1. Home>
2. Specialties>
3. Women's Health>
4. Summary and Comment

Underlying Cause of Preeclampsia?

It might be angiotensin-receptor-agonistic antibodies.

The underlying cause of preeclampsia has been difficult to identify. Recent cellular and molecular discoveries have determined that women with preeclampsia have increased calcium levels in blood cells and show antibodies against angiotensin-II type I (AT₁) receptors. These investigators examined whether angiotensin-receptor-activating antibodies cause the increased intracellular calcium seen in preeclampsia. Serum samples from pregnant women with and without preeclampsia were added to Chinese hamster ovary cells that had been transfected with rat angiotensin-II type 1A receptors, and changes in intracellular calcium were measured.

Immunoglobulin from all 16 patients with preeclampsia stimulated calcium mobilization in a dose- and time-dependent manner. Conversely, immunoglobulin from 10 of 14 normotensive women did not stimulate calcium mobilization, and immunoglobulin from the remaining 4 increased calcium mobilization through a non-AT₁-receptor mechanism. Further, the researchers determined that the transcription factor (nuclear factor of activated T cells) for the luciferase reporter gene was activated by preeclamptic immunoglobulin through increased intracellular calcium.

Comment: These findings highlight the possibility that angiotensin-receptor-agonistic antibodies serve as the mechanism underlying preeclampsia. We need additional studies to determine the presence of receptors on multiple target organs and to track the timing and initiation of antibody production. Such experiments might lead to effective targeted treatment of this serious condition.

— Marian C. Limacher, MD

Published in Journal Watch Women's Health November 23, 2004

Citation(s):

Thway TM et al. Antibodies from preeclamptic patients stimulate increased intracellular Ca2+ mobilization through angiotensin receptor activation. Circulation 2004 Sep 21; 110:1612-9.

• Original article (Subscription may be required)
• Medline abstract (Free)