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PubMed1991

[Somatomedin C level and stimulation of growth hormone and adrenal cortex function by administration of releasing hormones and physical exertion in patients with obesity].

In a clinical study on potential determinants underlying the impairment of growth hormone stimulation in obese human subjects, we examined in 20 otherwise healthy adult obese subjects (14 females, six males, age 18 to 40 years, body mass index greater than 29 kg/m2) the responses of growth hormone (hGH), adrenocorticotropic hormone (ACTH) and cortisol to releasing hormone stimulation (growth hormone-releasing hormone and corticotropin-releasing hormone) and the responses of hGH, ACTH, cortisol and free fatty acids (FFA) to physical exercise. Subjects with somatomedin-C levels less than or equal to 0.7 U/ml (group 1) were more obese than subjects with somatomedin-C levels greater than 0.7 U/ml (group 2) (p less than 0.01). In group 1, hGH increased by 4.3 +/- 1.2 ng/ml in response to releasing hormone administration and by 0.9 +/- 0.3 ng/ml in response to physical exercise (normal responses, increase by greater than 7 ng/ml), in group 2, hGH increased by 6.7 +/- 1.4, and 2.4 +/- 0.8 ng/ml, respectively (p less than 0.05 vs. group 1). Moreover, FFA stimulation by physical exercise was blunted in group 1 (p less than 0.05 vs. group 2). In contrast, ACTH stimulation was found increased in group 1 in comparison to group 2, particularly in response to physical exercise (p less than 0.01), and resulted in enhanced cortisol stimulation (p less than 0.05). Thus, impaired hGH stimulation in obese human subjects is not explained by an altered relationship between hGH and somatomedin-C levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

[Nervous system changes in adrenal failure].

AIM: To study nervous systems in chronic adrenal failure (CAF). MATERIAL AND METHODS: 262 patients with CAF were studied clinically, biochemically and electrophysiologically before and after treatment. RESULTS: The patients were found to have syndromes of vegetovascular dystonia by hypotonic type, syncopal paroxysms, myastenic, minor strokes, dyscirculatory-dysmetabolic encephalopathy, polyneuropathy. A direct correlation was established between the severity and duration of adrenal failure (AF), lowering of adrenal cortex hormones, coefficient Na/K and clinical manifestations of the neurological syndromes. Adequate hormone replacing and symptomatic therapy promoted a regress of neurological disorders in most of the patients especially in mild and moderate AF. CONCLUSION: Adequate therapy corrects neurological disturbances in patients with chronic NN.

Adolescent↗