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Mild Gestational Diabetes Raises Risk of Cryptorchidism

Posted: Friday, February 02, 2007

Minor elevations in glucose during pregnancy are associated with a significantly increased risk of having an infant with an abnormal testicular descent, also known as congenital cryptorchidism, the results of a case-control study suggest.

"Cryptorchidism is the most common malformation in newborn boys," Dr. Helena E. Virtanen from University of Turku, Finland, and colleagues note in the Journal of Clinical Endocrinology and Metabolism for December. In one epidemiological study, maternal diabetes was shown to be a risk factor for this disorder

Dr. Virtanen's group evaluated postnatally the prevalence of glucose metabolism disorders during pregnancy of mothers of 1163 boys who had normal testicular descent at birth and mothers of 125 boys with abnormal testicular descent.

They report that after adjustment for possible confounders -- maternal smoking during pregnancy and older age at delivery -- as well as previously described risk factors for cryptorchidism -- prematurity and low birth weight for gestational age -- abnormal maternal glucose metabolism was still significantly more common in the boys with cryptorchidism compared with the boys with normal testicular descent.

For women with diet-treated gestational diabetes, the odds ratio of having a child with cryptorchidism was 3.98. The risk of cryptorchidism was also increased by more than twofold when all mothers with only an abnormal oral glucose tolerance test result were included in the group with diabetes, the authors note.

"It remains to be elucidated how mildly abnormal glucose metabolism during pregnancy increases the risk for congenital cryptorchidism," Dr. Virtanen and colleagues say.

One possibility, they suggest, is that mildly abnormal maternal glucose metabolism during pregnancy fuels an imbalance between fetal estrogen and androgen action, which interferes with the descent of the testes, given that testicular descent is influenced by the effect of both androgens and estrogens.

Source: Diabetes In Control: J Clin Endocrinol Metab 2006;91:4862-4865