R. N. M. Macsween

Histological grading and staging of chronic hepatitis

‘Armed Forces instifute of Pathology, Washington, USA, 2University of Lisbon. Lisbon, Portugal, -‘Hofstetten, Switzerland, 4Servizio di Anatomia e Istologia Patologica. Spedali Civili, Brescia, Italy, 5Department of Medicine, University of Leuven, Leaven, Belgium, 61nstitute for Pathology, University of Basel, Basel, Switzerland, 7Department of Pathology, University of Graz. Graz, Austria, 8Department of Pathology, University of Leuven, Leuven, Belgium. 9 Weiden, Germany, ‘ODepartment of Pathology, Western Infirmary, University of Glasgow, Glasgow, UK, “Department of Pathology, ~osp~talfor Sick Children, University of Toronto, Toronto, Canada, ~‘~nstitute of Liver Studies, King’s College Hospital, London, UK, 13Frederiksberg, Denmark, Is Watt, Switzerland, “Vienna, Austria

Breast cancer in women with primary biliary cirrhosis

melphalan. He required hospital admission on the occasions of his chemotherapy and for eight episodes of peritonitis related to the dialysis. The last four episodes of peritonitis were within two months of his death. Other than this he lived an independent life. He finally succumbed to a Gram negative septicaemia associated with myelosuppression and hypercalcaemia 55 months after presentation. We suggest that chronic dialysis should be offered to patients with myeloma on their individual merits rather than adopting the pessimistic view expressed by Dr Hamblin. A R MORTON AM HOLMES S WALDEK Departnment ofMedicine and Renal Unit, Hope Hospital, Salford M6 8HD

Hepatic vein lesions in alcoholic liver disease: retrospective biopsy and necropsy study.

Obliteration of the terminal hepatic venules with perivenular fibrosis (phlebosclerosis) is a well recognised feature in alcoholic liver disease. Veno-occlusive lesions with intimal obliteration of hepatic veins and a lymphocytic phlebitis of hepatic veins may also be present. We looked for these lesions in 256 liver biopsies and 50 livers obtained at necropsy from patients with alcoholic liver disease. Phlebosclerosis was a universal finding in alcoholic hepatitis and cirrhosis and showed increasing severity with progressive liver injury. Veno-occlusive lesions, however, were found in only 25 of 256 (9.8%) of biopsies and 11 of 50 (22%) of livers obtained at necropsy, showing alcoholic hepatitis or cirrhosis: lymphocytic phlebitis was found in 10 of 256 (3.9%) and two of 50 (4%), respectively. Moreover, veno-occlusive lesions were generally mild. The prevalence of veno-occlusive lesions and lymphocytic phlebitis was considerably less than has been previously documented. Phlebosclerosis may have a different mechanism and be a more important contributory factor in progressive liver injury.

Histopathology of portal hypertension: a practical guideline

T Roskams, A Baptista, L Bianchi, A Burt, F Callea, H Denk, J De Groote, V Desmet, S Hubscher, K Ishak, R MacSween, B Portmann, H Poulson, P Scheuer, L Terracciano & H Thaler Department of Pathology, K.U. Leuven, Leuven, Belgium, Hospital de Santa Maria, Lisboa, Portugal, University of Basel, Basel, Switzerland, University of Newcastle, Newcastle, UK, Spedali Civili of Brescia, Brescia, Italy, University of Graz, Graz, Austria, Department of Hepatology, K.U. Leuven, Leuven, Belgium, Department of Pathology, University of Birmingham, Birmingham, UK, Armed Forces Institute of Pathology, Washington, DC, USA, Department of Pathology, Western Infirmary, University of Glasgow, Glasgow and Institute of Liver Studies, Kings College Hospital, London, UK, Frederics Berg, Denmark, Department of Pathology, Royal Free Hospital, London, UK, and Wien, Austria

Hepatitis Bs antibody in alcoholic cirrhosis.

Sera from patients with chronic liver disease were tested for antibody against hepatitis B surface antigen by radioimmunoassay. The antibody was found in 25% of patients with alcoholic cirrhosis and in 52% when alcoholic cirrhosis was associated with portal hypertension, these results being significantly higher than in a matched control population. Other forms of chronic liver disease did not differ from the control population. Hepatitis B virus infection might be a factor in determining which alcoholic patients go on to develop chronic liver disease and cirrhosis.

Expression of tissue polypeptide antigen (TPA) in fetal and adult liver: changes in liver disease.

The distribution of tissue polypeptide antigen (40 kD molecular weight) in normal adult and fetal liver, and in liver disease was investigated and compared with the distribution of low and high molecular weight cytokeratins. In normal liver tissue polypeptide antigen was found only in bile duct epithelium; this distribution is similar to that of high molecular weight cytokeratin, but differs from that of low molecular weight cytokeratins. In liver disease it was found in areas of ductular transformation; in Mallorys bodies; and in alcoholic liver disease and primary biliary cirrhosis in some hepatocytes that did not contain Mallorys bodies.

Angiosarcoma of the liver in Great Britain, 1963-73.

Deaths attributed to primary angiosarcoma of the liver (ASL) in Great Britain between 1963-73 were reviewed by submitting available histological material to a panel of histopathologists and by obtaining full occupational and residential histories for the cases agreed as ASL by the panel. On average four recorded cases of ASL occurred a year, but in only one-third of the cases submitted did the panel agree with the original diagnosis. Only one of the agreed cases could be confidently associated with exposure to vinyl chloride.

An appraisal of the relationship between primary hepatocellular carcinoma and hepatitis B virus

The association between hepatitis B virus infection and primary hepatocellular carcinoma is reviewed. On the basis of serological and tissue examination there is a close link between virus infection and the tumour. While there is evidence to favour an oncogenic role for virus this is not conclusive, and other possible explanations for the relationship are discussed.

Serum glutamate dehydrogenase as a marker of hepatocyte necrosis in alcoholic liver disease.

Serum glutamate dehydrogenase concentration was assessed as a marker of the degree of hepatocyte necrosis found at liver biopsy in 95 patients suspected of having alcoholic liver disease. Although the serum concentration was raised in 54 patients, no relation between it and the severity of hepatocyte necrosis could be established. Glutamate dehydrogenase was therefore not confirmed to be a useful indicator of hepatocyte necrosis in patients with chronic alcoholism.

Unusual variant of primary sclerosing cholangitis.

Two cases of primary sclerosing cholangitis are described, in which the characteristic bile duct lesions were unusual because there was an exuberant and exaggerated fibrous replacement of the ducts which produced dense fibrotic scars in portal tracts.