No abstract

Objective: To assess the efficacy of pleural fluid cholesterol in differentiating transudates and exudates as compared with Light's criteria. Methods:Patients with pleural effusion during a 6-month period were enrolled in the study and underwent thoracentesis. Pleural fluid was analyzed for the levels of protein, lactate dehydrogenase (LDH), and cholesterol. Etiological diagnosis, which was established after considering clinical and biochemical factors, was the gold standard for comparison. Cut-off values for pleural fluid cholesterol were taken as 60 mg/dL and 45 mg/dL. Results:A total of 53 patients were included for final analysis. Of them, 19 were with transudates and 34 with exudates in their pleural fluids. The sensitivity, specificity, positive predictive value, and negative predictive value of the pleural fluid cholesterol (cut-off >45 mg/dL) were 97.06%, 94.74%, 97.06%, and 94.74%, respectively, for identifying exudates. These values were differentiating better than those obtained by Light's criteria for pleural fluid cholesterol (cut-off >60 mg/dL) (p<0.0001). Combining pleural fluid protein with pleural fluid cholesterol (>45 mg/dL) gave a higher specificity (100%) and positive predictive value (100%) but a lower sensitivity (82.93%) and negative predictive value (63.16%). Conclusion:Pleural fluid cholesterol is better than Light's criteria for the differentiation of transudates and exudates and is less cumbersome as it does not require a simultaneous blood sampling. Cut-off value of pleural fluid cholesterol for differentiating transudates and exudates should be 45 mg/dL. Further studies are warranted to assess the efficacy of the combination of pleural fluid protein and cholesterol as criteria for classifying effusions.

Proton Pump Inhibitors (PPIs) are widely used in the treatment of peptic ulcer disease, Helicobacter pylori (H pylori) gastritis and gastro-esophageal reflux disease. PPIs are known to be relatively safe medications, with the most common adverse reactions reported as diarrhea, nausea, vomiting, abdominal pain and headache. Thrombocytopenia has not been found to be a significant side effect of PPI use. Furthermore, successful treatment of H pylori associated immune thrombocytopenic purpura (ITP) with PPI therapy has been reported in the literature. In clinical practice, however, PPI use has been thought to be associated with medication-induced thrombocytopenia, although the precise prevalence of this consequence has not been quantified. The purpose of this study is to determine the prevalence of thrombocytopenia in hospitalized patients treated with pantoprazole, a commonly prescribed PPI, compared to non-medicated controls. In this retrospective, case-controlled analysis, we analyzed the platelet counts of 626 patients between 18 and 80 years of age who were admitted to an urban, community-based hospital and were medicated with pantoprazole for at least three days during their hospital stay. Thrombocytopenia was defined as a drop in the platelet count to below 150,000/ml, or a drop of at least 50% from baseline. Patients who had a platelet count below 150,000/ml on admission or were hospitalized for less than 3 days were excluded from the study. A control group of 560 patients with the same inclusion criteria who had not been prescribed pantoprazole was analyzed for comparison. 626 patients were included in the study group and 560 patients in the control group. The median age was 67 years in study group, and 61 years in the control group. The mean platelet count on admission was 260,00/ml in the study group, and 257,000/ml in the control group. Of the subject group, 39 patients (6.2%) met our definition of thrombocytopenia, which was not statistically different from the 35 patients (6.2%) with thrombocytopenia in the control group (p=0.90). Our study compared patients who received PPI therapy with pantoprazole for at least three hospital days to patients without treatment. We found no difference in the rate of thrombocytopenia between hospitalized patients treated with pantoprazole and the non-medicated controls. The rate of thrombocytopenia that we observed is probably an estimate of the overall thrombocytopenia rate in hospitalized patients irrespective of specific medications. While our report did not control for variables such as concurrent medication use, comorbid illnesses, and patient demographics, we are confident that the sample size selected for this study is large enough to provide sufficient evidence that thrombocytopenia is not a significant side effect of pantoprazole therapy.