Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen patients with clomiphene-resistant hypothalamic anovulation were given tamoxifen 10 mg per day from cycle day 5 to 9 during two consecutive menstrual cycles. Not included were patients with hyperprolactinemia and PCOD. Treatment was monitored using measurement of follicle size by ultrasound and assessment of serum estradiol. Failure to ovulate persisted in 15 patients. Of the two patients who ovulated, one received hCG on day 16, and became pregnant. We were unable to demonstrate that clomiphene-resistant patients were likely to ovulate with tamoxifen. Forty-five patients with hypothalamic anovulation not previously treated were then given tamoxifen in the same dosage. This part of the study indicated that tamoxifen was successful in inducing ovulation in 84% of the cycles. There was marked improvement in cervical mucus in tamoxifen cycles as compared with clomiphene cycles. Tamoxifen was effective, and had some advantages compared with clomiphene in patients responding to both drugs. This preliminary study suggests that tamoxifen may be a useful addition to the treatment of ovulatory failure.
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PMID:Tamoxifen in clomiphene-resistant hypothalamic anovulation. 288 87

Clomiphene is a first line treatment for anovulation, a common cause of infertility. Response to clomiphene is variable and unpredictable. Tamoxifen is structurally related to clomiphene, and also shows considerable variation in response. CYP2D6 and CYP3A4 are major contributors to the metabolism of tamoxifen. The aim of the present work was to define the role of CYP2D6 and CYP3A4 in the in vitro metabolism of enclomiphene, regarded by some as the more active isomer of clomiphene. Enclomiphene (25 microM) was incubated with human liver microsomes (from 4 extensive (EM) and 1 poor metaboliser with respect to CYP2D6) and with microsomes from lymphoblastoid cells expressing CYP2D6. Microsomes from all the EM livers and recombinant CYP2D6 metabolised enclomiphene (the disappearance of drug ranged from 40-60%). No metabolism was detected in microsomes from the PM liver. Quinidine (1 microM) completely inhibited the metabolism of enclomiphene by all the EM livers and by recombinant CYP2D6 (p<0.001, one way ANOVA). Ketoconazole (2 microM) had no significant effect on enclomiphene metabolism in 3 out of the 4 EM livers. The extent of enclomiphene metabolism was correlated with the amount of CYP2D6 present (p<0.001, Pearson correlation test). The findings indicate that CYP2D6 is primarily responsible for the metabolism of enclomiphene.
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PMID:CYP2D6 is primarily responsible for the metabolism of clomiphene. 1844 89