Aim Coronavirus disease 2019 (COVID-19) is a recently encountered disease that was declared a pandemic by WHO in 2020. Obesity and other components of the metabolic syndrome may aggravate the severity of COVID-19. Nonalcoholic fatty liver disease (NAFLD) represents the hepatic manifestation of metabolic syndrome. The aim of this study was to investigate a possible association between MAFLD and COVID-19 severity. Methods We performed a retrospective, case-control study, enrolling 71 consecutive COVID-19 patients who were divided into two groups according to the presence or absence of fatty liver by computed tomography scan. All medical records of eligible patients were reviewed including demographic, clinical, laboratory parameters and data regarding the presence of NAFLD and COVID-19 severity. Results NAFLD was identified in 22/71 (31%) of the study group. Out of 71, thirteen suffered from severe COVID-19. NAFLD patients had more severe COVID-19 compared with non-NAFLD subjects, 8/22 (36.3%) vs. 5/49(10.2%), ( P < 0.005), respectively. Multiple logistic regression analysis showed that NAFLD subjects were more likely to have severe COVID-19 disease (odds ratio 3.57, 95% confidence interval: 1.22, 14.48, P = 0.0031). Conclusion NAFLD represents a high risk for severe COVID-19 irrespective to gender, and independent of metabolic syndrome specifically in male gender. Moreover, obesity, hypertension and metabolic syndrome were also significantly associated with severe COVID-19.

Background and aim The progression of nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH) is believed to be the driver for future development of fibrosis and cirrhosis. Nevertheless, there remains a lack of noninvasive methods for the diagnosis of NASH. The aim of the present study was to determine the role of neutrophil-to-lymphocyte ratio (NLR) in predicting histological severity in NAFLD. Patients and methods We performed a single-center retrospective study in EMMS Nazareth Hospital from July 2014 to May 2017. Liver biopsies were evaluated using the steatosis, activity, and fibrosis scoring system, which includes three components: (i) steatosis (0–3), (ii) activity grade (0–4), and (iii) fibrosis (0–4). Patients were divided into two groups. The first group was considered to have NAFLD when fibrosis grade was 0–1 and inflammatory activity was 0–1, whereas the second group included patients with fibrosis grade of 2–4 and inflammatory activity grade of 2–3, considered to have NASH. Results Ninety-one (91) patients with biopsy-proven fatty liver were included. The average age was 42.13 ± 11.5 (18–74) years. Fifty-seven (62.6%) patients were male. Univariate analysis revealed several factors to be associated with advanced fibrosis and inflammatory activity, including NLR, C-reactive protein, and HOMA-IR, which correlated with fibrosis [odds ratio (OR): 1.405, 95% confidence interval (CI): 1.21–1.63, P < 0.0001; OR: 1.329, 95% CI: 1.05–1.68, P = 0.016; and OR: 1.922, 95% CI: 1.18–3.11, P = 0.007, respectively], and NLR, triglycerides, and HOMA-IR, which correlated with hepatocyte inflammation (OR: 1.210, 95% CI: 1.08–1.35, P = 0.0009; OR: 0.984, 95% CI: 0.97–0.99, P = 0.01; and OR: 2.069, 95% CI: 1.28–3.34, P = 0.003, respectively). On multivariate logistic regression analysis, NLR remains independently associated with advanced fibrosis grade and inflammatory activity (OR: 0.734, 95% CI: 0.631–0.854, P < 0.0001, area under the curve: 0.8622 and OR: 0.836, 95% CI: 0.74–0.95, P = 0.006, area under the curve: 0.7845, respectively). Our second major finding was defining an NLR cut-off point that was associated with inflammatory activity and fibrosis grade using receiver operating characteristic analysis based on the Youden index (J), which is defined by the maximal sensitivity and specificity. Conclusion NLR showed significant independent correlation with advanced inflammation and fibrosis in patients with NAFLD. This simple available laboratory tool may be incorporated into future diagnostic scores.

Background Abdominal aortic aneurysm (AAA) and fatty liver disease are both associated with the metabolic syndrome (MS); the aim of this study was to investigate whether patients with AAA are also at a higher risk for fatty liver disease. Methods A case-control retrospective study. Patients diagnosed with AAA were compared with age- and sex-matched controls regarding the prevalence of fatty liver disease. Extracted data include anthropometric parameters, clinical and laboratory data, and liver imaging. Results 995 patients were enrolled in the final analysis, 495 patients with AAA and 500 age- and sex-matched controls. The prevalence of fatty liver disease among AAA subjects was 48.9% compared with 21.2% among the controls ( P <0.005). After adjusting for age, smoking, body mass index, and MS components, the logistic regression analysis indicates that AAA (men: OR 1.29, 95% CI 1.17, 1.49, P =0.001; women: OR 1.23, 95% CI 1.06, 1.43, P =0.002), obesity (men: OR 1.32, 95% CI 1.17, 1.59, P <0.001; women: OR 1.32, 95% CI 1.07, 1.52, P =0.012), hypertension (men: OR 1.23, 95% CI 1.13, 1.46, P =0.001; women: OR 1.13, 95% CI 1.00, 1.33, P =0.045), MS (men: OR 1.31, 95% CI 1.19, 1.53, P =0.001; women: OR 1.28, 95% CI 1.16, 1.42, P =0.002) were associated with non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH). The prevalence of liver cirrhosis was 1.23%; subjects with obesity, diabetes, hypertension, and AAA had increased risk for cirrhosis (OR 1.89, 95% CI 1.18, 3.22, P =0.014; OR 1.27, 95% CI 1.09, 2.72, P =0.0027; OR 2.08, 95% CI 1.29, 3.42, P =0.004; OR 1.73, 95% CI 1.08, 2.87, P =0.027, respectively). Conclusion AAA patients are at increased risk for NAFLD/NASH, may predict advance liver disease and liver cirrhosis.