Fenofibrate of gemfibrozil for treatment of types IIa and IIb primary hyperlipoproteinemia: a randomized, double-blind, crossover study.

OBJECTIVE: To compare the hypolipidemic effects of gemfibrozil and micronized fenofibrate in patients with primary hyperlipoproteinemia, phenotypes IIa and IIb, with emphasis on their cholesterol-lowering effectiveness. METHODS: A randomized, double-blind, double-dummy, crossover study was performed to assess the effects of gemfibrozil (900 mg) and micronized fenofibrate (200 mg), administered once daily, to 21 patients (45 to 70 years old)-16 with type IIa and 5 with type IIb primary hyperlipidemia. The two treatment periods lasted 6 weeks each; the run-in and washout periods were 4 weeks. RESULTS: Both drugs significantly reduced total cholesterol, calculated low-density lipoprotein (LDL) cholesterol, triglycerides, apolipoprotein B, and fibrinogen (P<0.01 for all calculations, except P<0.05 for fibrinogen with gemfibrozil therapy) and increased high-density lipoprotein (HDL) cholesterol (P<0.01). Neither drug affected Lp(a) lipoprotein, whereas uric acid was reduced only by fenofibrate (P<0.01). The percentage decrease in total cholesterol and LDL cholesterol was greater with fenofibrate than with gemfibrozil (-22% versus -15%, P<0.02; and -27% versus -16%, P<0.02, respectively). In contrast, reductions in levels of triglycerides (-54% versus -46.5%), apolipoprotein B, and fibrinogen, as well as the increase in HDL (+9% for both drugs), showed no significant difference between treatments. Separate analysis of patients with type IIb hyperlipoproteinemia showed essentially the same plasma lipid changes as for the overall group, but with greater modifications in triglyceride and HDL concentrations. CONCLUSION: Fenofibrate and gemfibrozil induced similar variations from baseline values in triglycerides, HDL cholesterol, apolipoprotein B, and fibrinogen, but the decreases in total and LDL cholesterol levels were greater with fenofibrate, in this group of patients with primary hyperlipidemia.

Efectos de la estrogenoterapia sobre la masa ósea en mujeres postmenopáusicas osteopénicas / Effects of estrogen therapy on bone mass in postmenopausal women with osteopenia

Estrogen treatment prevents early postmenopausal bone loss. The aim of this study was to evaluate the effects of estrogen-progestogen therapy on bone mass in elderly osteopenic postmenopausal women. Fifteen women with a mean age of 58 +/- 6 (R +/- SD) years and 12 +/- 7 (5-31) years from menopause were evaluated. Bone mineral density (BMD) was assessed by dual R-ray absoptiometry (DXA) with 1.7 percent variation coefficient at lumbar spine (L2-4) and 1.9 percent at femur neck. Measurements were done at both sites before and after a 12 month treatment. At the beginning of the study lumbar spine BMD (LS BMD) was low: < 0.9 grs/cm2; z-score: -1.4 +/- 0.17 (X +/- SEM). Treatment consisted in transdermal 17beta estradiol (50 microg/day) (n=10) or an equivalent natural estrogen oral dose (n=5). Variable doses of medroxiprogesterone acetate were added on an individualized basis to women with an intact uterus (n=12). Calcium intake was increased up to a median of 1200 mg/day (800-1600). After a one year treatment LS BMD was increased by 8.4 +/- 1.1 percent (X +/- SEM) (95 percent CI: 6-10.8), from 0.748 +/- 0.02 to 0.810 +/- 0.02 gr/cm2 (p <0.0001). A less marked gain in femur neck bone mineral density (FN BMD) was also noticed: 3.9 +/- 1.5 percent (95 percent CI: 0.6-7.2); 0.671 +/- 0.02 vs 0.697 +/- 0.02 gr/cm2 (p < 0.05). Patients treated with transdermal and oral routes showed similar results. Percentage variations in LS BMD and FN BMD were positively correlated (r : 0.53; p < 0.05). Six patients were treated for 2 years; LS BMD continued to rise, the additional gain being 5.1 +/- 2.2 percent (p < 0.05), while a non significant increase in FN BMD was observed (7.5 +/- 3.5 percent; p = 0.06). In the early postmenopausal period, hormonal replacement therapy (HRT) produces either a stabilization or a slight increase (2-4 percent) in BMD. In contrast, a significant augmentation of bone mass (especially at the spine) seems to occur in osteopenic women when THR is administered in the late postmenopausal period. This suggests that HRT could be used for the prevention as well as for the treatment of postmenopausal osteoporosis. Further studies should be done to evaluate whether HRT reduces the incidence of osteoporotic fractures in elderly osteopenic women.

Efectos de la estrogenoterapia sobre la masa ósea en mujeres postmenopáusicas osteopénicas / Effects of estrogen therapy on bone mass in postmenopausal women with osteopenia

Estrogen treatment prevents early postmenopausal bone loss. The aim of this study was to evaluate the effects of estrogen-progestogen therapy on bone mass in elderly osteopenic postmenopausal women. Fifteen women with a mean age of 58 +/- 6 (R +/- SD) years and 12 +/- 7 (5-31) years from menopause were evaluated. Bone mineral density (BMD) was assessed by dual R-ray absoptiometry (DXA) with 1.7 percent variation coefficient at lumbar spine (L2-4) and 1.9 percent at femur neck. Measurements were done at both sites before and after a 12 month treatment. At the beginning of the study lumbar spine BMD (LS BMD) was low: < 0.9 grs/cm2; z-score: -1.4 +/- 0.17 (X +/- SEM). Treatment consisted in transdermal 17beta estradiol (50 microg/day) (n=10) or an equivalent natural estrogen oral dose (n=5). Variable doses of medroxiprogesterone acetate were added on an individualized basis to women with an intact uterus (n=12). Calcium intake was increased up to a median of 1200 mg/day (800-1600). After a one year treatment LS BMD was increased by 8.4 +/- 1.1 percent (X +/- SEM) (95 percent CI: 6-10.8), from 0.748 +/- 0.02 to 0.810 +/- 0.02 gr/cm2 (p <0.0001). A less marked gain in femur neck bone mineral density (FN BMD) was also noticed: 3.9 +/- 1.5 percent (95 percent CI: 0.6-7.2); 0.671 +/- 0.02 vs 0.697 +/- 0.02 gr/cm2 (p < 0.05). Patients treated with transdermal and oral routes showed similar results. Percentage variations in LS BMD and FN BMD were positively correlated (r : 0.53; p < 0.05). Six patients were treated for 2 years; LS BMD continued to rise, the additional gain being 5.1 +/- 2.2 percent (p < 0.05), while a non significant increase in FN BMD was observed (7.5 +/- 3.5 percent; p = 0.06). In the early postmenopausal period, hormonal replacement therapy (HRT) produces either a stabilization or a slight increase (2-4 percent) in BMD. In contrast, a significant augmentation of bone mass (especially at the spine) seems to occur in osteopenic women when THR is administered in the late postmenopausal period. This suggests that HRT could be used for the prevention as well as for the treatment of postmenopausal osteoporosis. Further studies should be done to evaluate whether HRT reduces the incidence of osteoporotic fractures in elderly osteopenic women.(AU)