A Modern View of the Pathogenesis of Allergy with Drug Etiology

Nowadays many diseases are associated with a high risk of drug allergy, and this risk can vary greatly depending on the type of disease. With the progression of disease in HIV-infected patients is increased IgE and decreased the number of CD4+ T-cells. In this case violated the ratio of interferon-gamma-producing (Th1 type) clones of CD4+ T-cells and IL-4 - producing (Th2 type) clones of CD4+ T-cells. In HIV-infected patients, there is the high risk of developing allergies in the form of skin rashes and temperature, and severe skin syndromes Stevens-Jones (SJS) and toxic epidermal necrolysis (TEN) in 6%-10% of cases. CD4+ T cells secrete cytokines, for instance Interleukin (IL-5), Gransim and Eotaxin involve eosinophils to be grown and differentiated. Studies on the antigenicity of antibiotics demonstrated the potential relevance of both categories of drug allergy: hapten and p-i models. In patients with allergic reaction to piperacillin, this medication acts as the hapten, with the formation of the immunogenic conjugate piperacillin - albumin, which stimulates the drug-responsive T-cells. Immunogenetic factors have been identified as risk indicators for the development of hypersensitivity reactions to the representatives of many classes of drugs, such as Abacavir and Nevirapine, Carbamazepine and Allopurinol, etc. Thus, considering the huge genetic polymorphism in systems of drug metabolism in the body and in the systems contributing immune response to the resulting products of conjugation of hapten-protein, evident is the need to further study the role of these systems in the occurrence of adverse reactions to drug therapy, in particular, in the development of allergic complications.