Alendronate increases spine and hip bone mineral density in women with postmenopausal osteoporosis who failed to respond to intermittent cyclical etidronate

• Published in: Bone (New York, N.Y.) N.Y.), 1999, Vol.24 (1), p.65-68
• Main Authors: Watts, N.B, Becker, P
• Format: Article
• Language: English
• Subjects: Absorptiometry, Photon; Aged; Aged, 80 and over; Alendronate; Alendronate - pharmacology; Alendronate - therapeutic use; Alkaline Phosphatase - blood; Amino Acids - urine; Biological and medical sciences; Bisphosphonate; Bone Density - drug effects; Bone mineral density; Bones, joints and connective tissue. Antiinflammatory agents; Drug Administration Schedule; Etidronate; Etidronic Acid - therapeutic use; Female; Femur - drug effects; Femur - physiology; Humans; Lumbar Vertebrae - drug effects; Lumbar Vertebrae - physiology; Medical sciences; Middle Aged; Osteoporosis, Postmenopausal - drug therapy; Pharmacology. Drug treatments; Responder; Space life sciences; Therapy; Treatment Outcome
• ISSN: 8756-3282; 1873-2763
• DOI: 10.1016/S8756-3282(98)00144-6

In a U.S. multicenter study of intermittent cyclical etidronate treatment for postmenopausal osteoporosis, approximately 20% of patients were nonresponders, defined as failure to increase spine bone mineral density. In contrast, essentially all patients who received 10 mg of alendronate daily in U.S. phase III trials showed some increase in spine bone mineral density. The current study was undertaken to determine the response to alendronate therapy in women with postmenopausal osteoporosis who were nonresponders to intermittent cyclical etidronate therapy. Twenty-five women with postmenopausal osteoporosis (mean ± SD: 65.1 ± 1.9 years of age), previously treated with intermittent cyclical etidronate with no increase of spine bone mineral density, and who agreed to be changed to alendronate, were recruited from a university out-patient clinic specializing in the treatment of osteoporosis for a prospective observational study. Measurements included bone mineral density of the lumbar spine and proximal femur (by dual-energy X-ray absorptiometry) and biochemical markers of bone remodeling (serum bone-specific alkaline phosphatase by immunoassay and urine deoxypyridinoline by high-pressure liquid chromatography). Patients had received intermittent cyclical etidronate for 3.3 ± 0.4 years, during which time their bone density declined at spine and hip sites. They were then changed to alendronate 10 mg/day, which they received for 1.3 ± 0.1 years; after treatment with alendronate, bone mineral density increased significantly at the lumbar spine (4.4 ± 0.7% annualized, p < 0.0001) and at all hip sites. Bone markers also changed significantly after alendronate treatment: urine deoxypyridinoline fell from 6.8 ± 0.8 to 5.5 ± 0.6 μmol/mol creatinine (p < 0.0001) and serum bone-specific alkaline phosphatase rose from 4.6 ± 0.5 to 11.9 ± 1.0 ng/mL ( p < 0.0001). Upper gastrointestinal side effects forced 4 of 25 patients (16%) to discontinue alendronate. Alendronate increases bone density at the spine and hip in patients who have not responded to intermittent cyclical etidronate therapy. Changes in bone markers suggest that alendronate causes more complete suppression of bone resorption and less inhibition (or stimulation) of bone formation.