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Infliximab has been shown to have beneficial effects on bone metabolism in patients with Crohn’s disease (CD) although as yet the exact mechanisms have not been fully elucidated. To evaluate the impact of adalimumab therapy on bone metabolism using a combined in vivo and in vitro model. Parathyroid hormone, vitamin D, bone formation markers, bone resorption marker, pro-inflammatory cytokines, anti-inflammatory cytokines, osteoprotegerin, and sRANKL were measured in control patients and pre- and post-treatment with adalimumab in CD patients. The effect of control patients’ and pre- and post-treatment CD patients’ sera on human osteoblasts (hFOB 1.19) in vitro cell viability and differentiation was also analyzed. There was a significant increase in bone formation markers osteocalcin (P

Summary Background Patients with inflammatory bowel disease (IBD) are at increased risk of osteoporosis. A number of studies have emerged in recent years indicating that tumour necrosis factor (TNF) blockade appears to have a beneficial effect on bone mineral density (BMD) in IBD patients. Aims To provide a review of the available data regarding the effect of the currently licensed anti-TNF-α therapies on bone metabolism and BMD in IBD patients. Methods A Medline search was performed using the search terms ‘infliximab’, ‘bone metabolism’, ‘IBD’, ‘BMD’, ‘bone markers’, ‘adalimumab’, ‘bone disease’, ‘Crohn’s disease’ and ‘ulcerative colitis’. Results Infliximab has a beneficial effect on bone turnover markers in Crohn’s disease (CD) patients in the short term. The longest study to date comprising 24 CD patients showed an overall improvement in two bone formation markers – b-alkaline phosphatase (P = 0.022) and osteocalcin (P = 0.008) at 4 months post-treatment. Moreover, the largest study to date comprising 71 CD patients showed significant improvement in sCTx, a bone resorption marker (P = 0.04) at week-8 post-treatment. There is little data looking at the effect of anti-TNF-α therapy on bone metabolism in ulcerative colitis. Moreover, the long-term effects of anti-TNF-α therapy on bone structure and fracture risk in IBD patients are currently not known. The effect of cessation of anti-TNF-α therapy on bone metabolism is also unknown. Conclusion Properly controlled long-term trials are needed to fully evaluate the impact of TNF blockade on bone mineral density.

Here we describe a patient with ulcerative colitis who developed alveolitis after infliximab therapy. With earlier case reports of development of alveolitis in rheumatoid arthritis patients after infliximab infusion, the temporal relationship between the infliximab therapy and the development of alveolitis in this case, raises the possibility that the two might be causally related. With an increasing trend towards treating moderate to severely active ulcerative colitis patients with infliximab as a rescue therapy, clinicians should be aware of this potentially serious complication.