Bengt-Ãke Bengtsson Division of Endocrinology, Sahlgren's Hospital, S-41345 GÃ¶teborg, Sweden Acromegaly was first described by Marie in 1886 /l/, although earlier reports exist. Minkowski in 1887 /2/ suggested a pituitary source of the disorder, which was later confirmed by Cushing in 1909 /3/, who postulated excessive secretion of a growth-promoting hormone by the pituitary gland. Acromegaly is a well established syndrome :aused by excessive secretion of GH, in more :han 99% of cases due to a pituitary adenoma. The acromegalic features result from overproduction of GH, as well as a related increase of GH-dependent tissue growth factors ;uch as insulin-like growth factor-I (IGF-1). Clinical manifestations of acromegaly are due Î¿ local effects of the pituitary mass and the ystemic effects of increased growth hormone ecretion. Symptoms consist of the typical coarsening of facial features, soft-tissue swelling, lerve compression, visceral enlargement, cardiac hypertrophy and metabolic changes such as liabetes mellitus and hyperlipidemia /4/. In 1980, Alexander et al /5/ published an pidemiological study of acromegaly based on a 2-year survey in the Newcastle region in Lngland. An incidence of 4.2 per million ^habitants was found, identical to the incidence 'e observed in Gothenburg, Sweden /6/. Our tudy comprised 166
Journal of Pediatric Endocrinology and Metabolism – de Gruyter
Published: Jan 1, 1993
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