Liver disease in the era of COVID-19: Is the worst yet to come?

The global social, economic and political crises related to coronavirus disease 2019 (COVID-19) presumably had more indirect than direct negative impacts on health systems. Drastic lifestyle changes, social isolation and distancing, and individual and global financial crises resulted in robust populations forfeiting healthy habits and seeking comfort in alcoholic beverages, drugs and unhealthy diets. The inevitable consequences are increases in the incidence of nonalcoholic fatty liver disease, viral hepatitis, acute alcoholic hepatitis, liver cirrhosis decompensation and ultimately liver-related mortality. The inaccessibility of regular clinical and sonographic monitoring systems has caused difficulties in the treatment of patients with chronic liver disease (CLD) and has prevented prompt hepatocellular carcinoma detection and treatment. A dramatic reduction in the number of liver donors and the transformation of numerous transplantation centers into COVID-19 units drastically decreased the rate of orthotopic liver transplantation. The indirect, unavoidable effects of the COVID-19 pandemic in the following years have yet to be determined. Substantial efforts in the management of patients with liver disease in order to overcome the inevitable COVID-19-related morbidity and mortality that will follow have yet to be initiated. Several questions regarding the impact of the COVID-19 pandemic on liver disease remain. The most important question for general CLD patients is: How will the modification of clinical practice during this pandemic affect the outcomes of CLD patients? This article reviews the influence of COVID-19 on patients with liver disease during the pandemic, with particular emphasis on the disease course associated with pandemic resolution.

Assessment of Steatosis and Fibrosis in Liver Transplant Recipients Using Controlled Attenuation Parameter and Liver Stiffness Measurements.

Aim: The primary objective of this study was to evaluate the prevalence of increased controlled attenuation parameter (CAP) and liver stiffness measurements (LSM) as surrogate markers of liver steatosis and fibrosis in liver transplant recipient (LTR). Secondary objectives were to determine the predictors of increased CAP and LSM in population of LTR. Methods: In this prospective, cross-sectional study, we have evaluated 175 LTRs' mean age as 61 (53-65) with a functioning graft for more than one year who came for regular outpatient examinations to the Department of Gastroenterology, University Hospital (UH) Merkur, Zagreb, Croatia. Results: Of 175 analyzed LTRs, 34.28% had obesity, 64.00% had hypertension, 38.28% had diabetes, and 58.85% had hyperlipidemia. The prevalence of liver steatosis was 68.57%, while the prevalence of severe liver steatosis was 46.85%. On multivariate analysis, independent factors associated with liver steatosis were male gender, total cholesterol as positive predictor, and HDL as negative predictor, and independent factors positively associated with severe liver steatosis were higher body mass index (BMI) and higher triglyceride levels. The prevalence of moderate liver fibrosis was 54.85%, while the prevalence of advanced liver fibrosis was 24%. On multivariate analysis, independent factors positively associated with moderate fibrosis were gamma-glutamyl transferase (GGT) and CAP, while the independent factor positively associated with advanced fibrosis was GGT. Conclusion: Our study showed high prevalence of increased CAP and LSM measurements as surrogate markers of liver steatosis and fibrosis. Metabolic syndrome components were highly present and were associated with CAP and LSM values as well as in the pretransplant setting. Due to high prevalence of metabolic comorbidities and nonalcoholic fatty liver disease in LTRs and the lack of the abnormal liver test in a significant number of these patients, TE with CAP may be a reasonable initial assessment for LTRs with one or more components of the metabolic syndrome.

EXPRESSION OF MUC2 GLYCOPROTEIN ANTIBODY AND VASCULAR ENDOTHELIAL GROWTH FACTOR IN BARRETT'S MUCOSA.

Higher expression of the mucin 2 (MUC2) glycoprotein and vascular endothelial growth factor (VEGF) in Barrett's mucosa may be associated with a higher risk of esophageal adenocarcinoma development. Thirty-six patients diagnosed with Barrett's esophagus (BE), short-segment, were included in the study due to unsuccessful treatment with proton pump inhibitors. The diagnosis was confirmed by histopathologic analysis of the tissue obtained by esophagogastric junction biopsy. Expression of MUC2 and VEGF was determined by immunohistochemistry. We found four patients in early stage of adenocarcinoma and 32 patients with BE; five of them had indication for argon plasma coagulation treatment, one for radiofrequency ablation and one for endoscopic mucosal resection; 25 patients were treated with proton pump inhibitors. Regression of BE occurred in 25 (69.44%) patients. MUC2 positivity is unique for goblet cells in patients with BE, but it is not the only marker. VEGF is an indicator of angiogenesis in the mucosa of patients with BE and adenocarcinoma.

Secondary hypertension due to isolated interrupted aortic arch in a 60-year-old person--one-year follow up.

Interrupted aortic arch (IAA) is a congenital defect characterized by loss of luminal continuity between the ascending and descending aorta1. It is a rare malformation with an estimated incidence of perinatally diagnosed cases of 3 per million live births3. The condition is considered extremely rare in adults. However, its true prevalence in this population is unknown. We have found 30 case reports of IAA in adults in literature, 5 of whom were older than 50 years. Four of them had type A IAA. Arterial hypertension is a typical co-morbidity. In this report we describe a 60-year-old male patient who had a type A asymptomatic IAA. Although we initially suspected the aortic coarctation, further invasive procedures revealed complete interruption of the aortic arch just distal to the origin of the left subclavian artery. The patient underwent surgical repair, followed by full recovery and near-normalization of blood pressure.