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Studies on the mechanisms of adverse reactions produced by diethylcarbamazine in patients with onchocerciasis—Mazzotti reaction
Author(s) -
GUERRACACERES J.G.,
BRYCESON A.D.M.,
QUAKYI I.,
SPRY C.J.F.
Publication year - 1980
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1980.tb00048.x
Subject(s) - diethylcarbamazine , onchocerciasis , immunology , immune reaction , immune system , antibody , eosinophil , onchocerca , brugia pahangi , local reaction , allergic reaction , immunoglobulin e , allergy , biology , medicine , filariasis , helminths , onchocerca volvulus , asthma
Summary The treatment of patients with onchocerciasis with diethylcarbamazine (DEC) can produce local or systemic reactions within a few hours—the Mazzotti reaction. In order to study the immunological mechanisms which could underly this reaction, three patients were studied who were undergoing treatment, and two normal subjects who had been treated successfully previously were controls. Blood eosinophils were vacuolated and a higher proportion than normal had Fc receptors. After taking 50 mg DEC orally, in parallel with the development of symptoms in the three patients, localised in two and generalized in one, there was a fall in blood eosinophil counts which were lowest at 12 h. Serum IgG levels fell slightly in all three patients, and the serum IgE level fell in one, but there were no changes in the titres of antimicrofilarial antibodies. Levels of circulating immune complexes were not elevated at any time, and complement levels did not alter during the reaction. From these findings and a review of previous work on the mechanisms of the Mazzotti reaction it is suggested that when microfilarae are damaged by DEC, an inflammatory reaction is produced which may be localised or generalized. The reaction does not appear to require the generation of circulating immune complexes, or systemic complement activation, even when the reaction is generalized. It is suggested that the clinical features of the reaction may be due to the effects of mediators secreted from inflammatory cells including eosinophils, in sites where microfilarae are being destroyed.