Diminished effect of etidronate in vitamin D deficient osteopenic postmenopausal women

Objective: The effects of vitamin D deficiency in osteopenic postmenopausal women treated with intermittent cyclical etidronate have been studied. Bone mass and biochemical parameters as bone markers were measured before and after one year of therapy with intermittent cyclical etidronate. Results: In 30 patients without vitamin D deficiency, bone mass in the lumbal spine and femoral neck was significantly increased compared to 28 vitamin D deficient patients. After cyclical intermittent etidronate therapy, serum osteocalcin and PTH were significantly increased in the vitamin D deficient patients, whereas in non-vitamin D deficient patients they did not change. Conclusion: It is worthwhile measuring serum vitamin D before starting etidronate therapy and, in case of deficiency, to give vitamin D. Received: 6 April 1995/Accepted in revised form: 23 April 1996     

In vitro studies of antiphospholipid antibodies and its cofactor, beta 2-glycoprotein I, show negligible effects on endothelial cell mediated protein C activation.

The effect of sera and purified IgG isolated from plasma of 46 patients with systemic lupus erythematosus (SLE) and 9 healthy donors on the endothelial cell (EC) mediated protein C activation was investigated. Out of the 46 SLE sera used, 19 were antiphospholipid antibodies (aPL) positive. From 12 patients IgG was isolated, of which 6 contained aPL. EC were first incubated with IgG (7 mg/ml) or serum (1:1 diluted) for 1 h and then tested for their ability to promote protein C activation by thrombin, with the cells either in a monolayer or in a suspension. The normal range (mean of control values +/- 2 SD) of protein C activation was 80-120%. In contrast to others, we could not detect an inhibition of protein C activation by any of the patient IgG's or sera. The recently described cofactor for binding of antiphospholipid antibodies to phospholipids, beta 2-glycoprotein I, was purified and added to the purified IgG's. A combination of these two components did not inhibit the EC mediated protein C activation by thrombin. This study suggests that the inhibition of the protein C activation, mediated by EC, is not a general mechanism by which aPL related thrombosis can be explained.