Adrenocorticotropic Hormone-dependent Cushing's Syndrome Research Articles

A simplified morning ovine corticotropin-releasing hormone stimulation test for the differential diagnosis of adrenocorticotropin-dependent Cushing's syndrome.

The objective of this study was to develop criteria for the interpretation of a morning ovine CRH stimulation test for the differential diagnosis of ACTH-dependent Cushing's syndrome. Its design was retrospective review, and its setting was the in-patient unit of a tertiary care center. One hundred and eighteen patients with proven Cushing's disease or ectopic ACTH secretion were studied. The percent change in plasma ACTH and cortisol levels after CRH administration (1 microgram/kg BW) was calculated for each patient using 3 combinations of pre-CRH values (-15, -10, -5, and -1 min) and 6 combinations of post-CRH values (15, 30, 45, and 60 min). The diagnostic performance of these 36 sets of response measures was compared. The mean ACTH concentrations 15 and 30 min after CRH increased by at least 35% above the mean basal value at -5 and -1 min in 93 of 100 patients with Cushing's disease, but in none of the 16 patients with ectopic ACTH secretion. This measure gave the best sensitivity (93%) and specificity (100%). The best cortisol criterion was a mean increase at 30 and 45 min of 20% or more above mean basal values at -5 and -1 min, which gave a sensitivity of 91% and a specificity of 88%. We developed a simplified diagnostic test with 100% specificity using ACTH measurements 5 and 1 min before and 15 and 30 min after CRH administration. Although all patients with ectopic ACTH secretion had less than a 35% increase in ACTH, the probability of Cushing's disease was high at all levels of response, indicating that other tests should be performed to confirm the diagnosis.

A simplified morning ovine corticotropin-releasing hormone stimulation test for the differential diagnosis of adrenocorticotropin-dependent Cushing's syndrome

A simplified morning ovine corticotropin-releasing hormone stimulation test for the differential diagnosis of adrenocorticotropin-dependent Cushing's syndrome

Elevated adrenocorticotropic hormone and cortisol levels in a patient with medullary carcinoma of the thyroid containing ectopic immunoreactive corticotropin-releasing hormone and bombesin.

Pituitary adrenocorticotropic hormone-dependent Cushing's syndrome due to ectopic production of corticotropin-refeasing hormone (CRH) or bombesin (gastrin-releasing peptide) is an extremely rare cause of pituitary adrenocorticotropic hormone (ACTH) hypersecretion. We report a patient with elevated ACTH and cortisol levels due to ectopic secretion of both bombesin and CRH by metastatic medullary carcinoma of the thyroid (MCT). A 45-year-old man was investigated because of diabetes insipidus and visual field disturbances due to suprasellar metastasis of the MCT. On physical examination, he was a chronically ill man with a body mass index of 18.5 and was darkly pigmented but without other features typical of Cushing's syndrome. Hypogonadotropic hypogonadism, thyroid-stimulating hormone (TSH) deficiency, and hyperprolactinemia were due to pituitary stalk disorder, in light of these deficiencies, we were surprised to find elevated plasma ACTH, cortisol, and growth hormone (GH) levels throughout the day. Plasma ACTH at 9AM was 118 pg/ml and plasma cortisol was 859 nmol/L. At 12PM, ACTH was 89 pg/ml whereas plasma cortisol was 540 nmol/L. Urinary 17 OH CS were elevated (38 nmol/24 hr). The mean of the four-point day curve for GH was elevated. Plasma electrolytes were normal. The presence of both CRH and bombesin was documented by immunocytologic studies in the metastases (lymph node and suprasellar biopsy). ACTH was not found in any of the metastases. Because of the close proximity of the suprasellar metastasis to the portal pituitary circulation, CRH and bombesin could have been readily provided to the pituitary corticotrophs.

A Case of Pituitary Adrenocorticotropin-Dependent Cushing's Syndrome in the Horse*

In the horse, a syndrome of hirsutism, hyperglycemia, glucosuria, polydipsia, polyuria, polyphagia, and progressive debilitation has been recognized. Most often the syndrome has been associated with adenomas of the pars intermedia of the pituitary and bilateral adrenal hyperplasia or nodular hyperplasia involving primarily the zona fasciculata. Previously, the syndrome has been ascribed to compression of the hypothalamus by an expanding but functionally inactive pituitary neoplasm. In the present case, with RIA determination of plasma ACTH concentrations, the syndrome was ascribed to pituitary ACTH-dependent hyperadrenocorticism and likened to human Cushing's disease.