Ismail Yilmaz

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

BACKGROUND: Mortality is high among patients admitted to intensive care units (ICUs). Several prognostic markers have been described in such patients, but the literature contains no data comparing C-reactive protein (CRP) and cardiac troponin T (cTn-T), nor of a combination of CRP and cTn-T in the same patient group in the ICU. METHODS: This was a retrospective electronic data review of patients who presented to the emergency department for respiratory reasons between December 2007 and December 2009 and in whom CRP and cTn-T levels were measured. Patients with a diagnosis of pulmonary embolism and acute coronary syndrome were excluded. We recorded demographics, chronic diseases, admission diagnosis, Simplified Acute Physiology Score II (SAPS II), ICU stay, and CRP and cTn-T concentrations. RESULTS: We included the records of 158 patients. Mean ICU stay was 9.9 days (range 1–65 d), and mean hospital stay was 14.1 days (range 1–72 d). For predicting mortality, receiver operating characteristic analysis gave a CRP cutoff value of ≥ 10 mg/dL, and a CTn-T cutoff value of ≥ 0.01 ng/mL. For CRP the mortality area under the curve was 0.691 (95% CI 0.608–0.775), the sensitivity was 65%, and the specificity was 70%. For cTn-T the mortality area under the curve was 0.733 (95% CI 0.655–0.812), the sensitivity was 78%, and the specificity was 56%. Of the patients who died, 65% had CRP ≥ 10 mg/dL and 78% had cTn-T ≥ 0.01 ng/mL. On multivariable regression analysis, CRP ≥ 10 mg/dL was associated with 6.6-fold higher (95% CI 1.7–21.3) ICU mortality. There was no advantage for models that combined CRP and cTn-T. CRP alone was more valuable in predicting ICU mortality than in combination with troponin or SAPS II. CONCLUSIONS: Elevated CRP is an independent early prognostic marker of mortality risk in ICU patients. We suspect that a CRP-based prognosis strategy may be useful.

Prognostic significance of PaO2/PaCO2 ratio in normotensive patients with pulmonary embolism.

Introduction:  Risk stratification remains controversial in patients with normotensive pulmonary embolism (PE). The debate has recently focused right ventricular dysfunction detected by echocardiography or spiral computed tomography (CT) and cardiac biomarkers.

Relation between inflammatory cytokine levels in serum and bronchoalveolar lavage fluid and gene polymorphism in young adult patients with bronchiectasis.

AIM Bronchiectasis develops as a result of genetic and environmental factors and its etiopathogenesis is not still clear. Recent studies have revealed that inflammatory cytokines, which are formed as a result of chronic infection and inflammation, play a role in the pathogenesis of bronchiectasis. For this purpose, the level of inflammatory cytokines in bronchiectasis and the presence or absence of a genetic predisposition with the gene polymorphism of these cytokines was investigated. MATERIAL AND METHODS A total of 60 patients, 40 study cases and 20 controls, which were monitored with the diagnosis of bronchiectasis were included in the study. In these individuals, cytokine levels [interleukin (IL)-6, IL-8, IL-10, and tumor necrosis factor (TNF)-α] in serum and bronchoalveolar lavage (BAL) fluid, along with the routine blood tests, were determined. Furthermore, the polymorphism in IL-6, IL-8, IL-10, and TNF-α cytokine genes and its frequency were studied in the obtained DNA by the automatic sequence analysis method and the results were compared. FINDINGS It was found that in serum and BAL fluid of the patient group, the IL-8 level was high, whereas the IL-10 level was low (P<0.05). No significant difference was detected in the other cytokines (P>0.05). It was found that in cytokine gene polymorphisms IL-8 -251 A/T, IL-10 -592 A/C, and IL-10 -819 T/C genotypes are associated with increased risk of bronchiectasis. It was detected that the IL-8 -251 A/T genotype increased the risk of having the disease by 4.19 fold. (OR =4.19, 95% CI =1.24-14.17, P=0.021). The IL-10 -592 C/A genotype increased the risk of having the disease by 5.71 fold (OR = 5.71, 95% CI =1.35-24.06, P=0.017) and the IL-10 -819 T/C genotype increased the risk of having the disease by 5.06 fold (OR =5.06, 95% CI =1.20-21.27, P=0.048). No significant correlation was found between the other polymorphisms and bronchiectasis. CONCLUSIONS The IL-8, IL-10 levels and the gene polymorphism of these cytokines differ. In addition to detecting higher levels of pro-inflammatory IL-8 and lower levels of anti-inflammatory IL-10, detection of gene polymorphism related to these two cytokines in bronchiectasis gives rise to the thought that cytokines may have role in a predisposition to bronchiectasis. However, as the number of patients is small, precise remarks could not be made on this subject. There is need for further studies include a larger number of patients.