• PDF / 175,873 Bytes
• 1 Pages / 595.245 x 841.846 pts (A4) Page_size
• 2 Downloads / 160 Views

DOWNLOAD

REPORT

---

1 S

JC-virus infection, HHV-6 infection and tumefactive multiple sclerosis: case report A 51-year-old man developed JC-virus infection during treatment with natalizumab and human herpesvirus 6 (HHV-6) infection following treatment with methylprednisolone. Additionally, he developed tumefactive multiple sclerosis (MS) during treatment with fingolimod [durations of treatments to reactions onsets not stated; not all dosages, routes and outcomes stated]. The man, with an 8-year history of relapsing-remitting MS (RRMS), was hospitalised with a suspicion of MS relapse. He had been diagnosed with MS in 2009, for which he had been treated with glatiramer-acetate. He had a significant family medical history of MS (mother and uncle). During treatment with glatiramer-acetate, he exhibited 4 relapses. Therefore, he received treatment with IV unspecified steroids initially with a good response. Based on an acute central vestibular syndrome, which led to dizziness and an ataxic gait dysfunction, he was diagnosed with a clinically isolated syndrome (CIS). At that time, he had first relapse and MRI showed multiple white matter lesions in the supratentorium, cerebellum and cervical as well as thoracic spinal cord. In 2012, due to an increased relapse rate and incomplete clinical remissions, he started receiving natalizumab. At that time, the last relapse while receiving glatiramer-acetate led to development of a residual paraparesis and a left side internuclear ophthalmoplegia. At the time of last relapse, brain MRI showed multiple white matter lesions with a cystic aspect and incomplete ring-like gadolinium enhancement. Following natalizumab initiation, his condition stabilised and he had no more relapses. However, he exhibited increased anti-JC virus (JCV) antibody level index to 4.5 (JC-virus infection). The man’s natalizumab was discontinued in 2017. He started receiving fingolimod 3 months prior to his current admission (i.e. after 4 weeks of discontinuation of natalizumab). Prior to 8 days of his admission, he exhibited a progressive left lower limb weakness and deterioration of walking ability became evident. He was able to stand without help and walk a few steps with unilateral assistance. At that time, his differential diagnosis included MS relapse or progressive multifocal leukoencephalopathy (PML). A MRI scan at the day of admission, showed bihemispheric confluent T2 white matter lesions without changes, consistent with PML. CSF examination showed mildly increased lactate and glucose levels with normal WBC count. His albumin quotient was normal; however, oligoclonal bands were positive with intrathecal synthesis of immunoglobulins G and M. The PCR, microbiological and serological examination including JC virus PCR, JCV CSF/serum antibody index, HSV-1 PCR, HSV-2 PCR, varicella-zoster virus PCR, Epstein–Barr virus PCR and HIV PCR were all negative. Subsequent evoked potentials showed an impairment of the corticospinal tract to the right leg, bilaterally impaired tibial nerve somatosensory reactions, and evidence of a bila