The impact of glycemic variability on length of stay and mortality in diabetic patients admitted with community-acquired pneumonia or chronic obstructive pulmonary disease.

AIM: To investigate the influence of glycemic variability (GV) on length of stay and in-hospital mortality in non-critical diabetic patients. METHODS: A observation retrospective study was performed. Diabetic patients admitted between January and June 2016 with the diagnosis of community-acquire pneumonia (CAP) and/or acute exacerbation of chronic obstructive pulmonary disease (COPD) were enrolled and glycemic control (persistent hyperglycemia, hypoglycemia, mean glucose level (MGL) and respective standard deviation (SD) and coefficient of variation (CV)) were evaluated. Primary outcomes were length of stay and in-hospital mortality. RESULTS: Data from 242 patients were analyzed. Fifty-eight percent of the patients were male, with a median age of 77 years (min-max, 29-98). Patients had on average 2.1 glucose readings-day and the MGL was 193.3 mg/dl (min-max, 84.3-436.6). Hypoglycemia was documented in 13.4% of the patients and 55.4% had persistent hyperglycemia. The median length of hospital stay was 10 days (min-max, 1-66) and in-hospital mortality was 7.4%. We found a significant higher in-hospital mortality in older patients, with history of cancer and with nosocomial infections. We did not find any correlation between MGL, SD, CV, hypoglycemia or persist hyperglycemia and in-hospital mortality. A longer length of stay was observed in patients with heavy alcohol consumption and nosocomial infections. The length of stay was negatively correlated with the mean glucose level (r2-0.147; p < 0.05) and positively correlated with the coefficient of variation (p 0.162; p < 0.05). CONCLUSION: This study confirmed the negative impact of the glycemic variability in the outcomes of diabetic patients admitted with CAP or acute exacerbation of COPD.

A new model of outbred genetically selected mice which present a strong acute inflammatory response in the absence of complement component C5.

OBJECTIVE: Mice selected for a strong (AIRmax) or weak (AIRmin) acute inflammatory response present different susceptibilities to bacterial infections, autoimmune diseases and carcinogenesis. Variations in these phenotypes have been also detected in AIRmax and AIRmin mice rendered homozygous for Slc11a1 resistant (R) and susceptible (S) alleles. Our aim was to investigate if the phenotypic differences observed in these mice was related to the complement system. MATERIAL: AIRmax and AIRmin mice and AIRmax and AIRmin groups homozygous for the resistance (R) or susceptibility (S) alleles of the solute carrier family 11a1 member (Slc11a1) gene, formerly designated Nramp-1. METHODS AND RESULTS: While no difference in complement activity was detected in sera from AIRmax and AIRmin strains, all sera from AIRmax Slc11a1 resistant mice (AIRmax(RR)) presented no complement-dependent hemolytic activity. Furthermore, C5 was not found in their sera by immunodiffusion and, polymerase chain reaction and DNA sequencing of its gene demonstrated that AIRmax(RR) mice are homozygous for the C5 deficient (D) mutation previously described in A/J. Therefore, the C5D allele was fixed in homozygosis in AIRmax(RR) line. CONCLUSIONS: The AIRmax(RR) line is a new experimental mouse model in which a strong inflammatory response can be triggered in vivo in the absence of C5.