In a hospital-based study from England, antiHelicobacter pylori ( H.p ylori) IgG antibodies were found in 13.6 % of children presenting with recurrent abdominal pain; however, on endoscopy, only 64 % of them were found to have H. pylori gastritis [2]. We present an interesting association of H. pylori gastritis and autoimmune hepatitis in a 13-year-old patient. A 13-year-old girl was referred to our Centre with an acute onset of jaundice. There was no history of blood transfusion or recent exposure to drugs or toxins. Apart from jaundice and mild hepatomegaly, clinical examination was unremarkable. Her blood investigations showed a conjugated hyperbilirubinaemia of 71 lmol/l with ALT and AST levels of 572 IU/l and 909 IU/l respectively, a gamma-glutamyl transpeptidase activity of 52 IU/l and a slightly deranged clotting profile (INR 1.64). She had negative hepatitis A, B, C and Epstein Barr virus screens and normal serum coeruloplasmin and alpha-1-antitrypsin levels and phenotype. An autoantibody screen was positive for antinuclear and smooth muscle antibodies (a titre of 1:640 for both) and the antidouble stranded DNA antibody level was 10 IU/ml (normal value <7 IU/ml). A serum immunoglobulin (Ig) profile showed raised total IgG and IgA levels of 40.5 g/l (reference range 6.26–13.9 g/l) and 3.64 g/l (reference range 0.39–2.52 g/l) respectively. IgG subclasses showed elevated IgG1 and IgG3 of 36.8 g/l (reference range 3.47–9.93 g/l) and 1.27 g/l (reference range 0.23–1.17 g/l) respectively. Ultrasonographic examination of the liver was normal and there was no evidence of ascites. A liver biopsy and oesophagogastroduodenoscopy were performed under general anaesthesia. There was evidence of duodenitis in the duodenal bulb (markedly erythematous and oedematous mucosa with no evidence of ulceration) and CLO test, routine histopathology and culture all indicated H. pylori colonisation. The liver histopathology showed plasma cell, lymphocyte and eosinophil infiltration in the portal tracts with prominent interface hepatitis and evidence of hepatocyte necrosis, regeneration, fibrosis and rosette formation consistent with autoimmune hepatitis. Unfortunately, we were unable to do PCR for H. pylori on the liver biopsy. She was given antiH. pylori triple therapy (amoxicillin, metronidazole and omeprazole) for 2 weeks and started on steroid and azathioprine for autoimmune hepatitis. A few weeks later, she was much better. She had a negative urea-breath test indicating H. pylori eradication and her ALT and AST levels improved (62 and 60 IU/l respectively) with a normal bilirubin of 11 lmol/l. The prevalence of serum antibodies to non-gastric Helicobacter species was significantly higher in patients with autoimmune chronic liver disease than in healthy blood donors [4]. Infection with Helicobacter hepaticus causes chronic hepatitis and hepatocellular carcinoma (HCC) in mice and H. pylori genomic sequences have been demonstrated in the liver of patients with cirrhosis. In a small adult case-control study from Italy, seroprevalence of antibodies to H. pylori was higher in patients with HCC than in controls (78.2% compared to 54%, P <0.05) [3]. In another adult study from the same Centre, the prevalence of H. pylori antibodies was higher in patients with autoimmune hepatitis compared to controls, but the difference was not statistically significant (64.5% compared to 53.2%, P =0.3). In both studies, infection with H. pylori was not confirmed by endoscopy. As autoimmunity is a feature of H. pylori [1], larger studies are needed to examine the role of H. pylori in the aetiology of autoimmune hepatitis. W. El-Matary (&) AE A. M. Dalzell Gastroenterology Unit, Royal Liverpool Children’s NHS Trust, Alder Hey, Eaton Road, L12 2AP Liverpool, UK E-mail: welmatary@yahoo.com Tel.: +44-151-2284811 Fax: +44-151-2280383