Immunoreactive Corticotrophin Levels in Adrenocortical Insufficiency

Gm, Besser; Cullen, Dana; Irvine, W. J.; Ratcliffe, J G; Landon, J.

doi:10.1136/bmj.1.5745.374

Cited by 63 publications

(26 citation statements)

References 9 publications

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“…Extensive suprasellar extrusion had caused a severe and permanent lesion of the optic chiasm. Surgical removal of the tumour and radiotherapy were followed by a sustained regression of hyperpig¬ mentation and by a lowering of plasma ACTH to levels within the range found in uncomplicated cases of treated Addison's disease (Besser et al 1971;Holdaway 1973;Krieger & Gewirtz 1974). By contrast, in case 2 (F.G.), an intrasellar eosinophilic microadenoma neither caused any neurolo¬ gical complications nor affected the secretion of other pituitary hormones. Although it consisted of ACTH-producing cells, its contribution to overall ACTH secretion might have been rather minor, since, after its removal, hyperpigmentation per¬ sisted and plasma ACTH concentration remained markedly elevated.…”

Section: Discussionmentioning

confidence: 85%

ACTH-producing pituitary adenomas in Addison's disease: two cases treated by transsphenoidal microsurgery

Krautli¹,

Müller²,

Landolt³

et al. 1982

Acta Endocrinologica

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In 2 women with known Addison's disease, progressive hyperpigmentation reappeared years after an initial remission under conventional substitution therapy with cortisone. Excessively elevated plasma ACTH concentrations and radiological evidence of sella turcica deformation led to the diagnosis of ACTH-producing adenomas and prompted their removal by transsphenoidal microsurgery. In one patient, a large Crooke's cell adenoma with extensive extrasellar expansion had caused severe and irreversible bilateral defects of the visual fields and unilateral optic atrophy. Surgical removal of the tumour and radiotherapy brought about a permanent disappearance of the hyperpigmentation, but eventually led to secondary hypothyroidism. In the second patient, the selective removal of a small intrasellar eosinophilic adenoma consisting of ACTH-producing cells did not alleviate the hyperpigmentation and did not lower the plasma ACTH concentration. However, hyperpigmentation regressed markedly within a year of treatment with a higher dose of cortisone. The rarity of similar cases in the literature seems to indicate that insufficient feedback suppression of ACTH-producing cells in treated Addison's disease does not by itself induce the development of a pituitary adenoma, but might promote the growth of an independently and coincidentally occurring microadenoma, which would have caused Cushing's disease in a person with intact adrenal glands.

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Section: Discussionmentioning

confidence: 85%

ACTH-producing pituitary adenomas in Addison's disease: two cases treated by transsphenoidal microsurgery

Krautli¹,

Müller²,

Landolt³

et al. 1982

Acta Endocrinologica

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“…The latter has been used previously as a criterion for a normal adrenal response in studies investigating the HPA axis during septic shock (19)(20)(21). High ACTH levels in the presence of relatively low cortisol values, that is a low cortisol/ ACTH, may be indicative of primary adrenal insufficiency, while low to normal ACTH levels in the presence of low cortisol values are principally indicative of secondary adrenal insufficiency (22,23).…”

Section: Methodsmentioning

confidence: 99%

Assessing adrenal status in patients before and immediately after coronary artery bypass graft surgery

Debono¹,

Sheppard²,

Irving³

et al. 2011

European Journal of Endocrinology

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Objective: Patients with cortisol deficiency poorly tolerate any systemic inflammatory response syndrome (SIRS), and may die if not treated with sufficient exogenous glucocorticoids. Controversy surrounds what constitutes a 'normal' adrenal response in critical illness. This study uses conventional tests for adrenal insufficiency to investigate cortisol status in patients undergoing elective coronary artery bypass surgery, a condition frequently associated with SIRS. Design: A prospective, observational study. Methods: Thirty patients with impaired left ventricular function (ejection fraction O23% !50%) underwent basal ACTH measurement, and a short cosyntropin test (250 mg, i.v.) 1 week preoperatively, and at C4 h following induction of general anaesthesia. Preoperatively, a 30 min cortisol level post cosyntropin O550 nmol/l was taken as a normal response. Results: Prior to surgery, all patients had a normal response to cosyntropin. Postoperatively, eight patients (26.7%) did not achieve stimulated cortisol levels O550 nmol/l and the mean peak cortisol postoperatively was lower (1048 vs 730 nmol/l; P!0.001). There was a significant rise in ACTH after surgery (21 vs 184 ng/l; PZ0.007) and reduction in D-cortisol post cosyntropin (579 vs 229 nmol/l; P!0.001). There was no change in basal cortisol pre-and post-operatively (447 vs 501; PZ0.4). All patients underwent routine, uneventful postoperative recovery. Conclusion: Up to one quarter of patients with a normal cortisol status preoperatively demonstrated a raised ACTH and deficient cortisol response postoperatively. Despite these responses, all patients had uneventful outcomes. These data reinforce the need for caution when interpreting results of endocrine testing following major surgery or in the intensive care environment, and that prognostic value of these results may be of limited use.

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“…In patients with primary adrenocortical insufficiency given a large dose of hydrocortisone, plasma ACTH levels fell exponentially. The rapid fall of plasma ACTH levels seen in this and other reports (Besser et al, 1971 ;Krieger and Gewirtz, 1974) suggests that the negative feedback control mechanism remains almost intact in primary adrenocortical insufficiency.…”

Section: Discussionmentioning

confidence: 58%

“…Blood samples were collected through the catheter at 15-30 min intervals. Plasma was immediately separated and frozen, and then assayed for ACTH with a radioimmunoassay kit (Radio Chemical Center) by the extraction procedure with porous glass (Ratcliffe et al, 1971), and for cortisol with Clark's acid fluorescent method (Clark, 1969 Hydrocortisone infusion (1.0mg/kg/1.5 hr -3 .0mg/kg/2 hr) Five patients with adrenalectomized Cushing's disease showed no significant suppression 30 min after the infusion (Table 2, Fig. 1).…”

Section: Methodsmentioning

confidence: 99%

Plasma Immunoassayable ACTH Levels during and after Hydrocortisone Infusion in Patients with Cushing's Disease

et al. 1976

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SynopsisThe plasma ACTH responses to hydrocortisone infusion were compared in patients with Cushing's disease and primary adrenocortical insufficiency. In 4 patients with primary adrenocortical insufficiency, plasma ACTH levels were suppressed exponentially after administration of a relatively large dose of hydrocortisone (1.0 mg/kg/1.5 hr-3.0mg/kg/2 hr). In patients with post-adrenalectomized Cushing's disease (4, bilateral; 1, unilateral), plasma ACTH suppression was delayed. Plasma ACTH levels, expressed as a percentage of the basal concentrations, were significantly less suppressed in patients with Cushing's disease than in patients with primary adrenocortical insufficiency 90 (p <0.05) and 120 (p <0.05) min after the beginning of infusion. When 0.5mg/kg hydrocortisone was infused over a period of 1.5 hr, suppression was also delayed in Cushing's disease, and plasma ACTH levels were less suppressed in 4 patients with Cushing's disease than in 4 patients with primary adrenocortical insufficiency at 30 (p> 0.05), 45 (p> 0.05), 60 (p <0.01) and 90 (p <0.05) min.

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Immunoreactive Corticotrophin Levels in Adrenocortical Insufficiency

Cited by 63 publications

References 9 publications

ACTH-producing pituitary adenomas in Addison's disease: two cases treated by transsphenoidal microsurgery

ACTH-producing pituitary adenomas in Addison's disease: two cases treated by transsphenoidal microsurgery

Assessing adrenal status in patients before and immediately after coronary artery bypass graft surgery

Plasma Immunoassayable ACTH Levels during and after Hydrocortisone Infusion in Patients with Cushing's Disease

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