Pre-eclampsia—also known as toxemia in pregnancy—is a condition that occurs during pregnancy. Typical clinical manifestations include high blood pressure and protein in the urine. The symptoms are often vague and may be diffuse swelling and headaches. In its most severe form, pre-eclampsia can develop into eclampsia—a life-threatening condition characterized by seizures, high blood pressure and general organ failure. In Sweden, approximately 5000 pregnant mothers suffer annually from pre-eclampsia, corresponding to approximately 3–7% of all pregnant women. Since the only cure today is to terminate the pregnancy, pre-eclampsia causes 15% of all premature deliveries.
Complications and deaths are rare in our country, but globally, pre-eclampsia is a medical problem of enormous proportions: it causes every fifth death among pregnant women worldwide. Today, there are no reliable diagnostic methods and only symptomatic treatment, reducing blood pressure, is available. The only curative treatment is to terminate pregnancy by inducing delivery.
The reasons why some women develop pre-eclampsia are still shrouded in mystery—which has sometimes led to pre-eclampsia being called “the disease of theories”. The first step in the development of the disease is suggested to be caused by inadequate development of the placenta. This leads to an inadequate blood supply, which in turn causes oxidative stress, which damages the placenta. Hitherto unknown “Factor Xs” and the breakdown products of placental cells, known as cellular debris, leak into the mother’s blood circulation and contribute to general inflammation and vascular injury which cause organ damage in general and kidney damage in particular.
Successful experiments with A1M
Two research teams at the Biomedical Center at Lund University recently showed that an important “Factor X” consists of free fetal hemoglobin. In a laboratory model, where the placenta was perfused with free hemoglobin, hypertension and placental damage were demonstrated, identical to those damages described in pre-eclampsia. Intravenous treatment was simulated by adding A1M to the perfused placenta. The results showed several beneficial effects: the structural damage was repaired and leakage of hemoglobin ceased. In a pregnant sheep pre-eclampsia model, A1M show similar therapeutic effects. None of the treated animals showed any side effects of A1M.
These results give hope that A1M may be used as a preventive or therapeutic drug for pre-eclampsia.