Objectives: This study aims to evaluate serum lipoprotein-associated phospholipase A2 (Lp-PLA2) level and carotid intima-media thickness in primary Sjögren syndrome (pSS) as an indicator of atherosclerosis. Patients and methods: Between July 2019 and July 2020, a total of 33 female pSS patients (mean age: 44.5±11.2 years; range, 23 to 60 years) and 37 female age- and sex-matched healthy individuals (mean age: 40.9±7.2 years; range, 25 to 54 years) were included. Carotid intima-media thickness and serum Lp-PLA2 levels were measured in the patient and control groups. Results: The patients had a higher median serum Lp-PLA2 of 560 (range, 108 to 1,222) ng/mL vs. 328 (range, 0 to 1,280) ng/mL in the controls (p=0.024) and a similar mean intima-media thickness of carotid artery (0.64±0.14 mm vs. 0.62±0.15 mm, respectively; p=0.595). Serum Lp-PLA2 was positively correlated with platelet count (r=0.411, p=0.018) and negatively correlated with erythrocyte sedimentation rate (r=-0.409, p=0.018). The mean value of carotid intima-media thickness was positively correlated with disease duration (r=0.316, p=0.074) and was negatively correlated with the level of leucocyte (r=-0.458, p=0.007). Conclusion: Our study suggests that the patients of pSS have a potential risk of atherosclerotic cardiovascular disease, independent of traditional cardiovascular risk factors and disease severity.

COVID-19 disrupts the balance between coagulation and fibrinolysis. Especially in the clinical course of serious disease, plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), and tissue plasminogen activator levels increase in association with hypercoagulable state and hypofibrinolysis. This explains the increased incidence of thrombosis seen in COVID-19 infection. In this study, we aimed to examine the changes in PAI-1 and TAFI levels of COVID-19 patients. Department of Infectious Diseases and Clinical Microbiology, University of Health Sciences, Dişkapi Yildirim Beyazit Training and Research Hospital—Ankara Turkey, between April 1 and May 7, 2021. Patients who were diagnosed with COVID-19 were included in this retrospective study. TAFI and PAI-1 levels were analyzed from the samples that had been stored at –80 °C formerly. One hundred thirty-five patients diagnosed with COVID-19 and followed up in the service or intensive care unit were included in the study. Thirty-four (25.2%) patients required follow-up in the intensive care unit. Mortality rate was 10.4%, the coagulation tests of these patients were also compared. PA1-1 levels were found to be statistically significantly higher in intensive care unit patients (median: 133 pg/mL vs 31 pg/mL; P < .001), and there was no significant difference in TAFI levels (median:7.31 ng/mL vs 9.80 ng/mL; P = .171) between the 2 groups. TAFI levels were found to be higher in patients who died. In COVID-19 infection, as the severity of the disease increases, the coagulation balance deteriorates and eventually a hypercoagulable state occurs with an increase in PAI-1 and TAFI levels. Markers such as PAI and TAFI can be illuminating in further studies in determining prognosis and mortality and developing new treatment options.

Objectives: Clinical biochemistry laboratories (CBL) are the most frequently utilized laboratory group in healthcare, and their significance in patient care is indisputable. This study investigated the frequency and pattern of test utilization rate in CBL at two large hospitals’ outpatient and inpatient clinics. Methods: A total of 43,732,428 CBL tests, including clinical chemistry, immunoassay, coagulation, specific proteins, CBC, and urinalysis, were conducted for 12,182,382 patients across two large hospitals in different settings between 2018 and 2022. These tests were analyzed alongside patient admissions data, with a focus on the distribution across various clinics. Results: A total of 94 % and 93 % of those admitted to Hospitals 1 and 2 were outpatients. They had applied to CBL laboratories for 27.1–30.3 % of outpatients and 81.2–88.7 % of inpatients for at least one test. When analyzing the rates at which laboratory tests were requested for outpatients, it was found that emergency departments had the highest test-requesting rates, ranging from 19.99 to 45.36 %. This was followed by internal medicine clinics, with rates ranging from 13.77 to 14.8 %, and inpatient intensive care units, with rates between 24.31 and 30.14 %. Outpatients had 10–11 test requests for each patient and 16–31 for inpatients. The most frequently requested laboratory tests were CBC, glucose, creatinine, urea, AST and ALT in two hospitals. Conclusions: Despite significant variations in location, structure, medical staff, and patient demographics, approximately one-third of outpatients and 85 % of inpatients at these hospitals undergo testing in CBL. CBLs are essential for screening, diagnosis, prognosis, and healthcare treatment.

Aim: Interleukin-38 has been involved as an inflammatory mediator in rheumatic diseases. However, little is known about the role of IL-38 in the development of primary Sjögren’s syndrome. The present study aimed to evaluate the role of IL-38 in primary Sjögren’s syndrome and its clinical relevance. Material and Method:Between 2019 and 2020, 40 patients with primary Sjögren’s syndrome and 39 healthy participants were included in the study. The serum IL-38 level was measured by ELISA in all participants. The serum levels of IL-38 were compared with clinical and laboratory features. Results:The serum IL-38 levels between the patients with primary Sjögren’s syndrome and the controls were similar (58.0 pg/ml, min-max: 0-641.0 vs. 55.0 ng/ml, min-max: 0-338.0; p=0.511). No significant correlations were found between serum IL-38 level and SSDAI (r=-0.104, p=0.523). IL-38 level was mildly negatively correlated with RF (r=-0.364, p=0.021) and positively correlated with CRP (r=0.321, p= 0.044). Conclusion:The correlation of IL-38 with CRP and RF should be considered because it might be important clues for contribution to the disease process. IL-38 might be relevant to the heterogeneous nature of PSS and the future role of IL-38 might be a biomarker for specific clinical manifestations of pSS.