PCOS: Diagnosis and contraceptive options
What tests are recommended to diagnose polycystic ovary syndrome (PCOS)? To determine chronic anovulation associated with polycystic ovary syndrome, Sarah Berga, MD, associate professor of OB/GYN and reproductive sciences at the University of Pittsburgh School of Medicine at Magee-Womens Hospital, uses the following diagnostic approach:
Take a good patient history and perform a reasonable physical exam. Upon the initial findings, order these five tests from one blood sample: luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), prolactin, and an androstenedione level. Be sure the blood sample is timed not to follow the physical exam. If a physical exam, Pap smear, and breast exam are done prior to the blood sample, the patient’s prolactin level is stimulated. If the sample is taken in a resting state, with a patient who has not just eaten, all the monitored levels should be normal. In the "first cut" for PCOS diagnosis, the LH/FSH ratio will be high, and the androstenedione will be high/normal or high, says Berga. At this point, the diagnosis is not confirmatory, but the provider will be able to exclude hyperprolactinemia, hypothyroidism, hyperthyroidism, and menopause. If the patient is believed to be ovulatory, but the provider is unsure, an estradiol/progesterone test can be performed to get a sense of the ovarian function. If the test confirms that the patient is ovulating, another condition outside of PCOS is most likely at play, she says. Because LH/FSH will vary when the patient is ovulating in an ovulatory cycle, Berga often adds the estradiol and progesterone tests to back up the LH/FSH tests. How ever, if the LH/FSH ratio is greater than 2.5 or 3, and the androstenedione is elevated, the vast majority of patients can be considered PCOS candidates. If PCOS is diagnosed, move forward to determine if the patient has glucose intolerance, impaired glucose tolerance, or frank diabetes. A two-hour post-glucose test should give an accurate depiction of those conditions.Although women with PCOS can have unpredictable ovulatory cycles, they should not be considered protected against unintended pregnancy by their condition.1 Low-dose oral contraceptives (OCs) provide birth control, lower free testosterone levels, relieve acne and hirsutism, and establish regular menses.
Because they restore regular cycles, prevent endometrial hyperplasia, and increase levels of sex hormone binding globulin, combination OCs are the contraceptive agent of choice in women with PCOS, says Andrew Kaunitz, MD, professor and assistant chair of the department of OB/GYN at the University of Florida Health Sciences Center in Jacksonville.
Use of a low-dose OC has shown reasonable suppression of the ovary, but with recovery occurring during the placebo phase.2 For that reason, Berga suggests either using OCs on a continuous basis, or prescribing Mircette (Organon, West Orange, NJ) because it minimizes return of ovarian function.
There has been some debate about whether OCs worsen insulin sensitivity in women with PCOS, says Richard Legro, MD, assistant professor of OB/GYN at Pennsylvania State University’s College of Medicine at the Milton S. Hershey Medical Center in Hershey, but he believes the benefits outweigh the risk.
What about the use of other contraceptives for birth control in women with PCOS? If depot medroxyprogesterone acetate (DMPA) is used, providers also may wish to add supplemental estrogen to increase levels of sex hormone- binding globulins and improve lipid profiles, Kaunitz says.
Legro questions the use of DMPA due to his concern that it may exacerbate already-irregular bleeding patterns. Intrauterine devices or barrier methods don’t address the symptoms often encountered by women with PCOS, he adds.
References
1. Hatcher RA, Trussell J, Stewart F, et al. Contraceptive Technology. 17th edition. New York City: Ardent Media; 1998.
2. Daniels TL, Berga SL. Resistance of gonadotropin releasing hormone drive to sex steroid-induced suppression in hyperandrogenic anovulation. J Clin Endocrinol Metab 1997; 82:4,179-4,183.
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