Management of prolactinomas—1986

At least one third of women with hyperprolactinaemia have a prolactinoma (Franks & Jacobs 1983) and whereas most are microadenomas (<lo mm in diameter), a few of the tumours are large and extend out of the pituitary fossa to compromise the optic chiasma or to compress or invade the cavernous sinus. The therapeutic approaches presently available for patients with prolactinomas are medical treatment with dopamine agonists such as bromocriptine, selective pituitary surgery or radiotherapy. The major advance in the last decade has been the realization that treatment with bromocriptine not only suppresses hypersecretion of prolactin, but it may also result in shrinkage of the tumour, largely through reduction in the size of the tumour cells (Tindall et al. 1982). A number of reports have shown that treatment with bromocriptine can improve visual field defects and those using computerized tomography have confirmed tumour shrinkage (McGregor et al. 1979; Tan & Jacobs 1986). It has now been established that 90% of prolactinomas regress on treatment with bromocriptine (Bergh & Nillius 1982); even very large tumours with serum prolactin concentrations of 80 000-120 OOO dl (2000-3000 nglml) may show remarkable shrinkage (Velentzas et al. 1981). In cases where no shrinkage occurs despite suppression of prolactin secretion, the tumour is usually not a prolactinoma, but has caused secondary hyperprolactinaemia by compressing the pituitary stalk or hypothalamus. The argument in favour of medical treatment is made more compelling by the results of longterm follow-up, an issue that we can now begin to address after a decade of use of bromocriptine (Tan & Jacobs 1985). At the present time the following conclusions can be drawn: (1) The clinical response to treatment with bromocriptine in women with hyperprolactinaemia and proven prolactinoma has been consistently favourable and is maintained during prolonged treatment. There have been no cumulative sideeffects and no reports of tumour progression or growth of proven prolactinomas during treatment with bromocriptine (Corenblum & Taylor 1983). The maintenance dose of bromocriptine is usually much lower than the dose needed to induce remission and in our experience is about 5 mg/day. (2) When medication has been stopped after treatment for several years, although in many cases serum prolactin concentrations returned to pretreatment levels, in the majority there has been no regrowth of the tumour. In a recent report, for instance, 15 patients with prolactinomas were treated for 1.5-7 (mean 3.7) years: when the bromocriptine was withdrawn the tumour or gland size remained unchanged in 13 of the 15 patients. One man had a marginal increase in tumour size, while in another it shrank (Johnston et al. 1984). Surgical management of prolactinomas has resulted in owlatory menstrual cycles in 40% of patients with macroadenomas and in 80% of patients with microadenomas (Hardy et al. 1978; Tucker et al. 1981; Richards et al. 1986). Operation does of course carry a risk of surgical complications, which necessarily includes hypopituitarism. In a review of the results of transsphenoidal surgery in eight series totalling 283 patients, the rate of cure, that is of persistent normalization of serum prolactin concentrations, ranged from 24 to 78% (Thorner et al. 1980). In general the larger the tumour, the smaller the chance of cure and bromocriptine is often needed postoperatively to normalize prolactin secretion and so induce ovulation. For