Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome.

BACKGROUND AND OBJECTIVES: Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by numerous episodes of absence of respiratory flow during sleep, which can be followed by a decrease in SaO2, which is rapidly normalized when ventilation resumes. We hypothesize that this hypoxia-reoxygenation phenomena may affect the generation of vascular endothelial growth factor (VEGF), erythropoietin (EPO), endothelin-1 (ENDO-1), and inducible nitric oxide synthase (iNOS). DESIGN AND SETTING: Prospective, patients referred to sleep disorders center. PATIENTS AND METHODS: The presence and severity of OSAS were determined using the standard overnight polysomnography. Diagnosis of OSAS was made when the apnea-hypopnea index (AHI) was ≥15, independent of the appearance of symptoms. Serum levels of VEGF, EPO, ENDO-1, and nitrite-nitrate were measured after overnight fasting in 69 patients with OSAS and in 17 healthy control subjects. Serum levels of VEGF and nitrite-nitrate were measured again after 12 weeks of treatment with continuous positive airway pressure (CPAP) in OSAS patients. RESULTS: Serum VEGF levels were found to be significantly higher and nitrite-nitrate levels were found to be significantly lower in OSAS patients than in controls (P=.003, .008, respectively), but no differences in EPO and ENDO-1 levels were found between the groups. We demonstrated that in OSAS patients, the serum VEGF levels were decreased and nitrate levels were increased after 12 weeks of CPAP treatment (P=.001, .002, respectively). CONCLUSION: According to our data, it is likely that hypoxia-reoxygenation phenomena affect the VEGF and nitrite-nitrate levels, which may be pathogenic factors in generating cardiovascular complications in OSAS.

[The effect of adhesion molecule CEACAM1 and chemokine receptor CXCR4 expression on prognosis of non-small cell lung cancer patients]. / Küçük hücreli disi akciger kanserli hastalarda adezyon molekülü CEACAM1 ve kemokin reseptörü CXCR4 ekspresyonunun prognoz üzerine olan etkisi.

Poor prognosis in the lung cancer result from early metastatic potential of the tumoral cells. The mechanisms of tumoral cell metastasis are complex. Adhesion molecules play an important role in metastatic process, which is cell-to-cell and cell-to-matrix interactions and chemokins which arrange the migration and growth of the cells are also important in metastatic biology. The aim of this study is to investigate the prognostic relevance of carcinoembrionic antigen cell adhesion molecule 1 (CEACAM1) and chemokine receptor CXCR4 expression in patients with non-small cell lung cancer (NSCLC). Using immunohistochemical analysis, we evaluated CEACAM1 and CXCR4 expression in parafine specimens from 50 patients with NSCLC confirmed histopathologically and the relationship between CEACAM1 and CXCR4 expression and the prognosis. Twenty-one (42%) patients were positive and 29 (58%) were negative for CEACAM1 expression. Patients whose tumors had CEACAM1-positive staining had a shorter duration of survival than patients whose tumors had no expression, but it was not significant statistically [8.93 ± 8, (median: 8) vs 12.3 ± 11.3, (median: 9), p> 0.36]. Twenty-three (46%) patients were positive and 27 (54%) were negative for CXCR4 expression. Patients whose tumors had CXCR4-positive staining had a longer duration of survival than patients whose tumors had no expression, but it was not significant statistically [12.8 ± 12.4, (median: 12) vs 9.3 ± 7.6, (median: 8), p> 0.14]. In conclusion, CEACAM1 and CXCR4 played a part in metastatic process in lung cancer may not affect on survival independently. The biologic mechanisms leading to the spread of tumor cells are complex and related multifactoriel process.

The role of plasminogen activator inhibitor-1 polymorphism, factor-V-Leiden, and prothrombin-20210 mutations in pulmonary thromboembolism.

Polymorphism in plasminogen activator inhibitor-1 gene is suggested to be associated with an increased risk of venous thromboembolism. The aim of this study was to investigate the association of plasminogen activator inhibitor-1 gene polymorphism and its coexistence with factor-V-Leiden and prothrombin-20210 mutations in pulmonary thromboembolism. The authors investigated plasminogen activator inhibitor-1 4G/5G polymorphism, factor-V-Leiden, and prothrombin-20210 mutations in 143 pulmonary thromboembolism patients and 181 controls. Plasminogen activator inhibitor-1 4G/4G, 4G/5G, and 5G/5G gene polymorphisms and prothrombin-20210 mutations were not different between cases and controls. Factor-V-Leiden mutation was present in 21.0% and 7.7% of the cases and controls, respectively, P = .001. Neither different plasminogen activator inhibitor-1 genotypes and 4G allele nor coexistence of the allele with factor-V-Leiden or prothrombin-20210 was associated with the risk of recurrence. As a result, plasminogen activator inhibitor-1 gene polymorphism or its concomitant presence with mentioned mutations was not found to be associated with increased risk for pulmonary thromboembolism or recurrent disease in this study.

Value of APACHE II, SOFA and CPIS scores in predicting prognosis in patients with ventilator-associated pneumonia.

BACKGROUND: Ventilator-associated pneumonia (VAP) is the most frequent infection with high mortality rates in intensive care units (ICUs) and the prediction of outcome is important in the decision-making process. OBJECTIVE: To assess the value of the Acute Physiology and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA) and Clinical Pulmonary Infection Score (CPIS) in the prediction of mortality during VAP episodes in pulmonary patients. METHODS: This study was a prospective observational cohort study. Sixty-three patients who were admitted to the ICU and developed VAP were included in the study consecutively. Clinical and laboratory data conforming to the APACHE II and SOFA scores were recorded on admission and APACHE II, SOFA and CPIS scores on the day of the diagnosis of VAP. The outcome measure was the ICU mortality. Logistic regression and receiver operating characteristic (ROC) curve analyses and the area under the curve (AUC) were used to estimate the predictive ability of the scoring systems. RESULTS: Mortality rate was 54%. The mean APACHE II (21 +/- 6, 14 +/- 5; p = 0.001), SOFA (7 +/- 3, 4 +/- 2; p = 0.002) and CPIS (8 +/- 2, 7 +/- 3; p = 0.025) scores determined at the time of VAP diagnosis were significantly higher in nonsurvivors than in survivors. Discrimination was excellent for APACHE II (ROC AUC: 0.81; p = 0.001) and acceptable for SOFA (ROC AUC: 0.71; p = 0.005) scores. Of the three scores only APACHE II >16 was an independent predictor of the mortality (OR: 5; 95% CI: 1.3-18; p = 0.019) in the logistic regression analysis. CONCLUSION: These results suggest that APACHE II determined at the time of VAP diagnosis may be useful in predicting mortality in the pulmonary ICU patient population who develops VAP.