Eleven (29%) of them had an incomplete form of the disease. Coronary artery abnormalities were found in 10 (26%) children, insignificantly more often among those with incomplete KD. Each day of treatment delay increased the complication rate by almost 1.5 (OR 1.45, p = 0.009). Treatment initiated 10 days after the onset of the disease increased

this risk almost nine times (OR 8.99, p = 0.007). No significant differences in respect to age (p = 0.431), gender (p = 0.744) and laboratory test results were found between the groups with and 432 without coronary complications. A complete regression of coronary artery involvement was seen in 7 children, and partial regression was seen in one child. One child died and another needed coronary artery bypass grafting. Conclusions: Coronary artery aneurysms developed at a similar rate in both complete and incomplete forms of KD and the only significant risk factor Protein Tyrosine Kinase inhibitor Silmitasertib Metabolism inhibitor was the timing of treatment initiation. In young children with

fever of unknown cause lasting longer than 5 days, echocardiography is warranted. Despite a tendency for coronary artery aneurysms to regress, late complications may occur and all children require long-term follow up in a cardiology clinic.”
“Aims: This meta-analysis aims to evaluate the effects of common polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene on the toxicity and clinical responses of irinotecan-based Natural Product Library supplier chemotherapy in patients with colorectal cancer (CRC). Methods: The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched from their inception through November 1st, 2013 without language

restrictions. Meta-analysis was conducted with the use of the STATA 12.0 software. Crude odds ratios (ORs) and their 95% confidence intervals (95% CIs) were calculated. Seven clinical cohort studies with a total of 815 CRC patients met the inclusion criteria. Two common polymorphisms (677 C bigger than T and 1298A bigger than C) in the MTHFR gene were assessed. Results: The results from our meta-analysis suggested that MTHFR genetic polymorphisms might significantly decrease the rate of grade 3/4 toxicity of irinotecan-based chemotherapy in CRC patients (OR=0.53, 95% CI: 0.32-0.89, p=0.015). Furthermore, we also demonstrated that MTHFR genetic polymorphisms strongly correlated with good clinical responses (complete response+partial response) to irinotecan-based chemotherapy in CRC patients (OR=1.47, 95% CI: 1.05-2.04, p=0.024). Conclusions: Our findings provide empirical evidence that MTHFR genetic polymorphisms may decrease the toxicity of irinotecan-based chemotherapy and increase the clinical benefits for CRC patients. Thus, MTHFR genetic polymorphisms may be screened to predict the clinical responses to irinotecan-based chemotherapy in CRC patients.