BackgroundThe men infected with COVID-19 have been shown to have more severe disease and a higher mortality rate. Morbidity and mortality associated with COVID-19 are mediated through intense viral inflammation and increased levels of inflammatory biomarkers. We aimed to retrospectively evaluate any gender difference in patients with severe COVID-19 pneumonia in terms of inflammatory biomarkers. MethodsOur study included 132 patients. The general characteristics, radiological features and laboratory parameters of the patients were recorded. ResultsNo difference was observed between the genders according to comorbidities, pulse steroid requirement and hypoxemia. There was no difference between the male and female participants in terms of age, white blood cell count, lymphocyte count, red cell distribution width, C-reactive protein, troponin, albumin and Ddimer. However, duration of hospitalization; percentage of polymorphonuclear leukocyte (PNL); and haemoglobin, alanine aminotransferase and ferritin values were higher in the males, and lymphocyte percentage and platelet count were higher in the women participants. ConclusionLarger studies with gender-specific reporting and robust analyses are required to clarify how gender alters the cellular and molecular pathways associated with COVID-19. This would improve the interpretation of biomarkers and the clinical management of COVID-19 patients by facilitating a personalised medical approach to risk stratification, prevention and treatment.

The COVID-19 infection causes involvements in many such as the central nervous system and causes prothrombotic complications. Viral neurotropism, endothelial dysfunction, coagulopathy, and inflammation are suggested mechanisms in the development of acute cerebrovascular disease in COVID-19 patients. The development of a neurological complication is a risk factor for mortality. Patients with high inflammatory markers need to be closely followed-up, because of the risk of the development of complications. It should be kept in mind that there may be neurological involvement in patients with symptoms such as headache, impaired consciousness, vertigo, drowsiness, and loss of strength. In this case, we aimed to present our patient who developed ischemic stroke while under treatment for severe COVID-19 pneumonia.

Background and aimSarcoidosis is a multisystem inflammatory disease of unknown aetiology. This study aimed to evaluate the relationship between systemic inflammatory parameters, the systemic immune-inflammation index (SII) and the lymphocyte-to-monocyte ratio (LMR), and disease stage, clinical findings, and 18F-fluoro-2-deoxy-D-glucose (18F-FDG) tomography/computed tomography (PET/CT) uptake. Materials and methodsOur study included 73 patients. The general characteristics, radiological features, spirometric tests, PET/CT findings, and laboratory parameters of the patients were recorded. ResultsRelapse and parenchymal fibrosis were not associated with metabolic parameters, such as LMR and SII. Serum angiotensin-converting enzyme (ACE) levels were lower in the relapsed group than in the non-relapse group. However, the patients' PET/CT images indicated that 18F-FDG parenchym maximum standard uptake value (SUV max), lymph node SUV max, lymph node short axis dimension, SII, and LMR were similar between all patients, relapsed or not. ConclusionAlthough found to be significant in other inflammatory diseases, we found that SII and LMR alone did not indicate disease prognosis in sarcoidosis due to the small number of patients and the lack of homogeneity between the groups in our study. The usefulness of these markers for clinical use should be investigated by studies that include those with extrapulmonary sarcoidosis, and that calculate these markers at the time of disease diagnosis and during the post-treatment period.

Aim:We aim to answer the question of "Can D-dimer be an indicator of prognosis and mortality in COPD exacerbations?" by doing retrospective research on the prognosis and mortality of patients who had high D-dimer levels in COPD exacerbations with no thromboembolism detected. Material and Method: Our research is retrospective and cross-sectional. A total of 115 patients who had applied to our hospital between January 2018 and January 2019 with COPD acute exacerbations and who had higher D-dimer levels detected than the 0.44 mg/L upper limit of our hospital's laboratory are included in this research. All patients have been previously diagnosed with COPD by a pulmonologist and have been undergoing treatment. Patients under the age of 18, patients whose information was not accessible through their files, pregnant patients, patients who have not been diagnosed with COPD by a pulmonologist, patients who had been diagnosed with lung malignancy through pathology, patients where pulmonary embolism was detected through pulmonary CT angiography, patients with renal function test disorder and patients with known renal failure are not included in this study. Results: A total of 115 patients were included in the study. Patients who developed mortality had statistically significant lower levels of OSAS, higher rates of pneumonia, anemia, and liver failure, higher numbers of applications to emergency services in 1 year, higher numbers of hospitalizations due to COPD acute exacerbations in 1 year, higher numbers of intensive care unit admissions due to COPD acute exacerbations in 1 year and lower survival time. In addition, patients who developed mortality had statistically significant lower rates of group B and C and higher rates of group D according to the classification of Global Initiative of Chronic Obstructive Lung Disease (GOLD). Although the D-dimer levels were higher in patients who developed mortality, there were no statistically significant differences between groups. No significant cut-off value for D-dimer was calculated. Conclusion: As a result, although our study has found higher D-dimer levels in patients who develop mortality, these results were not statistically significant.