Acth, LPH and Related Peptides in the Ectopic Acth Syndrome

Pullan, P.T.; Clement‐Jones, Vicky; Corder, Roger; Lowry, P. J.; Besser, G. M.; Rees, Lesley

doi:10.1111/j.1365-2265.1980.tb03409.x

Cited by 32 publications

(12 citation statements)

References 20 publications

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“…The maximum level of ACTH, in the six patients in whom it was measured (three of whom failed to suppress after dexamethasone), before and after dexamethasone was 29 pg ml -1 and 13 pg ml -1 respectively. These levels are lower than those recognized to be associated with ectopic production of ACTH, characteristically greater than 200 pg ml -1 (Besser and Landon, 1968;Ratcliffe et al, 1972;Pullan et al, 1980;Howlett et al, 1986) and suggest an alternative pathogenesis for the hyperplasia and resistance to dexamethasone. An ectopic source of ACTH is also discounted by the rarity of this syndrome being recorded with haematological malignancies which accounted for the majority of our patients.…”

Section: Discussionmentioning

confidence: 59%

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy

et al. 1999

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The aim of this study was to further elucidate the activity of the hypothalamo–pituitary–adrenal (HPA) axis in patients with malignancy and to correlate this with the size of the adrenal glands. Fourteen patients with a variety of malignancies were studied prior to receiving cytotoxic chemotherapy. During routine staging computerized tomographic (CT) scans, the size of the body, medial and lateral limbs of the adrenal glands were measured and compared with those of a normal group of patients studied previously. Measurements of 09:00 h serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels were made before and after the administration of dexamethasone (0.5 mg 6-hourly for 48 h) in addition to the peak cortisol response to i.v corticotropin releasing hormone (CRH). Overall, patients with malignancy had significantly larger adrenal glands than patients without malignancy; those with non-haematological malignancies had larger glands than patients with haematological malignancies. Following dexamethasone to suppress circulating cortisol levels, nine patients (64%) demonstrated abnormal resistance with cortisol levels > 50 nmol l −1 : mean value 294 nmol l −1 (range 67–1147). Those patients who failed to suppress after dexamethasone had significantly larger adrenal glands than those that did suppress and tended to have non-haematological malignancies. ACTH levels were undetectable or low in three patients in whom it was measured and who did not suppress with dexamethasone. Following CRH, the cortisol levels were highest (823 and 853 nmol l −1 ) in two of these patients. Malignancy is associated with diffuse enlargement of the adrenal glands and resistance to dexamethasone-induced suppression of the HPA axis, which is not due to ectopic ACTH secretion. This disturbance of the normal control of the HPA axis is unexplained and its functional significance remains uncertain. © 1999 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 59%

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy

et al. 1999

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“…the nature of which was probably identical to hypothalamic CRF, since immunological and chromatographic similarities to the syn thetic human peptide were observed. Nearly all previous cases of ectopic Cushing's syn drome have been reported to be due to secre tion of ACTH by a non-pituitary site [2][3][4], However, a few cases have been described in which ACTH secretion was found in con junction with the secretion of substances with CRF activity [23][24][25] which conceiva bly may have stimulated the pituitary corticotrophs. More recently, however, since an tisera to CRF have become available, cases of Cushing's disease due solely to ectopic production of CRF [6,8] or excessive pro duction of CRF by an intrasellar gangliocytoma [7] have been described.…”

Section: Discussionmentioning

confidence: 98%

Ectopic Corticotrophin-Releasing-Factor and Growth Hormone Releasing Factor Secretion: Diagnosis Using Human Pituitary Cell Culture

et al. 1987

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Cell culture of human pituitary tissue has been used to diagnose a patient with Cushing’s syndrome due to ectopic secretion of corticotrophin-releasing factor (CRF; case 1) and a case of acromegaly associated with ectopic secretion of a growth-hormone releasing factor (GRF; case 2). In both patients a pituitary tumour was not detected. Case 1 had a small cell carcinoma and symptoms of the ectopic ACTH syndrome, but in culture the carcinoma failed to secrete detectable ACTH. However, the culture medium used to maintain this carcinoma in vitro was found to contain a substance which stimulated ACTH secretion by human pituitary corticotrophs in cell culture. Radioimmunoassays and HPLC indicated that this substance had similar elution characteristics to human CRF and cross-reacted with antiserum to ovine CRF. Case 2 was found to have a lung tumour, the removal of which led to regression of her acromegalic symptoms. In culture, this tumour did not secrete GH, but did secrete a GRF. We conclude that the Cushing’s syndrome and acromegaly, in cases 1 and 2, respectively, were due to ectopic secretion of CRF and GRF leading to hyperstimulation of the pituitary gland.

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“…These peptides have been found in extracts of ACTH-producing carcinoid tumours [2] and were demonstrable in this patient's tumour.…”

Section: Discussionmentioning

confidence: 95%

Actopic ACTH production by a thymic carcinoid tumour

McCaughey¹,

Walker²,

Rolles³

et al. 1987

Eur J Pediatr

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Acth, LPH and Related Peptides in the Ectopic Acth Syndrome

Cited by 32 publications

References 20 publications

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy

Ectopic Corticotrophin-Releasing-Factor and Growth Hormone Releasing Factor Secretion: Diagnosis Using Human Pituitary Cell Culture

Actopic ACTH production by a thymic carcinoid tumour

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