Mifepristone Side-Effects, 2000-2012
RU-486 also blocks cortisol, a critical molecule in the functioning of the innate immune system, a biological defense mechanism that protects the body against bacterial infections. Mothers recovering from chemical abortion suffer 150% greater E.R. admissions than for surgical abortion. One-third of RU-486 abortions require later surgical intervention.
On April 30, 2011 the United States Food and Drug Administration (FDA) staff completed a one-page assessment of the adverse event reports (AERs) it had collected on mifepristone (RU-486; Mifeprex®), the primary drug in the only medical abortion regimen approved in the United States.+ Senator Orrin Hatch (R-Utah) requested a copy of the assessment and subsequently made it available to the Family Research Council (FRC) in the summer of 2011. FRC has studied the RU-486 regimen’s approval process and has tracked the drug’s side-effects since mifepristone’s FDA approval on September 28, 2000 . In the decade following the regimen’s approval, FRC has continued to analyze the abortion regimen’s side-effects as described in the RU-486 AERs and other public sources – both domestic and international. The FDA estimates that as of the end of April 2011, 1.52 million American women had taken RU-486 to induce an abortion. While the loss of 1.52 million preborn children is inherently a moral tragedy, this paper focuses on the additional medical hazards that many women face when using RU-486 to induce an abortion.
To have a well-grounded understanding of the FDA’s RU-486 safety statistics, one first must have some basic knowledge about how RU-486 causes a medical abortion. Progesterone is one of the most important hormones affecting human pregnancy. It prepares the uterus for embryonic implantation and plays an essential role in maintaining an established pregnancy. RU-486 acts as a progesterone blocker or antagonist because it prevents progesterone from binding to its receptors located in critical cells of the uterine lining (i.e., endometrium).
One can understand how mifepristone functions by using the following analogy. RU-486 is like a blank key that fits into a key hole but cannot turn the lock. A blank is the specific type of key for a lock but one that has not yet been cut by the locksmith to turn the lock. This useless blank key, RU-486, prevents a working key (progesterone) from entering the key hole and turning the lock’s mechanism. RU-486’s blockage of progesterone receptors leads to the deterioration of the uterine wall in which an embryo is implanted. As this deterioration worsens, the uterus is no longer able to sustain the pregnancy and the embryo dies.
Additionally, RU-486 is not sufficiently potent to reliably kill the developing embryo and expel the dead embryo or fetus. Accordingly, a second drug, misoprostol, is taken one to two days after RU-486 to trigger the uterine contractions needed to expel the remaining “products of conception” or viable embryo. FDA’s approval mandated a mifepristone-misoprostol regimen to induce an abortion. Misoprostol, marketed as Cytotec®, is a prostaglandin approved to prevent ulcers in certain patients who take NSAIDs. However, powerful and often painful uterine contractions commence very soon after a pregnant woman ingests misoprostol. Obstetricians commonly use misoprostol now to induce labor in women reaching the end of their pregnancies.
We return to our lock and key model. The chemical-biological world contains many locks (chemical receptors) and the RU-486 blank key fits into two very important locks. As noted above, one is the lock – the receptor – for progesterone. The second is the lock for cortisol, a critical molecule in the functioning of the innate immune system, a biological defense mechanism that protects the body against bacterial infections. RU-486 fits into both locks because cortisol closely resembles progesterone in its molecular structure.