Sự thay đổi đầu tiên là một xơ cứng của venules cổng thông tin tại vùng 1 của gan với những thay đổi lâm sàng của splenomegaly và cao huyết áp cổng thông tin. Sau đó các hiệp hội bao gồm angiosarcoma gan và gan peliosis. Thay đổi chỉ mang tính mô học sớm tiếp xúc với monomer | 348 Chapter 20 may enhance the toxicity of another for instance 6-mercaptopurine effects are worsened by doxorubicin. Long-term use of cytotoxic agents in recipients of renal transplants or in children with acute lymphatic leukaemia leads to chronic hepatitis fibrosis and portal hypertension. Arsenic The organic trivalent compounds are particularly poisonous. Arsenic trioxide 1 Fowler s solution given for long periods for the treatment of psoriasis has resulted in non-cirrhotic portal hypertension 100 . Acute probably homicidal arsenic poisoning can cause perisinusoidal fibrosis and VOD 66 . Arsenic in drinking water and native drugs in India may be related to idiopathic portal hypertension. The liver Fig. . Arsenic hepato-toxicity following treatment of psoriasis. Zone 1 is expanded by fibrosis and sclerosis of portal vein radicles. Mallory s trichrome stain. Peliosis hepatis Adenoma Portal zone Hepato-cellular carcinoma Fig. . Toxic effects of vinyl chloride arsenic and thorotrast on the liver. shows portal tract fibrosis and sclerosis of the portal vein branches fig. . Angiosarcoma is a complication. Vinyl chloride Workers exposed to vinyl chloride monomer over many years develop hepato-toxicity fig. . The earliest change is a sclerosis of portal venules in zone 1 of the liver with the clinical changes of splenomegaly and portal hypertension. Later associations include angiosarcoma of the liver and peliosis hepatis. Early histological alterations indicative of vinyl monomer exposure are focal hepato-cellular and focal mixed hepatocyte and sinusoidal cell hyperplasia. These are followed by sub-capsular portal and perisinusoidal fibrosis. Vitamin A Vitamin A is being increasingly used in dermatology by food faddists in cancer prevention and for hypogonadism. Toxicity develops with as little as 25 000 iu daily over 6 years or 50000iu daily for 2 years 42 . It is potentiated by alcohol abuse. The patient presents with nausea vomiting .
