Background and Aim:Studies on potential biomarkers in experimental models of acute lung injury (ALI) and clinical samples from patients with ALI have provided evidence to the pathophysiology of the mechanisms of lung injury and predictor of clinical outcome. Because of the high mortality and substantial variability in outcomes in patients with acute respiratory distress syndrome (ARDS), identification of biomarkers such as cytokines is important to determine prognosis and guide clinical decision-making.Materials and Methods:In this study, we have included thirty patients admitted to Intensive Care Unit diagnosed with ARDS, and serum samples were collected on day 1 and 7 and were analyzed for serum interleukin-6 (IL-6) and IL-8 by ELISA method, and Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring was done on day 1.Results:The mortality in the patients observed with ARDS was 34%. APACHE II score was significantly higher in nonsurvivors as compared to survivors. There were no significant differences in gender and biochemical and hematological parameters among the survivors and nonsurvivors. Serum IL-6 and IL-8 levels on day 1 were significantly higher in all the ARDS patients as compared to healthy controls and these levels were returned to near-normal basal levels on day 7. The serum IL-6 and IL-8 levels measured on day 7 were of survivors. As compared to survivors, the IL-6 and IL-8 levels were significantly higher in nonsurvivors measured on day 1. Spearman's rank correlation analysis indicated a significant positive correlation of APACHE II with IL-8. By using APACHE II score, IL-6, and IL-8, the receiver operating characteristic curve was plotted and the provided predictable accuracy of mortality (outcome) was 94%.Conclusion:The present study highlighted the importance of measuring the cytokines such as IL-6 and IL-8 in patients with ARDS in predicting the clinical outcome.

We aimed to assess whether measuring carotid intima-media thickness (CIMT) and oxidative stress markers such as protein carbonyls, malondialdehyde, nitrate and glutathione in plasma of elderly patients without and with coronary artery disease (CAD) identifies early risk for CAD. A total of 50 cases with cardiovascular risk factors over the age of 60 years without CAD, and 50 patients with angiographically documented CAD over the age of 60 years were included in the study. Control group consists of 200 healthy individuals without the risk factors. Demographic details were obtained from all the subjects and CIMT measured by high frequency ultrasound and oxidative stress markers such protein carbonyls, malondialdehyde and total glutathione were determined in plasma by spectrophotometric methods. The distribution of cardiovascular risk factors in without CAD and CAD cases were smokers (16 vs 56 %), hypertension (26 vs 64 %), diabetes (16 vs 56 %) and dyslipidemia (18 vs 58 %) and positive family history (4 vs 38 %). None of the control group had any cardiovascular risk factors. Among the CAD cases, 16 % had single vessel disease, 44 % had double vessel disease and 40 % had triple vessel disease. The CIMT was significantly increased in CAD cases as compared to cases without CAD and healthy controls. On the other hand, CIMT was significantly increased in cases without CAD as compared to healthy controls. CIMT also increased with the duration of diabetes in patients without CAD and severity of disease in CAD cases. The levels of oxidants like plasma malondialdehyde, protein carbonyls, were significantly elevated and antioxidant glutathione levels and nitrate levels were significantly reduced in cases with and without CAD as compared to healthy controls. Oxidative stress markers and CIMT was found to be significantly increased in patients with cardiovascular risk factors like diabetes, family history of CAD, dyslipidemia, hypertension and smoking when compared to patients without risk factors. In patients with diabetes, CIMT increased as duration of disease increases and also in poorly controlled diabetes. In CAD group, when number of vessel involvement (severity of coronary disease) increases, the CIMT also increases confirming that CIMT is a quantifiable risk factor for CAD.