Elsevier

The Lancet

Volume 352, Issue 9138, 31 October 1998, Pages 1455-1461
The Lancet

Seminar
Growth-hormone and prolactin excess

https://doi.org/10.1016/S0140-6736(98)03356-XGet rights and content

The treatment of acromegaly and hyperprolactinaemia has been improved by the availability of effective and welltolerated slow-release somatostatin analogues and dopamine agonists with long-lasting activity, such as cabergoline. The use of these drugs has extended the possibility of treatment to patients who would have responded poorly to the previously available compounds, such as octreotide or bromocriptine, and to those who were intolerant to pharmacotherapy. Moreover, the improvement in the management of acromegaly has enabled the reversal, at least partly, of cardiomyopathy and sleep apnoea, two important risk factors for morbidity and mortality in these patients.

Section snippets

Epidemiology

The prevalence of GH-secreting adenomas is 50–80 cases per million, and the incidence is three to four new cases per million per year.1, 2 In less than 2% of patients, excessive GH secretion may be the consequence of a hypothalamic or ectopic tumour (gangliocytoma, bronchial, or pancreatic) that produces GH-releasing hormone (GHRH); such tumours lead to somatotroph hyperplasia or a well-defined adenoma. The ectopic secretion of GH itself is even rarer.1

Diagnosis

The clinical features of acromegaly

Epidemiology

The aetiology of pathological hyperprolactinaemia is diverse (panel). Any process interfering with dopamine synthesis, its transport to the pituitary gland, or its action at lactotroph dopamine receptors can lead to hyperprolactinaemia.3 Once drugs are excluded, microprolactinomas (<10 mm) or macroprolactinomas (>10 mm) are the most common causes of hyperprolactinaemia. The prevalence of prolactinomas is unknown; in necropsy series, the rate varies between 23% and 27% for microadenomas.44, 45

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