Insulin Hypoglycemia Test and Releasing Hormone (Corticotropin-Releasing Hormone and Growth Hormone-Releasing Hormone) Stimulation in Patients with Pituitary Failure of Different Origin

Abstract

To investigate the efficacy of endocrine evaluation in diagnosing and localizing the cause of anterior pituitary failure, 17 patients with suprasellar space-occupying lesions, 4 patients with intrasellar tumors, 8 patients with no detectable anatomical lesion, 1 patient with posttraumatic failure and 1 patient with septooptical dysplasia were investigated. Endocrine evaluation consisted of measuring adrenocorticotropic hormone (ACTH), cortisol, and growth hormone (GH) levels during insulin hypoglycemia test (IHT) and after administration of corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GRH). In addition, basal prolactin levels, gonadal and thyroid function were evaluated. The results showed that 4 of 17 patients with suprasellar tumors had normal ACTH and GH responses during IHT and after releasing hormone (RH) administration. Five of these patients had a normal ACTH or cortisol rise but no GH response during IHT. All 5 had a normal ACTH and 3 had normal GH rise after RH. Seven patients with suprasellar tumors had no ACTH or GH response during IHT, but all had an ACTH response to CRH. Only 3 of this group had a GH response to GRH. There was one exception of a patient who showed a GH and ACTH rise during IHT but only a blunted ACTH and no GH rise after RH administration. Four patients with pituitary failure and no demonstrable lesion had an ACTH rise after CRH but no GH rise after GRH, whereas in 3 patients with isolated ACTH deficiency no ACTH rise after CRH was seen. In 4 patients with nonsecreting pituitary tumors normal ACTH responses to IHT and CRH were seen, whereas GH rose during IHT only in 1 patient. Thirteen of all patients had elevated prolactin levels above 500 µU/ml. Eight of these patients had ACTH and GH secretion patterns compatible with a hypothalamic defect, i.e. no response during IHT but an ACTH or GH response or both after RH administration. However, 5 patients with a bonafide pituitary tumor and nonresponsiveness to the releasing hormone had also elevated prolactin levels. In 2 patients with moderate hyper-prolactinemia, ACTH and GH responses to IHT and RH were completely normal. Our findings show that the endocrine function tests used in this study are not always reliable in locating the hypothalamo-pituitary defect.

The overnight single‐dose metyrapone test is a simple and reliable index of the hypothalamic‐pituitary‐adrenal axis

“…Side-effects are minimal using CRH in doses of 100 pg or less and the test is as useful as hypoglycaemia in assessing the function of the HPAA in patients on long-term corticosteroid therapy (Schlaghecke et al, 1992). However, the CRH test is costly, requires frequent blood sampling, and the assessments of its value in differentiating hypothalamic from pituitary causes of secondary adrenal insufficiency are conflicting (Muller et al, 1987;Lytras et al, 1984;Stalla et al, 1985Stalla et al, , 1988Taylor & Fishman, 1988). Some patients with an isolated hypothalamic defect give a normal response to CRH and this may be misleading if this diagnosis is not suspected.…”

A comparison of pituitary-adrenal responses to corticotropin-releasing hormone, hypoglycaemia and metyrapone in children with brain tumours and growth hormone deficiency

“…There are few reports regarding hormonal assessments in children with brain neoplasms using CRH other than in those with Cushing disease [4,20]. In the present study, we evaluated pituitary-adrenal function by performing a CRH stimulation test in children following treatment for brain tumours and compared the release of adrencorticotropin (ACTH) and cortisol with that in growth hormone deficient (GHD) children whose pituitary ACTH secretion was normal.…”

Inhibition of lnterleukin-2-Mediated Lymphocyte Activation in Patients with Cushing’s Syndrome: A Comparison with Hypocortisolemic Patients

“…Plasma cortisol concen trations were 66 ± 17 nmol/1 (p < 0.001 vs. normal subjects). Diag nosis was confirmed by low or undetectable basal plasma ACTH lev els (1.1 ± 0 .4 pmol/1, p < 0.001 vs. normal subjects) and the failure to respond appropriately to ACTH stimulation and insulin-hypoglyce mia [31,32], All hypocortisolemic patients were on oral 25 mg corti sol substitution therapy, distributed as four dosages per day, but on the day of testing, blood samples were taken before the 10 mg morn ing cortisol administration. Because of ethical considerations and the danger of causing an acute adrenal crisis, patients were not studied without adequate cortisol substitution for a longer period of time.…”