The change of bone mineral density according to treatment agents in patients with ankylosing spondylitis.
OBJECTIVE
The aim was to access the effects of treatment on bone mineral density (BMD) by treatment agents in patients with ankylosing spondylitis (AS).


METHODS
We analyzed clinical characteristics of 90 AS patients. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and x-ray of lumbar spine (L-spine) and sacroiliac joint were included in the baseline assessment. The BMDs of right femur and L-spine were measured annually using dual x-ray absorptiometry (DXA). The patients were divided into one of the following four groups by agents exposed for the follow-up period: conventional treatment, bisphosphonate, anti-TNF-α agent or bisphosphonate + anti-TNF-α agent. We evaluated the changes of BMD according to treatment groups.


RESULTS
The average age of disease onset was 30 years and the mean disease duration was 8.2 years. The patients who were assigned to the groups of conventional treatment, bisphosphonate, anti-TNF-α agents and bisphosphonate + anti-TNF-α agents were 40, 20, 19 and 11. BMDs values of both L-spine and femur showed tendencies to the most increase in the group treated with concurrent bisphosphonate and anti-TNF-α agent. However, the change of BMD by treatment agents was significant different only in trochanter (P = 0.001). In patients without syndesmophyte, there was significant difference of BMD change in both L-spine and total proximal femur (P = 0.001, 0.004). The BMD change of trochanter was correlated with the reductions of ESR and CRP (r = 0.239, P = 0.035 and r = 0.233, P = 0.040).


CONCLUSIONS
The BMDs of AS patients increased more by the treatment of concurrent bisphosphonate and anti-TNF-α agents. The gain of bone mass was associated with the reduction of inflammation.
Kang
Kwi Young
KY
Division of Rheumatology, Department of Internal Medicine, Medical College, Chungbuk National University, Cheongju, South Korea. kykang@catholic.ac.kr
Lee
Kwan Yong
KY
Kwok
Seung-Ki
SK
Ju
Ji Hyeon
JH
Park
Kyung-Soo
KS
Hong
Yeon Sik
YS
Kim
Ho-Youn
HY
Park
Sung-Hwan
SH
D015502:Absorptiometry, Photon; D000068879:Adalimumab; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D015519:Bone Density / Q000187:drug effects / Q000502:physiology*; D004164:Diphosphonates / Q000494:pharmacology / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D005269:Femur / Q000503:physiopathology; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology / Q000627:therapeutic use; D000069285:Infliximab; D008159:Lumbar Vertebrae / Q000503:physiopathology; D008297:Male; D008727:Methotrexate / Q000494:pharmacology / Q000627:therapeutic use; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012189:Retrospective Studies; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000503:physiopathology*; D012460:Sulfasalazine / Q000494:pharmacology / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D004164:Diphosphonates; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D012460:Sulfasalazine; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D008727:Methotrexate