The prevalence and geographic distribution of Crohn's disease and ulcerative colitis in the United States
ABSTRACT Previous US studies of inflammatory bowel disease (IBD) prevalence have sampled small, geographically restricted populations and may not be generalizable to the entire nation. This study sought to determine the prevalence of Crohn's disease (CD) and ulcerative colitis (UC) in a large national sample and to compare the prevalence across geographic regions and other sociodemographic characteristics.
We analyzed the health insurance claims for 9 million Americans, pooled from 87 health plans in 33 states, and identified cases of CD and UC using diagnosis codes. Prevalence was determined by dividing the number of cases by the number of persons enrolled for 2 years. Logistic regression was used to compare prevalence estimates by geographic region, age, sex, and insurance type (Medicaid vs commercial).
The prevalence of CD and UC in children younger than 20 years was 43 (95% confidence interval [CI], 40-45) and 28 (95% CI, 26-30) per 100,000, respectively. In adults, the prevalence of CD and UC was 201 (95% CI, 197-204) and 238 (95% CI, 234-241), respectively. The prevalence of both conditions was lower in the South, compared with the Northeast, Midwest, and West. IBD appears to be more common in commercially insured individuals, compared with those insured by Medicaid.
This estimation of the prevalence of IBD in the US should help quantify the overall burden of disease and inform the planning of appropriate clinical services.
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ABSTRACT: Interleukin-8 (IL-8) plays key roles in both chronic inflammatory diseases and tumor modulation. We previously observed that IL-8 secretion and function can be modulated by nucleotide (P2) receptors. Here we investigated whether IL-8 release by intestinal epithelial HT-29 cells, a cancer cell line, is modulated by extracellular nucleotide metabolism. We first identified that HT-29 cells regulated adenosine and adenine nucleotide concentration at their surface by the expression of the ectoenzymes NTPDase2, ecto-5'-nucleotidase, and adenylate kinase. The expression of the ectoenzymes was evaluated by RT-PCR, qPCR, and immunoblotting, and their activity was analyzed by RP-HPLC of the products and by detection of Pi produced from the hydrolysis of ATP, ADP, and AMP. In response to poly (I:C), with or without ATP and/or ADP, HT-29 cells released IL-8 and this secretion was modulated by the presence of NTPDase2 and adenylate kinase. Taken together, these results demonstrate the presence of 3 ectoenzymes at the surface of HT-29 cells that control nucleotide levels and adenosine production (NTPDase2, ecto-5'-nucleotidase and adenylate kinase) and that P2 receptor-mediated signaling controls IL-8 release in HT-29 cells which is modulated by the presence of NTPDase2 and adenylate kinase.Mediators of Inflammation 07/2014; 2014:879895. DOI:10.1155/2014/879895 · 2.42 Impact Factor
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ABSTRACT: Background: There is increasing interest in investigating genetic risk models in empirical studies, but such studies are premature when the expected predictive ability of the risk model is low. We assessed how accurately the predictive ability of genetic risk models can be estimated in simulated data that are created based on the odds ratios (ORs) and frequencies of single-nucleotide polymorphisms (SNPs) obtained from genome-wide association studies (GWASs). Methods: We aimed to replicate published prediction studies that reported the area under the receiver operating characteristic curve (AUC) as a measure of predictive ability. We searched GWAS articles for all SNPs included in these models and extracted ORs and risk allele frequencies to construct genotypes and disease status for a hypothetical population. Using these hypothetical data, we reconstructed the published genetic risk models and compared their AUC values to those reported in the original articles. Results: The accuracy of the AUC values varied with the method used for the construction of the risk models. When logistic regression analysis was used to construct the genetic risk model, AUC values estimated by the simulation method were similar to the published values with a median absolute difference of 0.02 [range: 0.00, 0.04]. This difference was 0.03 [range: 0.01, 0.06] and 0.05 [range: 0.01, 0.08] for unweighted and weighted risk scores. Conclusions: The predictive ability of genetic risk models can be estimated using simulated data based on results from GWASs. Simulation methods can be useful to estimate the predictive ability in the absence of empirical data and to decide whether empirical investigation of genetic risk models is warranted.Frontiers in Genetics 06/2014; 5:179. DOI:10.3389/fgene.2014.00179
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ABSTRACT: The biological therapy of Crohn's disease, such as infliximab is a powerful approach in the therapy of inflammatory bowel diseases. However, in some patients with aggressive disease course, even a combined immunosuppressive therapy will not result in permanent remission. Hematopoietic stem cell transplantation has emerged as a new potential therapeutic tool for inflammatory bowel diseases. The authors report the case of a 15-year-old boy with severe Crohn's disease resistant to combined immunosuppressive therapy. After a 3-years course of unsuccessful conventional therapy including infliximab, autologous hematopoietic stem cell transplantation was performed which resulted in a complete remission. One year after transplantation the patient has relapsed, but he could be treated effectively with conventional therapy regiments. To the best of knowledge of the authors, this is the first report in Hungary presenting hematopoietic stem cell therapy in patient with severe Crohn's disease. Orv. Hetil., 2014, 155(20), 789-792.Orvosi Hetilap 05/2014; 155(20):789-92. DOI:10.1556/OH.2014.29892