title: The effect of monthly ibandronate on bone mineral density and bone turnover markers in patients with haemophilia A and B and increased risk for fracture.
abstract: Haemophilia A and B have been associated with increased prevalence of low bone mineral density (BMD). However, no study has so far evaluated the effects of anti-osteoporotic therapy on BMD in haemophilia.The primary endpoint of this prospective study was to estimate the effect of 12-month therapy of oral ibandronate 150 mg/month on BMD in patients with haemophilia A and B. Secondary endpoint was its effect on turnover markers (BTM) of bone resorption [serum C-terminal telopeptide of type 1 collagen (sCTX), tartrate-resistant acid phosphatase band 5b] and bone formation (osteocalcin and bone-specific alkaline phosphatase. Ten adult patients with T-score < -2.5 SD or Z-score < -2 and/or increased risk of fracture according to FRAX model were included. All received 1,000 mg/day calcium carbonate with 800 IU/d cholecalciferol. Males with haemophilia A (n=7) or B (n=3) (mean age 43.5 ± 13.5 years) were studied. Ibandronate resulted in an increase in lumbar BMD (from 0.886 ± 0.169 to 0.927 ± 0.176 g/cm2, 4.7%, p=0.004). No change in BMD of total hip (from 0.717 ± 0.128 to 0.729 ± 0.153 g/cm2, p=0.963) or femoral neck (0.741 ± 0.135 to 0.761 ± 0.146 g/cm2, p=0.952) was noticed. Ibandronate led to a decrease in sCTX (from 0.520 ± 0.243 to 0.347 ± 0.230 ng/ml, -29.9%, p=0.042). No change was observed in other BTM. Ibandronate was generally well-tolerated. In conclusion, ibandronate significantly improved BMD in lumbar spine and reduced bone resorption in adults with haemophilia at increased risk of fracture. Its effect on hip BMD and bone formation markers was not significant.
authors.affiliation: 2nd Propedeutic Department of Internal Medicine, Sarantaporou 10, Greece. anagnwstis.pan@yahoo.gr
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Anagnostis
authors.forename: Timoleon-Achilleas
authors.initials: TA
authors.lastname: Vyzantiadis
authors.forename: Maria
authors.initials: M
authors.lastname: Charizopoulou
authors.forename: Fotini
authors.initials: F
authors.lastname: Adamidou
authors.forename: Spyridon
authors.initials: S
authors.lastname: Karras
authors.forename: Dimitrios G
authors.initials: DG
authors.lastname: Goulis
authors.forename: Asterios
authors.initials: A
authors.lastname: Karagiannis
authors.forename: Vasilia
authors.initials: V
authors.lastname: Garipidou
authors.forename: Sofia
authors.initials: S
authors.lastname: Vakalopoulou
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects*; D050071:Bone Density Conservation Agents / Q000008:administration & dosage*; D001851:Bone Diseases, Metabolic / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D016723:Bone Remodeling / Q000187:drug effects*; D004164:Diphosphonates / Q000008:administration & dosage*; D004334:Drug Administration Schedule; D050723:Fractures, Bone / Q000517:prevention & control; D006467:Hemophilia A / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D002836:Hemophilia B / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D000077557:Ibandronic Acid; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D000077557:Ibandronic Acid