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Objective. —To evaluate the effect of treatment with alendronate sodium, a potent aminobisphosphonate, on the incidence of nonvertebral fractures in postmenopausal women with osteoporosis. Data Sources. —Published data and data on file at Merck Research Laboratories. Study Selection. —All completed prospective, randomized, placebo-controlled alendronate trials of at least 2 years' duration (5 studies). Data Extraction. —All subjects were women with osteoporosis between the ages of 42 and 85 years, postmenopausal at least 4years with lumbar spine bone mineral density (measured using dual-energy x-ray absorptiometry) at least 2.0 SD below the mean for young adult women. All women randomized to treatment with placebo or alendronate at a dose higher than 1 mg per day for at least 2 years were included. Data Synthesis. —In the placebo group (n=590), 60 women reported nonvertebral fractures during 1347 patient-years at risk (overall rate, 4.45 women with fractures per 100 patient-years at risk). In the alendronate group (n=1012), 73 women reported nonvertebral fractures during 2240 patient-years at risk (overall rate, 3.26 women with fractures per 100 patient-years at risk). The estimated cumulative incidence of nonvertebral fractures after 3 years was 12.6% in the placebo group and 9.0% in alendronate group. The relative risk for nonvertebral fracture estimated using the Cox proportional hazards model was 0.71 (95% confidence interval,0.502-0.997) (P=.048). A reduction in risk was consistent across each of the studies and at each major site of osteoporotic fracture, including the hip and wrist. Conclusion. —In postmenopausal women with osteoporosis, treatment with alendronate reduces the risk of nonvertebral fractures over at least 3 years.

RICKETS ICKETS in the growing child and osteomalacia in the adult are now rarely due to simple vitamin-D deficiency. Renal tubular defects and intestinal malabsorption are frequently associated with the clinical picture of rickets, and large doses of vitamin D are usually required for healing. One syndrome, familial vitamin D resistant rickets, is well characterized genetically and clinically. 1,2 This disease is inherited as a sex-linked dominant. The children present a picture of rickets, which is usually more marked in the lower extremities. Large doses of vitamin D are necessary for treatment, but the results have not been especially satisfactory. 3,4,5 Although active rickets cease at the time of closure of the epiphyses, these patients remain dwarfed with deformities of the lower extremities, and have been confused with achondroplastic dwarfs. The clinical picture of osteomalacia, with roentgenographic evidence of decreased bone density and pseudofractures, is unusual in adults with familial

In a sensitive method for measuring both cortical and trabecular bone mass in the radius, bone mass is determined by measuring the photon energy absorbed by bone from a monochromatic gamma-ray source, 125 I. The method is quite reproducible, with a coefficient of variation of about 2.5%. Measurements of bone mass were performed on 169 white women older than 50 years of age who were divided into two groups: those with (56 women) and those without collapsed vertebrae (113 women). Measurements of both trabecular and cortical bone mass were significantly less in the group with collapsed vertebrae. This method is capable of providing objective, reproducible measurements of bone mass in man. It appears to be a very promising tool for the study of the natural history of diseases of demineralization and for providing data on the response to therapy.