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The pathological findings are described in three cases of infectious canine hepatitis in free-ranging red foxes (Vulpes vulpes) in England. The foxes died after short periods of clinical illness. Mild jaundice and hepatic congestion were evident grossly. On histopathological examination, intranuclear inclusion bodies were visible in hepatocytes, in association with hepatocyte dissociation and necrosis, as well as in renal glomeruli, renal tubular epithelial cells and vascular endothelial cells. Canine adenovirus type 1 (CAV-1) was isolated from all three foxes. In a serological study, antibodies to CAV-1 were detected in tissue fluid extracts taken from 11 of 58 (19 per cent) frozen red fox carcases from England and Scotland.

Acetaminophen-induced liver injury (AILI) is a significant health problem and represents the most frequent cause of drug-induced liver failure in the United States. The development and implementation of successful therapeutic intervention strategies have been demanding, due to significant limitations associated with the current treatment for AILI. Lactoferrin (Lac), a glycoprotein present in milk, has been demonstrated to possess a multitude of biological functions. Our study demonstrated a profound protective effect of Lac in a murine model of AILI, which was not dependent on its iron binding ability, inhibition of acetaminophen (APAP) metabolism, or a direct cytoprotective effect on hepatocytes. Instead, Lac treatment significantly attenuated APAP-induced liver sinusoidal endothelial cell dysfunction and ameliorated hepatic microcirculation disorder. This protective effect of Lac appeared to be dependent on hepatic resident macrophages (Kupffer cells, KC). Collectively, our data indicated that Lac, through activation of KC, inhibited APAP-induced liver sinusoidal endothelial cell damage and improved hepatic congestion, thereby protecting against AILI. These findings reveal the significant therapeutic potential of Lac during AILI and other types of liver diseases.

Secondary tricuspid regurgitation is a common finding in dilated cardiomyopathy, being present in up to 90% of patients studied with Doppler echocardiography. It appears to be primarily due to annular dilatation and loss of the sphincter-like action of the tricuspid annulus during systole. Apical displacement of the papillary muscle and increased chordal tension may also contribute to mal-coaptation of the tricuspid leaflets in systole. Hepatic pulsations generally occur late in dilated cardiomyopathy, indicating hepatic congestion due to progressive biventricular failure. These are thought to result from secondary tricuspid regurgitation and transmission of the regurgitant v wave to the liver. Careful pulsed-Doppler studies of the timing of hepatic pulsations in dilated cardiomyopathy often show them to be presystolic, rather than systolic, suggesting that a mechanism other than tricuspid regurgitation may be responsible. (ECHOCARDIOGRAPHY, Volume 8, March 1991)

The features of hepatic congestion on computed tomography, ultrasound and nuclear medicine sulphur colloid scans have been reviewed. Hepatic congestion may not be appreciated clinically, especially in the elderly, but the features described should be sufficiently characteristic to establish the diagnosis. The CT appearance may be confused with neoplastic infiltration, so that recognition of the condition may avoid further unnecessary investigations.