Washington (H24N). Among some women whose pregnancies fail in the last trimester some common genetic threads have appeared, according to a study published in The New England Journal of Medicine.

Researchers in Milan, Italy, have discovered that the small number of women who carry the Factor V Leiden or prothrombin-gene mutations (which may cause blood clots in the veins) can develop abnormal placentas and lose their babies in the last trimester of pregnancy.

Ida Martinelli, MD, and Pier M. Mannucci, MD, were originally studying a gene mutation that causes high concentrations of the amino acid homocysteine in the body’s fluids and is associated with late fetal loss (death of a baby in the last four months before birth). They wondered whether this mutation might also cause blood clots in the placenta, and decided to include two other gene mutations (Factor V Leiden and the prothrombin-gene) they knew could cause clots to form and see if any of the three affected the health of unborn children.

Between 1995 and 1998, 67 women who were referred to the two main obstetrical hospitals in Milan for fetal loss in the last trimester of pregnancy took part in the study. None of the women had lost other children before birth, their placentas were in normal position in the uterus and their uteri were normally shaped. None had Rh blood factor incompatibilities and they did not abuse drugs or alcohol. None of the fetuses had congenital malformations or abnormal genetic readings.

Women who had problems with blood clots were excluded from the study, as were non-white women because the targeted genetic abnormalities are rare in non-white populations. A group of 232 women who had one or more normal pregnancies during the same period of time was used as control. Complete histories were taken from all the women, and blood samples were drawn and analyzed for genetic mutations and clotting abnormalities. The placentas of the babies who died were analyzed by pathologists who were not part of the study team and were unaware of possible genetic problems.

The researchers found that, while the original gene that caused homocysteine buildup was not connected with blood clots in the placenta, the Factor V Leiden and prothrombin-gene mutations were. Only 16 percent of the 67 women who had lost their babies had one of the two mutations (which are never seen together), but nearly 80 percent of the placentas in this group were abnormal. The risk of late fetal loss in women with Factor V Leiden or prothrombin-gene mutations was calculated at three times higher than that of women who did not carry the mutations.

Since anticoagulation therapy is successful in reducing problems in pregnant women with another blood clotting condition, called antiphospholipid-antibody syndrome, the authors suggest that this therapy might also keep women with either of the two gene mutations from developing blood clots in their placentas and losing their babies.

However, researchers said further study is needed to determine whether the gene mutations can produce multiple fetal deaths. Some of these women had had healthy children before the fetal deaths that brought them to the study, so the gene does not cause this event in every pregnancy. Although the authors recommend screening for the mutations if fetal death occurs, they also say that further studies of the risks and benefits of anticoagulation therapy (which can cause bleeding and loss of calcium from the bones) should be conducted before it is recommended for women carrying mutations of the Factor V Leiden or prothrombin genes.

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