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Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Luteal phase defect is an ovulatory disorder of considerable clinical importance that is implicated in infertility and recurrent spontaneous abortion. As a subtle disruption of ovulatory or luteal function, it may be the most common ovulatory disorder in women. Pathophysiologic alterations of the complex reproductive process that lead to delayed endometrial maturation characteristic of LPD include disordered folliculogenesis, defective corpus luteum function, and abnormal luteal rescue by the early pregnancy. A variety of clinical conditions, such as hyperprolactinemia, hyperandrogenic states, weight loss, stress, and athletic training may result not in overt oligo- or anovulation, but rather may be manifest as LPD. Reasonable consensus exists regarding the use of endometrial biopsy for diagnosis of LPD, although issues regarding timing, number of samples needed, method of interpretation, and the adjunctive use of hormone assay and ultrasonography are still not settled. Other tests, including assay of progesterone-associated endometrial protein, analysis of decidual steroid receptors, or determination of decidual prolactin production, may in the future contribute to the accurate diagnosis of this condition. In the absence of an identifiable correctable underlying cause of LPD, progesterone replacement and clomiphene citrate are the usual treatment options for consideration. Combination therapy, gonadotropins, and other treatments are reserved for refractory cases. No data at present suggest a difference in efficacy between progesterone and clomiphene. When abnormal luteal endometrial biopsy is corrected, conception and live birth rates are high.
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PMID:Luteal phase defect. Etiology, diagnosis, and management. 157 84

Obesity, which disturbs lipid and glucose metabolism, is a recent medical concern. It threatens human health and also has adverse effects on reproductive functions by causing insulin resistance/hyperinsulinemia, especially in women with polycystic ovary syndrome (PCOS). For PCOS patients to prevent these adverse effects, it is important to take into account improving their lifestyles by exercise and proper diets. The relationship between insulin resistance/hyperinsulinemia and reproductive disorders should be understood as fully as possible in order to provide effective treatment. It is well known that insulin resistance and compensatory hyperinsulinemia can be triggered by obesity with visceral fat accumulation. Hyperinsulinemia affects granulosa cells in small follicles and theca cells. This condition induces early response to luteinizing hormones on granulosa cells of small follicles and causes premature differentiation of these cells, which eventually results in anovulation. For improvement of anovulation because of hyperinsulinemia, insulin-sensitizing agents (biguanide and thiazolidinedione derivatives) are useful. Hyperinsulinemia may adversely affect the endometrial functions and environment, and evoke implantation disturbance. Treatment with an insulin-sensitizing agent (metformin) improves the levels of glycodelin, insulin-like growth factor binding protein 1, and blood flow in spiral arteries during the peri-implantation period. It supports endometrial function, improves the endometrial environment, and facilitates embryo implantation. The rate of early pregnancy loss during the first trimester is 30-50% in women with PCOS, which is threefold higher than for normal women. Metformin treatment improves the levels of insulin, the homeostasis model assessment for insulin resistance, and plasminogen activator inhibitor activity, and decreases early pregnancy loss. It goes without saying that lifestyle change is fundamental for improving reproductive performance in addition to treatment with insulin-sensitizing agents.
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PMID:Insulin resistance/hyperinsulinemia and reproductive disorders in infertile women. 2969 42