Direct health care costs of Crohn's disease and ulcerative colitis in US children and adults.

Division of Pediatric Gastroenterology, Department of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
Gastroenterology (Impact Factor: 13.93). 09/2008; 135(6):1907-13. DOI: 10.1053/j.gastro.2008.09.012
Source: PubMed

ABSTRACT Data regarding the health care costs of inflammatory bowel disease (IBD) in the United States are limited. The objectives of this study were to estimate the direct costs of Crohn's disease (CD) and ulcerative colitis (UC) in the United States, describe the distribution of costs among inpatient, outpatient, and pharmaceutical services, and identify sociodemographic factors influencing these costs.
We extracted medical and pharmacy claims from an administrative database containing insurance claims from 87 health plans in 33 states, occurring between 2003 and 2004. We identified cases of CD and UC using an administrative definition. For each case, we selected up to 3 non-IBD controls. Claims were classified as inpatient, outpatient, or pharmaceutical according to Current Procedural Terminology codes or National Drug Codes. Costs were based on the paid amount of each claim. IBD-attributable costs were estimated by subtracting costs for non-IBD patients from those for patients with IBD. Logistic regression was used to identify the sociodemographic factors affecting these costs.
We identified 9056 patients with CD and 10,364 patients with UC. Mean annual costs for CD and UC were $8265 and $5066, respectively. For CD, 31% of costs were attributable to hospitalization, 33% to outpatient care, and 35% to pharmaceutical claims. The corresponding distribution for UC was 38%, 35%, and 27%, respectively. Costs were significantly higher for children younger than 20 years compared with adults, but this did not vary substantially by sex or region.
This study demonstrates a substantial economic burden of IBD and can be used to inform health policy.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Caveolin-1 (Cav-1) is a multifunctional scaffolding protein serving as a platform for the cell's signal-transduction and playing an important role in inflammation. However, its role in inflammatory bowel disease is not clear. A recent study showed that Cav-1 is increased and mediates angiogenesis in dextran sodium sulphate-induced colitis, which are contradictory to our pilot findings in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis. In the present study, we further clarified the role of Cav-1 in TNBS-induced colitis. In BALB/c mice, acute colitis was induced by intra-rectal administration of one dose TNBS, while chronic colitis was induced by administration of TNBS once a week for 7 weeks. To assess the effects of complete loss of Cav-1, Cav-1 knockout (Cav-1-/-) and control wild-type C57 mice received one TNBS administration. Body weight and clinical scores were monitored. Colon Cav-1 and pro-inflammatory cytokine levels were quantified through ELISAs. Inflammation was evaluated through histological analysis. Colon Cav-1 levels were significantly decreased in TNBS-induced colitis mice when compared to normal mice and also inversely correlated with colon inflammation scores and proinflammatory cytokine levels (IL-17, IFN-γ and TNF) significantly. Furthermore, after administration of TNBS, Cav-1-/- mice showed significantly increased clinical and colon inflammatory scores and body weight loss when compared with control mice. Cav-1 may play a protective role in the development of TNBS-induced colitis. Our findings raise an important issue in the evaluation of specific molecules in animal models that different models may exhibit opposite results because of the different mechanisms involved.
    PLoS ONE 03/2015; 10(3):e0119004. DOI:10.1371/journal.pone.0119004 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: & Aims: There is controversy over the best treatment for patients with Crohn's disease, due to the lack of direct comparative trials. We compared therapies for induction and maintenance of remission in patients with Crohn's disease, based on direct and indirect evidence. We performed systematic reviews of MEDLINE, EMBASE, and Cochrane Central databases, through June 2014. We identified randomized controlled trials (n=39) comparing methotrexate, azathioprine/6-mercaptopurine, infliximab, adalimumab, certolizumab, vedolizumab, or combined therapies with placebo or an active agent for induction and maintenance of remission in adult patients with Crohn's disease. Pairwise treatment effects were estimated through a Bayesian random-effects network meta-analysis and reported as odds ratios (OR) with a 95% credible interval (CrI). Infliximab, the combination of infliximab and azathioprine (infliximab+azathioprine), adalimumab, and vedolizumab were superior to placebo for induction of remission. In pair-wise comparisons of anti-tumor necrosis factor agents, infliximab+azathioprine (OR, 3.1; 95% CrI, 1.4-7.7) and adalimumab (OR, 2.1; 95% CrI, 1.0-4.6) were superior to certolizumab for induction of remission. All treatments were superior to placebo for maintaining remission, except for the combination of infliximab and methotrexate. Adalimumab, infliximab, and infliximab+azathioprine were superior to azathioprine/6-mercaptopurine: adalimumab (OR, 2.9; 95% CrI, 1.6-5.1), infliximab (OR, 1.6; 95% CrI, 1.0-2.5), infliximab+azathioprine (OR, 3.0; 95% CrI, 1.7-5.5) for maintenance of remission. Adalimumab and infliximab+azathioprine were superior to certolizumab: adalimumab (OR, 2.5; 95% CrI, 1.4-4.6) and infliximab+azathioprine (OR, 2.6; 95% CrI, 1.3-6.0). Adalimumab was superior to vedolizumab (OR, 2.4; 95% CrI, 1.2-4.6). Based on a network meta-analysis, adalimumab and infliximab+azathioprine are the most effective therapies for induction and maintenance of remission of Crohn's disease. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
    Gastroenterology 10/2014; 148(2). DOI:10.1053/j.gastro.2014.10.011 · 13.93 Impact Factor
  • Source
    European Journal of Gastroenterology & Hepatology 01/2013; 25(7):790-797. DOI:10.1097/MEG.0b013e32836019b9 · 2.15 Impact Factor


Available from

Similar Publications