• The Journal of Korean Obstetrics and Gynecology
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• v.31 no.3
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• pp.152-163
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• 2018

Objectives: In recent studies, increased AMH level has been suggested as objective surrogate marker for diagnosis PCOS, one of the major causes of oligomenorrhea. The purpose of this study is to report the clinical effect of Korean medicine treatment on oligomenorrhea patient with increased Anti-mullerian hormone level, who can be diagnosed who can be ruled out PCOS. Methods: A 27 year old woman with oligomenorrhea was enrolled in this study. We measured serum hormone levels and ruled out PCOS. The patient received Korean medicine treatment for 3 months, we assessed the result of treatment through observation of the menstrual cycle and follow-up measurements of serum hormone levels. Results: 1. The patient had menstrual cycle regularly. 2. Increased serum AMH level of the patient decreased from 12.16 ng/ml to 8.51 ng/ml. 3. The other serum hormone levels such as testosterone, LH/FSH ratio decreased Conclusion: This case shows that Korean medicine treatment could have a beneficial effect on menstrual cycle and decrease the increased serum hormone levels of ruled out PCOS patient.

• Journal of Genetic Medicine
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• v.5 no.2
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• pp.139-144
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• 2008

We report on two cases of pericentric inversion of X chromosome. The cases were found in a 40-year-old man with azoospermia and in a family of a 38-year-old pregnant woman. The first case with 46,Y,inv(X)(p22.1q27) had concentrations of LH, prolactin, estradiol, and testosterone that were within normal ranges; however, FSH levels were elevated. Testis biopsy revealed maturation arrest at the primary and secondary spermatocytes without spermatozoa. There were no microdeletions in the 6 loci of chromosome Y. For the second case, the cytogenetic study of thepregnant woman referring for advanced maternal age and a family history of inversion X chromosome was 46,X,inv(X)(p22.11q27.2). The karyotype of her fetus was 46,X,inv(X)(p22.1q27). Among other family members, the karyotypes of an older sister in pregnancy and her fetus were 46,X,inv(X)(p22.11q27.2), and 46,Y,?inv(X), respectively. The proband's father was 46,Y,inv(X)(p22.11q27.2). All carriers in the family discussed above were fertile and phenotypically normal. In addition, the ratio of inactivation of inv(X) by RBG-banding was discordant between the two sisters, with the older sister having only 4.1% of cells carrying inactivated inv(X) while the proband had a 69.5% incidence of late replicating inv(X). Therefore, we suggest that the cause of azoospermia in the first case might be related to inversion X chromosome with positional effect. Also, the family of the second case showing normal phenotype of the balanced inv(X) might be not affected any positional effect of genes.