Background: Because of the lack of sufficient data, we aimed to investigate the role of serum 25(OH) vitamin D level on COVID severity and related mortality. Methods: This was a retrospective observational study. Data, including sociodemographic features, clinical characteristics, and laboratory data, and 25(OH) vitamin D levels were recorded for each study participant. Patients were stratified into different vitamin D groups; Normal (Serum 25(OH) vitamin D level >30 ng/mL), Vitamin D insufficiency (21-29 ng/mL), and deficiency (<20 ng/ mL). The severity of COVID was classified according to the Chinese Clinical Guideline for classification of COVID-19 severity. Mortality data were determined for participants. Univariate and multivariate Logistic regression analysis was performed to determine independent predictors of in-hospital mortality. Results: Overall, 149 COVID-19 patients (females 45.6%, mean age 63.5 ± 15.3 (range 24-90 years) years) were included. Fortyseven patients (31.5%) had moderate COVID-19, whereas 102 patients (68.5%) had severe-critical COVID-19. The mean 25(OH) vitamin D level was 15.2 ± 10.3 ng/mL. Thirty-four (22.8%) and 103 (69.1%) patients had vitamin D insufficiency and deficiency, respectively. Mean serum 25(OH) vitamin D level was significantly lower in patients with severe-critical COVID-19 compared with moderate COVID-19 (10.1 ± 6.2 vs. 26.3 ± 8.4 ng/mL, respectively, p<0.001). Vitamin D insufficiency was present in 93.1% of the patients with severe-critical COVID-19. Multivariate logistic regression analysis revealed that only lymphocyte count, white blood cell count, serum albumin and, 25(OH) vitamin D level were independent predictors of mortality. Conclusion: Serum 25(OH) vitamin D was independently associated with mortality in COVID-19 patients.
In this study, we aimed to evaluate the relationship between the laboratory parameters of platelet volume / lymphocyte ratio (PLR) and systemic inflammatory index (SII) with prognosis and mortality in patients with hospitalized GFR (Glomerular filtration rate) <60 ml / min and a diagnosis of acute myocardial infarction (AMI). This study was designed as a retrospective cohort study. 235 myocardial infarction (MI) patients over the age of 18 and with GFR <60 ml / min, hospitalized in our hospital between January 01, 2016 and January 01, 2019, were included in the study. The patients were divided into 2 groups as survival and mortality group. The two groups were compared in terms of demographic characteristics, clinical laboratory data (symptoms, comorbidities, laboratory findings, GFR, coronary angiography, medications and complications). Platelet -lymphocyte ratio (PLR) was obtained by dividing platelet count to lymphocyte count. Systemic inflammatory index (SII) was found by multiplying neutrophil count and PLR value. The mean age of the survival group was 67.1±12,8 years. In the mortality group, the mean age was 69.55±11,1 years. PLR and SII levels were significantly higher in the mortality group compared to the survival group (p=0.002, p=0.029, respectively). According to the results of ROC analysis in mortality group patients, it was found that sensitivity 59.1% and specificity 70.4% for PLR (p=0.002); sensitivity 54.5% and specificity 60.9% for SII (p=0.
Background: Serum C-reactive protein (CRP) to albumin ratio (CAR) has been defined as an inflammation-based prognostic marker. We evaluated the association and prognostic value of CRP/albumin ratio in patients with pulmonary embolism (PE).Methods: A total of 256 patients with acute PE who were hospitalized between March 2016 and December 2020 were retrospectively reviewed. PE severity index (PESI) was calculated. Serum levels of CRP and albumin that were obtained at the time of admission were used for calculation. CAR was evaluated for correlation with PESI, and thus, foresee the risk of death due to PE. Results: There were 186 patients eligible for inclusion. 54 patients were in intermediate, 34 patients were in high risk and 98 patients were in very high-risk group according to PESI score. In the correlation analysis, we observed moderate positive correlations between CRP/albumin ratio, troponin and PESI score (r = 0.584, p < 0.0001; r = 521, p < 0.0001, respectively). Regression analysis revealed that only CRP/albumin ratio and PESI score were independent risk factors associated with 6-month mortality of acute PE patients. The AUC for CRP/albumin ratio was 0.643, 0.751, and 0.763 for 30-day, 90-day, and 6-month mortality, respectively (95% CI: 0.550-0.737, 0.672-0.830, 0.687-0.838]. A cut-off value of 5.33 for CRP/albumin ratio was associated with 65.3% sensitivity and 65.6% specificity in predicting 6-month mortality. Conclusion:The CRP/albumin ratio, an inexpensive and easily measurable laboratory variable, may be a useful prognostic marker of PE, especially when other causes that alter serum levels are excluded from the study. (REV INVEST CLIN. [AHEAD OF PRINT]
OBJECTIVE: This preliminary study aims to examine a change in the blood levels of irisin in patients with acute pericarditis (AP) and acute myopericarditis (AMP) and examine the diagnostic value of the serum irisin level in AP and AMP. METHODS: 10 patients, who applied to the emergency service and cardiology clinic with chest pain and who were diagnosed with AP and 5 patients, who were diagnosed with AMP as a result of routine examinations, were included in the study. The basal laboratory parameters, echocardiography fi ndings and serum irisin levels of the patients and during check one month later were examined. RESULTS: While the basal irisin levels were found to be signifi cantly low in the AMP group and high during the check (6.6 ± 1.58, 8.19 ± 1.43, respectively), no statistically signifi cant difference was determined (p = 0.23). It was observed that the basal and control irisin levels did not vary signifi cantly in the AP group (8.03 ± 1.6, 8.19 ± 1.43, respectively) (p = 0.84). CONCLUSION: In this preliminary study, the basal irisin levels were found to be signifi cantly low in the AMP group, while there was no statistically signifi cant difference between the basal irisin levels and control irisin levels in the AP and AMP groups (Tab. 5, Ref. 17).
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