An unusual pattern of delayed enhancement in a patient with a focal hepatic defect due to amyloidosis is presented. Without the aid of region-of-interest density measurements, the lesion was not appreciated on unenhanced computed tomography scans

The effect of cholestyramine and bile acid feeding upon fecal, red blood cell, and plasma protoporphyrin levels was evaluated in a patient with erythropoietic protoporphyria and evidence of hepatic damage. After a basal period on a controlled diet, bile acids alone were administered (300-900 mg) daily for 9 days, followed by cholestyramine (12 g) plus bile acids (900 mg) daily for 7 days, and cholestyramine alone (12 g) daily for 6 days. There was no substantial change in either the red blood cell or plasma protoporphyrin concentrations during any treatment period. However, cholestyramine and cholestyramine combined with bile acids caused a threefold increase in fecal protoporphyrin excretion, whereas bile acids alone had no effect in this regard. After 1 yr of cholestyramine therapy, fecal excretion of protoporphyrin remained elevated with concurrent improvement in liver function tests and photosensitivity. This study indicates that cholestyramine but not bile acids can substantially increase protoporphyrin excretion and therefore may be capable of ameliorating the hepatotoxicity that may occur in selected patients with erythropoietic protoporphyria.

Rats were given intravenous injections of either physiologic saline or trypan blue dye suspended in saline. After 24 hours, the livers of these animals were sampled for light and electron microscopic study. The livers of the saline treated rats showed no morphologic alterations. The livers of the trypan blue injected animals exhibited no structural abnormalities in the hepatic parenchymal cells, but their sinusoidal lining cells were hypertrophied, mainly due to the appearance of numerous phagosomes, increased quantities of rough endoplasmic reticulum, and prominent Golgi zones.