The effect of low dosage glucocorticoids on bone mass in rheumatoid arthritis: a cross-sectional and a longitudinal study using single photon absorptiometry.

The cross-sectional study of patients with RA receiving LDGC, compared with those on NSAID alone (or patients with AS) showed that LDGC significantly affects bone mass at midshaft and even more so at the distal radius. The loss of bone seems to be brisk but continuous on the long run, at least at the distal scanning site, and thus increases the C/T ratio, especially in aged men. The loss of bone mass in the LDGC group correlates with the duration of the disease as well as with carpal destruction (especially at mid shaft radius), with both parameters being correlated with one another. At equal carpal destruction, LDGC still affects bone mass. Whether receiving NSAID alone or LDGC in addition, patients with RA, as compared with controls, are more liable to lose bone when they grow older. In a longitudinal study, premenopausal women were unaffected by the administration of LDGC at both scanning sites. In contrast, postmenopausal women receiving LDGC lost at least twice as much bone as did normal women after the menopause. Men of all ages on LDGC lost bone at a rate equal to that of normal women after the menopause. Men with RA or with AS on NSAID alone did not significantly lose bone. It is concluded that LDGC may be given to premenopausal women without harm to their bone mass. After the menopause, hormonal replacement therapy, if not contra-indicated, should be given in association with LDGC. Men fortunately have a higher peak bone mass and therefore can afford to lose bone during a decade before they attain the same situation as women at the time of their menopause. If treatment is then continued for another two decades, their bone mass might behave as does that of postmenopausal women if bone loss is continuous over such long periods of time. This latter assumption has yet to be verified.

[Effects of 1,25(OH)2D3 on bone mineralization in vitamin D deficiency (author's transl)]. / Effets du 1,25 (OH)2D3 sur la minéralisation osseuse dans l'ostéomalacie vitaminoprive.

Two cases with vitamin D-deficient osteomalacia of digestive origin (coeliac disease) have been treated orally with 1,25(OH)2D3 in dosages of respectively 8 and 3 microgram/24 h. Serial transiliac bone biopsies have been performed. Mineralization fronts were normalized after respectively 4 and 1.5 months, whereas mineralization rates, as demonstrated by double tetracycline labeling, were normalized respectively after 2 and 1.5 months. In both cases osteomalacia healed completely despite persistently low 25(OH)D levels in the serum. It is obvious from these studies that 1,25(OH)2D3 per se is able to cure vitamin D-deficient osteomalacia, a finding that has been disputed. Whether 25(OH)D acts more rapidly on bone, as suggested by the studies performed in one case with anticonvulsant osteomalacia, remains to be proven.