Mistakes in alcoholic liver disease and how to avoid them

you pay a little more attention to the patient. He is presenting with jaundice (total bilirubin 5.4 mg/dL) and mildly elevated transaminase levels (with an AST:ALT ratio >2), is a little more thrombocytopenic than you would expect (45,000/mcL) and leukocytosis is slightly more pronounced than anticipated (12.4 x10 cel/L). Over the days that follow, his bilirubin level goes up (19 mg/dL) and his INR and creatinine levels also worsen. The patients is now in grade Mistake 1 Not recognizing alcoholic hepatitis in a patient who has multiple chronic liver disease aetiologies A male patient with longstanding cirrhosis and documented chronic hepatitis C (nonviraemic after treatment one year before) is admitted to the emergency department with haematemesis but no haemodynamic compromise. As anticipated, oesophageal variceal bleeding is confirmed and successfully managed by band ligation. A straightforward Alcohol consumption is the most prevalent aetiology for liver cirrhosis in Europe and the third leading risk factor for overall mortality.1,2 In fact, alcoholic liver cirrhosis accounts for almost half a million deaths a year worldwide, corresponding to 50% of all cases of cirrhosis, according to the World Health Organization (WHO). 3 Alcoholic liver disease (ALD) is multifaceted, with several cofactors influencing its progression. Patients abusing alcohol can simultaneously have viral hepatitis B or C, or a genetic disease, such as alpha-1 antitrypsin deficiency or haemochromatosis. Alcohol consumption is usually assessed in pure grams per day and has a direct relationship with liver damage. Daily alcohol consumption of >30 g for men and >20 g for women is considered the cut-off volume at which there is a risk of developing alcohol-related liver disease.4 Besides volume, the pattern of consumption is also a significant factor, with heavy episodic drinking (HED) defined as an intake of 60 g or more of pure alcohol on at least one occasion in the past 30 days. Regarding HED, there is scarce information on the threshold to be applied to this pattern of drinking.5 Although the relationship between alcohol consumption and ALD is well defined, it must be acknowledged that severe disease only develops in a fraction of those who consume excessive amounts of alcohol. Nonetheless, the disease course is very much influenced by the pattern of drinking, with periods of abstinence or heavy drinking clearly altering its progression.5 ALD can present in different stages, ranging from steatosis to more severe disease, such as the clinical syndrome of alcoholic hepatitis, or decompensated liver cirrhosis, which is sometimes complicated by liver cancer. In the setting of alcoholic hepatitis, several scores, such as the Maddrey discriminant function, Glasgow alcoholic hepatitis score (GASH) and ABIC, may be used to evaluate disease severity, predict short-term survival, and decide on the need for specific treatment. Later on, the Lille score, which includes the reduction in serum bilirubin levels at day 7, evaluates the response to prednisolone after one week, in order to decide whether to continue or stop treatment.5 Despite being a frequent disease, the different aspects of ALD mean that its management still poses many difficulties and pitfalls. In this article we discuss frequent mistakes in ALD, based on the current guidelines and some paradigmatic real-life cases. III–IV hepatic encephalopathy. Now you start to wonder: has anything gone wrong? Why is he in acute-on-chronic liver failure (ACLF)? Is he infected? What about alcohol? In fact, his previous registries state he misused alcohol and was referred to a rehabilitation program a couple of years earlier. On admission, the patient denied he was misusing alcohol, but his wife confirms he had gone back to drinking heavily. So is this alcoholic hepatitis? Alcoholic hepatitis is a clinical syndrome. Most of its clinical features are present in this patient (jaundice, AST:ALT elevation 2–5 times the upper limit of normal (ULN) in a ratio of 2:1 and an inflammatory response syndrome). The clinical picture frequently worsens with progression to ACLF and is associated with complications such as gastrointestinal bleeding, encephalopathy and hepatorenal syndrome. In fact, the presenting symptom may well be one of these complications. Histologically-proven severe alcoholic hepatitis is estimated to comprise 6% of patients with decompensated cirrhosis and up to a quarter of ACLF patients. Diagnosis based on classic clinical criteria such as those mentioned above were found to misdiagnose alcoholic hepatitis in up to 25% of cases, thus addressing the question of alcohol consumption is essential. Questionnaires such as CAGE and AUDIT (alcohol use disorders inventory test), or the shorter version AUDIT-C, will help identify harmful and hazardous drinkers with good sensitivity and specificity. A thorough anamnesis will help tie up the loose ends, but as discussed later, liver biopsy can