Rh Incompatibility Could
Up Schizophrenia Risk
Excerpt By Merritt McKinney, Reuter's Health

NEW YORK (Reuters Health) - A blood mismatch between a pregnant woman and her fetus may double the risk of schizophrenia, according to the results of a new study.

But all of the children in the study were born before 1970, when a preventive treatment for the mismatch became available, so more research is needed to see whether it continues to affect schizophrenia risk, the study authors report in the December issue of the American Journal of Human Genetics.

The blood mismatch called Rh incompatibility occurs when a fetus's red blood cells have a surface protein called Rh factor and the mother does not. The mother's immune system may produce antibodies to attack the Rh factor in the fetus, which can cut off the brain's oxygen supply and cause jaundice. Since 1970, an injection has been available to keep a woman's immune system from launching this attack.

Schizophrenia is thought to be caused by both genetic and environmental factors, and several studies based on birth records have suggested that Rh incompatibility may increase the risk of the mental illness. Dr. Christina G.S. Palmer of the University of California, Los Angeles, and colleagues conducted a gene-based study to evaluate this risk. The study included 181 Finnish families in which at least one family member had schizophrenia. Only three patients were born after it was possible to prevent Rh incompatibility.

The researchers found that children who were Rh incompatible with their mothers were more than twice as likely to develop schizophrenia.

The study "provides additional compelling evidence that Rh-positive children of Rh-negative mothers are at increased risk for schizophrenia," Palmer told Reuters Health.

"It shows that genes that relate to immunological pathways can be involved in the development of schizophrenia," she said.

Despite the increased risk associated with Rh incompatibility, the researchers stress that the absolute risk of schizophrenia remains low. It is possible, they suggest, that schizophrenia develops after Rh incompatibility when a person has other genes that increase their susceptibility to the illness. The findings may help researchers identify other such genes, according to the report.

According to Palmer, it will be important to conduct a study in a group of children born after the development of a treatment that prevents mothers' immune system from rejecting Rh-positive fetuses.

"We just don't know the extent to which prophylaxis has reduced Rh incompatibility as a risk factor for schizophrenia," she said.

SOURCE: American Journal of Human Genetics 2002;71.

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