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P651 Transient acute cerebellitis with hepatitis a virus infection in a 3 years old child on nitrofurantoin prophylaxis

Background Hepatitis A Virus (HAV) Infection is prevalent worldwide. HAV is well known to cause extra hepatic involvement by autoimmune mechanisms. This case highlights the importance of how two autoimmune inciting factors working together could lead to transient cerebellitis, which has not been reported in association with either of them singly. Case report A three year old female child presented with gait imbalance and jaundice for last three days. She had visited her GP two weeks previously with complaints of mild fever, vomiting and diarrhoea which had resolved with oral rehydration in a week time. She had also complained of mild upper abdominal pain in last 2 days. She had suffered 2 episodes of urinary tract infection in recent past and her GP had commenced her on nitrofurantoin prophylaxis since last 3 months. DMSA scan of the kidney was due in a month time. Past history was not relevant and had no sick contacts in recent past. Examination revealed jaundice and tender right upper quadrant of the abdomen. Neurological examination revealed wide based mildly ataxic gait with past pointing of left hand on cerebellar examination. Rest of the neurological and other systemic examination were within normal limits. Blood tests revealed normal full blood counts, electrolytes and inflammatory markers. Liver function tests (LFT) was deranged with total bilirubin 52 micromole/L, conjugated bilirubin 20micromol/L, GGT 36 IU/L, ALP 140 IU/L, ALT 74, AST 60 and Albumin 38. Prothrombin time and INR were within normal limits. Ultrasound of the abdomen revealed mildly echogenic liver suggestive of acute inflammatory changes with slightly oedematous gall bladder wall. MRI of the brain revealed small hyper intense signal in the right cerebellar hemisphere. Blood tests for viral serology were positive for anti HAV IgM antibody. Diagnosis of hepatitis A virus infection with cerebellitis was made based on all these results. Subsequently nitrofurantoin was stopped and she was treated conservatively. LFT was repeated weekly which normalized completely within next three weeks and her ataxic gait improved gradually. Conclusion Nitrofurantoin has been linked in past with autoimmune organ injury. Transient cerebellitis has well been associated with several infections and autoimmune processes. Neither Nitrofurantoin nor HAV in isolation has been reported to cause cerebellitis. Barring the possibility of chance association, this case adds to the medical literature, the association of cerebellitis with HAV infection in isolation or in combination with concomitant autoimmune triggering factors such as medication.