The Effects of Hormones of the Hypothalamo-Hypophyseal-Adrenal, Renin-Angiotensin, and Thyroid Hormone Systems on the Formation of Dyscirculatory Encephalopathy

Abstract

Measurements were made of plasma levels of free (f) thyroxine (fT4), triiodothyronine (fT3), thyrotropic hormone (TSH), adrenocorticotrophic hormone (ACTH), aldosterone, and renin in patients with dyscirculatory encephalopathy (DE). Their influences on the development of chronic circulatory insufficiency were assessed. A total of 39 patients were studied (aged 45-73 years) with DE stages I and II, without acute or chronic (in the exacerbation phase) somatic illness. These observations showed that diffuse lesions of brain tissues of different severities were accompanied by the following changes in thyroid homeostasis: 1) significant combined increases in TSH without alteration to the "fT3-TSH" negative feedback regulatory mechanism in patients with stage I DE; 2) significant combined decreases in TSH levels with marked suppression of the conversion of thyroxine into triiodothyronine and an interaction with impairments in the "fT3-hypophysis" system in patients with stage II DE. In addition, there were changes (increases) in cortisol levels with simultaneous decreases in renin levels in patients with stage II DE as compared with patients with stage I DE. Correlation analysis demonstrated the absence of any relationship between the age of the patients, the state of hormonal homeostasis, and the extent of vascular stenosis. These results suggest a role for hormones of the hypothalamo-hypophyseal-adrenal, thyroid, and renin-angiotensin systems in the mechanism by which DE develops as well as the possibility of using tests for these hormones as additional criteria for assessing the severity of diffuse brain lesions.

Angiotensin‐converting enzyme genotype and encephalopathy in Chernobyl cleanup workers

“…Thus, activation of the brain RAS, triggered by diverse stimuli, may mediate the late cerebral complications seen in CCW which would be consistent with the demonstrated association of the ACE D‐allele and the development of DE in our cohort. In support, plasma renin activity is suppressed by increased ACE activity and ang II generation, and lower circulating renin levels have been associated with DE progression [55]. Moreover, the ACE inhibitor captopril has been successfully used to treat DE arising in patients with hypertension [56].…”