Estudo dos hormônios tireoideanos, de polimorfismos dos genes das desiodases e da dor crônica como preditores dos desfechos do tratamento da depressão maior

• Ano de defesa: 2023
• Autor(a) principal: Martini, Murilo
• Orientador(a): Wajner, Simone Magagnin
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Hormônios tireóideos; Polimorfismo genético; Dor crônica; Prognóstico; Transtorno depressivo maior; Testes de função tireóidea; Terapêutica
• Link de acesso: http://hdl.handle.net/10183/271246

Major depression has an annual incidence of approximately 6% and is the third leading cause of years of life lost due to disability in the world. Neurobiological and clinical factors, associated with biopsychosocial contributors, are involved in the pathogenesis of depression, which can be a cause or consequence of many organic diseases. Depression and chronic pain are often comorbid. Depression can be a cause of somatic pain as much as pain of any etiology increases the risk of depression, and the presence of one of these morbidities increases the severity of the other. Depression is also associated with hypothyroidism. Even in situations of systemic euthyroidism, intratissue changes in thyroid metabolism, due to changes in the activity of deiodinases and in the expression of thyroid hormone transporters, can predispose to depressive-anxious behavior. In the first piece of this thesis, 346 patients with depression were genotyped for the single nucleotide variant rs225014-T/C (also known as Thr92Ala) and 285 for the rs974453-A/G variant. The first is a polymorphism of the type 2 deiodinase gene (DIO2), and we found that patients with the Ala/Ala genotype had a better response to depression treatment within 6 months, in terms of reducing signs of psychomotor disturbance and severity of symptoms. The latter is a polymorphism of the gene that encodes a thyroid hormone transporter (SLCO1C1), mainly responsible for the passage of T4 across the blood-brain barrier, and in our study, it was not associated with the severity of depression or response to treatment. The second study of this thesis retrospectively evaluated 88 patients with depression and found a prevalence of 47.7% of comorbid chronic pain. Patients with chronic pain had a worse response to treatment at 6 months. There was a 72% difference in the reduction of the Hamilton score, which measures the severity of symptoms, and patients with pain did not show any improvement in signs of psychomotor disturbance (melancholia). Almost all patients were euthyroid and T3, T4, and TSH levels were not confirmed as modulators of the difference in response to treatment between patients with and without chronic pain.