cirrhosis of the liver Cirrhosis is the diffuse proliferation of liver fibrous tissue, leading to the formation of nodules and pseudo-lobules on the basis of extensive hepatocyte necrosis, thereby disrupting the normal structure and blood supply of the liver. Cirrhosis is the end stage of a chronic, progressive, and diffuse liver disease resulting from long-term exposure to various disease factors affecting the liver.

Cirrhosis is characterized by the diffuse proliferation of fibrous tissue in the liver, leading to the formation of nodules and pseudo-lobules, thereby disrupting the normal structure and blood supply of the liver. It is the end-stage of a chronic, progressive, and diffuse liver disease caused by various pathological factors acting on the liver over an extended period.

According to the etiology of cirrhosis, it can be classified into viral cirrhosis, cholestatic cirrhosis, alcoholic cirrhosis, autoimmune cirrhosis, congestive cirrhosis, and cryptogenic cirrhosis (cirrhosis of unknown cause), among others.

According to the disease's progression, it can be divided into compensated cirrhosis and decompensated cirrhosis.

Based on its pathological features, it can be categorized into micronodular cirrhosis, macronodular cirrhosis, and mixed nodular cirrhosis.

Here, we will primarily discuss cirrhosis classified based on its pathological type.

Micronodular Cirrhosis

Macroscopically, the liver appears reduced in size and weight, with increased hardness. The liver capsule is thickened, and the surface shows diffuse granules of equal size, typically less than 3mm in diameter. Microscopically, pseudo-lobule formation is observed, with absent, displaced, or increased central veins. This type is commonly seen in patients with alcoholic, cholestatic, hemochromatosis, and congestive cirrhosis.

Macronodular Cirrhosis

The liver generally appears reduced in size and weight, with various atypical nodules and depressed areas on the surface, with nodule diameters mostly exceeding 3mm. Microscopically, different-shaped pseudo-lobules are divided by fibrous septa. There is a collection of ductules in the connective tissue, along with bile duct proliferation and mononuclear cell infiltration. This type is frequently observed in patients with chronic hepatitis B and C-related cirrhosis.

Mixed Nodular Cirrhosis

This type is characterized by an equal proportion of small and large nodules. It can be observed in genetic metabolic disorders such as alpha-1 antitrypsin deficiency (α1-AT deficiency), some ketone metabolism disorders (Wilson's disease), and cirrhosis caused by hepatitis B infection.

Viral Hepatitis

Hepatitis B, C, D, and a small proportion of hepatitis E can progress to cirrhosis, with hepatitis B being the predominant cause in China, accounting for over half of the cases. The main reasons for the progression from hepatitis to cirrhosis include persistent presence of the hepatitis virus, moderate to severe liver necrosis, and fibrosis. Overlapping infections of different types of hepatitis can accelerate the progression to cirrhosis.

Alcoholic Liver Disease

Chronic alcohol abuse is the most common cause of cirrhosis in Western countries, accounting for approximately 50% to 90% of cases, but it is relatively less common in China, constituting only about 10%.

Non-alcoholic Fatty Liver Disease

It is the second most common cause after viral hepatitis and chronic alcoholic liver disease, and its incidence is increasing.

Chronic Cholestasis

Primary and secondary cholestatic cirrhosis, the latter mostly caused by biliary obstruction due to various reasons. The toxic effects of high concentrations of bile acids and bilirubin can accelerate hepatocyte degeneration, leading to cirrhosis.

Medications or Toxins

Long-term use of certain drugs (such as antifolate antitumor drugs, isoniazid, etc.) and repeated exposure to certain chemical toxins (such as arsenic, carbon tetrachloride, etc.) can cause related hepatitis, ultimately progressing to cirrhosis.

Hepatic Blood Circulatory Disorders

Long-term intrahepatic congestion and hypoxia caused by various factors can lead to necrosis and fibrosis of corresponding areas, eventually progressing to cirrhosis.

Genetic and Metabolic Disorders

Cirrhosis caused by factors related to genetics and metabolism. In China, Wilson's disease, characterized by copper metabolism disorder, is the most common. In Western countries, cirrhosis caused by hemochromatosis (iron metabolism disorder) and alpha-1 antitrypsin deficiency (α1-AT deficiency) is more prevalent. In addition, tyrosinemia caused by tyrosine metabolism disorders can also lead to cirrhosis.

Immune Disorders

Autoimmune hepatitis and primary sclerosing cholangitis can both progress to cirrhosis.

Parasitic Infections

Schistosoma egg obstruction of specific veins may cause eosinophil infiltration and related fibrous tissue proliferation, leading to the development of schistosomal cirrhosis.

Unclear Causes

There is a category of cirrhosis patients with an unknown medical history, making it impossible to identify the cause. Clinically, this is often referred to as cryptogenic cirrhosis, accounting for about 5% to 10% of cases.

Compensated Stage

This includes clinical stages 1 and 2. Patients in stage 1 do not have varices or ascites, while those in stage 2 do not have ascites or bleeding, but esophageal varices can be detected through endoscopy. Approximately 10% to 20% of patients in the compensated stage may have no symptoms, or they may present with nonspecific manifestations such as decreased appetite, weight loss, weakness, and diarrhea.

Decompensated Stage

Mainly includes clinical stages 3, 4, and 5, with specific features as follows:

Stage 3 involves ascites without bleeding, with or without esophageal varices.

Stage 4 is primarily characterized by esophageal varices, with or without ascites.

Stage 5 mainly involves sepsis and hepatorenal syndrome.

In addition to the above characteristics, the following manifestations may also occur in these stages:

Decreased appetite, abdominal distension, abdominal pain, diarrhea, weakness, and weight loss.

Bleeding tendency: gingival and nasal bleeding, excessive menstrual bleeding in women, skin and mucous membrane petechiae and ecchymoses.

Endocrine system imbalance: reduced male sexual function, gynecomastia, infertility, and amenorrhea in females.

Chronic illness appearance: manifested as dark complexion, angular stomatitis, and facial telangiectasia.

Skin manifestations: spider nevi, palmar erythema.

Estrogen inactivation disorders: manifested as gynecomastia in males.

Chest and abdominal wall varices: in severe cases, varicose veins can form around the umbilicus, and vascular murmurs can even be heard on the varicose veins.

Jaundice: the appearance of jaundice indicates further progression of the disease to the middle stage, characterized by yellowing of the skin, mucous membranes, and sclera.

Fever: irregular fever may be present in approximately one-third of patients, mainly related to infection and disease activity.

Positive shifting dullness: if ascites is present, it may manifest as positive shifting dullness in the abdomen.

Hepatic hydrothorax: more common on the right side (85%), occasionally on both sides (2%), and on the left side (13%).

Hepatic encephalopathy: as the disease progresses to the late stage, hepatic encephalopathy may occur, characterized by hepatic fetor and asterixis.

Hepatomegaly and splenomegaly: in general, the liver is enlarged in the early stage, but in the late stage, it becomes firm, shrinks, and is not easily palpable below the ribs. If liver cancer occurs, the liver may become firm as a rock and increase in size. 35% to 50% of cirrhosis patients have splenomegaly, mostly moderate, with occasional severe cases.

Some Chinese herbal medicines with hepatoprotective, enzyme-lowering, choleretic, and dampness-eliminating effects can be used, but they are ineffective against antiviral treatment. It is recommended to seek treatment at a regular medical institution under the guidance of a physician.

Antifibrotic Drugs

Certain Chinese medicines such as Salvia miltiorrhiza, peach kernel extract, and capsules for regulating vital energy and removing stasis have a certain antifibrotic effect.

Diet

Ensuring nutritional intake and adhering to necessary dietary restrictions are fundamental measures to improve liver function and slow disease progression. Patients with esophageal varices should consume mashed vegetables, minced meat, and soft foods, chewing slowly and thoroughly to prevent injury to the varicose veins.

Recommended diet

Protein: Essential for liver cell repair and maintaining normal plasma albumin levels. Protein intake should be ensured through consumption of soy products, milk, eggs, fish, chicken, and lean pork. When blood nitrogen levels are elevated, protein intake should be limited or avoided, and plant-based proteins such as soy products should be chosen.

Vitamins: Fresh fruits and vegetables are rich in vitamins, such as tomatoes and citrus fruits containing vitamin C, which should be consumed regularly to ensure adequate vitamin intake.

Dietary restrictions

Alcohol restriction: Regardless of the cause of cirrhosis, alcohol consumption should be avoided, as it can lead to further liver damage.

Low-sodium diet: Cirrhosis patients should primarily follow a low-sodium diet. Excessive sodium can cause fluid retention, exacerbating ascites and lower limb edema. Foods low in sodium include grains, melons, fruits, while high-sodium foods to be avoided include salted meats, pickles, soy sauce, canned foods, and foods containing monosodium glutamate.

Healthy eating

Cirrhosis patients may experience malnutrition. They should consume plenty of fruits and vegetables, opt for lean protein sources such as legumes, poultry, or fish, and avoid consuming raw seafood.

Preventing infection

Cirrhosis patients are more susceptible to infections, so they should adopt good personal hygiene habits, such as frequent handwashing, and consider vaccinations against hepatitis A, hepatitis B, influenza, and pneumonia.

Careful use of medications

Consult a doctor before taking any medication and avoid using hepatotoxic drugs. Refrain from using unverified drugs, unregulated traditional Chinese remedies, and health supplements. Patients with insomnia should use sedatives cautiously. Antiviral drugs such as entecavir and tenofovir should not be stopped without medical advice, as doing so may lead to acute or chronic liver failure.

Viral hepatitis is the most common cause of cirrhosis. Studies show that hepatitis B and C viruses are independent risk factors for cirrhosis. Vaccination, avoiding high-risk behaviors for virus transmission, and early screening can prevent viral hepatitis infections and subsequent cirrhosis. Additionally, alcohol abuse is a significant cause of cirrhosis and should be avoided. Balancing diet, controlling weight, and maintaining a healthy lifestyle can also reduce the risk of cirrhosis.