PubMed · 9510785
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E Ben-Sefer. Running on empty.. https://pubmed.ncbi.nlm.nih.gov/9510785/
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Functional hypothalamic amenorrhea are frequently observed. Body weight, body composition, eating attitudes, exercise are potent modulators of gonadotrop axis. Animal studies and clinical observations stress the fact of a major impact on ovary function of starvation or caloric restriction, weight loss and fat mass deficiency, eating disorders, stress or high intensive exercise training. From a pathophysiological point of view, insulin, IGF's system, leptine and central neuromediators are a link between nutrition and the gonadotropic axis. Initial clinical evaluation may strongly suggest the environmental origin of the amenorrhea. Basal hormonal evaluation (gonadotropins, prolactin, androgens ...) excludes other diseases and specialised evaluations [basal metabolic rate (BMR), Free T3 ...] could confirm the diagnosis. A low BMR, and a low Free T3, a normal FSH level with a low LH level suggest the nutritional origin of the amenorrhea. Improvement of nutritional intake and body composition with a psychological follow up may reverse the gonadotropin deficiency. If this deficiency persists hormonal replacement therapy is added in order to prevent the short or long term consequences (osteoporosis) of hypoestrogenism.
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Until the introduction of the first atypical antipsychotic, clozapine, in 1975, hyperprolactinemia was assumed to be an inevitable consequence of treatment with any antipsychotic agent. Now we know that atypical antipsychotics such as clozapine, olanzapine, quetiapine, sertindole, and ziprasidone are not associated with significant prolactin increase. These new antipsychotics appear to spare dopamine blockade within the brain's tubero-infundibular tract, a dopamine pathway that also controls prolactin secretion. Since the release of prolactin is tonically inhibited by the hypothalamus, with dopamine acting as the prolactin release-inhibiting factor, any disruption of the connection between the hypothalamus and the pituitary gland is associated with hyperprolactinemia. Other factors that can increase prolactin secretion are also reviewed (e.g. estrogens, thyroid-releasing factor, vasoactive intestinal peptides, opioids, surgery, illness such as epilepsy or herpes zoster infection, and psychic or physical stress). Prolactin levels are at their highest 1-2 hours before waking, and early waking interrupts its secretion. The major effects of hyperprolactinemia in women are amenorrhea, cessation of normal cyclic ovarian function, loss of libido, occasional hirsutism, and increased long-term risk of osteoporosis. The effects in men are impotence, loss of libido, and hypospermatogenesis. Current data indicate that conventional antipsychotics, as well as high doses of risperidone (> 6 mg/day), increase prolactin levels to a range associated with sexual dysfunction in nonpsychiatric patients. The lack of prolactin elevation reported with the atypical antipsychotics is believed to be due to their much greater specificity, which results in less blockade of dopamine receptors in the tubero-infundibular pathway.