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Título

Miller Fisher syndrome (MFS) associated with Hepatitis B virus (HBV) infection: a case report.

RESUMO

Case-report: A 55-year-old female presenting an acute onset of bilateral ptosis, ophthalmoparesis, bilateral fixed mydriasis, limb ataxia and neck pain. Serum serology demonstrated B virus antigen.A ENMG and CSF analysis were normal in the first week Because of the acute onset and pupil involvement, anti botulinum toxin serum was administered. However, in 3 days, the patient still presented worsening symptoms with new onset bulbar signs. Another CSF analysis identified protein-cytologic dissociation. Plasmapheresis was started suspecting MFS. Five sessions were performed and, after that, the patient improved from symptoms and remained in hospital for dysautonomia surveillance. Treatment with tenofovir was also initiated for Hepatitis B, considering the patient's clinical condition was an extrahepatic manifestation . Due to improvement of dysautonomia and neurological symptoms, the patient was discharged from hospital, after another ENMG, that showed typical signs of Miller Fisher Syndrome.
Discussion: In MFS there is an acute polyneuritis, characterized by a triad of areflexia, ophthalmoplegia and ataxia. These last two signs were present in the patient in question. Anti-ganglioside antibodies are found in CSF analysis of patients with MFS in more than 90% of cases. This anti-GQ1b inflicts immune-mediated damage on target tissue found in cranial nerves III, IV and VI, which causes the characteristic ophthalmoplegia. Plasmapheresis, and intravenous human immunoglobulin are first line treatments. There are few case-reports of Hepatitis B Virus and MFS association in literature, with no evidence of direct cause-effect correlation. However, Guillain Barre syndrome has been reported as extra hepatic manifestation of hepatitis B, with viral antigen present in CSF and nerve biopsy.

Final comments: The relative rarity of MFS and the variety of diagnoses make it difficult to plan and implement procedures and treatments. It is assumed that the anti-GQ1b antibody is the mediator of such syndrome. Thus, early recognition and prompt plasmapheresis therapy can decrease the severity and duration of the disease. Furthermore, there is still a need for unpublished treatments that are evidenced in terms of their effectiveness and availability.

Palavras Chave

Miller Fisher Syndrome, Hepatitis B