PubMed · 4769711
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A D Lauta. [Experiments on hypothalamic effect on metabolic endocrine processes].. https://pubmed.ncbi.nlm.nih.gov/4769711/
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Cushing's syndrome, characterized by unregulated cortisol secretion, may be caused by a variety of adrenal, pituitary, or other tumors. The best biochemical test for establishing the diagnosis is determination of 24-h urinary free cortisol. The specific causes for Cushing's syndrome may be further differentiated by plasma adrenocorticotrophic hormone (ACTH). Primary adrenal cortical diseases are associated with low levels of ACTH and are considered ACTH-independent. Pituitary disease and the ectopic ACTH syndrome are associated with normal or elevated ACTH levels and are considered ACTH-dependent. Adrenal forms of Cushing's syndrome may result from either adenoma or carcinoma. The diagnostic approach to Cushing's syndrome and the clinical, biochemical, and radiographic features that distinguish adrenal adenoma and carcinoma are the subjects of this paper. 65-75% of CS [14, 15]. Most cases of Cushing's disease are the result of pituitary adenomas; however, corticotrope hyperplasia is responsible for a small minority of cases. Ectopic production of ACTH from a variety of tumors (bronchial carciniod, thymoma, oat-cell carcinoma, pheochromocytoma, islet-cell tumor, and prostate cancer) accounts for 10-15% of CS. Primary adrenocortical diseases account for the remaining 20-30% of CS, including benign adenoma (10-15%), adrenocortical carcinoma (5-10%), and adenomatous hyperplasia (5%). The purpose of this review is to present a contemporary approach to the evaluation and management of patients with Cushing's syndrome, emphasizing the primary adrenal etiologies pertinent to urologists.
Hypertension is a common medical disorder in pregnancy that may predate or first appear in pregnancy. Endocrine disorders rarely are the cause of the elevated blood pressure. However, it is essential to have a high index of suspicion because they carry much higher fetal and maternal morbidity and mortality risks. Endocrine disorders presenting as hypertension are primarily the result of autonomous production of renin, aldosterone, cortisol, or catecholamines. This report discusses the physiological changes in pregnancy, presentation, investigation, and management of these disorders.
The pertinent literature on the prevalence, clinical manifestations and pathogenic mechanisms of sleep apnoea (SA) in endocrine diseases, namely acromegaly, Cushing syndrome, hypothyroidism and diabetes mellitus was reviewed. An increased prevalence is well documented in patients with active and treated acromegaly. While most authors report peripheral obstruction, due to hypertrophy of tongue and pharyngeal tissues, to be the cause of SA in acromegaly, some findings argue for a role of hormone-induced changes of central respiratory control. SA is also more common in hypothyroidism, especially when myxedema is present. The associated edema and myopathy appear to be of pathogenic importance. Thyroxin substitution is frequently effective for the treatment of SA but nCPAP can be necessary initially and in some patients even after remission of clinical signs of hypothyroidism. In Cushing disease and syndrome, parapharyngeal fat accumulation can cause SA, but no epidemiological information is available. In non insulin dependent diabetes (NIDDM), obesity is the common risk factor for both, nocturnal hypoxia and insulin resistance. In IDDM, the development of autonomic neuropathy may predispose to SA. Where treatment of the underlying endocrine disease is unable cure the associated SA, nCPAP is usually the treatment of first choice. More prospective studies are clearly needed to establish prevalences and resolve the controversies regarding pathogenesis.