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PubMed1981

Erythromelalgia-like eruption in parkinsonian patients treated with bromocriptine.

In a previous report about the chronic use of bromocriptine in Parkinson disease, a distinctive cutaneous eruption was noted and termed "erythromelalgia." This eruption has occurred in 9 of 110 patients on chronic bromocriptine therapy; histopathologic examination in 3 patients showed a prominent perivascular lymphocytic infiltration and perivascular edema of the dermis, without frank vasculitis. This is a reversible unwanted effect of bromocriptine therapy.

Aged↗
PubMed1985

Parkinson's disease and hypertension: chronic bromocriptine treatment.

We studied the effects of bromocriptine therapy (mean dosage, 56.0 mg daily) for 12 months in five patients with both Parkinson's disease and hypertension. Therapy improved neurologic manifestations and reduced both supine and standing systolic blood pressures and standing diastolic blood pressure with no consistent change in heart rate. Transient episodes of orthostatic hypotension appeared in two cases. Domperidone (60 mg daily for 1 month) did not abolish the antihypertensive effect of bromocriptine, suggesting that central dopaminergic or alpha-adrenolytic mechanisms are involved in this effect. Bromocriptine may be useful in the treatment of hypertension in patients with Parkinson's disease.

Aged↗
PubMed1985

Combined bromocriptine-levodopa therapy early in Parkinson's disease.

Compared with levodopa, treatment of parkinsonism for 3 years with bromocriptine alone resulted in less fluctuation and peak-dose dyskinesia, but also less improvement in parkinsonian disability. Only a few of the 76 patients had long-term benefit on chronic bromocriptine therapy. However, combined bromocriptine and levodopa therapy had a therapeutic response equal to that of levodopa alone, with fewer fluctuations and peak-dose dyskinesias. Treatment should begin with a low dose of levodopa and a dopamine agonist.

Bromocriptine↗
PubMed1986

Bromocriptine holiday: effects on dopamine receptors and turning behavior in rats.

In experimental Parkinson's disease, we studied the effects of chronic administration (30 days), withdrawal, and reinstitution of bromocriptine. Dopamine (DA) receptor supersensitivity was produced by 6-hydroxydopamine and reversed by chronic bromocriptine administration. Drug holiday reestablished sensitivity of DA receptors, but reinstitution of bromocriptine again downregulated receptors. The effects of a drug holiday on DA receptors are short-lived, and long-term clinical improvement cannot be expected. Apomorphine-induced contralateral turning produced by the lesion was unaffected by any drug regimen.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Early combination of bromocriptine and levodopa in the treatment of Parkinson's disease: a 5-year follow-up.

Compared with levodopa, long-term bromocriptine treatment of parkinsonian patients for 5 years resulted in fewer fluctuations of disability and peak-dose dyskinesias, but also less improvement in parkinsonian disability. Combination of low-dose bromocriptine and levodopa resulted in a therapeutic response equal to that of levodopa alone but with fewer end-of-dose disturbances and peak-dose dyskinesias. I believe that treatment should begin promptly with a low dose of levodopa, combined with a dopamine agonist such as bromocriptine.

Bromocriptine↗
PubMed1995

A randomized, double-blind, placebo-controlled study of bromocriptine in nonfluent aphasia.

We carried out a double-blind and placebo-controlled study of the efficacy of bromocriptine in the treatment of nonfluent aphasia. Seven patients received bromocriptine (up to 60 mg/d) and an identical placebo in a randomized order. End points were the number of content words, content units, and pauses > 3 seconds during the description of a figure; verbal naming; and verbal fluency. There were no significant benefits of bromocriptine over placebo in any of the variables examined.

Adult↗
PubMed1988

Pituitary apoplexy manifested during a bromocriptine test in a patient with a growth hormone- and prolactin-producing pituitary adenoma.

This report describes the clinical course of pituitary apoplexy induced by a single dose of bromocriptine in a 50-year-old woman with acromegaly. The patient suddenly complained of diminished vision and headache 2 hours after the oral administration of 2.5 mg of bromocriptine. Her visual symptoms and headache persisted for several days. The basal plasma GH concentration decreased from 76.2 ng/ml to 37.2 ng/ml the day after the attack of apoplexy and to 3.0 ng/ml on the 9th day. The authors assess the changes in endocrine findings related to pituitary apoplexy and also emphasize the necessity to view with caution any symptomatic change during bromocriptine therapy.

Adenoma↗
PubMedDate not supplied

Bone calcium turnover, formation, and resorption in bromocriptine- and prolactin-treated lactating rats.

To evaluate the effect of endogenous prolactin (PRL) on bone metabolism, we studied bone calcium turnover by the (45)Ca kinetic method and bone formation and resorption by bone histomorphometry and biochemical markers in 13-wk-old lactating Wistar rats. For 1 wk, the animals received daily administration of 0.9% NaCl (control) intraperitoneally, 6 mg of bromocriptine/ kg of body wt intraperitoneally, or 6 mg of bromocriptine/kg of body wt plus 2.5 mg of ovine PRL/kg of body wt subcutaneously. Bromocriptine, a dopaminergic inhibitor of endogenous PRL secretion, significantly decreased calcium ion deposit rate and calcium resorption rate in femur, tibia, vertebrae 5 and 6, and sternum by 20- 42%. By contrast, calcium resorption rate of the vertebrae and the sternum of the PRL-treated group was higher than that of controls, whereas the tibia and sternum exhibited a greater net loss of calcium. The suppression of bone calcium turnover in the bromocriptine-treated group was further supported by a significant decrease in the urinary deoxypyridinoline, a biochemical index of bone resorption, and the histomorphometric data, which showed changes indicative of suppressed bone resorption and formation. The histomorphometric data from the PRL-treated group were not different from those of the control group with the exception of an increase in the longitudinal growth rate. The results suggested a role of endogenous PRL in the stimulation of bone turnover during lactation.

Animals↗
PubMed1990

[Comprehensive approach to clinical background and effect of bromocriptine administration in patients with endocrinological polycystic ovarian disease].

Present study was performed to elucidate the clinical features and the treatment of so-called endocrinological polycystic ovarian disease (PCO). 36 cases out of 189 infertile patients who had various ovulatory disturbances were subjected during past four years. They were selected by the definitions as follows; 1) serum LH levels greater than or equal to 30 mIU/ml and serum FSH levels less than or equal to 15 mIU/ml, 2) hyper-response of LH secretion by LH-RH (100 micrograms) loading test; maximum values greater than or equal to 250 mIU/ml. Serum androstenedione (ASD), dehydroepiandrosterone-sulfate (DHA-S), estrone (E1), estradiol (E2), progesterone (P, in the mid-luteal phase) and testosterone (T) levels were examined by RIA method for the purpose of the evaluation of the endocrinological background of the PCO in Japanese women. The same examinations were also done in 8 volunteer women who had normal ovulatory menstrual cycles for the control study. In 6 cases of the PCO patients who showed biphasic BBT charts, the endometrial biopsy was done in the mid-luteal phase at the same time of the blood sampling. And the correlation between various serum hormone levels and the endometrial morphology in the PCO patients was also discussed. Then bromocriptine (5 mg/day) was administered in these patients for more than 30 days and the effect of the treatment was investigated. Serum ASD levels in the PCO patients were significantly higher than those in the control (2.52 +/- 1.30 vs. 1.43 +/- 1.21 ng/ml, M +/- S.D., p less than 0.05), while serum E2 and P levels in the patients were significantly lower than those in the control (E2: 118.6 +/- 39.5 vs. 192.5 +/- 53.9 pg/ml, p less than 0.005. P: 7.26 +/- 5.08 vs. 124.4 +/- 4.6 ng/ml, p less than 0.005, respectively). There were no significant differences in serum levels of the other hormones. By the administration of bromocriptine, serum ASD levels decreased (1.62 +/- 1.34 ng/ml, p less than 0.05), and E2 (177.9 +/- 48.6 pg/ml, p less than 0.025) and P (11.8 +/- 4.3 ng/ml, p less than 0.005) levels increased significantly into the levels of control. Serum LH levels of the patients were also suppressed by the treatment of bromocriptine (42.5 +/- 13.7 vs. 27.4 +/- 12.0 mIU/ml, p less than 0.005), however there was no change in serum FSH levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

Prolactin and bromocriptine induced changes in liver, adipose tissue and blood lipids of mature male bonnet monkeys, Macaca radiata (Geoffroy).

Effects of prolactin and bromocriptine on neutral and phospholipids of liver, adipose tissue and serum were studied in mature male bonnet monkeys. Hyperprolactinemia (ovine prolactin, 250 micrograms/kg body weight/day, i.p. for 30 days) elevated hepatic total lipids and phospholipids and decreased total and free cholesterol. While triacyl glycerol accumulated, mono-and diacyl glycerols diminished in liver and adipose tissues of prolactin treated monkeys. Concentrations of all phospholipid fractions, except sphingomyelin and cardiolipin in adipose tissue accrued in both tissues. Serum triacylglycerol, phosphatidyl ethanolamine, phosphatidyl choline and phosphatidyl inositol showed a significant increase in hyperprolactinaemic monkeys. Bromocriptine (1 mg/kg body weight/day for 30 days) treatment reduced serum phospholipids without altering hepatic or adipose tissue lipids. The present study indicates that hyperprolactinaemia leads to hyperlipidemia due to accretion of hepatic and adipose tissue triacyl glycerol and certain phospholipid fractions. Bromocriptine has a specific inhibitory effect on serum phospholipids.

Adipose Tissue↗
PubMed1995

Normal growth and pubertal development during bromocriptine therapy in two patients with prolactinoma.

The cases of two boys, a 14 years 10 months old and an 18-year-old, with delayed puberty are presented. The first patient also had a short stature. Both patients had a pituitary adenoma, as shown by computed tomography, with high prolactin levels. After bromocriptine therapy was started, there was a spontaneous progression of normal puberty. The first patient used a synthetic growth hormone together with bromocriptine, however, even after the growth hormone was stopped progression in puberty and gain in height continued. The favorable response obtained in these patients implies that bromocriptine can be an effective therapy for adolescent patients with prolactinoma.

Adolescent↗
PubMed1997

Octreotide and bromocriptine suppress thyroid hormone levels and thyroid nodule in an acromegalic patient with nontoxic autonomous goiter.

An acromegalic patient with nontoxic autonomous goiter was sequentially treated with octreotide and bromocriptine. Before therapy, serum GH, PRL and insulin-like growth factor-I (IGF-I) levels were increased. Free T3 and free T4 were within the normal range with suppressed TSH levels, whereas 123Iodine-uptake of thyroid was 5.6% after 24 h. During treatment with octreotide and bromocriptine, serum GH, PRL, and IGF-I became normal and free T3 and free T4 were slightly but significantly decreased, but TSH levels remained very low. After thyroidectomy, thyroglobulin, free T3 and free T4 were further decreased, and the TSH levels were recovered to normal. These findings suggested that octreotide and bromocriptine inhibit the release of thyroid hormones from the autonomous thyroid gland directly or indirectly through the decline in IGF-I.

Acromegaly↗
PubMed1987

Decrease in serum prolactin during bromocriptine-induced pregnancy and subsequent restoration of reproductive function in some hyperprolactinemic women.

Twenty-two women with hyperprolactinemia and amenorrhea were followed up for at least 18 months after 22 bromocriptine-induced full term pregnancies. Return of menstruation occurred in 9 of the 22 patients after pregnancy. Five of them conceived subsequently without any treatment. The prolactin (PRL) concentration before or during bromocriptine treatment was not significantly different between the patients who conceived spontaneously and those who did not. However, the PRL concentration after weaning was significantly lower in the patients who conceived spontaneously than in those who did not. Serum PRL levels were normal or only slightly elevated in the patients who conceived spontaneously. In 11 of the 22 patients, PRL levels were serially determined during bromocriptine-induced pregnancies. In 7 of the 11 patients, serum PRL levels fell during the second or third trimester. Spontaneous pregnancy occurred in 3 of the 7 patients who showed a decrease in PRL values during pregnancy, but in none of the 4 patients who did not. Furthermore, PRL levels after weaning correlated with PRL levels during the third trimester in these 11 women. Consequently, a decrease in PRL values during pregnancy may result in a fall in PRL levels after pregnancy, which in turn leads to the restoration of reproductive function in some subjects.

Adult↗
PubMed1988

A case of large prolactinoma supposed to be cured by bromocriptine therapy.

The authors reported a patient with a large prolactinoma (PRL 1,716 ng/ml) who was treated with bromocriptine for two years and followed up for a subsequent 36 months. After the start of the therapy, the tumor size was dramatically reduced, and finally the disappearance of the tumor was confirmed by high resolution coronal CT. The serum prolactin level and pituitary function were normalized. The tumor has not regrown and the blood prolactin level has remained normal for 36 months since the discontinuation of bromocriptine administration. This is a very rare case report on the eradicative effect of bromocriptine on such a large prolactinoma. Another characteristic of this case was that the prolactin reserve was maintained not only before the therapy but also during the early stage of the therapy.

Adult↗
PubMed1990

Reduction of pituitary tumor size with clinical and biochemical improvement with bromocriptine in a normoprolactinemic Cushing's disease.

We report a 37-year old Japanese female patient with Cushing's disease who was treated with a large daily dose of bromocriptine, which resulted in the reduction of the pituitary tumor size with clinical and biochemical improvements. On admission, the pituitary tumor size detected by magnetic resonance imaging (MRI) was 12.4 x 11.1 x 6.2 mm. Both the basal plasma prolactin level and its response to TRH test were normal. The patient was treated with bromocriptine at 5 to 35 mg/day. With 35 mg daily, 24-h urinary free cortisol started to decrease and eventually became normal. Four months after initiation of treatment with the drug, there was clinical remission with normalization of suppressibility of plasma cortisol with 1 mg dexamethasone. Repeated examination of the pituitary fossa by MRI showed a marked reduction in the tumor size (6.3 x 6.2 x 2.4 mm). This is a very rare case in which treatment with bromocriptine resulted in a reduction of the pituitary tumor size as well as clinical and biochemical improvements in a patient with normoprolactinemic Cushing's disease.

Adrenocorticotropic Hormone↗
PubMed1977

Hypogonadism, galactorrhoea and hyper-prolactinaemia: Evaluation of pituitary gonadotrophins reserve before and under bromocriptine.

Twenty patients with hypogonadism (19 women with amenorrhoea and 1 man with impotence and infertility), galactorrhoea and hyper-prolactinaemia (range: 36 to 344 ng/ml) were studied. The radiological study of the sella turcica, including in all cases hypocycloidal tomograms, allowed classification of the patients into 3 groups: group I (n = 4) had a grossly enlarged sella turcica, group II (n = 12) had localized alterations indicating the probable existence of a prolactin-secreting microadenoma ("microdeformation") while group III patients presented no radiological abnormality. Before treatment, all the patients were submitted to a complete evaluation of the function of their anterior pituitary, including the LH and FSH responses to iv administration of Gn-RH. All the group I patients had low basal LH levels and a blunted response to Gn-RH. The basal LH and in response to Gn-RH were normal in most of the group II patients and in all of the group III patients. An exaggerated FSH response to Gn-RH was observed in 6/12 patients with microdeformation (group II) but not in groups I and III patients. A low LH and a blunted LH response to Gn-RH is highly suggestive of the existence of a pituitary prolactin-secreting adenoma in case of amenorrhoea and hyper-prolactinaemia patients; a normal response does not however rule out such a diagnosis. The reasons for a exaggerated FSH response to Gn-RH in patients with suspected prolactin-secreting microadenoma remain to be investigated though this pattern can also occur in other cases of amenorrhoea. Hence the Gn-RH test might contribute to the assessment of the hypothalamo-pituitary axis of patients with hyper-prolactinaemia. Six patients treated for 4 months with bromocriptine (CB-154) were submitted to re-evaluation of their pituitary gonadotrophins reserve. All the women experienced restoration of menses with 39 days of treatment and the male patient regained potency. It was observed that bromocriptine treatment and subsequent normalized prolactin levels in the 4 group II women tested were associated with normalization of their previously exaggerated FSH response to Gn-RH; LH responses were also diminished in these cases. These data are compatible with the hypothesis that hyper-prolactinaemia per se could interfere with the endogenous secretion of Gn-RH at the hypothalamic level. In one patient with grossly enlarged sella turcica and a previous lack of an LH and FSH response to Gn-RH, bromocriptine treatment restored a normal gonadotrophins response, confirming that, in this case, the alteration of this response was indeed due to a prolonged lack of endogenous Gn-RH secretion.

Adolescent↗
PubMed1978

Long-term treatment of acromegaly with bromocriptine.

Treatment with bromocriptine, 30-55 mg daily, in 13 acromegalics for 1-15 months, resulted in a 60% decrease in growth hormone secretion, as judged from the excretion of growth hormone in 24-h urine. Normal excretion was obtained in 10 patients, while 1 patient showed no response. The plasma growth hormone response to O-GTT was improved, but not normalized, in 4 of 7 patients treated for more than 6 months, and marked glucosuria disappeared in two diabetics. While the secretion of TSH, LH and FSH was unchanged, the prolactin secretion was inhibited. The urine excretion of free cortisol showed a 30% decrease, possibly due to a direct effect of bromocriptine on the ACTH-secretion. Hypercalcaemia was never seen, but the initial hypercalcuria showed a modest decrease without measurable changes in the creatinine clearance. The subjective relief during long-term treatment was marked in 10 of 11 patients and the dominating symptoms disappeared in 40-67%, whereas heal-pad thickness, enlarged sellae, and visual fields remained unchanged. No serious side effects were observed. Treatment with bromocriptine seems effective and should be considered as a remedy amongst others, in suitable cases of acromegaly.

Acromegaly↗
PubMed1981

Effect of short-term bromocriptine treatment on amniotic fluid prolactin concentration in the first half of pregnancy.

The effect of short-term bromocriptine treatment on amniotic fluid and maternal prolactin concentrations was studied in 9 pregnant women in the first half of pregnancy. Bromocriptine suppressed the maternal serum prolactin level, but had no effect on the amniotic fluid level. Since both foetal and maternal prolactin secretion are suppressed by bromocriptine our results suggest that amniotic fluid prolactin is produced by extrapituitary tissues, which do not contain dopamine receptors.

Amniotic Fluid↗