Dunbar Syndrome and Hypoxic Hepatitis: An Unusual Presentation

Hypoxic hepatitis, also known as ischemic hepatitis, is characterized by acute hepatocellular injury due to inadequate oxygen delivery to the liver. Celiac trunk stenosis can lead to hepatic ischemia and subsequent liver damage. We present the case of an 81-year-old patient with a history of hypertension, ischemic heart disease, hypothyroidism, and biliary lithiasis, who developed hypoxic hepatitis secondary to Dunbar syndrome and a stenosis of the superior mesenteric artery. The patient improved symptoms and liver function tests with conservative management, including intravenous fluids and supportive care. Long-term management involved continued antiplatelet therapy and statins, with consideration of further interventions for celiac trunk stenosis. This case underscores the importance of recognizing Dunbar syndrome as well as superior mesentery trunk stenosis as a potential cause of hypoxic hepatitis. It highlights the need for multidisciplinary management in such cases.

Low serum albumin predicts early mortality in patients with severe hypoxic hepatitis

To evaluate the incidence, etiology, and predictors of mortality of severe hypoxic hepatitis. METHODSWe used computerized patient records to identify consecutive cases of severe hypoxic hepatitis admitted to a tertiary hospital in Singapore over a one-year period. We defined severe hypoxic hepatitis as elevation of serum transaminases more than 100 times upper limit of normal in the clinical setting of cardiac, circulatory or respiratory failure after exclusion of other causes of hepatitis. We used multivariable regression analysis to determine predictors for mortality. RESULTSWe identified 75 cases of severe hypoxic hepatitis out of 71380 hospital admissions over one year, providing an incidence of 1.05 cases per 1000 admissions. Median age was 65 years (range 19-88); 57.3% males. The most common etiologies of severe hypoxic hepatitis were acute myocardial infarction and sepsis. Fifty-three patients (71%) died during the hospitalization. The sole independent predictive factor for mortality was serum albumin measured at the onset of severe hypoxic hepatitis. Patients with low serum albumin of less than 28 g/L have more than five-fold increase risk of death (OR = 5.39, 95%CI: 1.85-15.71). CONCLUSIONSevere hypoxic hepatitis is uncommon but has a high mortality rate. Patients with low serum albumin are at highest risk of death.

COVID-19 and liver injury: An ongoing challenge

The new coronavirus severe acute respiratory syndrome coronavirus 2(SARSCoV-2)was identified in December 2019,in Wuhan,China.The virus was rapidly spread worldwide,causing coronavirus disease 2019(COVID-19)pandemic.Although COVID-19 is presented,usually,with typical respiratory symptoms(i.e.,dyspnea,cough)and fever,extrapulmonary manifestations are also encountered.Liver injury is a common feature in patients with COVID-19 and ranges from mild and temporary elevation of liver enzymes to severe liver injury and,even,acute liver failure.The pathogenesis of liver damage is not clearly defined;multiple mechanisms contribute to liver disorder,including direct cytopathic viral effect,cytokine storm and immune-mediated hepatitis,hypoxic injury,and druginduced liver toxicity.Patients with underlying chronic liver disease(i.e.,cirrhosis,non-alcoholic fatty liver disease,alcohol-related liver disease,hepatocellular carcinoma,etc.)may have greater risk to develop both severe COVID-19 and further liver deterioration,and,as a consequence,certain issues should be considered during disease management.The aim of this review is to present the prevalence,clinical manifestation and pathophysiological mechanisms of liver injury in patients with SARS-CoV-2 infection.Moreover,we overview the association between chronic liver disease and SARS-CoV-2 infection and we briefly discuss the management of liver injury during COVID-19.

Anabolic steroid-induced cardiomyopathy underlying acute liver failure in a young bodybuilder

Heart failure may lead to subclinical circulatory disturbances and remain an unrecognized cause of ischemic liver injury. We present the case of a previously healthy 40-year-old bodybuilder, referred to our Intensive-Care Unit of Hepatology for treatment of severe acute liver failure, with the suspicion of toxic hepatitis associated with anabolic steroid abuse. Despite the absence of symptoms and signs of congestive heart failure at admission, an anabolic steroid-induced dilated cardiomyopathy with a large thrombus in both ventricles was found to be the underlying cause of the liver injury. Treatment for the initially unrecognized heart failure rapidly restored liver function to normal. To our knowledge, this is the f irst reported case of severe acute liver failure due to an unrecognized anabolic steroid-induced cardiomyopathy. Awareness of this unique presentation will allow for prompt treatment of this potentially fatal cause of liver failure.