed over a period of 3 years. Using repeated oral food challenges we were able to identify kiwi fruits as a causal elicitor of allergic vasculitis. The presence of Act c 1-specific IgG strongly supports an antigen-specific process, but food-specific IgG antibodies are also frequent finding in healthy individuals (1). Foodstuff is rarely considered as a cause for allergic vasculitis in clinical practice and is reported only anecdotally in current literature (rye, carrot, cow’s milk, hen’s egg, cocoa products and additives) (2–4). Strikingly, in our patient mainly dependent body regions like legs and feet were affected by vasculitis and therefore, the formation of IgG immune complexes with kiwi antigen and their deposition in dermal postcapillary venules can be assumed as pathogenic process (5). The authors report no conflict of interest. J.G., S.K., and J.R. cared for the patient. J.G. and S.K. wrote the manuscript. M.O., M.M. and J.R. reviewed the manuscript. M.O. performed the western blot.