The aim of this study was to perform a meta-analysis of controlled clinical trials of glucocorticoid treatment in clinical alcoholic hepatitis, adjusting for prognostic variables and their possible interaction with therapy, because these trials have given appreciably different results. Weighted logistic regression analysis was applied using the summarised descriptive data (for example, % with encephalopathy, mean bilirubin value) of the treatment and control groups of 12 controlled trials that gave this information. Despite evidence of publication bias favouring glucocorticoid treatment, its overall effect on mortality was not statistically significant (p = 0.20)--the relative risk (steroid/control) was 0.78 (95% confidence intervals 0.51, 1.18). There was indication of interaction between glucocorticoid therapy and gender, but not encephalopathy. Thus, the effect of glucocorticoid treatment may be different (beneficial or harmful) in special patient subgroups. These results do not support the routine use of glucocorticoids in patients with alcoholic hepatitis, including those with encephalopathy. Whether other subgroups may benefit needs further investigation using the individual patient data from the published trials and testing in new randomised trials.

Susceptibility to primary biliary cirrhosis (PBC) may be partly inherited although instances of PBC within families are only infrequently described. The records of 736 patients with PBC seen over a 25 year period were examined to identify those with a positive family history. Ten patients originating from eight families were identified, giving a frequency of 1.33%. They comprised mother and daughter pairs; in two families both mother and daughter had been seen at our clinic. The daughters presented at an earlier age, median 36 years (range 24-54), than the mothers, 52 years (50-81). During follow up one daughter (45 years) and six mothers have died (range 53-81 years) and two mothers and one daughter have had a transplant aged 57, 57, and 30 years respectively. It is concluded that familial PBC is not rare, that it is related to maternally inherited factors, and that disease tends to present earlier in the second generation.

A 51 year old woman with a two year history of ulcerative colitis developed a wide spread gastrointestinal non-Hodgkin's lymphoma of low grade malignancy (MALT-lymphoma) involving upper and lower gastrointestinal tract, spleen, and bone marrow. After chemotherapy, clinical symptoms improved and lymphocytic infiltrates disappeared. Thirty nine cases of ulcerative colitis and 22 cases of Crohn's disease complicated by gastrointestinal lymphomas reported in published works are reviewed. In inflammatory bowel diseases any dense lymphocytic infiltrates seen in biopsy specimens obtained from ulcerative colitis or Crohn's disease should be assessed to exclude gastrointestinal lymphoma.

A case of a middle aged woman with weight loss, ascites, and a pleural effusion is presented where a clinical diagnosis of ovarian cancer was made. Her CA 125 was greatly increased at 873 IU/ml and the ascites was a lymphocytic exudate but cytology failed to show malignant cells. Operative biopsy showed numerous noncaseating granulomas in the omentum but no mycobacterial organisms were seen. Empiric antituberculous treatment was started before positive culture results were received and when treatment had ended both the ascites and pleural effusion had resolved and the CA 125 had fallen to 7 IU/ml. Review of published works showed several other examples of tuberculous peritonitis associated with increased CA 125 and the possible cause of raised CA 125 in this condition is discussed.

Continued bleeding or early rebleeding is associated with a poor prognosis in patients with variceal haemorrhage. It is not clear why bleeding stops in some patients and continues or restarts in others. It is suggested that secondary haemodynamic changes in the splanchnic circulation after a bleed may contribute to the risk of further bleeding. These changes include the effects of hypotension on portocollateral resistance, the effects of blood in the gut on splanchnic blood flow, and the effects of blood volume expansion on portal venous pressure during resuscitation. These factors, working in concert, cause a secondary rise in portal venous pressure, which may precipitate further bleeding. Treatment aimed at preventing these secondary haemodynamic changes may be beneficial. It is probable that somatostatin and octreotide could act in this way, which may explain their therapeutic efficacy.