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The influence of lithium chloride on experimental autoimmune thyroid disease.

1985; National Institutes of Health; Volume: 61; Issue: 1 Linguagem: Inglês

R Hassman, John H. Lazarus, Carlos Diéguez, A P Weetman, R Hall, Anthony McGregor,

Genetics and Neurodevelopmental Disorders

Lithium administration is known to be associated with the development of thyroid dysfunction; it also exerts an effect on the immune system. The effect of lithium on experimental autoimmune thyroid disease was studied in female August rats. Following immunization with rat thyroglobulin in Freund's complete adjuvant, lithium chloride was administered i.p. for 30 days to four groups at varying stages of the disease. Control animals received i.p. saline. Anti-thyroglobulin antibody levels (measured by ELISA) were significantly increased in rats given lithium immediately post-immunization (group B) compared to control animals (661 +/- 42 OD vs 448 +/- 68; mean +/- s.e., P less than 0.02). In contrast, animals which received lithium during the spontaneous resolution of the disease (group D) showed a significant fall in anti-TG antibody compared to controls (99 +/- 15 vs 27 +/- 15; P less than 0.001). Anti-TG antibody levels remained undetectable in animals which received lithium but were not immunized. The splenic T cell blastogenic response (as measured following phytohaemagglutinin stimulation) was significantly increased in rats receiving lithium prior to and during immunization (group A) (stimulation index 63.4 +/- 6.9 vs 10.2 +/- 2.4; P less than 0.001). Spontaneous cell proliferation of splenic lymphocytes was decreased in two lithium treated groups (group A P less than 0.005, group C P less than 0.05). There was no alteration in splenic weight or the degree of thyroid lymphocytic infiltration in any of the treated group. Lithium exerted both positive and negative influences on the immune system in rats immunized with thyroglobulin in adjuvant but did not induce autoantibody production in normal rats.