Introduction and Aim: Hepatocellular carcinoma (HCC) is a deadly complication among patients with chronic liver disease (CLD). Controversies on the efficacy and safety of statin to prevent HCC among patients with CLD remain despite the growing evidences. We aim to investigate the efficacy and safety of using statin for HCC prevention among adult with CLD. Methods: We performed a systematic search of 4 electronic databases (PubMed/MEDLINE, EMBASE, Cochrane library, and ClinicalTrial.gov) up to April 15, 2020. We selected all types of studies evaluating the statin use and the risk of HCC among CLD patients, regardless of language, region, publication date, or status. The primary endpoint was the pooled risk of HCC. The secondary endpoint was the risk of statin-associated myopathy. Result: From 583 citations, we included a total of 13 studies (1,742,260 subjects, 7 types of statins), fulfilling the inclusion criteria, evaluating efficacy and safety of statin in CLD patients for HCC prevention. All studies were observational (2 nested case-control studies, 11 cohort studies), and no randomised trial was identified. We found that statin user has a lower pooled risk of HCC development (hazard ratio=0.57, 95% confidence interval: 0.52-0.62, I 2=42%). HCC reduction was consistent among statin users in cirrhosis, hepatitis B virus, and hepatitis C virus infections. The risk of statin-associated myopathy was similar between statin user and nonuser (hazard ratio=1.07, 95% confidence interval=0.91-1.27). Conclusion: Statin use was safe and associated with a lower pooled risk of HCC development among adults with CLD. Given the bias with observation studies, prospective randomised trial is needed to confirm this finding.

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Background Painless aortic dissection presenting with seizure and acute liver failure is uncommon. We described a case of early recognition leading to successful treatment of painless aortic dissection with atypical presentation. Case summary A young lady presented with generalized tonic-clonic seizures coupled with hepatitic pattern of deranged liver function test. Examination revealed blood pressure of 99/75 mmHg and hepatic flap. Electrocardiography showed sinus tachycardia. Urgent bedside echocardiography showed preserved cardiac function without significant valvular pathology, but noted a moderate pericardial effusion. Abdominal Ultrasound excluded liver cirrhosis or biliary obstructions. Viral hepatitis serologies and anti-liver panel were negative. She was progressively hypotensive with concurrent acute liver failure and oliguric acute kidney injury. Despite no chest pain, her rising serum troponin and widened mediastinum prompted an urgent computed-tomography aortogram, which showed a 4.3 cm dilatation of ascending thoracic aorta with acute haemopericardium and cardiac tamponade. She was diagnosed with malperfusion syndrome from Stanford type A aortic dissection. She underwent emergent ascending aorta and aortic arch repair and dialysis. She experienced complete recovery in her kidney, liver, and neurological function post-operatively. Discussion Painless aortic dissection masquerade as acute liver failure is uncommon. We describe a successful early recognition of malperfusion syndrome from painless aortic dissection, thus providing window for timely, life-saving intervention. Clinical challenges in this case include: (i) atypical presentation of aortic dissection, (ii) worsening acute liver failure which could lead to unnecessary liver transplantation, and (iii) risk of contrast-induced nephropathy in the setting of acute renal failure.