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Biomedical subjects

R C Mellinger

Publications and source records attributed to R C Mellinger.

At least 19 recordsLinked to original sources
PubMed1991

Cushing's disease: dilemmas of diagnosis and management.

Determining the cause of Cushing's disease and correcting the abnormality presents a continuing challenge to the clinician despite remarkable advances in diagnostic and therapeutic techniques. We present seven cases to illustrate 1) the classic disorder cured by pituitary adenomectomy; 2) persistence of the disease after adenomectomy; 3) Cushing's disease manifesting in the puerperium and remitting with dopamine agonist therapy; 4) a patient whose disease relapsed at least five times during 20 years of treatment by adrenalectomy, pituitary radiation, mitotane, and pituitary adenomectomy; 5) the Nelson syndrome; 6) the ectopic adrenocorticotropic hormone (ACTH) syndrome in a patient with dexamethasone suppressible urinary cortisol who had a pituitary adenoma which stained positively for ACTH but who was not cured by total hypophysectomy; and 7) a patient whose ACTH-secreting tumor proved fatal despite repeated surgical, radiologic and pharmacologic measures.

Adrenocorticotropic Hormone↗
PubMed1991

Hyperandrogenemia and virilization with simultaneous pituitary and adrenal adenomas.

We describe a postmenopausal woman who presented with virilizing hyperandrogenemia and was found to have an intrasellar tumor and a large left adrenal mass. Pathologic studies showed on undifferentiated hypophyseal adenoma with immunostaining for chromogranin only and a benign adrenocortical adenoma. In light of current understanding of the regulation of adrenal androgen secretion and adrenocortical mitogenesis, we postulate that this case may be explained by secretion of adrenal androgen-stimulating and mitogenic factors by the pituitary tumor.

Adenoma↗
PubMed1990

Colon cancer and polyps in acromegaly: increased risk associated with family history of colon cancer.

A cohort of 52 subjects diagnosed with acromegaly in southeastern Michigan and northern Ohio between 1935 and 1985 were followed to determine the incidence of colon cancer and polyps. Medical records were reviewed, subjects or their next-of-kin were interviewed, and screening examinations of the colon were offered to the living patients who were located. Data on demographics, personal histories of cancer and colon polyps, family history of colon cancer, and cure from acromegaly were obtained for both living and deceased subjects. The risk for colon cancer compared to the general population was estimated using standardized incidence ratios (SIRs). The expected number of cases was determined utilizing age, sex and race-specific rates provided by the cancer registry in southeastern Michigan. Among the 52 subjects, one could not be located and nine were deceased, none from colon cancer, with one known to have a history of colon polyps. Of 13 (31%) who declined the screening physical, one had a history of polyps and none reported a history of colon cancer. Two of 29 screened patients were found to have right-sided adenocarcinoma of the colon. Of the entire cohort, eight people (including one deceased) had a current or previous diagnosis of polyps, with five known to be histologically adenomatous. The SIR for colon cancer was 4.7 (95% confidence interval 0.6-17.1). Seven subjects, including the two with detected adenocarcinoma and four of the six living subjects with polyps only, reported a family history of colon cancer. The SIR for the subset of subjects with a family history of colon cancer was 29.1 (95% confidence interval of 3.5-104.6).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1989

Marked elevation of serum dehydroepiandrosterone sulphate in Cushing's disease with macronodular adrenocortical hyperplasia.

A 30-year-old man presented with longstanding hypercortisolism and biochemical studies typical of pituitary-dependent Cushing's disease. After unsuccessful transsphenoidal surgery, plasma ACTH transiently became undetectable and adrenal computed tomography (CT) was consistent with macronodular hyperplasia. Serum dehydroepiandrosterone sulphate (DHEA-S) exceeded 10,000 ng/ml (normal 2,000-3,350 ng/ml). Despite either transient adrenal autonomy or variable adrenocortical ACTH hyperresponsiveness, urinary cortisol normalized within eight months following pituitary irradiation alone. Serum DHEA-S fell progressively but remained mildly elevated (4,000 ng/ml). Follow-up CT showed minimal residual adrenal nodularity. Given these findings and a review of the literature, we propose that chronic cosecretion of non-ACTH proopiomelanocortinderived peptides may have stimulated both hypersecretion of DHEA-S and adrenocortical macronodularity in this patient.

Adrenal Cortex Diseases↗
PubMed1989

Hypersecretion of growth hormone and prolactin in McCune-Albright syndrome.

Acromegaly and hyperprolactinemia have been reported in association with the McCune-Albright syndrome, but the pathophysiology of the GH and PRL hypersecretion that occurs in patients with this disorder has not been defined. We studied GH and PRL secretory dynamics in three patients with McCune-Albright syndrome and hypersecretion of these hormones. Each patient had excessive linear growth, glucose-non-suppressible plasma GH concentration, and GH responsiveness to TRH and GHRH. In response to exogenous GHRH, plasma GH concentrations rose approximately 2-fold in all three patients. Plasma GHRH levels were 20-40 ng/L (normal, less than 30). Study of the spontaneous GH secretory pattern in two patients indicated nocturnal augmentation of GH release. Bromocriptine therapy failed to reduce plasma GH in all patients; in one patient treatment with octreotide, a long-acting somatostatin analog, partially suppressed plasma GH and insulin-like growth factor I levels. These results suggest that hypersecretion of GH in the McCune-Albright syndrome is not due to ectopic GHRH production or autonomous somatotroph function. The results are similar to those described in classic acromegaly due to GH-secreting pituitary tumors. However, the lack of radiographic pituitary enlargement, the variable pituitary pathology reported in similar patients, and frequent concordance of GH and PRL excess suggest that the pathogenesis of this disorder may differ fundamentally from other forms of acromegaly or gigantism. The pathophysiology may reflect abnormal hypothalamic regulation and/or an embryological defect in pituitary cellular differentiation and function.

Adolescent↗
PubMed1987

Malignant somatostatinoma presenting with diabetic ketoacidosis.

High circulating levels of somatostatin (SRIF) were detected in a patient with a metastatic tumour after development of diabetic ketoacidosis (DKA). Fasting insulin and C-peptide levels were markedly suppressed, but plasma glucagon was not suppressed below normal. Progressive cachexia ensued; at autopsy a poorly differentiated non-small cell neuroendocrine carcinoma metastatic to liver was found. Small gallstones were noted. Electron microscopy of tumour tissue showed neurosecretory granules and tonofilament bundles. Immunohistochemical staining of tumour cells was diffusely positive for carcinoembryonic antigen, bombesin-like immunoreactivity, and calcitonin with focal immunoreactivity for SRIF, serotonin, neuron-specific enolase, chromogranin, and epithelial membrane antigen. Column chromatography of plasma and tumour extract revealed five or more peaks of material with SRIF-like immunoreactivity (SRIF-LI): predominantly SRIF-28 and intermediates in tumour extract, and SRIF-14 and an intermediate between SRIF-28 and SRIF-14 in plasma, DKA in this case of somatostatinoma syndrome may reflect differential effects of tumour production of larger molecular weight SRIF forms on insulin and glucagon secretion.

Adenoma, Islet Cell↗
PubMed1985

Effect of bromocriptine treatment on the aldosterone response to angiotensin II and adrenocorticotropin in idiopathic hyperaldosteronism.

Bromocriptine can prevent an increase in plasma aldosterone during the infusion of angiotensin II in normal subjects and during upright posture in some patients with idiopathic hyperaldosteronism. To determine if bromocriptine prevents the increase in plasma aldosterone concentration during angiotensin II infusion in idiopathic hyperaldosteronism, we infused angiotensin II in five patients with idiopathic hyperaldosteronism, before and after treatment with bromocriptine (2.5 mg, three times daily for 5 days), and measured the resulting plasma aldosterone and angiotensin II concentrations. We also determined the adrenal response to ACTH infusion before and after bromocriptine treatment in four of these patients. Bromocriptine treatment did not significantly change the plasma concentrations of aldosterone before or during the infusions of angiotensin II and ACTH. It did significantly decrease mean blood pressure and increase the plasma corticosteroid concentrations in the preinfusion periods, but it did not alter the response of blood pressure to angiotensin II or of plasma corticosteroid concentrations to the ACTH infusions.

Adrenal Cortex Hormones↗
PubMed1983

Primary polydipsia. Syndrome of inappropriate thirst.

A patient with lifelong severe polyuria and polydipsia had normal serum antidiuretic hormone (ADH) levels and responded to water deprivation with a prompt increase in urine osmolality and maintenance of normal plasma osmolality (less than 290 mOsm/kg), despite extreme thirst. When treated with desmopressin acetate and allowed free access to water, she was able to reduce plasma osmolality below 270 mOsm/kg, and her compelling thirst disappeared. The disorder is interpreted to be the result of excessive fluid intake in response to a thirst stimulus that was not inhibited by normal plasma osmolality. This study indicates that osmoreceptor control of ADH secretion is normal. Continued administration of vasopressin has relieved the symptoms and has not resulted in water intoxication.

Adult↗
PubMed1983

Failure of angiotensin II to stimulate increases in concentrations of adrenal androgens, 17-hydroxyprogesterone, or adrenocorticotropin in congenital 21-hydroxylase deficiency.

To determine if angiotensin II stimulates an increase in the plasma concentration of androstenedione, dehydroepiandrosterone, 17-hydroxyprogesterone, or ACTH in a patient with congenital 21-hydroxylase deficiency, we measured these plasma concentrations before and after the plasma angiotensin II concentration was increased by upright posture and angiotensin II infusion in a surgically castrate XX adult patient with this disorder. The patient was studied before treatment, after treatment with 1 mg dexamethasone daily for 3 weeks, and after treatment with both dexamethasone and 0.2 mg fludrocortisone daily for 3 weeks. The plasma concentrations of androstenedione, dehydroepiandrosterone, and 17-hydroxyprogesterone did not change consistently during increases in the angiotensin II concentration. The ACTH concentration did not increase in response to raised angiotensin II concentrations before or after steroid treatment. During the infusion of angiotensin II, blood pressure increased and renin activity decreased appropriate in degree to the preinfusion concentration of angiotensin II. The results from the study of this patient do not support the hypotheses that in congenital 21-hydroxylase deficiency, angiotensin II directly stimulates adrenal androgen secretion or that angiotensin II stimulates ACTH secretion.

17-alpha-Hydroxyprogesterone↗
PubMed1980

Pituitary carcinoma mimics the ectopic adrenocorticotropin syndrome.

A middle-aged man presented with weight loss, hypokalemic alkalosis, diabetes, hypertension, and generalized melanosis. Marked elevation of urinary free cortisol (655 micrograms/24 h) and plasma ACTH (2445 PG/ML) SUGGESTED THE DIAGNOSIS OF ECTOPIC ACTH syndrome. The plasma concentrations of cortisol and urinary 17-hydroxycorticosteroids increased paradoxically during the administration of dexamethasone without a corresponding change in the plasma ACTH level. Metyrapone administered over 24 h also markedly incrased both urinary free cortisol and 17-hydroxycorticosteroids. Selective venous sampling of plasma ACTH did not reveal a gradient between jugular vein and peripheral venous blood. The laboratory findings supported the diagnosis of ectopic ACTH syndrome. However, belated occurrence of visual changes necessitated surgical exploration, resulting in the diagnosis of pituitary carcinoma. A fluorescent antibody to ACTH reacted strongly with the atypical pituitary cells. This rare case documents that severe melanosis in Cushing's disease can occur without prior adrenalectomy and is consistent with the diagnosis of pituitary carcinoma. Furthermore, melanosis observed in patients with pituitary carcinoma is associated with ACTH levels similar to those occurrring in the ectopic ACTH or Nelson's syndrome.

17-Hydroxycorticosteroids↗
PubMed1979

Acromegaly associated with a bronchial carcinoid tumor: evidence for ectopic production of growth hormone-releasing activity.

A patient with acromegaly, pituitary enlargement, and elevated plasma GH levels also had a bronchial carcinoid tumor. Signs and symptoms of active acromegaly along with elevated GH levels persisted for 11 yr after hypophysectomy and pituitary stalk section. Resection of the bronchial carcinoid reduced plasma GH to barely detectable levels. Extracts of the frozen carcinoid tumor were devoid of significant GH, but when added to isolated pituitary cells of estrogen-primed male rats in 4-day primary culture exhibited specific GH-releasing activity in vitro. These findings strongly suggest that the patient's acromegaly resulted from continual stimulation of pituitary somatotrophs by a GH-releasing factor secreted by the bronchial carcinoid.

Acromegaly↗