Increase in bone mass after correction of vitamin D insufficiency in bisphosphonate-treated patients.
OBJECTIVE
To assess the relative contribution of vitamin D insufficiency to loss of bone mineral density (BMD) in patients taking bisphosphonates.


METHODS
Patients were eligible for inclusion if they had osteoporosis or osteopenia and demonstrated a decline in BMD during the preceding year while taking stable doses of alendronate or risedronate, plus supplemental calcium and vitamin D. Patients with previously known secondary causes of osteoporosis were excluded from the study. Eligible patients underwent prospective measurement of bilateral hip and lumbar spine BMD by dual-energy x-ray absorptiometry, serum 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D, intact parathyroid hormone, osteocalcin, and thyroid-stimulating hormone (thyrotropin), and urinary calcium:creatinine ratio.


RESULTS
Annual BMD was assessed in 175 previously bisphosphonate-responsive patients with low BMD. Of the 175 patients, 136 (78%) had either a significant interval increase or no change in BMD, whereas 39 (22%) had a significant decrease. Of the 39 patients who lost BMD, 20 (51%) had vitamin D insufficiency (25-OHD <30 ng/mL). After a single course of orally administered vitamin D2 (500,000 IU during a 5-week period), the 25-OHD level returned to normal in 17 of the 20 vitamin D-insufficient patients and was associated with significant (P<.02) 3.0% and 2.7% increases in BMD at the lumbar spine and the femoral neck, respectively. Failure to normalize the serum 25-OHD level was associated with further loss of BMD.


CONCLUSIONS
Vitamin D insufficiency was the most frequently identified cause of bone loss in patients with declining BMD during bisphosphonate therapy. Correction of vitamin D insufficiency in these patients led to a significant rebound in BMD.
Geller
Jordan L
JL
Burns and Allen Research Institute and Cedars-Sinai Medical Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90048, USA.
Hu
Bei
B
Reed
Susan
S
Mirocha
James
J
Adams
John S
JS
D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D019386:Alendronate / Q000494:pharmacology / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects* / Q000502:physiology; D050071:Bone Density Conservation Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001851:Bone Diseases, Metabolic / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D015331:Cohort Studies; D004164:Diphosphonates / Q000494:pharmacology / Q000627:therapeutic use*; D012968:Etidronic Acid / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D012189:Retrospective Studies; D000068296:Risedronic Acid; D016896:Treatment Outcome; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood; D014808:Vitamin D Deficiency / Q000097:blood / Q000150:complications / Q000188:drug therapy*
D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D014807:Vitamin D; C104450:25-hydroxyvitamin D; D000068296:Risedronic Acid; D012968:Etidronic Acid; D019386:Alendronate