• 1 January 1982
    • journal article
    • research article
    • Vol. 83  (4) , 786-796
Abstract
The nature and significance of vascular lesions in alcoholic liver disease were studied in 200 autopsies. Principal types of lesions were recognized: lymphocytic phlebitis, consisting of a chronic inflammatory cell infiltrate of the wall of terminal hepatic venules (central veins) or intercalated (sublobular) veins, was noted in 16.7% of patients with precirrhotic alcoholic hepatitis and 4.3% of patients with cirrhosis, phlebosclerosis, consisting of perivenular scarring with gradual obliteration of the lumen of terminal hepatic venules and sometimes intercalated veins was found to some degree in all patients with alcoholic hepatitis or cirrhosis and veno-occlusive lesions, consisting of intimal proliferation, fibrosis and narrowing of the lumen of terminal hepatic venules, intercalated veins and occasionally portal veins were found in 52.1% of cases of precirrhotic alcoholic hepatitis with total occlusion of some terminal hepatic venules or intercalated veins, or both, in 14.6%. In alcoholic cirrhosis, veno-occlusive lesions were present to some degree in 74.1% with totally occluded vessels found in 46.8%. Evidence of portal hypertension was present in 47.9% of patients with precirrhotic alcoholic hepatitis and was significantly associated with the degree of veno-occlusive change and phlebosclerosis, which tend to occur together. Veno-occlusive lesions and phlebosclerosis contributed to the development of portal hypertension in alcoholic liver disease. Veno-occlusive lesions in the cirrhotic liver may have contributed to atrophy, with loss of functioning parenchyma. The etiopathogenesis of the vascular lesions in alcoholic liver disease requires further investigation.