Divergence between growth hormone responses to insulin‐induced hypoglycaemia and growth hormone‐releasing hormone in patients with non‐functioning pituitary macroadenomas and hyperprolactinaemia

Abstract

This study demonstrates that ITT and GHRH tests cannot be used interchangeably in diagnosing GH deficiency in patients with non-functioning pituitary macroadenoma and hyperprolactinaemia. If the ITT is considered to be the reference test, GH deficiency as assessed by GHRH can be missed in patients with hyperprolactinaemia. This disparity is probably due to a different mechanism of action of these stimuli. Hyperprolactinaemia may be associated with a diminished somatostatin tone, leading to a higher basal and GHRH-stimulated GH, without having an effect on peak GH to ITT.

Reduced capillary permeability and capillary density in the skin of GH‐deficient adults: improvement after 12 months GH replacement

“…The seven patients (two women) who participated had severe GHD, defined as a peak GH level < 6 mU/ l in response to insulin-induced hypoglycaemia (venous blood glucose ≤ 2·2 mmol / l and the presence of hypoglycaemic symptoms) (The Growth Hormone Research Society Workshop on Adult Growth Hormone Deficiency, 1998). Soluble insulin was intravenously administered in a dose of 0·15 -0·20 U / kg body weight (Beentjes et al , 1996), and the insulin tolerance test was performed within 3 months before the start of the study. Each GH-deficient patient was matched with two healthy control subjects with respect to age (within 5 years) and body mass index (weight divided by height squared, within 2 kg / m 2 ).…”

Decreased plasma cholesterol esterification and cholesteryl ester transfer in hypopituitary patients on glucocorticoid replacement therapy

“…Hypopituitarism had been diagnosed to result from a pituitary or hypothalamic disorder which had been previously treated depending on its cause. All patients were growth hormone (GH) de®cient, de®ned as a peak GH v5 mg/l (10 mU/l) in response to insulin-induced hypoglycaemia (blood glucose nadir ¦2.2 mmol/l) [26]. Secondary adrenal insuf®ciency was de®ned as a peak serum cortisol response to insulin-induced hypoglycaemia ¦500 nmol/l [26,27] in the absence of an elevated corticotropin (ACTH) levels.…”

“…All patients were growth hormone (GH) de®cient, de®ned as a peak GH v5 mg/l (10 mU/l) in response to insulin-induced hypoglycaemia (blood glucose nadir ¦2.2 mmol/l) [26]. Secondary adrenal insuf®ciency was de®ned as a peak serum cortisol response to insulin-induced hypoglycaemia ¦500 nmol/l [26,27] in the absence of an elevated corticotropin (ACTH) levels. Secondary hypothyroidism was de®ned as a low free thyroxin (free T4) level (v9.0 pmol/l, reference range 9.0 ± 26.0) or a low free triiodothyronine (free T3) level (v3.0 pmol/l, reference range 3.0 ± 8.4) without an elevated thyrotropin (TSH) level [27].…”

“…Plasma insulin was measured by radioimmunoassay (Novo Nordisk Immunochemical Department, Copenhagen, Denmark). Serum GH, free T4, free T3, TSH, cortisol, gonadotropins and testosterone were assayed using routinely performed procedures as described [26]. Urinary steroid metabolites were analysed by gaschromatography [39].…”

Role of prolactin/adenoma maximum diameter and prolactin/adenoma volume in the differential diagnosis of prolactinomas and other types of pituitary adenomas

“…Pituitary adenoma-associated hyperprolactinemia is usually considered to be caused by prolactinoma, but other types of pituitary adenomas may also cause secondary hyperprolactinemia. For example, the incidence of non-functional pituitary large adenoma-associated secondary hyperprolactinemia is 34.8-41.2% (3)(4)(5)(6)(7)(8). The presence of secondary hyperprolactinemia makes it difficult to differentiate prolactinoma from other types of pituitary adenomas (9)(10)(11)(12).…”