Exploration of eosinopenia as a diagnostic parameter to differentiate sepsis from systemic inflammatory response syndrome: Results from an observational study.

AIM OF THE STUDY: Initial differentiation of sepsis from systemic inflammatory response syndrome (SIRS) is of prime importance for early institution of appropriate treatment. This study aimed to compare the differential diagnostic efficacy of absolute eosinophil count (AEC - a routinely available economic marker) with total leukocyte count (TLC) and procalcitonin (PCT - a costly marker available only in specialized settings). MATERIALS AND METHODS: In this prospective observational study, 170 patients of sepsis (severe sepsis = 125; SIRS = 45) were enrolled. AEC, TLC, and PCT were measured in the blood of all patients at the time of admission and data analyzed statistically. RESULTS: Median AEC was 0 cells/mm(3) in both SIRS and sepsis. TLC and PCT levels were significantly higher (P < 0.001) in culture negative, culture positive, and overall sepsis groups in comparison to SIRS group. At a cutoff of < 50 cells/mm(3), AEC demonstrated a sensitivity and specificity of 23% and 68%, respectively. The sensitivity, specificity, positive predictive value, and negative predictive value of TLC were 57%, 71%, 85%, 37% and of PCT were 82.4%, 82.2%, 93%, and 63%, respectively with area under curve of 0.455 for AEC, 0.640 for TLC, 0.908 for PCT. CONCLUSIONS: This study suggests that eosinopenia is not a reliable diagnostic tool to differentiate sepsis from SIRS. PCT and TLC are better differential diagnostic biomarkers.

Oxidative damage of plasma proteins and lipids in epidemic dropsy patients: alterations in antioxidant status.

Epidemic dropsy is an acute food adulterant disease caused due to consumption of edible mustard oil contaminated with argemone oil. Our in vitro studies have shown that the toxicity of argemone oil is due to the production of reactive oxygen species. The present study was aimed to evaluate the development of oxidative stress in terms of oxidation of plasma proteins and lipids and its correlation to enzymatic and non-enzymatic antioxidants in epidemic dropsy patients. Total plasma protein and globulin contents were found to be significantly (P<0.05) enhanced with a concomitant decrease (P<0.05) in albumin/globulin ratio in dropsy patients when compared to controls. Total cholesterol, triglycerides, low density lipoprotein cholesterol and very low density lipoprotein cholesterol were found to be significantly (P<0.05) increased with a simultaneous decrease (51%) in high density lipoprotein cholesterol in dropsy patients. The oxidation of plasma proteins and lipids were substantially enhanced (162-175%) in dropsy patients when compared to controls. Further, significant (P<0.05) decrease in superoxide dismutase, catalase, glutathione reductase and glutathione-s-transferase with a concomitant increase (69%) in glutathione peroxidase activity was noticed in dropsy patients. A significant reduction in plasma total antioxidant capacity, alpha-tocopherol, glutathione, retinol and retinyl esters content was observed in dropsy patients when compared to healthy controls. The results suggest that there exists an unproportionate equilibrium between free radicals formation and enzymatic and non-enzymatic antioxidant scavengers, which may cause oxidative damage to proteins and lipids in dropsy patients.

Analysis of the apo(a) size polymorphism in Asian Indian populations: association with Lp(a) concentration and coronary heart disease.

Most studies aiming to detect associations of genetic variation with common complex diseases, e.g. coronary heart disease (CHD) have been performed in populations with a western lifestyle but it is unclear whether associations detected in one geographic group exist also in others. We here have determined lipoprotein(a) levels and apo(a) K-IV-2 repeat genotypes in CHD patients (N=254) and controls (N=480) from two Asian Indian populations (Tamil Nadu and New Delhi). In both populations and also in the pooled dataset median Lp(a) levels were significantly elevated in the patients (27.4 mg/dl) compared with the controls (17.6 mg/dl). Apo(a) K-IV-2 allele frequencies were not different between the CHD patients and controls and thus did not explain the increased Lp(a) levels in CHD patients. Contrary to what has recently been observed in Black and White men short (K-IVor=30) apo(a) alleles were all associated with higher Lp(a) levels in the patients. Accordingly relative risk (estimated as odds ratio) for CHD rose continuously with increasing Lp(a) but was independent of apo(a) allele length. Together with previous studies our results indicate that the relation between apo(a) genotypes, Lp(a) levels, and CHD may be heterogeneous across ethnic groups and that it depends on the genetic architecture of the Lp(a) trait in a given population whether an association of K-IV-2 repeat length with CHD exists or not.