Acute onset distal symmetrical vasculitic polyneuropathy associated with acute hepatitis B Manmohan Mehndiratta a , Sanjay Pandey a , Rajeev Nayak a,⇑ , Ravindra K. Saran b a Department of Neurology, Room 511, Academic Block, G.B. Pant Hospital, J.L.N. Marg, New Delhi-2 110002, India b Department of Pathology, G.B. Pant Hospital, New Delhi, India article info Article history: Received 6 January 2012 Accepted 3 March 2012 Keywords: Extrahepatic manifestations Hepatitis B Mononeuritis multiplex Neuropathy Vasculitis abstract Hepatitis B can have varied extrahepatic manifestations involving the skin, renal, haematological and nervous systems. Neurological manifestations in hepatitis B may take the form of Guillain-Barré syn- drome and secondary systemic vasculitis-related mononeuritis multiplex. The clinical course of hepa- titis B-related, vasculitis-related neuropathy is usually subacute to chronic and clinical evolution is relatively benign. To our knowledge, acute hepatitis B-associated vasculitis manifesting as acute distal symmetric polyneuropathy has not been reported. We report a 60-year-old man who presented with fever, mild hepatomegaly, skin lesions in the form of non-palpable purpura and acute onset distal sym- metric sensorimotor polyneuropathy. Serum transaminase levels were raised and viral serological markers revealed acute hepatitis B. The patient remained anicteric throughout his clinical course. Nerve conduction studies showed severe axonal sensorimotor polyneuropathy and histopathological examina- tion of sural nerve biopsy was suggestive of vasculitic neuropathy. The patient was first given a course of intravenous immunoglobulin with the antiviral drug entecavir. The fever subsided after 1 week of treatment. The patient was started on prednisolone in addition to the entecavir, and showed significant improvement in motor power and marked resolution in paresthesia after 2 weeks of treatment. Thus, acute onset distal symmetric sensorimotor polyneuropathy of vasculitic etiology can be a manifestation of acute hepatitis B. Ó 2012 Elsevier Ltd. All rights reserved. 1. Introduction Hepatitis B can have varied extrahepatic manifestations involv- ing the skin, renal, haematological and nervous systems. Neurolog- ical manifestations in the form of Guillain-Barré syndrome (GBS) and secondary systemic vasculitis-related mononeuritis multiplex have been well reported. 1–4 We report a patient with hepatitis B virus (HBV)-associated acute distal symmetric sensorimotor vascu- litic polyneuropathy. Although rare, peripheral neuropathy is an important, and often the only, presenting clinical feature of HBV- associated vasculitis. Its recognition can be important for early diagnosis because the clinical outcome may be influenced by early therapeutic intervention. 2. Case report A 60-year-old man without any premorbid illness presented with a 1 week history of intermittent high grade fever, and acute onset motor weakness, paresthesias and marked diffuse sensory loss of all modalities in both hands and feet. The symptoms pro- gressed rapidly within 5 days in a distal symmetrical pattern. The fever continued even after progression to maximal deficit. Initially he denied having any pain, but subsequently developed severe burning paresthesias. He was a known smoker and occa- sionally consumed alcohol. There was no history of drug or toxin exposure, or any recent vaccination. His general examination re- vealed non-palpable, non-tender purpuric skin lesions over both legs (Fig. 1C). His systemic blood pressure was normal. Neuro- logical examination was suggestive of severe weakness (muscle power, Medical Research Council [MRC] grade 0/5) of bilateral wrist dorsiflexors, palmer flexors and small muscles of the hands. Examination in the lower limbs showed weakness (mus- cle power MRC grade 0/5) of bilateral ankle dorsiflexors, planter flexors and toe weakness. Muscle strength at shoulder, elbow, hip, and knee was normal in all groups of muscles. Supinator and ankle jerks were absent and the rest of the deep tendon re- flexes were normal. Sensory examination demonstrated sensory loss for touch, pain, temperature, joint position and vibration sense in the upper limbs up to the wrist and up to the ankle in lower extremities. Abdominal, chest and cardiovascular sys- tem examination was within normal limits. Hematological investigations revealed high erythrocyte sedi- mentation rate (60 mm at the end of the first hour) and leuko- cytosis (21,500 cells /cm 2 with neutrophilic leukocytosis). Serum transaminase levels were raised (aspartate aminotransfer- ase ([SGOT] 100 U/L and alanine aminotransferase [SGPT] 172 U/ L). Renal function tests, coagulation profile, urine analysis and serum bilirubin levels were normal on admission and also during serial testing. Abdominal ultrasonography showed mild homoge- nous hepatomegaly. Virological markers showed positive hepati- tis B surface antigen (HBsAg), positive immunoglobulin (Ig)M antibody to hepatitis B core antigen (anti HBc), positive hepatitis Be antigen (HBeAg) and negative anti HBeAg antibody. Antibody against hepatitis C and human immunodeficiency virus (HIV) were non-reactive. The concentration of C-reactive protein was also elevated. Antinuclear antibody tests, perinuclear antineutro- phil cytoplasmic antibody and cytoplasmic antineutrophil cytoplasmic antibody tests were negative. Cerebrospinal fluid (CSF) examination showed 30 cells, all of which were lympho- cytes, with normal glucose and protein concentration. The nerve conduction study revealed severe axonal sensorimotor polyneuropathy. Histopathological examination of the sural nerve biopsy was suggestive of vasculitic neuropathy with axonal loss in a zonal pat- tern (Fig. 1A, B). The patient was first given a course of intravenous immunoglobulin (2 g/kg in divided doses over 5 days) with the antiviral drug entecavir (0.5 mg/day). The fever subsided after 1 week of treatment. The patient was then started on prednisolone (1 mg/kg of body weight daily) along with entecavir (0.5 mg/day). ⇑ Corresponding author. Fax: +91 1123234350. E-mail address: nayakdrrajeev79@yahoo.com (R. Nayak). Case Reports / Journal of Clinical Neuroscience 20 (2013) 331–332 331