PubMed · 6368054
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S Franks, H S Jacobs. 1983. Hyperprolactinaemia.. https://doi.org/10.1016/s0300-595x(83)80059-0
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Classically, sports activities are thought to have a beneficial effect on bone tissues. Actually, there are many interactions between sports activities and bone tissue and in certain cases complex hormone disorders may develop. Recent progress in the evaluation of bone structure (absorptiometry) and better understanding of the neuroendocrine functions have improved our knowledge of these interactions and helped provide answers as to the true effect of sports, and particular high-level training, on bone tissue. Mechanical stimulation of bone increases the level of both cortical and cancellous bone formation. The mechanical effect is localized in areas under particular constraint such as the lower limbs in runners and the upper predominant limb in tennis players. Inversely, hypoestrogenism, similar to anorexia nervosa, has been observed to be the cause of general bone loss and increased risk of osteoporosis in certain high level athletes. When these two opposing phenomena occur simultaneously, there is generally an overall loss of cancellous bone mass while bones submitted to major mechanical stress may be relatively protected. Amenorrhoea, particularly in long distance runners, generally occurs when training exceeds 30 km per week. Menarche may be delayed by 1 or 2 years when training begins early and dismenorrhoea is seen in 50% or more of the athletes. Amenorrhoea results from a central disorder due to insufficient pulsatile secretion of luteo-releasing hormone and subsequent hypogonadism. The role of beta-endorphins or catelestrogens on hypothalamic receptors has been suggested as the underlying mechanism. These different observations help provide answers to the different problems raised when providing counselling and care for high level athletes.
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Following presentation and diagnosis, microprolactinomas usually follow a benign course and rarely progress to macroprolactinomas. However, clinically significant enlargement of prolactinomas during pregnancy, presumably related to estrogen stimulation, has been reported. This report describes a patient with amenorrhea and hyperprolactinemia and a microadenoma by computed tomography scan who developed a macroprolactinoma within 10 months after being placed on estrogen therapy. We propose that exogenous estrogen administration in this patient most likely promoted growth from a microprolactinoma to a macroprolactinoma. This case emphasizes the primary role of dopaminergic agonist therapy in the management of pathological hyperprolactinemia and suggests that estrogen therapy should not be casually given to patients with known prolactinomas to avoid the possibility of promoting tumor growth. A correlate of this approach is that caution regarding estrogen therapy should also be exercised in patients with idiopathic hyperprolactinemia who might have an occult microprolactinoma which could grow following estrogen stimulation. If estrogen treatment is deemed necessary, dopaminergic agonist therapy should also be used prophylactically to prevent potential tumor growth due to estrogen. The patient should then be carefully monitored with periodic serum PRLs and for the development of clinical manifestations suggesting pituitary growth. An imaging study should be performed when there is a significant increase in serum PRL or the development of new clinical manifestations.