PurposeThe underlying biological mechanisms of the frequent exacerbator phenotype of COPD remain unclear. We compared systemic neutrophil function in COPD patients with or without frequent exacerbations.MethodsWhole blood from COPD frequent exacerbators (defined as ≥2 moderate–severe exacerbations in the previous 2 years) and non-exacerbators (no exacerbations in the preceding 2 years) was assayed for neutrophil function. Neutrophil function in healthy ex-smoking volunteers was also measured as a control (reference) group.ResultsA total of 52 subjects were included in this study: 26 frequent exacerbators, 18 non-exacerbators and 8 healthy controls. COPD frequent exacerbators had blunted blood neutrophil fMLP-stimulated oxidative burst compared to both non-exacerbators (p < 0.01) and healthy controls (p < 0.001). There were no differences between COPD frequent exacerbators and non-exacerbators in blood neutrophil PMA-stimulated oxidative burst, but both COPD groups had reduced responses compared to healthy controls (p < 0.001). Bacterial-stimulated neutrophil degranulation was greater in frequent exacerbators than non-exacerbators (p < 0.05).ConclusionThis study is the first to report aberrant receptor-mediated blood neutrophil function in the frequent exacerbator of COPD.

BACKGROUNDMicroalbuminuria is an emerging risk factor in evaluation of inhospital coronary events and long-term morbidity and mortality in patients with acute myocardial infarction. The primary aim of this study is to determine the prognostic significance and the predictive value of microalbuminuria for complications in patients with non-diabetic, non-hypertensive acute myocardial infarction. MATERIALS AND METHODSA cross sectional study was done on 100 non-diabetic, non-hypertensive patients admitted for acute myocardial infarction. Spot urine sample was taken for measuring albumin creatinine ratio. Patients were followed up and observed for complications related to acute myocardial infarction like left ventricular dysfunction, cardiac failure, LV clot, recurrence of angina, occurrence of arrhythmias and death for a period of one year. RESULTSAmong the 100 patients included in the study group 71% had microalbuminuria while 29% were normoalbuminuric. The difference was statistically significant, and it shows that there is definite association between acute myocardial infarction and microalbuminuria.Post myocardial infarction complications were also higher in the group with microalbuminuria indicating its efficacy as a prognostic marker in patients with acute myocardial infarction. CONCLUSIONMicroalbuminuria is a marker of endothelial dysfunction and its level rises in patients with acute myocardial infarction by various mechanisms, most prominent being as a part of systemic inflammatory response. KEYWORDSAcute Myocardial Infarction, Microalbuminuria, Endothelial Dysfunction. HOW TO CITE THIS ARTICLE:Mohamed P, Lorenz T, Bagialakshmi G. A study on association of microalbuminuria in nondiabetic and non-hypertensive patients with acute myocardial infarction.

BACKGROUNDAcute kidney injury following administration of iodinated contrast (CI-AKI) has been referred to as contrast induced nephropathy (CIN). Ischemic preconditioning (IPC), transient brief episodes of ischemia before a subsequent prolonged ischemia/reperfusion injury, has been shown to reduce the extent of organ damage. Several studies have demonstrated the tissue-protective effects of remote ischemic preconditioning (RIPC) in various target organs, including the kidneys. The aim of this study is to assess if remote ischemic preconditioning reduces the incidence of contrast induced AKI in patients with STEMI undergoing coronary angiogram. MATERIALS AND METHODSThe study was conducted in 100 patients (50 cases and 50 control) who were undergoing coronary angiogram (CAG) following acute ST elevation myocardial infarction in Govt. Rajaji Medical College, Madurai. Test group underwent RIPC (Remote Ischemic preconditioning) and control group underwent sham preconditioning prior to procedure whereas both test and control groups received normal saline infusion-1 ml/kg/hr, beginning 12 hours before CAG till 12 hours after coronary angiogram (CAG). Both groups were followed with serial renal function tests for next 72 hrs after CAG.