Primary cirrhosis syndrome

Introduction to primary intrahepatic sclerosis syndrome Primary intrahepatic cirrhosis (Hanot) syndrome refers to a group of syndromes caused by non-specific inflammation of the intrahepatic bile duct, fibrosis leading to intrahepatic cholestasis, cirrhosis with nodular hyperplasia. Nowadays used to be called primary biliary cirrhosis, another name is chronic non-suppurative cholangitis, biliary hepatitis, biliary biliary cirrhosis, intrahepatic obstructive biliary cirrhosis. Intrinsic may be due to autoimmune abnormalities, bile duct and interlobular bile duct non-suppurative destructive inflammation, with bile duct hyperplasia; destruction, scar formation; hepatic lobular structure destruction, regeneration nodule formation; liver with obvious biliary stasis Hardened histological changes. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: Osteoporosis Upper gastrointestinal bleeding Hepatic encephalopathy Ascites

The cause of primary intrahepatic sclerosis syndrome

Cause:

May be due to autoimmune abnormalities, bile duct and interlobular bile duct non-suppurative destructive inflammation, with bile duct hyperplasia; destruction, scar formation; hepatic lobular structure destruction, regenerative nodule formation; cirrhotic tissue with obvious biliary stasis Learn to change.

Primary intrahepatic sclerosis syndrome prevention

The liver is the main hub of human metabolism and synthetic protein. When hepatocytes are separated by proliferating fibrous tissue to form nodular pseudo-lobules, that is, cirrhosis, the normal relationship between various types of blood vessels will be lost. Dysfunction, resulting in a series of physiological lesions. Retention is better than drug treatment, which can improve the liver's own immunity and prevent the development of cirrhosis. Rest is one of the important measures to protect the liver. When the patient is lying down, the blood of the liver is increased by 40% than when standing, which is beneficial to the recovery of hepatocytes and at the same time, the pressure of the portal vein can be lowered. Rest can also vary from person to person depending on the condition. Maintain normal living and good sleep to develop good habits, regular living, ensure sleep, help liver disease nursed back to prevent complications. Diet should provide adequate nutrition, food should be diversified, supply high-priced protein containing amino acids, multi-vitamins, low-fat, less slag diet, to prevent rough multi-fiber food damage to the esophageal vein, causing major bleeding.

Primary intrahepatic sclerosis syndrome complications Complications Osteoporosis Upper gastrointestinal bleeding Hepatic encephalopathy Ascites

Bile stasis can cause steatorrhea, white clay-like stool, osteoporosis, pathological fractures, hemorrhage, etc. In severe cases, complications such as upper gastrointestinal bleeding, hepatic encephalopathy and ascites may occur.

Symptoms of primary intrahepatic sclerosis syndrome Common symptoms Biliary cirrhosis, biliary stasis, liver area, friction sound, skin itching, liver splenomegaly, fatty diarrhea, osteoporosis, jaundice

Clinically more common in female patients, insidious onset, generalized skin itching, followed by jaundice and gradually deepened to severe, biliary stasis can cause steatorrhea, white clay-like stool, osteoporosis, pathological fractures, hemorrhage, etc., hepatosplenomegaly Large and obvious, the skin is yellow.

Examination of primary intrahepatic sclerosis syndrome

Laboratory tests for elevated serum bilirubin, mainly elevated bilirubin, elevated alkaline phosphatase, cholesterol, IgM, anti-mitochondrial antibodies, smooth muscle antibodies and anti-nuclear antibodies, albumin reduction, gamma-sphere The protein is elevated.

Diagnosis and diagnosis of primary intrahepatic sclerosis syndrome

Liver biopsy has characteristic pathological changes that can be diagnosed in patients with extrahepatic obstructive jaundice and secondary biliary cirrhosis.

It is differentiated from extrahepatic obstructive jaundice and secondary biliary cirrhosis.

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