Background: Patients with severe acute respiratory distress syndrome (ARDS) have high mortality rates; therefore, new biomarkers are necessary to predict the prognosis in the early stages. Serum lactate dehydrogenase (LDH) level is a specific marker of lung damage, but it is not sensitive because it is affected by several factors. This study aimed to determine whether the LDH/albumin ratio could be used as a prognostic biomarker in patients with severe ARDS due to COVID 19. Methods: Tertiary intensive care unit (ICU) patients with severe ARDS and confirmed COVID-19 diagnosis between August 1, 2020, and October 31, 2021, were included. The demographic and clinical characteristics of the patients were recorded from the hospital databases, together with laboratory results on the day of admission to the ICU and the length of stay in the ICU and hospital. LDH/albumin, lactate/albumin, C-reactive protein (CRP)/albumin, and BUN/albumin ratios were calculated. Logistic regression analysis was performed to determine independent risk factors affecting mortality. Results: Nine hundred and five patients hospitalized in a tertiary ICU were evaluated. Three hundred fifty-one patients with severe ARDS were included in this study. The mortality rate of the included patients was 61.8% (of 217/351). LDH/albumin, lactate/albumin, and BUN/albumin ratios were higher in the nonsurvivor group (P < .001). The area under the curve (AUC) from the receiver operating characteristic analysis that predicted in-hospital mortality was 0.627 (95% confidence intervals (CI): 0.574–0.678, P < .001) for the LDH/albumin ratio, 0.605 (95% CI: 0.551–0.656, P < .001) for lactate/albumin, and 0.638 (95% CI: 0.585–0.688, P < .001) for BUN/albumin. However, LDH/albumin ratio was independently associated with mortality in multivariate logistic regression analysis. Conclusion: LDH/albumin ratio can be used as an independent prognostic factor for mortality in patients with severe ARDS caused by COVID-19.

One of the most common causes of mortality and morbidity in elderly patients is sepsis. Malnutrition is widespread in elderly patients, affecting mortality and morbidity. The present study aimed to evaluate the clinical features of patients hospitalized in the tertiary intensive care unit with the diagnosis of sepsis, as well as the effects of the Sequential Organ Failure Assessment (SOFA) score, prealbumin, albumin, and other laboratory parameters on hospital mortality. The patients were divided into two groups according to their survival. The demographic and clinical characteristics of the two groups were compared. Independent risk factors affecting mortality were determined by logistic regression. A total of 653 patients admitted to the medical ICU were evaluated out of which 254 geriatric patients with sepsis and septic shock were included. There was in-hospital mortality in 122 (48%) patients. There was no difference in age in both groups (76 (71-84) vs. 76 (70-84), p=0.896). BUN (p=0.013), LDH (p=0.014), LDH/albumin (p<0.001), BUN/albumin (p<0.001), lactate/albumin (p= 0.007), and CRP/albumin (p=0.001) was higher in deceased patients compared to surviving patients. Prealbumin and albumin were lower in non-survivors (p=0.001). When the factors affecting mortality were examined by multivariate analysis, it was determined that none of the laboratory parameters alone predicted mortality. SOFA score was the only independent risk factor indicating mortality in the geriatric patient population with sepsis (OR=1.886 (1.410-2.510), p<0.001). In conclusion, we demonstrated that high age and parameters of nutrition indicators did not affect mortality in geriatric patients hospitalized in the intensive care unit due to sepsis. In our study, the SOFA score was an independent risk factor affecting mortality in geriatric patients with sepsis, as in all sepsis cases.

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.

Background and Objectives: The use of additional biomarkers to predict clinical course in diabetic ketoacidosis (DKA) is becoming increasingly important. The aim of this study was to investigate the relationship between interleukin-6 (IL-6) levels and the length of stay in the intensive care unit (ICU) in patients with DKA without signs of infection and to investigate the relationship between the neutrophil–lymphocyte ratio (NLR) and C-reactive protein (CRP) albumin ratio (CAR). Materials and Methods: This retrospective, single-center study included 78 patients with DKA without infection who were treated in the Medical ICU between July 2022 and June 2024. The patients were divided into two groups: moderate DKA (Group 1) and severe DKA (Group 2). The patients’ IL-6 levels, peripheral blood inflammatory markers (CAR, NLR), Acute Physiology and Chronic Health Evaluation (APACHE) II scores, and the duration of ICU stay were recorded. Results: The median duration of stay in the ICU was 2.00 (1–6) days in group 1 and 3.00 (1–26) days in group 2 (p = 0.001). The mean pH, HCO₃, and CO₂ values in Group 1 were 7.20 ± 0.07, 13.58 ± 2.11 mEq/L, and 29.45 ± 6.27 mmHg, while the mean pH, HCO₃, and PCO₂ values in Group 2 were 7.01 ± 0.11, 7.11 ± 1.91 mEq/L, and 20.35 ± 4.91 mmHg (p < 0.001, p < 0.001, p < 0.001, respectively). There was a strong positive correlation between IL-6 levels and the length of stay in the ICU (r = 0.813, p < 0.001). Additionally, there was a moderate positive correlation between the length of stay in the ICU with the severity of DKA (r = 0.475, p < 0.001), CAR (r = 0.336, p < 0.001), and NLR (r = 0.562, p < 0.001). Conclusions: Inflammatory markers such as NLR and CAR, and more specifically IL-6, were found to be associated with the clinical course and duration of stay in the ICU in patients with DKA.

Introduction Familial Mediterranean fever (FMF) is a recessively inherited disease characterized by recurrent attacks of fever and sterile polyserositis. Recently, some proteins originating from adipose tissue have been demonstrated to play a critical role in the inflammatory process. Asprosin is a new adipokine secreted by adipose tissue, and proinflammatory cytokines have been determined to increase with the decrease of circulating asprosin. This study was designed to evaluate the level of asprosin in the acute attack and attack-free period in FMF patients. Materials and methods A total of 65 FMF patients were evaluated for this cross-sectional case-control study. Those who were obese and had concomitant diabetes mellitus, hypertension, heart failure, and rheumatological disease were excluded from the study. The patients were divided into two groups: attack-free period and attack period. Fifteen healthy individuals who were not obese and had no additional disease were included as the control group. Demographic data, gene analyses, laboratory findings, and symptoms were recorded at the time of diagnosis. Serum asprosin level was studied by enzyme-linked immunosorbent assay test in the outpatient clinic controls of the patients. Asprosin levels and other laboratory findings were compared between the attack, attack-free, and control groups. Results Of the patients included in the study, 50% were in the attack period, and 50% were in the free-attack period. The mean age of the FMF patients was 34±10 years. Asprosin level in the control [median (interquartile range (IQR))=30.4 (21.5-57.7) ng/mL] group was significantly higher than the attack [median (IQR)=21.5 (17.5-28) ng/mL] and attack-free [median (IQR)=19(18.7-23) ng/mL] groups (p=0.001). C-reactive protein and sedimentation levels were significantly higher in the attack group compared to the other two groups (p<0.001). There was a moderate correlation between C-reactive protein and asprosin levels (Ro=-0.314, p=0.01). The cut-off value of serum asprosin level was determined as 21.6 ng/mL; sensitivity was 78%, and specificity was 77% (p<0.001). Conclusion The study demonstrated that the serum asprosin levels of FMF patients with acute attack were lower than those in the attack-free periods and healthy controls. Asprosin is likely to have a role in the anti-inflammatory cascade.