Table 2.

Factors predictive of poor outcome in autoimmune hepatitis.

	At presentation	During the treatment phase	On treatment withdrawal
Relapse when off treatment (50–90% of patients)	Prolonged symptomatic course Anti-LKM-1 positive* Anti-SLA/LP positive Nonconventional antibodies (anti-ASPGR, chromatin) Male sex HLA DRB1*03	Treatment nonadherence Short treatment duration Prolonged time to achieve remission Persistent portal inflammation or interface hepatitis Azathioprine-free maintenance regimens	Increasing duration since stopping treatment (50% relapse at 6 months; 80% at 3 years)
Progressive fibrosis/cirrhosis (10–50%)	Hypoalbuminaemia$ Coagulopathy$ Confluent necrosis	Treatment nonadherence Persistent inflammatory change on biopsy Increasing time to biochemical remission (>24 months) Persistently abnormal liver biochemistry Number of relapses per decade (>4)	Multiple relapses (38% progress to cirrhosis)
Liver-related death or OLT (10–20%)	Fulminant presentation Confluent necrosis Cirrhosis Female sex Anti-LKM-1, LC-1 or SLA/LP positive	Treatment nonadherence Poor responders (failure of transaminases to fall after 6 months; persistently raised ALT or AST) Frequent relapses Nontreatment with azathioprine	Multiple relapses Development of cirrhosis

Modified from Gleeson et al. [2011].

^*Relapse is near universal in type-II/anti-LKM-1 positive patients without corticosteroids, and these patients often require low-dose, maintenance prednisolone.

^$May reflect the presence of cirrhosis at baseline rather than risk of development.

ALT, alanine transaminase; ASPGR, asialoglycoprotein receptor; AST, aspartate transaminase; LC, liver cytosol; HLA, human leukocyte antigen; LKM, liver kidney microsomal; SLA/LP, soluble liver/pancreas antigen.