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Background: Risk adjustment is a critically important aspect of outcomes research. Racial, geographic, cultural, and socioeconomic differences are nonclinical parameters that can affect clinical outcomes measurement after gastric bypass surgery., Methods: A single surgeon's experience with 217 consecutive laparoscopic gastric bypass patients in private practice in Southern California was compared with the same surgeon's experience with 124 consecutive patients in an academic institution in Philadelphia., Results: Of the Southern California and Philadelphia groups, 89%, 1%, 9%, and 1% and 55%, 38%, 6%, and 0% were white, black, Hispanic, and Asian, respectively. The average number of co-morbidities was 7.8 in the Southern California group versus 14.4 in the Philadelphia group (P <.001). The 60-day readmission to the hospital rate and emergency room admission rate was 1.4% versus 10.4% and 1.4% versus 18.5%. The insurer mix of private pay, private insurer, and federally funded insurer was 20%, 80%, and 0% in the Southern California group and 0.8%, 71%, and 28% in the Philadelphia group, respectively. Multivariate logistic regression analysis found Medicaid status and practice location independently predicted for the 60-day readmission rate (odds ratio [OR] 3.7, P = .04 and OR 5.6, P = .04, respectively) and a return to the emergency room (OR 3.2, P = .03 and OR 16.3, P <.001). Race, income, and the presence of diabetes were not independent predictors. Variables with nonsignificant differences between the Southern California and Philadelphia cohorts included average age, average body mass index, and major complications (return to surgery and intensive care unit admissions)., Conclusion: The results of this study have shown that in comparing and predicting the outcomes after bariatric surgery, adjustment for demographic and insurance variables might be necessary to improve accuracy.

A common haplotype spanning 250 kb on chromosome 5q31 is strongly associated with Crohn disease (CD). Recently, two functional variants within the SLC22A4 and SLC22A5 genes at this locus (IBD5), L503F (c.1507C > T) and G-207C (c.-207G > C), have been proposed to contribute directly to susceptibility to CD. However, extensive linkage disequilibrium at the IBD5 locus has complicated efforts to distinguish causal variants from association of the general risk haplotype. We genotyped the SLC22A4 and SLC22A5 variants and other polymorphisms across the risk haplotype in four populations of European origin, and applied regression-based haplotype analysis to over 1,200 fully genotyped case-control pairs, modeling case/control status on the presence of one or more SNPs to test for conditional association and to identify risk haplotypes. We found highly significant association of SNPs at the IBD5 locus with Crohn disease in all populations tested. However, the frequencies of L503F and G-207C in individuals who did not carry the general IBD5 risk haplotype were not significantly different in cases and controls, with associated disease odds ratios (ORs) of 0.90 (95% CI, 0.57-1.40) and 0.90 (95% CI, 0.65-1.23), respectively. Haplotype analysis showed that addition of the SLC22A4 and SLC22A5 variants to a null model that included the background risk haplotype did not significantly improve the model fit. In addition to the common risk haplotype, several rare haplotypes had an increased frequency in cases compared to controls. This study suggests that the molecular basis for Crohn disease susceptibility at the IBD5 locus remains to be defined, and highlights the challenge of the identification of causal variants in a complex disease in regions of extensive linkage disequilibrium.

Evidence from four independent linkage studies and two meta-analyses of genome-wide data support the existence of a locus conferring susceptibility to inflammatory bowel diseases (IBD) in chromosomal region 19p. Identification of a susceptibility allele in this approximately 28.5 Mb region with over 600 genes is a formidable task. To tackle this problem, we undertook two approaches: (1) haplotype-based candidate-gene screen, and (2) evaluation of previously reported associations. For the former, we selected genes with potential implication in IBD pathogenesis based on published functional and expression data, typed SNPs, constructed haplotypes, screened for association in 180 IBD trios, and followed up preliminary associations in 343 IBD patients and 207 control individuals. Overall, we analyzed 465 SNPs, and 260 haplotypes distributed across 56 candidate genes. We found suggestive evidence of association (nominal P<0.01) with four genes (C3, FCER2, IL12RB1, and CRLF1) in a screening stage, but were unable to confirm these preliminary observations at follow-up. In the second approach, we typed four nonsynonymous polymorphisms in genes C3 (R102G and L314P) and ICAM1 (G241R and K469E) in four independent cohorts totaling 2178 IBD cases. We evaluated these data together with previously published reports for three of these variants (C3-Gly102, ICAM1-Arg241, and ICAM1-Glu469), in a meta-analysis. Our pooled meta-analysis provides compelling evidence against association of these variants with disease. Overall, we performed the most comprehensive candidate-gene association study for IBD to date. The information hereby generated constitutes a valuable resource to investigate other common genetic immune diseases, such as celiac disease.

As a cohort of the vulnerable populations, African Americans have the poorest health status indicators of all ethnic groups. Using a vulnerable populations theoretical framework, the reasons for the disparities are discussed.

Because clinicians control more than 70% of the total costs of medical care, the success of managed care systems in containing expenditures depends to a large degree on their leadership. Clinicians must make cultural changes and develop core competencies and technical skills to promote the continuous improvement needed for the success of managed care.

Previous studies have shown that supplementation of the diet with oat bran may lower serum cholesterol levels. However, it is not known whether oat-bran diets lower serum cholesterol levels by replacing fatty foods in the diet or by a direct effect of the dietary fiber contained in oat bran. To determine which is the case, we compared the effect of isocaloric supplements of high-fiber oat bran (87 g per day) and a low-fiber refined-wheat product on the serum lipoprotein cholesterol levels of 20 healthy subjects, 23 to 49 years old. After a one-week base-line period during which they consumed their usual diets, the subjects were given each type of supplement for six-week periods in a double-blind, crossover trial. Mean serum cholesterol levels (+/- SD) were not significantly different during the high-fiber and low-fiber periods: total cholesterol, 4.44 +/- 0.73 and 4.46 +/- 0.64 mmol per liter (172 +/- 28 and 172 +/- 25 mg per deciliter); low-density lipoprotein, 2.69 +/- 0.63 and 2.77 +/- 0.59 mmol per liter (104 +/- 24 and 107 +/- 23 mg per deciliter); and high-density lipoprotein, 1.40 +/- 0.39 and 1.32 +/- 0.39 mmol per liter (54.2 +/- 15.0 and 50.9 +/- 15.2 mg per deciliter), respectively. However, both types of supplements lowered the mean base-line serum cholesterol level, 4.80 +/- 0.80 mmol per liter (186 +/- 31 mg per deciliter), by 7 to 8 percent (95 percent confidence interval for high fiber, 11 to 4 percent, and for low fiber, 11 to 3 percent). The subjects ate less saturated fat and cholesterol and more polyunsaturated fat during both periods of supplementation than at base line. Those changes in dietary fats were sufficient to explain all of the reduction in serum cholesterol levels caused by the high-fiber and low-fiber diets. The average blood pressure was 112/68 mm Hg at base line and did not change during either dietary period. We conclude that oat bran has little cholesterol-lowering effect and that high-fiber and low-fiber dietary grain supplements reduce serum cholesterol levels about equally, probably because they replace dietary fats.

The changes in serum total CPK and its isoenzymes have not been delineated in acute mesenteric infarction. As measurement of serum CPK levels could conceivably be a useful diagnostic test for bowel infarction, this experiment was performed to assess changes in serum CPK levels in bowel infarction in dogs, using sham operation and talc peritonitis as controls. Laparotomies were performed in 20 dogs, and each was as signed randomly to one of three groups: those having laparotomy (LAP), talc peritonitis (PER), and superior mesenteric artery infarction (MAI). Mixed venous blood samples were obtained from all subjects for 30 hours after surgery. All animals were killed, and complete autopsies were performed. Confirmation of infarction and determination of its extent were obtained through both gross and microscopic examination of the gut in canines subjected to arterial infarction. Total serum CPK levels were determined by spectrophotometric analysis. Agarose gel electrophoresis was used to determine the levels of each of the isoenzymes. Significant elevations of CPK and CPK-MM occurred nine hours after injury. CPK-BB reached maximum elevation by six hours, while CPK-MB did not reach its maximum until 24 hours after injury. From data in the study we conclude that total CPK and its isoenzymes become elevated in the serum of canines subjected to experimental superior mesenteric artery infarction. That CPK-BB elevations peak in the first 12 hours after injury and CPK-MB in the second 12 hours after injury may be of particular diagnostic significance.