Introduction: Sepsis and septic shock are important causes of mortality in intensive care unit patients, hence early diagnosis and therapy are important in management of their treatment. The available information on sepsis patients is not enough to recommend or to discard the routine evaluation of triglyceride (TG) levels at the onset of sepsis. The aim of this study was to investigate the association of hypertriglyceridemia and clinical outcome (or mortality) in patients with severe sepsis. Materials and methods: Between January 1 and December 31, 2011, a total of 84 patients with sepsis from the intensive internal care unit at the Kayseri Training and Research Hospital, Kayseri, Turkey, were investigated retrospectively. Sepsis was defined according to the American College of Chest Physicians/Society of Critical Care Medicine/European Society of Intensive Care Medicine consensus conference definitions. For each patient, survival was recorded at the end of the last day of hospitalization as dead or alive. The TG values were taken retrospectively from the records, which were performed routinely for each patient with sepsis at the time of diagnosis. TG >150 mg/dL was considered as hypertriglyceridemia. Results: The percentages of male and female patients were 44% and 56%, respectively. The mean age of patients was 71.49±11.071 years. The percentage of patients with TG values more than 150 mg/dL was 81% (25/31) in the non-survivor group and 19% (6/31) in the survivor group. There was a significant difference regarding TG values between groups (P=0.039). Discussion: It was observed in this study that patients in the intensive care unit with sepsis had high TG levels. We also observed that the TG level >150 mg/dL at 0 hour (onset of sepsis) was a significant predictive marker of sepsis mortality rate. The contribution of hypertriglyceridemia to mortality might be modest compared to increase in severity of illness, but, nevertheless, these simple measurements represent a potential therapeutic target in sepsis.

Peer reviewed article authored by (Erden A, Esmeray K, Karagöz H, Karahan S, Gümüşçü HH, Başak M, Çetinkaya A, Avci D, Poyrazoglu OK). Read article or submit your manuscript for publishing.

Objectives: Antiphospholipid antibodies (APAs) increase the risk of excessive blood clotting, but their role in COVID-19 remains unclear. We aimed to investigate the presence of conventional APAs used in the classification of antiphospholipid antibody syndrome in patients with severe lung infection with SARS-CoV-2 and to compare these results with non-COVID-19 critically ill patients Methods: Thirty-one COVID-19 patients (COVID group) and 28 non-COVID-19 critically ill patients (non-COVID group), were included in the study. Anti-cardiolipin (ACA) (IgG, IgM), anti-β2-glycoprotein 1 (Anti-β2GPI) (IgG, IgM, and IgA), and if the patient had not received any anti thrombotic agent before blood collection, lupus anticoagulant (LAC) tests were studied from the plasma of the patients. For testing ACA and Anti-β2GPI, ELISA method was used, while fully automated coagulometer device was used for LAC test. Results: APAs were positive in 25.81% in the COVID group (8/31) and 25% in the non-COVID group (7/28). LAC was the most common APA present in 23.08% of the COVID-19 group, who underwent measurement (6/26), while 3.57% of the non-COVID group was LAC positive (1/28) (p = .047). In the COVID group, ACA IgM, and IgG were positive in 6.45% and 0%, respectively (2/31 vs 0/31). In the non-COVID group, ACA IgM was not positive in any patient, while ACA IgG was positive in 7.14% (2/28). Anti-β2GPI IgG and IgM tests were not positive in any patient in either the COVID or the non-COVID group. Anti-β2GPI IgA were positive in 6.45% and 14.29%, respectively (2/31 vs 4/28). Conclusion: In this study, APAs were equally positive in critically ill patients among COVID-19 or non-COVID-19 patients. Only LAC was more observed in COVID-19 patients. Key messages:

Various scoring systems and cytokines have been cited as predicting disease severity in COVID-19 infection. This study analyzed the link between mortality rate, levels of cytokines, and scoring systems such as the Glasgow Coma Scale (GCS), Acute Physiologic Assessment and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA), and Charlson Comorbidity Index in patients infected with COVID-19. Adult patients infected with COVID-19 were followed up in the intensive care unit (ICU) and analyzed prospectively. We measured serum cytokine levels (Interleukin-10 (IL-10), Interleukin-8 (IL-8), Interleukin-6 (IL-6), Interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α) and High mobility group box 1 (HMGB-1)) and recorded GCS, APACHE II, SOFA, and Charlson comorbidity index scores on admission to the ICU. Receiver operating curve (ROC) analysis was performed to predict mortality from IL-1β, IL-6 IL-10, IL-8, TNF-α, and HMGB-1 values. Study participants were grouped as follows: Group A, survivors, and Group B, deceased, during the 28-day follow-up. The mean age was 65.69 (±13.56) in Group A (n = 36) and 70.85 (±10.06) in Group B (n = 27). The female/male ratio was 23/40. Age, sex, body mass index (BMI), comorbid illnesses, GCS, APACHE II, SOFA, and Charlson scores, duration of hospitalization or ICU admission, therapeutic choices, and lymphocyte, PMNL, NLR, platelet, D-dimer, fibrinogen, GGT, CRP, procalcitonin, and lactate levels were similar between the groups. The frequency of acute kidney injury (AKI) was higher in Group B (p = 0.005). Serum IL-10, IL-8, IL-6, IL-1β, TNF-α, HMGB-1, ferritin, and LDH values were higher, and PaO₂/FiO₂ was lower in Group B than in Group A. ROC analysis showed that there was an association between serum IL-1β (>1015.7), serum IL-6 (>116.7), serum IL-8 (>258.4), serum IL-10 (>247.5), serum TNF-α (>280.7), and serum HMGB-1 (>23.5) and mortality. AKI gave rise to a greater risk of mortality (odds ratio: 7.081, p = 0.014). Mortality was associated with serum IL-10, IL-8, IL-6, IL-1β, TNF-α, and HMGB-1 but not with GCS, APACHE II, SOFA, or Charlson comorbidity index scores. AKI increased the risk of mortality by seven times. Our findings suggest that cytokine levels (serum IL-10, IL-8, IL-6, IL-1β, TNF-α, and HMGB-1) were predictors of mortality in COVID-19 infection. In addition, our results might give an opinion about the course of COVID-19 infection.

To compare patients with COVID-19 in intensive care units (ICUs) to healthy controls using nailfold videocapillaroscopy (NVC), offering standardised findings about micro-circulation. A descriptive, cross-sectional study. Medical Intensive Care Unit, Kayseri City Education and Research Hospital, Kayseri, Turkey between January and May 2021. The NVC parameters-capillary morphology, loop diameter, capillary density, dilated capillaries, giant capillaries, avascular areas, microaneurysms, and micro-hemorrhages of 32 patients with COVID-19 and 29 controls were recorded. The most common capillary morphology in the COVID-19 group (18/32, 56.2%) was serpentine, which also characterised some (6/29, 20.7%) patients in the non-COVID-19 group (p <0.001). The median capillary loop diameter was 77.78 ± 3.63 µm in the COVID-19 group and 71.67 ± 2.19 µm in the non-COVID-19 group (p=0.030). Mean capillary density was 6.41 ± 1.21/1 mm in the COVID-19 group and 8.55 ± 1.12/1 mm in the non-COVID-19 group (p <0.001). The COVID-19 group had significantly more enlarged capillaries (p = 0.001), giant capillaries (p = 0.025), avascular areas (p = 0.028), micro-aneurysms (p <0.001), and micro-hemorrhages (p = 0.011). Mean capillary density was 5.50 ± 0.19/1 mm among deceased patients with COVID-19, but 6.71 ± 0.25/1 mm among survivors (p = 0.011). NVC findings differed between patients with COVID-19 and controls, and capillary density was less among deceased patients with COVID-19 than survivors. Capillaries, COVID-19, İntensive care unit, Micro-circulation, Nailfold videocapillaroscopy.

Peer reviewed article authored by (Erden A, Karagöz H, Başak M, Karahan S, Çetinkaya A, Avci D, Buğday İ). Read article or submit your manuscript for publishing.