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Low Levels of Two Proteins Raise Miscarriage Risk

Women with polycystic ovary syndrome face greater chance of losing baby

WEDNESDAY, Feb. 11, 2004 (HealthDayNews) -- Low levels of two key proteins in the uterine lining may be linked to early miscarriages in women with polycystic ovary syndrome (PCOS).

So says an international study in the February issue of the Journal of Clinical Endocrinology & Metabolism.

The findings from researchers at the Virginia Commonwealth University (VCU) Medical Center may help identify women at risk.

PCOS is an endocrine system disorder that causes hormonal imbalances and infertility. It affects about 10 percent of women. Miscarriage rates are three times higher for women with PCOS than for healthy women.

The study included 134 pregnant women in Venezuela who were examined during the first trimester of pregnancy. Of those women, 72 had PCOS and 62 did not have the disorder. All the women were similar in age and body mass index.

Researchers measured the women's concentrations of glycodelin and IGF binding protein-1 (IGFBP-1). These proteins are secreted during pregnancy by the membrane that lines a woman's uterus (endometrium). It's believed the proteins play an key role in implantation of the embryo and maintenance of the pregnancy.

Both proteins were markedly lower in pregnant women with PCOS.

Of the 134 women in the study, 12 had miscarriages in the first trimester. Of those 12 women, 10 had PCOS. The rate of miscarriage was 14 percent for women with PCOS compared with 3 percent for healthy women.

"These findings are significant because they may provide a mechanism for first-trimester miscarriage in PCOS and help us identify pregnant women with PCOS who are at increased risk for miscarriage," Dr. John E. Nestler, chairman of the division of endocrinology and metabolism and vice chairman of the department of internal medicine at VCU, says in a prepared statement.

More information

Here's where you can learn more about miscarriage.

SOURCE: Virginia Commonwealth University, news release, Feb. 4, 2004
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