Bromocriptine treatment of acromegaly.

Thorner, Michael O.; Chait, Alan; Aitken, Maureen M.; Benker, G.; Bloom, Stephen R.; Mortimer, C. H.; Sanders, Paul W.; Mason, April C.; Besser, G. M.

doi:10.1136/bmj.1.5953.299

Cited by 201 publications

(63 citation statements)

References 19 publications

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“…The present findings might be of therapeutic importance, since suppression of the release of diabetogenic hormones like hOR and hPRL with bromocriptine in endocrine disturbances like acromegaly [20], hyperprolactinaemia or juvenile-type diabetes mellitus (Landgraf et al, unpublished observation) might improve the metabolic disturbances seen in these patients.…”

Section: Discussionmentioning

confidence: 64%

Prolactin: A diabetogenic hormone

Landgraf

Mm²,

Weißmann³

et al. 1977

Diabetologia

174

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Summary. During an oral glucose tolerance test (OGTT) glucose and insulin levels were measured in 26 patients with prolactin-producing pituitary tumours without growth hormone excess. Basal glucose and insulin levels did not differ from the values of an age-matched control group. After glucose load the hyperprolactinaemic patients showed a decrease in glucose tolerance and a hyperinsulinaemia. Bromocriptine (CB 154), which suppressed PRL, improved glucose tolerance and decreased insulin towards normal in a second OGTT. -Human PRL or CB 154 had no significant influence on insulin release due to glucose in the perfused rat pancreas. -These findings suggest a diabetogenic effect of PRL. CB 154 might be a useful drug in improving glucose utilization in hormone-active pituitary tumours.Key words: Prolactin, insulin release, glucose tolerance, pituitary tumours, pancreas perfusions, bromocriptine.Acute administration of ovine prolactin (PRL) has been shown to influence glucose metabolism in animals [1,2], to impair glucose tolerance in hypopituitary dwarfs and in hypophysectomized juvenile-type diabetics [3], and to stimulate lipid metabolism [4]. In order to study the long term effects of endogenous PRL on glucose tolerance and glucose-induced insulin secretion, patients with hyperprolactinaemia were investigated. In vitro experiments with the isolated perfused rat pancreas were undertaken to elucidate the direct effect of hPRL on insulin release. * Presented in part at the 11 th Annual Meeting of the European Association for the Study of Diabetes (EASD), Munich, September 4-6, 1975, and published in abstract form in Diabetologia 11, 357 (1975) Material aud Methods a. In vivo-StudyFifteen female and 11 male patients with hyperprolactinaemia were studied (Tab. 1). Twenty-four patients had a pituitary tumour, one had a craniopharyngioma and one had anormal sella turcica. A galactorrhoeaamenorrhoea syndrome was observed in 9 women.The average body weight was 13 ± 4 % above the ideal body weight and the average age was 34 ± 2 years (mean ± SEM). None of the patients had elevated plasma growth hormone concentrations. Eighteen patients had blunted hGH-secretion after insulin-induced hypoglycaemia. In six subjects TSH levels before and after TRH stimulation were below the lower limit of detection; six patients showed TSH values which were subnormal and two suffered from primary hypothyroidism. Thirteen had secondary hypogonadism, eleven had a latent or manifest secondary adrenal insufficiency and three had diabetes insipidus. The mean basal PRL level (x ± SEM) measured by radioimmunoassay [5] was 2422 ± 800 ng/ml ranging from 47 to 18 860 ng/ml. Our normal range for men is 8.5 to 25 ng/ml and for women up to 37.5 ng/ml. Fourteen patients were on appropriate hormone replacement therapy at the time of the study. Hypothyroidism was treated in all cases except two (Tab. 1) in order to avoid effects of low thyroid hormone levels on glucose tolerance.Fifteen patients (nine females and six males) were treated with bromocripti...

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Section: Discussionmentioning

confidence: 64%

Prolactin: A diabetogenic hormone

Landgraf

Mm²,

Weißmann³

et al. 1977

Diabetologia

174

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“…Though many investigators (Thorner et al, 1975;Halse et al, 1977;Eskildsen et al, 1978;Dunn et al, 1977;Meneschi, 1980) reported that without long-term treatment, a responder to bromocriptine cannot be separated from a non-responder in acromegaly, other authors (Nortier et al, 1984;Belforte et al, 1977;Oppizzi et al, 1984) GH responses to the TRH test in evaluating the effect of bromocriptine therapy. In the present study, we observed that the effects of bromocriptine diminished in 2 of 18 patients during long-term therapy.…”

Section: Discussionmentioning

confidence: 99%

Long-term bromocriptine therapy and predictive tests in acromegaly.

et al. 1986

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“…Dopamine agonists Dopamine D 2 receptor agonists have been used to treat acromegaly since the 1970s (52,53). Their overall efficacy is, however, limited in comparison with other therapeutic modalities.…”

Section: Gh Receptor Antagonistmentioning

confidence: 99%

Predictors and rates of treatment-resistant tumor growth in acromegaly

2005

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Background: Multimodal therapy for acromegaly affords adequate disease control for many patients; however, there remains a subset of individuals that exhibit treatment-resistant disease. The issue of treatment-resistant pituitary tumor growth remains relatively under-explored. Methods: We assessed the literature for relevant data regarding the surgical, medical and radiotherapeutic treatment of acromegaly in order to identify the factors that were predictive of aggressive or treatment-resistant pituitary tumor behavior in acromegaly and undertook an assessment of the rates of failure to control tumor progression with available treatment modalities. Results: Young age at diagnosis, large tumor size, high growth hormone secretion and certain histological markers are predictors of future aggressive tumor behavior in acromegaly. Significant tumor regrowth occurs in less than 10% of cases thought to be cured surgically, whereas failure to control tumor growth is seen in less than 1% of patients receiving radiotherapy. Somatostatin analogs induce a variable degree of tumor shrinkage in acromegaly but up to 2.2% of somatostatin analog-treated tumors continue to grow. Relative to other therapies, limited data are available for pegvisomant, but these indicate that persistent tumor growth occurs in 1.6 -2.9% of cases followed up regularly with serial magnetic resonance imaging scans. Conclusions: Treatment-resistant tumor progression occurs in a small minority of patients with acromegaly, regardless of treatment modality. Young patients with large tumors or those with high pre-treatment levels of growth hormone particularly warrant close monitoring for continued tumor progression during treatment for acromegaly.

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Bromocriptine treatment of acromegaly.

Cited by 201 publications

References 19 publications

Prolactin: A diabetogenic hormone

Prolactin: A diabetogenic hormone

Long-term bromocriptine therapy and predictive tests in acromegaly.

Predictors and rates of treatment-resistant tumor growth in acromegaly

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