Abstract
Dilantin therapy has been associated with immunoglobulin deficiency. An 11 year old male, treated for 8 months with dilantin for post-traumatic seizures, presented with an acute onset of fever, rash and diffuse lymphadenopathy. Serum IgA, IgM and IgE were virtually absent and IgG levels were very low (200 mg.%); circulating B-cells were markedly reduced with less than 0.2% of the mononuclear cells stained for sIgM/sIgD; T-cell numbers were normal. Using an antigen-specific hemolytic plaque assay, it was found that fresh, patient T-cells were able to suppress immunoglobulin secretion in normal as well as autologous B lymphocytes, sensitized in vitro. This spontaneous suppressor activity, previously described in some patients with X-linked agammaglobulinemia, was inhibited by lithium, a putative blocker of cyclic AMP generation. (J. Immunol. 121: 2097, 1978). Two weeks following cessation of dilantin therapy, clinical signs of illness disappeared, suppressor cells were no longer detectable and B lymphocytes began to re-appear. Normal numbers of circulating B lymphocytes were restored by 4 weeks and serum IgG, IgA, IgM and IgE levels were normalized by 8 weeks. These data suggest that in susceptible individuals, dilantin therapy may result in hypogammaglobulinemia. The coincidence of drug-induced antibody deficiency and the emergence of spontaneous suppressor cells supports the concept that abnormal suppressor T cells may play a role in certain antibody deficiency syndromes.
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Dosch, HM., Jason, J. & Gelfand, E. 907 DILANTIN-INDUCED SPONTANEOUS SUPPRESSOR (T) CELL, ACTIVITY AND HYPOGAMMAGLOBULINEMIA. Pediatr Res 15 (Suppl 4), 593 (1981). https://doi.org/10.1203/00006450-198104001-00932
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DOI: https://doi.org/10.1203/00006450-198104001-00932