a.続発性無月経の臨床的意義(1.内分泌)

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We review the hormonal situations in common endocrine disorders which produce secondary amenorrhea-eating disorder, stress, exercise, polycystic ovary syndrome (PCOS), hyperprolactinemia, hyper or hypothyroidism, and diabetes mellitus (DM). How these endocrine disorders affect on the pregnancy outcomes is also discussed. Eating disorder, stress and exercise affect the reproductive function due to physiologic and psychologic stresses. Increase of corticotropin-releasing hormone (CRH) and β-endorphin in the hypothalamus suppress gonadotropin-releasing hormone (GnRH) secretion, resulting in gonadal dysfunciton. Recent studies also indicate the importance of the change in leptin production in weigh-loss-induced gonadal dysfunction. These endocrine disorders also cause hypercortisolism (due to increased CRH) and hypothyroidism (due to decreased TRH). These changes may be viewed as a functionally adaptive phenomenon-an energy-saving strategy to protect more important biologic processes. It is possible to induce ovulation in such women. By doing so, however, an increase is more likely in maternal and fetal morbidity, mortality and long term developmental difficulties in infant. Recent reports suggest the importance of hyperandrogenism and insulin resistance in the pathogenesis of PCOS. Hyperinsulinemia and elevated serum LH act synergistically and stimulate hyperandrogenism which may lead to follicular atresia. It has been reported that the use of antidiabetic drugs to correct insulin resistance could improve associated endocrine-metabolic effects. PCOS does not affect the pregnancy outcome once ovulatory cycles are induced. The most important regulatory factor of prolactin production is dopamine (PRL inhibiting factor). Prolactin-associated menstrual abnormalities are secondary to a derangement of ovarian function or to an inhibition of GnRH production caused by a dopamine rise induced by hyper PRL. Prolactin is also mildiy elevated in hypothyroidism, PCOS and stress. Hyperprolactinemia doses not affect the pregnancy outcome. Thyroid dysfunction and diabetes mellitus cause menstrual disorders. Anovulatory cycles are common in thyroid dysfunction. It has been reported that thyroid hormone and insulin amplify the FSH action in granulosa cells. However, mechanisms by which gonadal dysfunction is produced in these disorders are still unclear. These endocrine-metabolic disorders are associated with increase in risks of fetal morbidity and mortality. Poor control of maternal thyroid dysfunction is associated with increase in risks of spontaneous abortion, preeclampsia, low-birth-weight infants. When thyroid deficiency occurs simultaneously in a pregnant woman and her fetus, the child's neuropsychological development is adversely affected. In diabetes mellitus, not only are there the perinatal risks of maternal and fetal complications, but also the risk of fetal anomalies when preconception glucose control is not intensively managed. It has recently been suggested that oxygen free radicals are involved in the high incidence of fetal anomaly associated with diabetic pregnancies. In view of the above mentioned facts, anovulation is considered to be one of the symptoms associated with hyper PRL and/or PCOS. Once ovulation is induced, pregnancy outcome is not miserable in these disorders. By contrast, gonadal dysfunction associated with hypothalamic amenorrhea, thyroid dysfunction and DM seems to be the protective reaction to avoid conception. Ovulation-induction is not recommended unless the patient has undergone a full recovery in these disorders.
社団法人日本産科婦人科学会の論文
2002-08-01

a.続発性無月経の臨床的意義(1.内分泌)

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