Bromocriptine treatment of prolactinomas.
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Biomedical subjects
Publications and source records attributed to T Eversmann.
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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.
Hyperprolactinemia can be treated medically. Thus all patients with a normal sella turcica and those patients with only slight enlargement of the sella turcica can be treated medically with the dopaminagonist bromocriptine. This treatment is also indicated in paitents with postoperative persisting hyperprolactinemia. In contrast to hyperprolactinemia medical therapy of acromegaly is still in the experimental stage, through the dopaminagonist bromocriptine induces a decrease of growth hormone levels and improvement of the disease in many patients with acromegaly.
The stress of motion sickness was experimentally provoked by Coriolis effect. Significant and reproducible increases from the basal serum level (delta mean +/- S.E.) of antidiuretic hormone delta - ADH: 48.2 +/- 4.6 pg/ml; p less than 0.0005), of growth hormone (delta - hGH: 10.0 +/- 1.2 ng/ml; p less than 0.0005), of prolactin (delta - hPRL: 186.5 +/- 29.9 muU/ml; p less than 0.0005), and of cortisol (delta - F; 12.3 +/- 0.9 microgram%; p less than 0.0005) were observed, whereas the luteinizing hormone levels did not change significantly. The stimulation of hormone secretion induced by different degrees of motion sickness seems to correlate with the severity of motion sickness. The secretion of antidiuretic hormones is the most sensitive indicator for the stress of motion sickness whereas growth hormone, prolactin, and cortisol responses to the stress of motion sickness are more delayed and less pronounced.
We exposed 35 male subjects to a rotary chair and motion sickness was provoked by Coriolis effect. This stress caused an increased excretion of urinary T3 and T4 and a decrease of TSH levels in serum. The increment in urinary excretion of thyroid hormones may serve as a very useful measure for the quantitation of physical stress. Although no statistically significant change of T3, T4, and TBG levels in serum could be observed by the employed techniques, the hypothesis is favoured that motion sickness probably causes an immeasurably small increase of the free thyroid hormone fraction in serum, thereby increasing urinary excretion of T3 and T4 and, in turn, decreasing TSH secretion. Physical or psychological stress situations involve most of the endocrine systems. Contadictory results have been reported in the literature concerning the relationship between thyroid function and stress.
A slight optokinetic stimulation induces a significant increase of serum levels of antidiuretic hormone 1,1 +/- 0.8 pg/ml (mean +/- SD) to 3,3 +/- 1,9 pg/ml (mean +/- SD). Serum levels of gGH and cortisol remain unchanged, whereas serum prolactin levels decrease slightly. The ADH secretion seems to be the most sensitive hormonal parameter of the stimulation of the vestibular nuclei induced either by the optokinetic stimulation or by the Coriolis effect.