bubble_chart Overview

Schistosomiasis-induced liver cirrhosis occurs in the advanced stage of schistosomiasis and is caused by the massive deposition of eggs.

bubble_chart Epidemiology

The schistosomiasis prevalent in our country is caused by Schistosoma japonicum.

bubble_chart Pathogenesis

The adult Chinese Taxillus Herb in the portal venous system causes lesions not due to the toxins secreted by the adult worms or the dead worms themselves, but rather due to the massive deposition of eggs. The eggs deposited in liver tissue form embryos within six days after being laid. Immature eggs elicit only very mild reactions, while mature eggs become surrounded by lymphocytes, macrophages, eosinophils, neutrophils, and plasma cells. These gradually develop into epithelioid cells, then fibroblasts. After the death of the miracidia inside the eggs, they gradually form pseudosubcutaneous nodules, which are eventually absorbed, leading to fibrous nodules and ultimately progressing to fibrosis.

bubble_chart Pathological Changes

Schistosomal cirrhosis occurs in the advanced stage of schistosomiasis, where a large number of eggs are deposited in the liver, particularly around the small branches of the portal vein system. This leads to fibrosis around the portal vein branches, especially the second, third, and fourth-order branches, resulting in so-called pipe-stem cirrhosis. Cross-sections show white fibrous masses of varying sizes surrounding the portal branches. Severe fibrosis can cause branch occlusion, and the contraction of these masses may deform the liver. The liver surface exhibits characteristic irregular grooves and uneven contours with indistinct boundaries. Since the main blood supply to the hepatic acinus comes from the small branches of the portal vein, poor blood supply can lead to hepatocyte atrophy, fatty degeneration, and nonspecific degeneration, with collapse of hepatic lobules and formation of fibrous septa. Some argue that although portal blood flow into the sinusoids is obstructed, causing portal hypertension, hepatic arterial flow can still enter the sinusoids, maintaining the blood supply and nutrition to the lobules. As a result, the hepatic lobules remain intact, and hepatocyte damage is minimal. The precise definition of cirrhosis involves hepatocyte degeneration and necrosis, residual hepatocytes forming regenerative nodules, collapse of the reticular protein scaffold, and connective tissue proliferation forming fibrous septa, ultimately destroying the original lobular structure and forming pseudolobules. From this perspective, some believe schistosomiasis only causes hepatic fibrosis.

bubble_chart Clinical Manifestations

Schistosomiasis-induced cirrhosis often presents with portal hypertension, which can lead to esophageal and gastric variceal bleeding. The degree of splenomegaly is more severe compared to post-hepatitis cirrhosis. In advanced stages, malnutrition exacerbates hepatocyte damage, manifesting as ascites and other signs of liver failure. Hypersplenism is associated with portal hypertension, splenic congestion, reduced blood flow, and the phagocytosis of blood cells by the mononuclear-macrophage system, resulting in pancytopenia.

bubble_chart Diagnosis

Diagnosis relies on medical history and physical examination. Type B ultrasound has special diagnostic significance, with its characteristic manifestation being a fibrous reticular image featuring rectangular linear fibrous structures.

bubble_chart Treatment Measures

1. Etiological treatment. Praziquantel is the drug of choice, as it offers high efficacy, short treatment duration, few adverse reactions, convenient administration, and broad-spectrum anti-parasitic activity. After oral administration, the drug is primarily absorbed from the intestines, reaching peak blood concentration within 30 minutes to 1 hour. The concentration in the portal vein is approximately 10 times higher than in peripheral blood, with the highest concentration found in the liver. It is metabolized in the liver and excreted via bile and urine, with no cumulative effect. The parasites die rapidly upon contact with the drug. Stool examinations typically turn negative about 2 weeks after medication. The adult dosage is 30 mg/kg per day, divided into three oral doses, for 2 consecutive days, with a total dose of 60 mg/kg. Alternatively, a single oral dose of 40–60 mg/kg may be administered. For mild cases, a single dose of 40 mg/kg is effective. The drug has no effect on the heart, liver, or kidneys but may cause dizziness, headache, lack of strength, and grade I abdominal pain. These symptoms usually appear about 1 hour after administration and resolve quickly after discontinuation, requiring no treatment. Rarely, syncope, mental disorders, hysteria or epileptic seizures, ataxia, frequent premature beats, bradycardia, atrial fibrillation, rash, etc., may occur.

2. Treatment of portal hypertension. Splenectomy may be considered for patients with massive splenomegaly. For recurrent bleeding due to esophageal varices, portosystemic shunt surgery or esophageal transection with gastric variceal ligation and stripping may be performed. Some advocate distal splenorenal shunt surgery, as it results in a lower incidence of encephalopathy and prevents parasite eggs from entering systemic circulation. Endoscopic sclerotherapy, propranolol, and calcium channel blockers can help prevent rebleeding from esophageal varices.

3. Treatment of complications, including ascites, hepatic encephalopathy, and spontaneous bacterial peritonitis.