Summary The CD14 receptor seems to be an important part of the innate immune system. A mutant CD14 can produce a reduced signal in response to infection, as a result of which an adequate inflammatory innate response is not induced, leading to a systemic infection. Defects in the innate immunity increase patient susceptibility to systemic infections and can produce a deregulated inflammatory response causing sepsis, organ failure or death in critically ill patients. We evaluated the CD14 ÿ260C>T polymorphism genotyping as a genetic tool for risk evaluation of critically ill patients admitted to an intensive care unit (ICU) in Southern Brazil. We monitored the patients daily during their entire ICU and post-ICU (hospital) stay (measured from the ICU admission day to a maximum of 224 days). A total of 85 patients, aged 19-95 years (mean = 56 years, median = 58 years), were included in this study. Patient mortality was 58.8%. The genotypic (TT = 0.27, TC = 0.41, CC = 0.32) and allelic (T = 0.48, C = 0.52) frequencies did not differ from the values expected by the Hardy-Weinberg model and genotype distribution was random for all clinical characteristics at ICU admission. We found a statistically significant difference favouring the survival of patients with TT genotype (P = 0.042), suggesting that this CD14 gene polymorphism could be a candidate for further study in the search for a complementary prognostic tool for patient risk evaluation. Our study describes, for the first time, the effect of the CD14 gene polymorphism in critically ill Brazilian patients. Our data suggest that patients carrying the TT genotype have a better survival outcome.
Blood groups ABO, MN, Rhesus, P, and Lewis, salivary ABH secretion, and at the HLA DQ alpha locus were studied in 65 Caucasian children of both sexes diagnosed as having acute febrile urinary tract infection in the 1st year of life, as well as in 60 Caucasian control children. No differences were observed between patients and controls. Results from patients with normal urinary tracts were also similar to those from patients with primary vesicoureteral reflux. We could not confirm previous findings suggesting different susceptibility to urinary tract infection based on phenotypes of several genetic markers.
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