Malnutritional cirrhosis is caused by long-term nutritional deficiencies. The reasons for malnutrition, aside from inadequate intake in some individuals, are often due to other diseases that restrict food consumption and absorption, such as after small intestine bypass surgery.

bubble_chart Pathogenesis

Malnutritional cirrhosis (Malnutrition Cirrhosis) is caused by long-term nutritional deficiencies. Animal experiments have confirmed that simple malnutrition, especially deficiencies in proteins, anti-fatty liver factors, and B vitamins, can lead to fatty liver, hepatocyte necrosis, degeneration, and ultimately cirrhosis. The mechanisms by which malnutrition leads to cirrhosis may include: ① When proteins containing cystine are deficient, the sources of cysteine and glutathione are reduced, affecting the generation and activity of enzymes in hepatocytes, making them susceptible to damage from various factors, leading to degeneration and necrosis. ② Choline is a lipotropic substance that can synthesize phospholipids with neutral fats in the liver, making hepatic fats easier to oxidize and utilize. If choline or the amino acids necessary for choline synthesis are severely deficient, fats will accumulate in hepatocytes, resulting in fatty liver. Fatty degeneration of hepatocytes can reduce their resistance to various harmful factors and may also cause cell volume enlargement, mutual compression, and pressure on liver blood sinuses, gradually leading to ischemia, necrosis, fibrous tissue proliferation, and ultimately cirrhosis.

The causes of malnutrition, aside from inadequate intake in some patients, are often due to other diseases that restrict food intake and absorption, such as after small intestine bypass surgery.

Similar to other types of cirrhosis, the development of nutritional cirrhosis is preceded by hepatocellular injury, such as fatty degeneration, accompanied by inflammatory cell infiltration and granuloma formation in the portal areas and hepatic lobules. This progresses to hepatic fibrosis. Like alcoholic liver injury, perivenular hepatic fibrosis is a hallmark of progression to cirrhosis. Prolonged and repeated liver damage ultimately leads to cirrhosis. The entire pathological process and the characteristics of liver lesions at various stages closely resemble those of alcoholic liver injury.

bubble_chart Clinical Manifestations

12 to 18 months after small intestine bypass surgery, changes in sexual characteristics may occur, such as decreased libido, gynecomastia in males, amenorrhea and altered secondary sexual characteristics in females. Other symptoms include loss of appetite, weakness, abdominal pain, nausea, and vomiting. Signs include jaundice, hepatosplenomegaly, ascites, and spider angiomas. Laboratory tests show elevated serum bile acids, increased AST, mostly normal ALT, prolonged prothrombin time, hypoalbuminemia, and liver biopsy may reveal hepatic steatosis and hepatitis manifestations.

Patients who have undergone small intestine bypass surgery for more than 7 years may develop cirrhosis. The progression to cirrhosis is insidious, with inconspicuous clinical manifestations, and occasional fatalities due to cirrhosis and liver failure.

bubble_chart Treatment Measures

Actively supplement nutrition with high protein and low fat, and intravenous nutrition can also be provided, which improves both liver function and histological changes in patients with cirrhosis.