NORMAL GROWTH AND PUBERTAL DEVELOPMENT DURING BROMOCRIPTINE TREATMENT FOR A PROLACTIN‐SECRETING PITUITARY MACROADENOMA
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SUMMARY An 11 ‐year‐old male presented with a 2‐year history of headache and lethargy. Serum PRL was elevated at 14 000 mU/1 and computerized tomography showed a pituitary macroadenoma. Visual fields and fundi were normal and the testes showed early pubertal changes. There was normal responsiveness of serum Cortisol but absence of GH response to hypoglycaemia. After bromocriptine therapy for 4 months serum PRL had fallen to 90 mU/1 and the tumour was not visible on repeat computerized tomography. After 7 months treatment, repeat pituitary function testing showed restoration of GH response to hypoglycaemia. Treatment with bromocriptine was continued and there was spontaneous progression of normal puberty; the serum testosterone continued to rise, and height maintained the 50th centile. Bromocriptine therapy should be considered as initial therapy in the management of prolactinomas in prepubertal patients.Keywords:
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To the Editor.—
We read with interest the article by Spark and co-workers (1982;247:311) about the effects of bromocriptine on the size of prolactin-secreting, human-growth-hormone-secreting and nonsecretory pituitary tumors and would like to make a comment about some of the issues raised therein. During the past five years, we administered bromocriptine (2.5 to 15 mg/day) for two to 46 months to 26 patients (12 females and 14 males) with prolactin-secreting pituitary macroadenomas with computed tomographic (CT) scan controls before, during, and after bromocriptine therapy. Eighteen of them had previously undergone pituitary surgery (by transsphenoidal or transfrontal route), telecobaltotherapy, or both, while eight had never been treated before. In our experience, the normalization of prolactin levels was not always related to the reduction of the tumor mass: in fact, bromocriptine normalized serum prolactin concentration in 19 cases (73%), while a shrinkage of the adenoma was documented at CT scan in onlyPituitary Tumors
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저자는 유즙분비 억제를 목적으로 Bromocriptine을 투여한 15예와 Estrogen을 투여한 10예에서 임상적 효과와 혈청 prolactin치의 변화를 수유군과 비교 관찰하여 다음과 같은 결론을 얻었다. 1. 분만직후 2시간 이내의 혈청 prolactin치는 분만전의 혈청 prolactin치보다 상승하였다.(p<0.01). 2. 수유군에서 혈청 prolactin치는 분만후 제 3 주경에 비임신시의 혈청 prolactin 치로 감소되었다. 3. Estrogen 투여시 유즙분비 억제효과는 부분적이었고 약 40%에서 rebound lactation이 나타났다. 4. Bromocriptine 투여시 유즙분비 억제효과는 우수하였고 7∼13%에서 유즙분비와 유방팽창이 나타 났으나 그 정도는 매우 경미하였다. 5. Bromocriptine 투여시 혈청 prolactin치의 감소는 수유군보다 현저한 차이를 나타내었다. (P<0.01). 6. Bromocriptine과 Estrogen 투여시 약물에 의한 부작용은 관찰할 수 없었다.
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In order to assess the possible antiproliferative action of bromocriptine on pituitary tumors, the effects of the drug on colony formation were studied using GH3 cells grown in double-layered agar. Bromocriptine (300 nM) clearly inhibited both the number of colonies arising from single tumor cells as well as the size of the tumor cell colonies (p<0.001). The drug did not inhibit colony formation by cells derived from 2 non-pituitary tumors. The data show that this dopamine agonist blocks proliferation of rat pituitary tumor cells in vitro and lend further support to the preliminary clinical observations of an anti-tumor effect of bromocriptine in man.
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herapy for large prolactinomas remains controversial. Surgery is often unsuccessful in restoring endocrine function to normal. However, medical therapy with bromocriptine, a dopamine agonist, not only suppresses PRL levels, but may also lead to a reduction in tumor size. Previous reports have demonstrated radiographic evidence of tumor regression only after 3 or more months of bromocriptine therapy. We have now documented, for the first time, objective evidence of extremely rapid reduction in tumor size in two patients harboring large PRL-secreting pituitary tumors (mean pretreatment serum PRL levels, 2350 and 3900 ng/ml) who were prospectively treated with bromocriptine (7.5 mg/day) in preference to surgical intervention despite marked visual impairment in one of the patients. After 2 and 6 weeks of therapy, respectively, marked reduction in tumor size was demonstrated radiographically in both patients. Headache, visual acuity, and visual fields had improved after only 3 days. Although the mechanism of bromocriptine's antitumor activity is unclear, we believe that a large prospective trial to study the effects of bromocriptine therapy on the size of PRL-secreting macroadenomas is urgently needed to determine whether medical therapy should become the primary modality of treatment to reduce tumor size as well as restore endocrine function.
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Bromocriptine treatment of lactating rats, or removal of the litter, led to a decrease in the number of insulin receptors in the mammary gland and an increase in the concentration of insulin in the serum. Bromocriptine also induced a decrease in the concentration of both prolactin and progesterone in the serum, whilst concurrent treatment with the former but not the latter prevented all the effects of bromocriptine for 48 h. Removal of the litter produced a similar decrease in the concentration in the serum of prolactin but not of progesterone. Treatment with prolactin prevented all of the effects of removal of the litter for 24 but not 48 h. This suggests that these effects of prolactin may require a mammary gland actually synthesizing milk since the gland rapidly fills with milk after removing the litter whereas milk removal continues to take place in bromocriptine-treated rats allowed to continue nursing their litters.
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The effect of bromocriptine withdrawal after long-term treatment on prolactin levels has been investigated in thirty-seven patients with prolactinomas. In ten patients with macroprolactinomas and post-operatively excessively high prolactin levels persisting suppression of prolactin secretion after bromocriptine withdrawal has been observed. This effect was not observed in patients with microprolactinomas or macroprolactinomas with only moderately elevated prolactin levels. The degree of persisting suppression correlated to the height of prolactin levels before treatment and to the duration of bromocriptine therapy. No correlation was found between the rise of prolactin levels after bromocriptine withdrawal and withdrawal time. It is suggested that the persisting suppression of prolactin levels is a sequence of reduction in tumour size. This anti-proliferative action of bromocriptine seems to be specific for the prolactin secreting cells in macroprolactinomas with high proliferation rate and high prolactin turn-over. These findings offer new possibilities in the management of patients with macroprolactinomas.
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Two women are described with Forbes-Albright syndrome in whom abnormally elevated serum prolactin levels were normal or undetectable following surgical removal of the pituitary tumors. One of the pituitaries contained prolactin bioactivity which could not be accounted for by the growth hormone content of this tumor. This bioactivity was localized to an electrophoretically slow moving protein, cathodal to growth hormone, on polyacrylamide gel. The second pituitary tumor produced a protein in vitro with a molecular weight close to that of growth hormone. Ninety five percent of this newly synthesized protein was immunologically distinguishable from growth hormone. Prolactin content of the culture medium of the latter tumor was significantly greater than that of normal human pituitaries and its growth hormone content was significantly smaller. These findings demonstrated that the pituitary tumors in these women were secreting prolactin. In one of the patients, it was possible to remove the tumor while leaving the normal anterior pituitary gland intact.
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