No abstract

Systemic lupus erythematosus (SLE) and primary anti-phospholipid syndrome (PAPS) are autoimmune diseases causing recurrent pregnancy loss. We hypothesized that anti-phospholipid antibodies (aPL), but not anti-Ro and anti-La antibodies, might have a role through direct placental damage. We cultured human placental explants in sera from women with SLE/PAPS with different antibodies. These sera were found to reduce placental growth and increase trophoblastic apoptosis. No effect was found on estradiol or progesterone secretion, but inhibition in betahCG secretion was detected. BetahCG was reduced in women with a history of recurrent pregnancy loss or thromboembolic events, and was also the most sensitive marker when examining the effects of specific antibodies. High titers of aPL were found to cause the largest reduction in betahCG. Anti-Ro and anti-La did not induce placental damage. A strong correlation was found between the rise in the number of different antibodies in the sera and the incidence of recurrent pregnancy loss, which was also accompanied by a decline in the betahCG levels. In conclusion, aPL, but not anti-Ro or anti-La, may cause placental damage in vitro. Thus betahCG levels might constitute a predictive marker for the risk of placental damage and pregnancy loss in women with SLE/PAPS.

No abstract

The effect of steroid structure on induction of chymotrypsinogen in embryonic chick pancreas was examined in vitro. In order of decreasing potency cortisol, corticosterone, and 21-deoxycortisol are classified as optimal inducers, whereas 11beta-hydroxyprogesterone, 11-deoxycortisol, cortisone, 11-deoxycorticosterone and 17-alpha-hydroxyprogesterone are classified as suboptimal inducers. Progesterone was inactive. It is concluded that the relative importance of the steroid hydroxyl groups for activity is 11beta greater than 21 greater than 17 alpha, and that their effect is cumulative.