Artificial neural network based prediction of the lung tissue involvement as an independent in-hospital mortality and mechanical ventilation risk factor in COVID-19.

INTRODUCTION: During COVID-19 pandemic, artificial neural network (ANN) systems have been providing aid for clinical decisions. However, to achieve optimal results, these models should link multiple clinical data points to simple models. This study aimed to model the in-hospital mortality and mechanical ventilation risk using a two step approach combining clinical variables and ANN-analyzed lung inflammation data. METHODS: A data set of 4317 COVID-19 hospitalized patients, including 266 patients requiring mechanical ventilation, was analyzed. Demographic and clinical data (including the length of hospital stay and mortality) and chest computed tomography (CT) data were collected. Lung involvement was analyzed using a trained ANN. The combined data were then analyzed using unadjusted and multivariate Cox proportional hazards models. RESULTS: Overall in-hospital mortality associated with ANN-assigned percentage of the lung involvement (hazard ratio [HR]: 5.72, 95% confidence interval [CI]: 4.4-7.43, p < 0.001 for the patients with >50% of lung tissue affected by COVID-19 pneumonia), age category (HR: 5.34, 95% CI: 3.32-8.59 for cases >80 years, p < 0.001), procalcitonin (HR: 2.1, 95% CI: 1.59-2.76, p < 0.001, C-reactive protein level (CRP) (HR: 2.11, 95% CI: 1.25-3.56, p = 0.004), glomerular filtration rate (eGFR) (HR: 1.82, 95% CI: 1.37-2.42, p < 0.001) and troponin (HR: 2.14, 95% CI: 1.69-2.72, p < 0.001). Furthermore, the risk of mechanical ventilation is also associated with ANN-based percentage of lung inflammation (HR: 13.2, 95% CI: 8.65-20.4, p < 0.001 for patients with >50% involvement), age, procalcitonin (HR: 1.91, 95% CI: 1.14-3.2, p = 0.14, eGFR (HR: 1.82, 95% CI: 1.2-2.74, p = 0.004) and clinical variables, including diabetes (HR: 2.5, 95% CI: 1.91-3.27, p < 0.001), cardiovascular and cerebrovascular disease (HR: 3.16, 95% CI: 2.38-4.2, p < 0.001) and chronic pulmonary disease (HR: 2.31, 95% CI: 1.44-3.7, p < 0.001). CONCLUSIONS: ANN-based lung tissue involvement is the strongest predictor of unfavorable outcomes in COVID-19 and represents a valuable support tool for clinical decisions.

Hepatotropic Properties of SARS-CoV-2-Preliminary Results of Cross-Sectional Observational Study from the First Wave COVID-19 Pandemic.

Liver injury-expressed as elevated liver enzymes-is common in patients with COVID-19. Little is known about the potential mechanisms of liver damage by SARS-CoV-2. A direct cytopathic effect on hepatocytes as well as injury related to hypoxia or hepatotoxicity are being considered. The aim of the study was to compare the clinical characteristic of COVID-19 disease in patients with normal and abnormal liver enzymes activity. A group of 150 patients with COVID-19, hospitalized in our center, was analyzed. Patients with the known liver comorbidities were excluded (n = 15). Clinical features and laboratory parameters were compared between patients with normal and abnormal aminotransferase values. Liver injury expressed as any alanine aminotransferase (ALT) elevation was noted in 45.6% of patients hospitalized due to COVID-19. The frequencies of aspartate aminotransferase (AST) elevation were lower. It was noted that elevated ALT/AST unfavorably affected other parameters related to liver function such as albumin level; gamma-glutamyl transpeptidase (GGTP); and partly, ALP activity and influenced inflammation-related parameters. The most probable cause of mild hepatitis during COVID-19 was anoxia and immune-mediated damage due to the inflammatory response following SARS-CoV-2 infection. A direct cytopathic effect of SARS-CoV-2 on hepatocytes, albeit less probable, can be considered as well. The use of potentially hepatotoxic drugs may contribute to liver damage.

Nosocomial COVID-19 Infection and Severe COVID-19 Pneumonia in Patients Hospitalized for Alcoholic Liver Disease: A Case Report.

BACKGROUND COVID-19 is an infectious disease caused by SARS-CoV-2. It has spread rapidly through the world, endangering human life. The main target of COVID-19 is the lungs; however, it can involve other organs, including the liver. Patients with severe COVID-19 have an increased incidence of abnormal liver function, and patients with liver disorders are considered to be at a higher risk of severe COVID-19 infection. The mechanism of liver injury reported in 14% to 53% of COVID-19 patients is poorly recognized and several possibilities need to be considered (cytokine storm, direct viral action, hypoxia). The incidence of underlying liver comorbidities in patients with a COVID-19 infection ranges from 1% to 11%. CASE REPORT This is a report of 2 nosocomial COVID-19 infections and severe COVID-19 pneumonia in 2 patients who were hospitalized during treatment for alcoholic liver disease (ALD). Case 1 and case 2 were a 31-year-old woman and a 40-year-old woman, respectively, with decompensated ALD and symptoms of the COVID-19 infection. Both patients were transferred from another hospital to our hospital after confirmation of COVID-19 during their hospitalization. The course of the infection progressed rapidly in both patients with the development of multiple-organ failure and death over a short period. CONCLUSIONS There are no clear recommendations on the management of ALD in the COVID-19 pandemic. Alcoholic hepatitis may be a risk factor for severe COVID-19 and a poor outcome. A high percentage of nosocomial COVID-19 infections are observed; therefore, special precautions should be taken to minimize the risk of COVID-19 exposure.