Presence of alcoholic steatohepatitis, but no selective histological feature, indicates an increased risk of cirrhosis and premature death

Abstract

Objective: The prognostic impact of early stages of histologically confirmed alcoholic liver disease is uncertain. Our aim was to determine the risk of cirrhosis and premature death, and identify prognostic markers, in patients with biopsy-proven alcoholic steatohepatitis – and to compare prognosis in patients with alcoholic pure fatty liver and the general population.

Material and methods: Patients with biopsy-proven alcoholic fatty liver disease diagnosed during 1976–1987 were identified. Data were collected from medical records, the Danish National Patient Registry and the Registry of Causes of Death. All biopsies were re-examined and morphological findings assessed. A reference cohort matched for age and gender was created. Cox proportional hazard models adjusted for age and gender were used to analyse differences in mortality and cirrhosis development, as well as the prognostic impact of histological and biochemical parameters.

Results: Two hundred and twenty-five patients with fatty liver and 111 with steatohepatitis were followed for median 13 and 9.7 years, respectively. There was a significantly higher risk of developing cirrhosis amongst patients with steatohepatitis compared to both patients with fatty liver (p < 0.001) and the reference cohort (p < 0.001). Mortality was significantly higher in patients with steatohepatitis compared to patients with fatty liver (p = 0.046) and the general population (p < 0.001). No histological or biochemical parameters with prognostic significance for mortality were identified.

Conclusion: Presence of steatohepatitis indicates an increased risk of cirrhosis and premature death. However, none of the histological parameters defining steatohepatitis can independently identify patients at risk for premature death.

keywords:

• Alcoholic fatty liver
• alcoholic liver disease
• alcoholic steatohepatitis
• cirrhosis
• prognosis

Disclosure statement

None to declare.

Funding information

The corresponding author has received funding from the Research Council at Hvidovre Hospital as well as from the ‘Hvidovre Hospital Foundation for the Study of Liver Disease’.