Trabecular Bone Score in Patients With Chronic Glucocorticoid Therapy-Induced Osteoporosis Treated With Alendronate or Teriparatide.
To determine the effect of alendronate (ALN) and teriparatide on trabecular bone score (TBS) in patients with glucocorticoid-induced osteoporosis.



Patients with chronic glucocorticoid therapy-induced osteoporosis (median 7.5 mg/day prednisone equivalent for ≥90 days) were randomized to receive oral ALN 10 mg/day (n = 214) or subcutaneous teriparatide 20 μg/day (n = 214) for 36 months; 118 patients in the ALN group and 123 patients in the teriparatide group completed treatment. Dual x-ray absorptiometry (DXA) results for 53 patients receiving ALN and 56 patients receiving teriparatide who had DXA scans with adequate resolution to perform TBS analysis and completed 36 months of therapy were blindly analyzed for TBS at baseline and 3, 6, 12, 18, 24, and 36 months.



In teriparatide-treated patients, TBS was significantly increased at 18 months compared to baseline, and by 36 months had increased 3.7% (P < 0.05). In ALN-treated patients, there was not a significant change in TBS compared to baseline at any time point. Changes in lumbar spine bone mineral density (BMD) measured by DXA in the subgroup with TBS data were similar to BMD results in the overall study population. At 36 months, increases in lumbar spine BMD were 5.5% and 10.3% in patients treated with ALN and teriparatide, respectively.



In patients with glucocorticoid-induced osteoporosis, both ALN and teriparatide increased lumbar spine BMD. However, trabecular bone score significantly increased with teriparatide but did not significantly change with ALN. The pathogenesis of glucocorticoid-induced osteoporosis is predominantly reduced bone formation. TBS may represent a sensitive measure to discriminate treatment effects of an anabolic versus an antiresorptive drug in glucocorticoid-induced osteoporosis.
University of Alabama at Birmingham.
Kenneth G
KG
Saag
Eli Lilly and Company, Indianapolis, Indiana.
Donato
D
Agnusdei
Lausanne University Hospital, Lausanne, Switzerland.
Didier
D
Hans
Spokane Osteoporosis Center, Spokane, Washington.
Lynn A
LA
Kohlmeier
Eli Lilly and Company, Indianapolis, Indiana.
Kelly D
KD
Krohn
University of Vermont College of Medicine, Burlington.
Edward S
ES
Leib
Cambridge, Maryland.
Edmund J
EJ
MacLaughlin
Eli Lilly and Company, Indianapolis, Indiana.
Jahangir
J
Alam
HealthEast Osteoporosis Care, St. Paul, Minnesota.
Christine
C
Simonelli
Eli Lilly and Company, Indianapolis, Indiana.
Kathleen A
KA
Taylor
Stanford University, Stanford, California.
Robert
R
Marcus
D019386:Alendronate / Q000627:therapeutic use*; D050071:Bone Density Conservation Agents; D000071556:Cancellous Bone / Q000187:drug effects*; D002908:Chronic Disease; D004311:Double-Blind Method; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced* / Q000188:drug therapy*; D011241:Prednisone / Q000009:adverse effects*; D019379:Teriparatide / Q000627:therapeutic use*
D050071:Bone Density Conservation Agents; D005938:Glucocorticoids; D019379:Teriparatide; D011241:Prednisone; D019386:Alendronate