Internal Diseases and Therapy · MU Sofia

97. Fatty liver. Alcoholic and nonalcoholic steatohepatitis

Covers fat accumulation in liver cells, distinguishing macrovesicular from microvesicular steatosis with their causes, then moves to alcoholic steatohepatitis, covering its mechanism, clinical signs, diagnostic AST/ALT ratio and treatment options. It closes with nonalcoholic fatty liver disease and NASH, including risk factors, pathogenesis, diagnosis where ALT exceeds AST, and management by weight loss, statins and vitamin E.

Inside: 1 section · 2 labelled pictures · 14 flashcards · 3 min

Topic 98 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 552 words (3 min of reading), with 14 flashcards.

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  1. Fatty liver. Alcoholic and nonalcoholic steatohepatitis

Fatty liver. Alcoholic and nonalcoholic steatohepatitis

Steatosis

This is fat accumulation in cells, in this case, hepatosteatosis, accumulation in liver cells. It can be macrovesicular (obesity, type 2 diabetes, metabolic syndrome, alcohol consumption, hep C, wilsons) or microvesicular (Reye syndrome, medications, fatty liver of pregnancy, inborn metabolic errors).

Image: “Histopathology of centrilobular steatosis of the liver” by Mikael Häggström , M.D. Author info - Reusing images - Conflicts of interest: None Mikael Häggström , M.D. Consent note , CC0, via Wikimedia Commons.

Alcoholic steatohepatitis

Develops in those who drink >6 drinks a day along with genetic predisposition, 50% of those who develop AASH have preexisting cirrhosis.

Mechanism is by effects of alcohol on hepatocytes, mediated by Kupffer cells. Hepatocytes undergo altered redox state due to alcohol and aldehyde dehydrogenase reactions causing oxidative stress and lipid peroxidation by enzyme induction. Chronic alcohol consumption

also increases gut permeability, causing portal toxicity, putting more stress on the kupffer cells, causing activation, leading to release of proinflammatory mediators.

All of this damage means that the hepatocytes are not able to properly metabolize fats as is their job, so, we end up with fat build up in the cells, leading to fatty liver. Clinical manifestations are generally that of alcoholism, look for palmar erythema, spider nevi, bilateral gynecomastia, testicular atrophy, parotid enlargement and dupuytren contractions (contraction of the hand, affecting little finger). The fatty liver itself doesn't give many symptoms, we may see anorexia, fatigue, right upper quadrant discomfort and tender hepatomegaly.

Diagnosis is based on history + liver disease. AST/ALT ratio of more than 2 is typical of excessive alcohol consumption (ALT rarely greater than 200 IU/L in such cases). Ultrasound will help to provide evidence of staging of hepatic steatosis and differentiate from other liver disorders.

Treatment

  • Abstinence, by far the most important and effective treatment
  • Prednisolone (corticosteroid) with IV of N-acetylcysteine can be given carefully for short time
  • Pentoxifylline is a possible second line to corticosteroids where steroids are contraindicated.
  • Vitamin E has hepatoprotective capabilities, although its use is controversial and benefits remain unproven

Nonalcoholic fatty liver disease (NAFLD or NASH)

NAFLD (of which NASH is the inflammatory form) is one of the most common causes of elevated liver enzymes in the western world. Due to obesity and type 2 diabetes increases, the condition is on the rise. The major risk factors are what you would expect, diabetes, obesity, metabolic syndrome, dyslipidemia, hypothyroidism, hypopituitarism and sleep apnea.

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