Case of Graves’ disease recovery

The pathogenesis of Graves’ disease (GD) is considered to be an etiologically multifactorial process of external influence on specific genes that are susceptible to the autoimmune reaction stimulating thyroid hormonogenesis. However, the mechanisms underlying gene loci activation in GD remain unknown. Since GD causes stress, which affects the autonomic nervous system (ANS), the ANS is postulated to be a pivotal link in GD pathogenesis. In this case study, we analyzed the diagnostic findings of a 40-year-old male patient with GD and evaluated the results of his ANS-focused treatment. We revealed the primary role of the ANS in hyperthyroidism development and the secondary (complementary) role of autoimmune processes in disease development. As illustrated by our patient's case, the factors related to pathogenesis were: (i) the influence of stressors, (ii) the ANS involvement in the regulation of the blood flow intensity and velocity through the thyroid gland, as established by the Doppler ultrasound investigation, (iii) the absence of the effect of anti-thyroid-stimulating hormone (TSH) antibodies on thyroid blood flow, and (iv) thyroid hormonogenesis during the presence of normal anti-TSH antibody levels and almost no TSH. Genetic predisposition to GD presumably hypersensitizes the ANS to stress, wherein stress readily excites the ANS, resulting in the inadequate overstimulation of the thyroid gland, with or without the involvement of autoimmune processes.