Autoimmunity and the endocrine system: Thyroid, hypophysis and pregnancy

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AUTOIMMUNE CONCEPT OF SCHIZOPHRENIA: HISTORICAL ROOTS AND CURRENT FACETS

Background: The review analyzes the possible role of autoimmune processes in the pathogenesis of schizophrenia and the evolution of concepts on this issue from its origin to the present. Results: Risks of autoimmune processes causing schizophrenia are associated with several factors: an impaired functioning of dopaminergic and glutamatergic systems in the brain, kynurenine pathway disorder with overproduction of quinolinic, anthranilic and kynurenic acids (possibly altering both neurons and T-regulators), increased intestinal permeability, as well as food antigens’ effects, stress and infections with various pathogens at different stages of ontogenesis. An increase in the levels of proinflammatory cytokines and chemokines as well as a decrease in the levels of anti-inflammatory ones also may contribute to schizophrenia risks. Schizophrenia often occurs in those patients having various autoimmune diseases and their first-degree relatives. Conclusion: Cases of schizophrenia resulted from autoimmune pathogenesis (including autoimmune encephalitis caused by autoantibodies against various neuronal antigens) are characterized by quite severe cognitive and psychotic symptoms and a less favorable prognosis. This severe course may result from the chronic immune damage of the neuronal receptors such as NMDA, GABA, and others and depend on hyperprolactinemia, induced by antipsychotics, but aggravating autoimmune processes

HYPERPROLACTINEMIA AND ANTIPSYCHOTIC THERAPY IN SCHIZOPHRENIC PATIENTS WITH HASHIMOTO\u27 S THYROIDITIS

Introduction: Hyperprolactinemia (HPRL) is known as a side effect of some antidepressants and antipsychotics. These medicines are common in treatment of schizophrenia. Thus, HPRL is often observed in schizophrenic patients. It is also known that HPRL can occur in Hashimoto\u27 s thyroiditis due to prolactoliberin effect of thyroliberin. The clinical pathophysiology of the patients with the comorbodity of schizophrenia and Hashimoto\u27s thyroiditis, receiving antipsychotics, is of special interest.It\u27s fair to assume that these patients have higher risks of HPRL. To analyze risks of HPRL with antipsychotic treatment, to identify an association between the antipsychotic therapy (AT) and HPRL in Hashimoto\u27s patiens receiving AT ,to explore the association of HPRL and other laboratory parameters in patients with Hashimoto\u27s thyroiditis and schizophrenia during AT. Subjects and methods: We studied 17 patients with HT in comorbidity with schizophrenia receiving AT (mean age 46,5+-12,8 years), all euthyroid or with light hypothyroidism. Different laboratory parameters such as anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) antibodies, blood levels of thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3) and prolactin (PRL) were analysed. Results: The study revealed the high levels of PRL, anti-TPO and anti-TG autoantibodies. Thus, patients were classified into 3 groups by the degree of expected HPRL risk from the antipsychotics used: without expected risk, with low and high expected risks. The correlation analysis detected an inverse significant correlation (R=-0.51; p=0.037) between expected level of drug-associated HPRL risk and actual PRL levels in studied group. At the same time, we detected a positive significant correlation between the levels of PRL and FT4 in the groups (R=0.53; p=0.03). The correlations between the levels of PRL and other parameters such as TSH, FT3, anti-TPO, anti-TG, anti-TSH receptor antibodies were not statistically significant. Conclusions: HPRL in the group was not associated with taking of antipsychotic drugs with high expected HPRL risk. Yet, a significant positive correlation existed between the levels of PRL and FT4.Hence, in Hashimoto\u27s thyroiditis accompanied with treated mental illness there are some non-iatrogenic stimulants of prolactogenesis. It cannot be ruled out that antipsychotics may interfere with prolactin metabolism, which creates a false effect of a positive correlation between prolactin and free thyroxine levels, in contrast to common HPRL of hypothyroidism