Endocrine Abstracts

Miscarriages are the most common form of pregnancy failure in humans. In general, genetic, endocrinologic, immunologic, anatomic or microbiologic causes account for the onset of a miscarriage. These factors have been completed by epidemiological studies which indicated the contribution of perceived stress to the onset of miscarriages.

Stress interferes with reproduction by altering the immune and endocrine system. Traditionally, progesterone is considered as the major hormone of pregnancy. Low progesterone levels will eventually lead to abortion. Progesterone has further been shown to exert an anti-abortive effect by inducing a protein called progesterone-induced blocking factor (PIBF), which favors the production of pregnancy-protective Th2 cytokines.

In an established murine model, abortions can be triggered by exposing the mice to stress during early gestation. Recent data from this model indicated that increased levels of abortogenic Th1 cytokines, a decrease of progesterone and thus, PIBF were incongruous with successful pregnancy maintenance. We now report that supplementation of progesterone in the murine model exerts a pregnancy protective effect by induction of a Th2 immune response. Further, we present data from a prospective cohort study on human pregnancy, which reveal that women with a clinically normally progressing pregnancy but high stress perception, accompanied by low levels of progesterone and PIBF during the first trimester, eventually suffered from a miscarriage.

These data indicate that stress may lead to an increased rate of miscarriages by altering the endocrine system, which then triggers an immune bias towards an abortogenic cytokine profile.