Acute abducens nerve palsy

Abstract

PAEDIATRICS AND CHILD HEALTH 17:10 42 12–84 μg/g). There was no evidence of significant iron deposition, nor did he have evidence of fatty liver. Further autoantibody profiling (Institute of Liver Studies, King’s College London) for antibodies implicated in cryptogenic autoimmune hepatitis demonstrated negative anti-liver cytosol type 1 (anti-LC1) and anti SLA/LP antibodies. On the basis of these results, a diagnosis of seronegative autoimmune hepatitis was made. He was commenced on 40 mg prednisolone, with a subsequent improvement in his liver function. This improvement was not sustained, which necessitated the introduction of azathioprine and finally mycophenolate mofetil before normalisation of LFTs. Conclusions: It has been proposed that a GFD is ‘protective’ against the development of autoimmune disease, but this and other cases described in the literature demonstrate that autoimmune hepatitis can occur after GFD has been commenced – in our case, the ALT changes were seen a year after gluten had been discontinued and having previously been normal. By using screening LFTs, we may well have avoided this patient developing cirrhosis, liver failure and subsequent liver transplant.