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Hyperprolactinaemia and impotence.

Abstract

Clinical, laboratory and radiological findings were evaluated in twenty-nine men who had raised serum prolactin concentrations and pituitary tumours. Twenty-one had functionless pituitary tumours ('prolactinomas') and eight had acromegaly. Supraseller extension was detected in twenty of the twenty-six men who had lumbar airencephalography. Three patients were studied before, sixteen before and after and ten only after pituitary ablative therapy. Seventeen of these men complained of complete lack of libido and impotence and six had impaired libido and sexual potency; only six patients in this series denied reproductive symptoms. Thirteen of the impotent subjects had small soft testes, ten reduced facial and body hair and three had marked gynaecomastia. No features of hypogonadism were noted in the six patients without reproductive symptoms and none of the patients had galactorrhoea. Serum prolactin concentrations were higher and serum testosterone concentrations lower in the impotent men compared with those with normal sexual potency. Serum LH and FSH (both basal and in response to LHRH) oestradiol and oestrone concentrations were not different between the two groups and, except in those with post-operative hypopituitarism, were within the normal range. Following successful lowering of prolactin concentrations by surgery or bromocripitine or both, serum testosterone rose and potency returned; by contrast failure to lower prolactin concentrations was associated with persistent impotence and hypogonadism. The endocrine profile of low serum testosterone concentrations with gonadotrophins which had not risen into the range usually seen in primary hypogonadism (together with the parallel increase of LH and testosterone in one patient studied sequentially during treatment which suppressed prolactin levels to normal), suggested that the impaired gonadal function was caused by a prolactin-mediated disturbance of hypothalamic-pituitary function.

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BibTeXRIS

S Franks, H S Jacobs, N Martin, J D Nabarro. 1978. Hyperprolactinaemia and impotence.. https://doi.org/10.1111/j.1365-2265.1978.tb02770.x

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Acromegaly↗

Acromegaly.

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Acromegaly↗

Carney complex: the first 20 years.

PURPOSE OF REVIEW: The purpose of this review is to comment on the current findings on Carney complex, a dominantly inherited disease and a unique multiple endocrine neoplasia syndrome. RECENT FINDINGS: Sequencing of the PRKAR1A gene in more than 150 kindreds has revealed a number of pathogenic mutations; in more than 90% of the cases, the sequence change was predicted to lead to a premature stop codon and, thus, mutant mRNAs were subject to nonsense-mediated mRNA decay. In Carney complex syndrome cells carrying these mutations, protein kinase A activity is irregularly stimulated by cAMP. Mutations that did not lead to a premature stop codon have also been described; these were also associated with abnormal protein kinase A activity. Animal models of the disease have been recently developed; they reproduced some of the stigmata of Carney complex syndrome but not all. Genetic testing of patients' family members has been introduced in recent years, leading to early detection and a better overall prognosis. SUMMARY: New treatments have yet to be applied; the elucidation of the molecular pathways regulated by PRKAR1A holds the promise of leading to molecularly designed therapies.

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