This study aims to reveal more effective clinical or laboratory markers for the diagnosis of acute appendicitis and to score the severity based on a sufficiently large number of patients with acute appendicitis.
We identified 1,195 patients with acute appendicitis after excluding those with other causes of hyperbilirubinemia among the 1,271 patients that underwent a laparoscopic or an open appendectomy between 2009 and 2010. A retrospective chart review of the medical records, including laboratory and histologic results, was conducted. We then analyzed the data using univariate and multivariate analyses.
Among the 1,195 patients, a laparoscopic appendectomy was performed in 685 cases (57.32%), and an open appendectomy was performed in 510 cases (42.68%). The univariate analysis demonstrated significant differences for white blood cell count (P < 0.0001), segmented neutrophils (P = 0.0035), total bilirubin (P < 0.0001), and systemic inflammatory response syndrome (SIRS) score between groups (P < 0.0001). The multivariate analysis demonstrated that total bilirubin (odds ratio, 1.772; 95% confidence interval, 1.320 to 2.379; P = 0.0001) and SIRS score (odds ratio, 1.583; 95% confidence interval, 1.313 to 1.908; P < 0.0001) have statistically significant diagnostic value for perforated appendicitis.
Hyperbilirubinemia is a statistically significant diagnostic marker for acute appendicitis and the likelihood of perforation.
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There have been studies on the relations between metabolic syndrome and colorectal cancer or on the relations between methylenetetrahydrofolate reductase (MTHFR) polymorphism and colorectal cancer, but reports on the relationship between metabolic syndrome, MTHFR polymorphism and colorectal cancer all together are rare. The aim of this study is to find the interrelation between metabolic syndrome and MTHFR polymorphism in colorectal cancer.
This study investigated 255 colorectal cancer patients (cancer group) who underwent surgery in our hospital from March 2003 to December 2008 and compared those patients to 488 healthy patients (control group). The diagnostic criterion for metabolic syndrome was based on the National Cholesterol Education Program-Adult Treatment Panel III (NCEP ATP III), and the MTHFR 677 polymorphism was analyzed.
When colorectal cancer patients and patients in the control group were classified as MTHFR 677 subtypes, there was no difference between the two groups: CC 87 (34.1%), CT 134 (52.6%), and TT 34 (13.3%) for the cancer group and CC 145 (32.4%), CT 238 (53.1%), and TT 65 (14.5%) for the control group. Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences. Moreover, we could find no differences in distributions of MTHFR 677C/T genotypes in the clinical and the biomedical variables of individuals with and without metabolic syndrome in the cancer group.
Our results show no relation between metabolic syndrome and MTHFR polymorphism in colorectal cancer. However, a further prospective study, based on a precise diagnostic criterion for metabolic syndrome, is needed.
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