Unusual reaction to hymenoptera sting: a case of Schönlein‐Henoch purpura

Abstract

Here is a case of Schonlein-Henoch syndrome, a secondary unusual reaction of allergy to the bite of a stinging hymenoptera. A 12-year-old patient has come under our observation for the appearance of nettle-rash papule and later on of palpable purpura with small bruises on the lower limbs and gluteuses, reporting nonspecific abdominal pains. After 3 days, we have observed association of arthralgias on both ankles and knees. A similar occurrence had already happened a year earlier and had been interpreted as secondary to acute streptococcal tonsillopharyngitis. To an accurate anamnesis following the second event, we found out that the patient had been stung by a bee just a few days earlier. The same thing had happened the year before but this detail at the time had not been considered important and therefore not studied more carefully. The patient though was normally tolerant to Dyptera bites. The skin tests with hymenoptera dehydrated extract (1) have been proved positive to 0,1 mcg/ml, with a 3rd Class RAST, to Apis mellifera, but negative to Vespula sp, Polistes dominulus and Tabanus sp. The skin biopsy specimen revealed a leukocytoclastic vasculitis (Fig. 1). All these clinical data, their follow-up and the bioptical result have enabled us to diagnose a SchonleinHenoch (SHP) relapsing purpura. The SHP is a form of vasculitis to hypersensitivity characterized by smallvessels inflammation, with a mainly cutaneous clinical interest, usually observed in children, with tissue depositing of immunocomplex (ICC) containing IgA. The main clinical manifestations are characterized by a symptomatological tetrad: (i) cutaneous purpura, a must criteria for the diagnosis, mainly on the lower limbs and glutaeuses; (ii) arthralgia, occuring in 75% of the cases; (iii) abdominal pain colitis type (in 70%) with intestinal bleedings (in 40%); (iv) kydney alterations nephritis like (in 30%) with hematuria episodes. The aetiology is unknown, but it is considered as main unleashing factors, the role played by viral and bacterial infections, the use of medicines and drugs, coldness, some nonspecific toxins, systemic diseases, tumoural pathologies and insect stings. A fundamental element of the damage because of ICC is the increasing vascular permeability, which allows their passage among the endothelium cells. Cochrane et al. (2) demonstrated that both histamine and serotonine are the chemical mediators responsible for the vessel-permeabilization process. They are also allowing to fix a considerable quantity of ICC. Furthermore, also mast cells, triggered eosinophils and basophiles are able to release externally a wide range of inflammation mediators such as vasoactive amines, metabolites of arachidonic acid, cytokines (3). The further activation of the complement amplifies the inflammatory process with the production of chemiotactic factors for neutrophiles, which once triggered releases lysosomial enzymes. We believe that this vasculitis has been secondary to the release of mediators from mast cells in an individual allergic to hymenoptera venom and not secondary to the toxicity of the venom itself. Our case is the third one reported in literature (4,5) of this unusual reaction triggered by an insect sting, but the first one reported after anhymenoptera sting in a patient allergic to Apis m. In fact, in our case, the urticaria has shortly preceeded the ourbreak of petechial eruption connected to the vasculitis pathology development, representing therefore an initial stage of hypersensitivity of the III type more than an aspect of the IgE-mediated reaction, which acted as a trigger factor. Even the histological examination gave evidence of a vasculitis but void of a relevant eosinophil reaction. This is why our patient underwent only one pharmacological treatment but has not been addressed to any specific immunotherapy (6).