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Objective To assess whether a combination of adalimumab and ciprofloxacin is superior to adalimumab alone in the treatment of perianal fistulising Crohn's disease (CD).Design Randomised, double-blind, placebo controlled trial in eight Dutch hospitals. In total, 76 CD patients with active perianal fistulising disease were enrolled. After adalimumab induction therapy (160/80mg week 0, 2), patients received 40mg every other week together with ciprofloxacin 500mg or placebo twice daily for 12weeks. After 12weeks, adalimumab was continued. Follow-up was 24weeks. Primary endpoint (clinical response) was defined as 50% reduction of fistulas from baseline to week 12. Secondary endpoints included remission (closure of all fistulas), Perianal Crohn's Disease Activity Index, Crohn's Disease Activity Index (CDAI) and Inflammatory Bowel Disease Questionnaire (IBDQ).Results Clinical response was observed in 71% of patients treated with adalimumab plus ciprofloxacin and in 47% treated with adalimumab plus placebo (p=0.047). Likewise, remission rate at week 12 was significantly higher (p=0.009) in the combination group (65%) compared with adalimumab plus placebo (33%). Combination treatment was associated with a higher mean CDAI change and mean IBDQ change at week 12 (p=0.005 and p=0.009, respectively). At week 24, no difference in clinical response between the two treatment groups was observed (p=0.22). No difference in safety issues was observed.Conclusions Combination therapy of adalimumab and ciprofloxacin is more effective than adalimumab monotherapy to achieve fistula closure in CD. However, after discontinuation of antibiotic therapy, the beneficial effect of initial coadministration is not maintained.Trial registration ClinicalTrials.gov Identifier: NCT00736983.

Item does not contain fulltext OBJECTIVE: The introduction of anti tumour necrosis factor-alpha (anti-TNFalpha) therapy might impact healthcare expenditures, but there are limited data regarding the costs of inflammatory bowel diseases (IBD) following the introduction of these drugs. We aimed to assess the healthcare costs and productivity losses in a large cohort of IBD patients. DESIGN: Crohn's disease (CD) and ulcerative colitis (UC) patients from seven university hospitals and seven general hospitals were invited to fill-out a web-based questionnaire. Cost items were derived from a 3 month follow-up questionnaire and categorised in outpatient clinic, diagnostics, medication, surgery and hospitalisation. Productivity losses included sick leave of paid and unpaid work. Costs were expressed as mean 3-month costs per patients with a 95% CI obtained using non-parametric bootstrapping. RESULTS: A total of 1315 CD patients and 937 UC patients were included. Healthcare costs were almost three times higher in CD as compared with UC, euro1625 (95% CI euro1476 to euro1775) versus euro595 (95% CI euro505 to euro685), respectively (p

Background: Celiac disease (GSE) and inflammatory bowel disease (IBD) are common gastrointestinal disorders. Both display enhanced intestinal permeability, initiated by gluten exposure (GSE) or bacterial interactions (IBD). Previous studies showed association of both diseases with variants in MYO9B , presumably involved in epithelial permeability. Aim: We hypothesized that genetic variants in tight junction genes might affect epithelial barrier function, thus contributing to a shared pathogenesis of GSE and IBD. Methods: We tested this hypothesis with a comprehensive genetic association analysis of 41 genes from the tight junction pathway, represented by 197 tag SNP markers. Results: Two genes, PARD3 (2 SNPs) and MAGI2 (2 SNPs), showed weak association with GSE in a Dutch cohort. Replication in a British GSE cohort yielded significance for one SNP in PARD3 and suggestive associations for two additional SNPs, one each in PARD3 and MAGI2 . Joint analysis of the British and Dutch data further substantiated the association for both PARD3 (rs10763976, P = 6.4 x 10-5; OR 1.23, 95% CI 1.11-1.37) and MAGI2 (rs6962966, P = 7.6 x 10-4; OR 1.19, 95% CI 1.08-1.32). Association was also observed in Dutch ulcerative colitis patients with MAGI2 (rs6962966, P = 0.0036; OR 1.26, 95% CI 1.08-1.47), and suggestive association with PARD3 (rs4379776, P = 0.068). Conclusions: These results suggest that celiac disease and ulcerative colitis may share a common etiology through tight junction-mediated barrier defects, although the observations need further replication.

We read with interest the comments of Buchan and Manuel concerning our risedronate intervention trial in osteopenic patients with Crohn's disease.1 ,2 They stipulated that exclusion of patients with vitamin D deficiency limited the significance of the performed study, as this deficiency is frequently observed in Crohn's disease. It is however well known that replenishment of vitamin D (and calcium) in patients with vitamin D deficiency would lead to a rapid improvement of bone density, irrespective of any effect of risedronate. As assessment of a therapeutic effect of the latter was our primary …

Coeliac disease (gluten-sensitive enteropathy; GSE) and inflammatory bowel disease (IBD) are common gastrointestinal disorders. Both display enhanced intestinal permeability, initiated by gluten exposure (GSE) or bacterial interactions (IBD). Previous studies showed the association of both diseases with variants in MYO9B, presumably involved in epithelial permeability.It was hypothesised that genetic variants in tight junction genes might affect epithelial barrier function, thus contributing to a shared pathogenesis of GSE and IBD.This hypothesis was tested with a comprehensive genetic association analysis of 41 genes from the tight junction pathway, represented by 197 tag single nucleotide polymorphism (SNP) markers.Two genes, PARD3 (two SNPs) and MAGI2 (two SNPs), showed weak association with GSE in a Dutch cohort. Replication in a British GSE cohort yielded significance for one SNP in PARD3 and suggestive associations for two additional SNPs, one each in PARD3 and MAGI2. Joint analysis of the British and Dutch data further substantiated the association for both PARD3 (rs10763976, p = 6.4 x 10(-5); OR 1.23, 95% CI 1.11 to 1.37) and MAGI2 (rs6962966, p = 7.6 x 10(-4); OR 1.19, 95% CI 1.08 to 1.32). Association was also observed in Dutch ulcerative colitis patients with MAGI2 (rs6962966, p = 0.0036; OR 1.26, 95% CI 1.08 to 1.47), and suggestive association with PARD3 (rs4379776, p = 0.068).These results suggest that coeliac disease and ulcerative colitis may share a common aetiology through tight junction-mediated barrier defects, although the observations need further replication.