Biomedical subjects

W Gallucci

Publications and source records attributed to W Gallucci.

6 recordsLinked to original sources

PubMed1991

Adrenal androgen secretion in postadolescent acne: increased adrenocortical function without hypersensitivity to adrenocorticotropin.

Basal and ACTH-stimulated plasma levels of cortisol, delta 4-androstenedione, and dehydroepiandrosterone (DHEA) were measured in a group of 11 female patients with postadolescent acne resistant to or relapsing after conventional therapy and in a group of 10 normal women without acne or hirsutism. Each patient received, in a blinded random fashion, a series of 5 1-h ACTH tests. For each test a different dose of ACTH-(1-24) was administered, ranging from 0-1 microgram/kg, given as an iv bolus. Blood samples were collected 0, 10, 30, and 60 min after ACTH bolus injection. Patients with acne had slightly higher concentrations of basal cortisol, delta 4-androstenedione, and DHEA than normal controls (P less than 0.05). After ACTH-(1-24) stimulation, the same patients had greater peak and time-integrated DHEA concentrations (P less than 0.03). The ED50 values of the cortisol dose-response curves were similar in patients and normal women (P less than 0.05), suggesting that there are no differences in the sensitivity of the adrenal cortex to ACTH between the acne patients and the controls studied. The ratio of DHEA to cortisol response was significantly elevated in women with acne compared to that in control women, suggesting some preponderance of the delta 5 pathway of steroidogenesis in acne (P less than 0.05). These findings of basal and ACTH-stimulated hypersecretion of delta 5-androgens in patients with postaldolescent acne are consistent with an increased volume of androgen-secreting tissue, rather than hypersensitivity of the adrenal zona reticularis to ACTH.

Acne Vulgaris↗

PubMed1988

The CRH stimulation test in bereaved subjects with and without accompanying depression.

We studied recently bereaved individuals with the corticotropin-releasing hormone (CRH) stimulation test. Subjects with a bereavement complicated by a depressive illness (n = 9) had significantly higher basal plasma cortisol levels and smaller plasma adrenocorticotropic hormone (ACTH) responses to CRH than either subjects with an uncomplicated bereavement (n = 19) or normal controls (n = 34). Subjects with depressed bereavement showed ACTH responses to CRH similar to those of depressed patients (n = 30). Bereaved subjects who had received psychotropic medications in the past (n = 13), compared with those who had not (n = 15), showed significantly smaller plasma ACTH responses to CRH. Significantly more subjects with bereavement complicated by depression, as compared to subjects whose bereavement was uncomplicated, had a past history of treatment for depression. These results suggest that predisposed individuals may respond to the stress of bereavement with a depressive illness accompanied by dysregulation of the hypothalamic-pituitary-adrenal axis.

Adjustment Disorders↗

PubMed1988

The antiglucocorticoid and antiprogestin steroid RU 486: its glucocorticoid agonist effect is inadequate to prevent adrenal insufficiency in primates.

The glucocorticoid receptor antagonist RU 486 has been used to treat the hypercortisolism of patients with nonpituitary Cushing's syndrome. Since endogenous cortisol production fluctuates in many patients with either the ectopic ACTH syndrome or adrenocortical tumors, treatment of these patients with a fixed dose of RU 486 introduces the risk of adrenal insufficiency. While RU 486 possesses some glucocorticoid agonist activity in addition to its potent antagonist effects, it is not known whether this intrinsic agonist activity is of sufficient magnitude to prevent adrenal insufficiency and sustain life. To answer this question three groups of bilaterally adrenalectomized cynomolgus monkeys (n = 5/group) were randomized to receive a daily injection of RU 486 (5 mg/kg.day), cortisol (1.25 mg/kg.day), or saline (placebo). All adrenalectomized monkeys received weekly im injections of deoxycorticosterone pivalate (1 mg) to prevent mineralocorticoid deficiency. Five sham-adrenalectomized monkeys served as controls and received im injections of saline (placebo). Blood was collected before adrenalectomy or sham operation and every 3 days postoperatively for measurement of serum electrolytes, blood urea nitrogen, and creatinine; plasma ACTH concentrations; and complete blood and differential cell counts. All sham-operated and cortisol-replaced adrenalectomized monkeys survived, and none developed overt biochemical evidence of adrenal insufficiency. All placebo and RU 486-replaced adrenalectomized monkeys expired within 33 days after adrenalectomy, presumably from adrenal insufficiency. These findings suggest that while RU 486 is a partial glucocorticoid agonist, its degree of glucocorticoid agonism is inadequate to prevent adrenal insufficiency and support life in adrenalectomized primates.

Adrenal Insufficiency↗

PubMed1986

Responses to corticotropin-releasing hormone in the hypercortisolism of depression and Cushing's disease. Pathophysiologic and diagnostic implications.

Primary depression can be associated with substantial hypercortisolism, thus prompting some researchers to suggest that depression shares pathophysiologic features with Cushing's disease. Clinically, depression can be difficult or impossible to distinguish from mild or early Cushing's disease that is associated with depressive features. The purpose of this study was to evaluate whether the pituitary-adrenal responses to ovine corticotropin-releasing hormone could help to clarify the mechanism of hypercortisolism in depression and in Cushing's disease and to assist in the differential diagnosis of these disorders. As compared with controls (n = 34), depressed patients (n = 30) had basal hypercortisolism (P less than 0.001) that was associated with attenuated plasma ACTH responses to ovine corticotropin-releasing hormone (P less than 0.001). This indicates that in patients with depression, the corticotroph cell in the pituitary responds appropriately to the negative feedback of high cortisol levels. In contrast, patients with Cushing's disease (n = 29) had plasma ACTH hyperresponsiveness to ovine corticotropin-releasing hormone (P less than 0.001), despite basal hypercortisolism (P less than 0.001), which indicates a gross impairment of the mechanism by which cortisol exerts negative feedback on the pituitary. Less than 25 percent of the patients with depression or Cushing's disease had peak ACTH responses that overlapped. We conclude that the pathophysiologic features of hypercortisolism in depression and Cushing's disease are distinct in each of the disorders and that the ovine corticotropin-releasing hormone stimulation test can be helpful in their differential diagnosis.

Adrenocorticotropic Hormone↗

PubMed1986

The corticotropin-releasing hormone stimulation test in chronic schizophrenia.

During a drug-free period a group of schizophrenic subjects (N = 9) showed normal mean basal plasma ACTH and cortisol levels in association with normal plasma ACTH and cortisol responses to an infusion of corticotropin-releasing hormone (CRH). Administration of fluphenazine had no effect on basal ACTH and cortisol levels or their responses to CRH (N = 8). These data differ from those previously reported in depressed patients, who showed elevated basal cortisol values in association with a blunted ACTH response to CRH, and add to a growing body of literature which suggests that hypothalamic-pituitary-adrenal regulation is less disturbed in schizophrenia than in depression.

Adrenocorticotropic Hormone↗

PubMed1986

The corticotropin-releasing hormone stimulation test in patients with panic disorder.

Eight patients with panic disorder had significantly lower ACTH and cortisol responses to corticotropin-releasing hormone and a significantly lower ratio of ACTH to cortisol response than 30 normal control subjects. These responses resemble those previously reported for depressed patients except that they occurred in the face of significantly elevated basal cortisol and ACTH levels. These results suggest that patients with panic disorder have an element of chronic hypercortisolemia, like depressed patients, but also a more acute perturbation in ACTH secretion, not previously seen in depressed patients.

Adrenocorticotropic Hormone↗