Liver disease ischemic hepatitis

Contraindications to treatment include autoimmune hepatitis, decompensated liver disease, women who are pregnant or patients whose female partners are pregnant, hemoglobinopathies, creatinine clearance <50 mL/ min, hemodialysis, or ischemic cardiovascular or cerebrovascular disease. 

A 39-year-old woman developed idiopathic thrombosis of the posterior tibial vein. Oral contraceptives and resistance to activated protein C were identified as risk factors. After initial treatment with intravenous heparin, she was given phenprocoumon and the oral contraceptive was withdrawn. After 4 months she developed subacute liver failure and phenprocoumon was withdrawn immediately. Autoimmune disease, viral hepatitis, toxic causes, and Budd-Chiari syndrome were excluded. Despite symptomatic treatment, she deteriorated further and orthotopic liver transplantation was performed. Histopathology of the explanted liver further excluded ischemic Uver cell necrosis and Budd-Chiari syndrome. 

Santra S, McKiernan P, Lander A, Dalzell AM, Baillie C, Beath S, Gupte GL. Ischemic hepatitis is a risk factor for progression of liver disease associated with parenteral nutrition in intestinal failure. J Pediatr Gastroenterol Nutr 2008 47(3) 367-9. 

Occasionally toxic compounds can directly damage the hepatic sinusoids and capillaries. One such toxic compound is monocrotaline, a naturally occurring pyrrolozidine alkaloid, found in certain plants (Heliotropium, Senecio, and Crotolaria species). Monocrotaline (Fig. 7.7) is metabolized to a reactive metabolite, which is directly cytotoxic to the sinusoidal and endothelial cells, causing damage and occlusion of the lumen. The blood flow in the liver is therefore reduced and ischemic damage to the hepatocytes ensues. Centrilobular necrosis results, and the venous return to the liver is blocked. Hence, this is known as veno-occlusive disease and results in extensive alteration in hepatic vasculature and function. Chronic exposure causes cirrhosis. 

The existence and the extent of glucose production from the small intestine, the muscle and the brain, therefore continues to be a matter of debate. Any advancement in this field, however, will have the potential to change the way we consider the concept of liver and kidney reciprocity, the physiological response to exercise and to feeding, and the pathogenesis of many conditions like diabetes, hypoglycecemia, liver and hepatic failure, ischemic and nerrrodegenerative diseases. 

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