Cohort study of internal malignancy in genetic hemochromatosis and other chronic nonalcoholic liver diseases.

The risk of hepatocellular carcinoma (HCC) and other internal malignancies was examined in patients with genetic hemochromatosis (GH) by following 208 patients from the time of diagnosis to June 1983 and by comparing the numbers of cancers they developed with expected values constructed from cancer registry incidence data by means of actuarial methods. In addition, cancers occurring in a comparison group of 148 subjects with other chronic nonalcoholic liver diseases (CLD) were determined. Among the GH group, 16 new cases of HCC occurred subsequent to the diagnosis of GH, together with 8 other malignancies. The 16 cases of HCC reflect a 200-fold excess risk, which from all indications represents the first quantitation of the risk of this tumor in GH. There appears to be no increased risk of other malignancies in this disease. Among the CLD group only 1 HCC and 1 other malignancy occurred.

Chronic hepatitis. Aetiology and current management.

The entity of chronic hepatitis has long been an enigma, and its treatment confusing. Recent studies have indicated the importance of excluding causes such as drugs, Wilson's disease and alpha 1-antitrypsin deficiency. After excluding such causes, there are 3 major groups--'autoimmune', hepatitis B, and non-A, non-B (NANB) in all of which an immunological basis for pathogenesis exists. The autoimmune group has been subdivided into a milder type (chronic persistent hepatitis) and a more severe type (chronic active hepatitis) on histological grounds. Corticosteroids are indicated in chronic active hepatitis if cirrhosis or bridging necrosis is present. However, corticosteroids are contraindicated in disease due to the hepatitis B virus where chronic active hepatitis correlates with the presence of replicating virus (serum positive for e antigen, DNA polymerase and HBV-DNA), and in such cases antiviral agents and immunomodulation are being studied. Very little is known about NANB hepatitis in the absence of an assay and there may be more than a single agent. In hepatitis B, the development of serological markers, molecular probes (HBV-DNA), natural animal hepatitis with near-identical viruses, and delta antigen (a virus requiring co-infection with hepatitis B) have all extended our knowledge so dramatically that it is hoped that the enigma of chronic hepatitis will be solved when an assay for NANB hepatitis becomes available.

Pyogenic liver abscess--a neglected diagnosis.

Twenty-five patients with pyogenic liver abscess admitted to the Royal Brisbane Hospital between 1970 and 1982 have been reviewed. The mortality rate was 32%; however, all patients who were diagnosed before death survived. In seven patients there was a history of biliary obstruction or biliary surgery of whom six died. The mean age of the patients who died was significantly higher than those surviving and it is suggested that this resulted from overdiagnosis of malignancy in the elderly, some hesitancy in investigating older patients, and a tendency to attribute multiple space-filling defects to metastatic tumour. If liver biopsy or even exploratory laparotomy have failed to confirm the diagnosis of hepatic abscess the clinician should not discard the possibility. It is concluded that the continuing high mortality from liver abscess is in large part due to lack of clinical awareness and failure in diagnosis rather than to inadequate therapy.

Are the causes and presentation of chronic hepatitis changing? An analysis of 104 cases over 15 years.

We describe the features at presentation of 104 patients with biopsy-proven chronic hepatitis who presented in Brisbane in the period 1968-32. The mean period of follow-up was 59 months. Sex ratio (female : male) was 70 : 34 and the mean age was 37 years (range 3-83). Eighty-five (82 per cent) were born in Australia. Serological evidence of hepatitis B (HBV) infection was present in 24 (23 per cent). Analysis of the HBV marker positive and negative (non-B) groups revealed that the clinical and laboratory features of HBsAg positive chronic hepatitis were much less florid than those of non-B patients. However, the disturbances seen in hepatic histopathology were similar in severity, and the mortality in the HBsAg positive group exceeded that in the non-B group. The relative risk calculated on an actuarial basis was higher in HBsAg positive patients. In contrast to the experience of others, severe chronic active hepatitis remains an important problem in Brisbane but some features of the disease are altering. Several changes may be attributable to the increasing incidence of HBV-associated disease, and in addition, patients aged under 20 with non-B chronic hepatitis are now rarely seen. This is of interest in view of recent reports of decreased incidence of another disease of disordered immune response, rheumatoid arthritis.

The prognosis of chronic active hepatitis without cirrhosis in relation to bridging necrosis.

Sixty-nine patients with chronic active hepatitis without cirrhosis were studied to define the prognostic implications of bridging necrosis of various types. There were 19 patients without bridging necrosis compared with 50 patients with bridging necrosis. The two groups did not differ significantly at presentation in age, sex, clinical or laboratory features. In the group without bridging necrosis, no patient died from the disease and none of 13 having a later biopsy developed cirrhosis. In the group with bridging necrosis, one patient died from hepatic failure and 7 of 36 developed cirrhosis (19%). When analyzed statistically, a significant (p less than 0.05) relationship is seen between increasing severity of initial lesion and the subsequent development of cirrhosis. It is concluded that patients with piecemeal necrosis without bridging should not be grouped together with patients with bridging necrosis or cirrhosis when considering management decisions.