cosyntropin and Adrenal-Cortex-Diseases

Topics: Adrenal Cortex Diseases; Adrenal Insufficiency; Cosyntropin; Glucocorticoids; Humans; Metyrapone

Tuberculosis is a major public health problem in Pakistan and adrenal involvement in long-standing tuberculosis has been found to be common. A multi-center study was conducted to assess the adrenal function using short Synacthen test in one hundred patients with tuberculosis of more than 6 months duration at three hospitals of Rawalpindi and Islamabad. Forty patients demonstrated impaired response to Synacthen test. In 21 (52.5%) the increment from basal level was less than 300 nmol/L with a peak level increasing to over 600 mmol/L in 15 (37.5%) patients, the increment from basal level was less than 300 nmol/L as well as the peak level was also less than 600 nmol/L. In 4 (10%) patients the increment was more than 300 nmol/L but they were not able to obtain a peak level of 600 nmol/L. No significant difference was found between the patients with normal response and the impaired response with regards to their clinical features, duration of illness, body mass index (BMI), blood pressure variation and routine biochemical profile. It is concluded that adrenal dysfunction is common in patients with long-standing tuberculosis. Diagnosis of hypoadrenalism is not possible on clinical grounds and routine biochemical examinations. Synacthen stimulation test is necessary for its diagnosis.

Topics: Adrenal Cortex Diseases; Adrenal Cortex Function Tests; Adrenal Glands; Adult; Chronic Disease; Cosyntropin; Female; Humans; Male; Middle Aged; Sensitivity and Specificity; Tuberculosis, Pulmonary

During a Phase I trial of suramin, a novel antineoplastic agent with activity against hormone-refractory prostate carcinoma, the authors observed two patients with clinical mineralocorticoid insufficiency in spite of hydrocortisone replacement therapy.. The authors retrospectively assessed adrenal cortical function in 20 such patients via adrenocorticotropic stimulation testing, measuring both cortisol and aldosterone responses, either at the time or treatment of immediately after discontinuation of treatment.. Two of 9 patients (22%) treated at relatively low dose levels (< or = 1200 mg/m2 on Day 1) demonstrated adrenal cortical insufficiency, as compared with 9 of 11 patients (32%) treated with relatively high doses (> 1200 mg/m2 on Day 1) (P = 0.03 by 1-tailed Fisher's exact test). There appeared to be a cumulative dose-response relationship to the development of glucocorticoid insufficiency, with no instances being observed at doses < 4.8 g/m2 and uniform toxicity occurring at doses > 7.6 g/m2. Long term glucocorticoid insufficiency was present in 1 of 5 patients (20%) tested at an interval of > 90 days after discontinuation of suramin treatment. All instances of glucocorticoid insufficiency were associated with mineralocorticoid insufficiency. Suramin did not affect the absorption or excretion of exogenously administered glucocorticoid in one patient.. Suramin causes both primary mineralocorticoid and primary glucocorticoid insufficiency. This may occur in a dose-dependent manner. Long term glucocorticoid insufficiency appears to occur in a minority of patients treated with low doses of suramin. Patients receiving high doses of suramin for treatment of advanced carcinoma should receive at least physiologic replacement doses of both mineralocorticoid and glucocorticoid. Higher doses of glucocorticoid may be required in selected patients.

Topics: Addison Disease; Adrenal Cortex Diseases; Adrenocorticotropic Hormone; Aged; Aldosterone; Antineoplastic Agents; Cosyntropin; Drug Administration Schedule; Humans; Hydrocortisone; Male; Middle Aged; Prostatic Neoplasms; Retrospective Studies; Suramin

Topics: Adrenal Cortex Diseases; Adrenal Cortex Function Tests; Adrenocorticotropic Hormone; Cosyntropin; Drug Administration Schedule; Female; Humans; Hydrocortisone; Male; Reproducibility of Results

Previous studies have shown that the rapid ACTH stimulation test using a low dose of 1 microg is more sensitive than that using 250 microg ACTH for detecting subtle cases of adrenal insufficiency. However, there are controversies for the reproducibility of the 1 microg-test. To evaluate the reproducibility of the 1 microg-test, we assessed both day-to-day and diurnal variations of cortisol responses to 1 microg ACTH injection. In addition, optimum sampling time for the 1 microg-test was also determined.. AND DESIGN Eight healthy volunteers and five patients with secondary adrenal insufficiency were recruited. Healthy subjects were given 1 microg ACTH 3 times in the morning (0800 h) and 2 times in the afternoon (1600 h). Patients with adrenal insufficiency had 2-tests in the morning and 2 in the afternoon. Serum cortisol levels were measured every 10 minutes for 1 h after the injection.. In healthy subjects, basal and peak serum cortisol levels were significantly higher in the morning (P < 0.05), whereas maximum cortisol increments were higher in the afternoon (P < 0.001). In patients with adrenal insufficiency, basal and peak serum cortisol levels in the morning were not different from corresponding values in the afternoon. Intra-individual coefficient of variation (CV) of peak serum cortisol response to 1 microg ACTH ranged from 3.0 to 16.4% in healthy subjects and 10.0-34. 4% in patients. Also, there was a significant correlation between peak morning or afternoon cortisol levels after 1 microg ACTH injection given in different days in both healthy subjects and patients. Twenty-six of the 40 studies in healthy subjects showed peak response at 20 minutes, while nine showed it at 30 minutes Using the data acquired at 20 and 30 minutes, all 40 studies in healthy subjects showed normal results while none of 20 studies in patients was normal.. We conclude that the cortisol response to 1 microg ACTH stimulation was reproducible in both healthy subjects and patients with secondary adrenal insufficiency. In order to assess adrenal function more accurately with the 1 microg ACTH stimulation test, serum cortisol should be measured before and 20 and 30 minutes after ACTH injection.

Topics: Adrenal Cortex Diseases; Adrenal Cortex Function Tests; Adrenal Insufficiency; Adult; Case-Control Studies; Circadian Rhythm; Cosyntropin; Drug Administration Schedule; Female; Humans; Hydrocortisone; Male; Middle Aged; Reproducibility of Results; Time Factors

In summary, maneuvers that affect the RAS stimulate or suppress solely aldosterone and 18-OHB and have little, if any, effect on DOC, 18-OHDOC, B, or cortisol. The magnitude of aldosterone response seems to be of equal magnitude for all stimulatory or suppressive maneuvers as used in the present protocols. Although primarily originating in the ZG, some secretion of 18-OHB from the ZF is evident by its disproportionate responses (in relation to aldosterone) to maneuvers challenging ACTH. The prompt and marked increases the 18-OHDOC and B after ACTH make them the most sensitive "markers" of the ZF steroid activity. The application of those maneuvers and MCH measurements to adrenal disorders should help to further characterize their pathophysiology.

Topics: Adolescent; Adrenal Cortex Diseases; Adult; Aldosterone; Angiotensin II; Corticosterone; Cosyntropin; Desoxycorticosterone; Diet, Sodium-Restricted; Female; Humans; Hydrocortisone; Male; Middle Aged; Mineralocorticoids; Posture; Potassium; Renin; Renin-Angiotensin System

Topics: Adrenal Cortex Diseases; Cosyntropin; Humans; Postoperative Complications

The putative stimulation of adrenal steroid production by immunoglobulins (Igs) of five patients with pigmented adrenocortical micronodular dysplasia and clinical Cushing's syndrome was investigated. Ascorbate depletion, a process linked to steroid production, was measured by a cyto-chemical bioassay employing guinea pig adrenal explants in organ culture and exposed to IgG from the patients and normal subjects. We also measured cortisol production by these segments during a 5-h culture period using a RIA. For positive reference values we studied the effects of ACTH-(1-39), ACTH-(1-24), ACTH-(11-24), and ACTH-(18-39) on in vitro ascorbate depletion and cortisol production. Both ACTH-(1-39) and ACTH-(1-24) depleted ascorbate and stimulated cortisol production in adrenal cells. The dose-response kinetics of the peptides were bell-shaped; maximal responses were reached in both instances at 1 fmol/L to 10 pmol/L. In all tests, stimulation of in vitro cortisol production was paralleled by ascorbate depletion. ACTH-(18-39) also stimulated ascorbate depletion and cortisol production, but at one concentration only (100 fmol/L), and TSH and LH had no effect. Protein-A-Sepharose-purified IgG preparations of the five patients stimulated ascorbate depletion and/or cortisol production in a dose-dependent fashion; however, the responses occurred over a narrow concentration range (15-150 micrograms IgG/mL culture fluid). These observations support the hypothesis that the hypercortisolism of the syndrome of pigmented adrenocortical micronodular dysplasia is due to circulating Igs that stimulate adrenal steroidogenesis.

Topics: Adolescent; Adrenal Cortex Diseases; Adrenocorticotropic Hormone; Adult; Ascorbic Acid; Biological Assay; Child; Cosyntropin; Cushing Syndrome; Dexamethasone; Female; Histocytochemistry; Humans; Hydrocortisone; Immunoglobulin G; Peptide Fragments

Topics: Adrenal Cortex Diseases; Adrenal Cortex Function Tests; Animals; Cattle; Cattle Diseases; Cosyntropin; Female; Pituitary-Adrenal Function Tests

Analysis of 24-h urinary steroid excretion was performed by capillary gas chromatography in six patients (five men, one woman) with adrenocortical insufficiency. Ten healthy subjects (five men, five women) served as controls. A complete absence of all 21-hydroxylated steroid metabolites was seen in patients with adrenocortical insufficiency, whereas the excretion of several steroids lacking hydroxylation in the 21-position (pregnenolone, pregnenetriol, and 11-ketoandrosterone) was markedly increased. In addition, the presence of 11 beta-hydroxyandrosterone was confirmed by mass-spectrometry in the urine of three patients. This pattern of steroid excretion was unchanged in patients with adrenocortical insufficiency, both after stimulation by 1-24 adrenocorticotropin (ACTH) and after short-term (3-d) suppression with dexamethasone. We conclude that patients with adrenocortical insufficiency present a pattern of steroid excretion characterized by the absence of 21-hydroxylated metabolites. In the absence of functional adrenocortical tissue, long-term pathologically elevated concentrations of ACTH apparently stimulate early steps of steroid synthesis, most likely in the gonads. In addition, the presence of 11-hydroxylated steroid metabolites (11-ketoandrosterone, 11 beta-hydroxyandrosterone) in the urine of patients with adrenocortical insufficiency demonstrates that chronic ACTH excess in this disorder may induce some activity of 11 beta-hydroxylase, an enzyme not found in the gonads under physiological conditions.

Topics: Adrenal Cortex Diseases; Adrenocorticotropic Hormone; Adult; Autoimmune Diseases; Chromatography, Gas; Cosyntropin; Cushing Syndrome; Dexamethasone; Female; Humans; Male; Middle Aged; Steroids

We report two children of a family with congenital adrenocortical unresponsiveness to ACTH. Repeated stimulation of the adrenal by Synthetic 1-24 ACTH (Synacthen) failed to increase cortisol secretion, but produced significant rises of serum aldosterone. This was, however, associated with increased plasma renin activity. Only when the renin-angiotensin effect was eliminated, by a converting enzyme blocker, did Synacthen fail to affect serum aldosterone. These data support the view that glucocorticoid deficiency in this disorder results from unresponsiveness to ACTH and that development of the zona glomerulosa and normal aldosterone secretion is achieved by action of the renin-angiotensin system.

Topics: Adrenal Cortex; Adrenal Cortex Diseases; Adrenal Cortex Function Tests; Aldosterone; Captopril; Cosyntropin; Glucocorticoids; Humans; Hydrocortisone; Infant; Infant, Newborn; Male; Renin; Syndrome

Diminished total plasma cortisol levels have been demonstrated in postmature neonates, suggesting that fetal glucocorticoids may be involved in the cause of postmaturity. This hypothesis was tested by adrenocortical stimulation in 32 newborns: 12 were postmature; 12 were postterm, but not postmature; and 8 were normal term neonates. The mean pre- and poststimulation total plasma cortisol levels were 3.9 and 50.9 microgram/100 ml, respectively, for the postmature newborns, 9.7 and 44.0 microgram/100 ml for the postterm, but nonpostmature newborns, and 9.8 and 37.1 microgram/100 ml for the normal term newborns. The differences in the poststimulation rise in plasma cortisol between the postmature and merely postterm infants or between the postterm and normal term infants were not statistically significant. The mean poststimulation cortisol rise in the postmature group exceeded that of the normal term group (P less than 0.05). The adequacy and promptness of response to adrenocortical stimulation eliminate the likelihood of adrenal insufficiency in postmature infants.

Topics: Adrenal Cortex; Adrenal Cortex Diseases; Adrenocorticotropic Hormone; Cosyntropin; Female; Humans; Hydrocortisone; Infant, Newborn; Placenta Diseases; Pregnancy; Pregnancy, Prolonged