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.
Background: Gastrointestinal (GI) dysfunction is common in the intensive care unit (ICU), although there is no consensus on biomarkers of GI dysfunction. We aimed to evaluate ultrasound-based gastric antrum measurements and serum intestinal fatty acid-binding protein (IFABP) and citrulline levels in relation to GI dysfunction in critically ill patients.Methods: Adult critically ill patients receiving enteral nutrition and stayed for in the ICU for ≥48 h was included. GI dysfunction was described using Gastrointestinal Dysfunction Score (GIDS). Gastric antrum measurements, including craniocaudal (CC) diameter, anteroposterior diameter, and antral-cross sectional area (CSA), as well as serum levels for IFABP and citrulline, were prospectively recorded at baseline and on day 3 and day 5 of enteral nutrition. The receiver operating characteristic (ROC) analysis was performed to evaluate gastric ultrasound parameters, serum IFABP, and citrulline concentrations in predicting GI dysfunction.Results: Thirty-nine participants with a median age of 60 years were recruited and 46.2% of participants had GI dysfunction. ROC analysis revealed that the cutoff value of CSA score to predict GI dysfunction was 4.48 cm 2 , which provided 72.7% sensitivity and 77.2% specificity (area under the curve = 0.768, 95% CI: 0.555-0.980). At baseline, gastric residual volume was highly correlated with CC diameter and CSA (r = 0.764, P < 0.001 and r = 0.675, P < 0.001, respectively). Serum IFABP and citrulline levels had no correlation with GI dysfunction or gastric ultrasound parameters (P > 0.05). Conclusion:CSA was associated with GI dysfunction in critically ill patients. Serum IFABP and citrulline concentrations were poor in predicting GI dysfunction.
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.
Asprosin, a new adipokine, is secreted by subcutaneous white adipose tissue and causes rapid glucose release. The skeletal muscle mass gradually diminishes with aging. The combination of decreased skeletal muscle mass and critical illness may cause poor clinical outcomes in critically ill older adults. To determine the relationship between the serum asprosin level, fat-free mass, and nutritional status of critically ill older adult patients, critically ill patients over the age of 65 receiving enteral nutrition via feeding tube were included in the study. The patients’ cross-sectional area of the rectus femoris (RF) of the lower extremity quadriceps muscle was evaluated by serial measurements. The mean age of the patients was 72 ± 6 years. The median (IQR) serum asprosin level was 31.8 (27.4–38.1) ng/mL on the first study day and 26.1 (23.4–32.3) ng/mL on the fourth study day. Serum asprosin level was high in 96% of the patients on the first day, and it was high in 74% on the fourth day after initiation of enteral feeding. The patients achieved 65.9 ± 34.1% of the daily energy requirement for four study days. A significant moderate correlation between delta serum asprosin level and delta RF was found (Rho = −0.369, p = 0.013). In critically ill older adult patients, a significant negative correlation was determined between serum asprosin level with energy adequacy and lean muscle mass.
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