Maintenance infliximab treatment is associated with improved bone mineral density in Crohn's disease

被引:78
作者
Bernstein, M [1 ]
Irwin, S [1 ]
Greenberg, GR [1 ]
机构
[1] Univ Toronto, Mt Sinai Hosp, Dept Med, Toronto, ON M5G 1X5, Canada
关键词
D O I
10.1111/j.1572-0241.2005.50219.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
OBJECTIVES: Diminished bone mineral density (BMD) is a recognized complication of Crohn's disease (CD). The mechanisms underlying bone loss are unclear but may include a direct effect of inflammatory cytokines related to disease activity. Because tumor necrosis factor alpha (TNF-alpha) plays a central role in the pathogenesis of CD inflammation, we evaluated the effect on BMD of maintenance treatment with infliximab in patients with CD. METHODS: BMD of the lumbar spine (L2-L4) and proximal left femur (neck and trochanter) were measured at baseline and 1 yr in 46 CD patients treated with infliximab (5 mg/kg) at 6-8 wk intervals for I yr. Thirteen patients received concurrent prednisone at a mean dose of 10 mg/day (range: 5-15). RESULTS: At baseline, reduced BMD (T-score <= 1) occurred in 43% of patients at the lumbar spine and 46% at the left femur. Between baseline and 1 yr, mean BMD increased at the lumbar spine by 2.4% +/- 0.7% (p = 0.002), at the femoral trochanter by 2.8% +/- 1.2% (p = 0.03), and at the femoral neck by 2.6% +/- 0.7% (p = 0.001). BMD gain at the lumbar spine and the left femur between the groups without and with osteopenia were not different. Changes in BMD were not correlated with concurrent corticosteroid therapy, calcium supplementation, or changes in C-reactive protein (CRP). CONCLUSIONS: Maintenance treatment with infliximab improves BMD in patients with CD and this effect is independent of corticosteroid administration. The BMD response after infliximab suggests that TNF-alpha plays a role in the bone loss associated with CD.
引用
收藏
页码:2031 / 2035
页数:5
相关论文
共 34 条
[1]
Dominant-negative IκB facilitates apoptosis of osteoclasts by tumor necrosis factor-α [J].
Abbas, S ;
Abu-Amer, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (22) :20077-20082
[2]
Abu-Amer Y, 2000, J BIOL CHEM, V275, P27307
[3]
Metabolic bone disease in adults with inflammatory bowel disease [J].
Adachi, JD ;
Rostom, A .
INFLAMMATORY BOWEL DISEASES, 1999, 5 (03) :200-211
[4]
Increase in bone mineral density of patients with spondyloarthropathy treated with anti-tumour necrosis factor α [J].
Allali, F ;
Breban, M ;
Porcher, R ;
Maillefert, JF ;
Dougados, M ;
Roux, C .
ANNALS OF THE RHEUMATIC DISEASES, 2003, 62 (04) :347-349
[5]
Transgenic mice expressing soluble tumor necrosis factor-receptor are protected against bone loss caused by estrogen deficiency [J].
Ammann, P ;
Rizzoli, R ;
Bonjour, JP ;
Bourrin, S ;
Meyer, JM ;
Vassalli, P ;
Garcia, I .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (07) :1699-1703
[6]
A randomized controlled trial of calcium with vitamin D, alone or in combination with intravenous pamidronate, for the treatment of low bone mineral density associated with Crohn's disease [J].
Bartram, SA ;
Peaston, RT ;
Rawlings, DJ ;
Francis, RM ;
Thompson, NP .
ALIMENTARY PHARMACOLOGY & THERAPEUTICS, 2003, 18 (11-12) :1121-1127
[7]
The association between corticosteroid use and development of fractures among IBD patients in a population-based database [J].
Bernstein, CN ;
Blanchard, JF ;
Metge, C ;
Yogendran, M .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2003, 98 (08) :1797-1801
[8]
Metabolic bone disease in patients with inflammatory bowel disease [J].
Bjarnason, I .
RHEUMATOLOGY, 1999, 38 (09) :801-804
[9]
CD4+CD45RBHi T cell transfer induced colitis in mice is accompanied by osteopenia which is treatable with recombinant human osteoprotegerin [J].
Byrne, FR ;
Morony, S ;
Warmington, K ;
Geng, Z ;
Brown, HL ;
Flores, SA ;
Fiorino, M ;
Yin, SL ;
Hill, D ;
Porkess, V ;
Duryea, D ;
Pretorius, JK ;
Adamu, S ;
Manuokian, R ;
Danilenko, DM ;
Sarosi, I ;
Lacey, DL ;
Kostenuik, PJ ;
Senaldi, G .
GUT, 2005, 54 (01) :78-86
[10]
Cino M, 2002, AM J GASTROENTEROL, V97, P915