[Thrombocytopenia associated with human immunodeficiency virus infection. Immunologic study of 60 patients addicted to parenteral drugs].

BACKGROUND

The immunologic study of 60 intravenous drug addict patients who were seropositive for the human immunodeficiency virus (HIV) and who developed thrombocytopenia (TP) is reported with the aim of establishing the relation of possible pathogenic factors which may trigger this complication.

METHODS

In all the patients the presence of antiplatelet antibodies was studied by direct and indirect immunofluorescence together with crypto-antibodies, immune complexes, lymphocytotoxic antibodies, antiphospholipid antibodies, immunoglobulins, lymphocytic populations and subpopulations and serology against different infectious agents.

RESULTS

Antiplatelet antibodies were detected in 71% of the patients of which 50% corresponded to immunoglobulins of IgG class, 12% to IgM, 21% to IgG plus IgM, 7% IgM plus IgA, 5% to IgG plus IgA and 5% IgG plus IgM plus IgA. In these patients a characteristic membrane fluorescence pattern was observed in which the fluorescein is distributed forming a thick, hard point. In 3 patients EDTA dependent crypto-antibodies were detected which in one case determined pseudothrombocytopenia. The immune complexes were demonstrated in 50% of the cases. Other findings were: hypergammaglobulinemia (86%), decrease in the CD4 population (47%), CD4/CD8 ratio < 1 (71%), lymphocytotoxic antibodies (70%), antiphospholipid antibodies (60%), and seropositivity for cytomegalovirus (62%), Epstein-Barr virus (10%) and hepatitis B virus (anti-HBc 75%, HBsAg 33%).

CONCLUSIONS

Thrombocytopenia associated to infection by the human immunodeficiency virus in intravenous drug addict patients is due to the concurrence of multiple factors. The relevance of each may vary according to the risk practice of the collective analysed and even within the same group of some individuals or others. The numerous serologic findings in these patients fundamentally express the existence of a chronic polyclonal stimulation of B cells which may be initiated by the action of the drug itself and which becomes aggravated during the course of the multiple acquired infections among which that due to the human immunodeficiency virus is of note.