Infliximab/methotrexate

Abstract

Dementia Scale score was 28 and cognitive function became normal. Two months after the discharge, MRI revealed slight S Infliximab/methotrexate improvement, and JC virus DNA in CSF was negative. At the last follow-up, she had been stable for over 6 months. Progressive multifocal leukoencephalopathy and Author comment: She had been treated with cryptococcal meningitis: case report methotrexate and infliximab for rheumatoid arthritis. A 65-year-old woman developed progressive multifocal Although concurrent [progressive multifocal leucoencephalopathy and cryptococcal meningitis during leukoencephalopathy] and cryptococcal meningitis is rare, it treatment with methotrexate and infliximab for rheumatoid should be considered in immunosuppressed patients. arthritis [not all routes stated; duration of treatments to reactions onsets not stated]. Nosaki Y, et al. Simultaneous development of progressive multifocal The woman was hospitalised for gait disturbance and leukoencephalopathy and cryptococcal meningitis during methotrexate and infliximab treatment. Internal Medicine 58: 2703-2709, No. 18, 2019. Available transient acute right upper limb weakness. At the age of from: URL: http://doi.org/10.2169/internalmedicine.2570-18 Japan 803437873 57 years, she was diagnosed with rheumatoid arthritis and had been receiving methotrexate and prednisolone. At the age of 61 years, due to remission she received methotrexate and prednisolone at reduced doses. At the age of 64 years, prednisolone was discontinued due to remission of symptoms. At the age of 65 years, she had been receiving infliximab 3 mg/kg and oral methotrexate 4mg. She had no medical history of diabetes mellitus. On current admission, her weight was 52.2kg. She was well oriented and alert. She had slight weakness of lower and right upper limbs and numbness of the right fingers. Her mini mental state examination score was 30 and Revised Hasegawa’s Dementia Scale score was 28 points. Brain MRI did not reveal abnormal intensity areas on diffusion-weighted imaging. On fluidattenuated inversion recovery (FLAIR) images revealed nonspecific lesions. After 4 days, she was discharged from the hospital. Following discharge, she reported general fatigue and headache. After 8 weeks, she was again hospitalised with nausea, weight loss, double vision, dizziness and headache. At that time, her cognitive function disturbed, Revised Hasegawa’s Dementia Scale score was 16 and weight decreased to 45kg. A neurological examination showed bilateral sixth nerve palsy and a drowsy state. Deep tendon reflexes were increased in the lower and upper extremities. She did not walk without assistance due to double vision, dizziness and headache. Blood tests revealed decreased lymphocytes. A CSF analysis showed an elevated WBC count with an opening pressure of over 30 cmH2O, increased protein concentration, glucose level 22 mg/dL and decreased CSF/ blood glucose ratio. Cryptococcal antigen was detected in the serum and CSF. CSF culture identified Cryptococcus neoformans infection. Brain MRI showed focal lesions in the white matter of the temporal and bilateral frontal lobes. On FLAIR and T2-weighted imaging, the lesions appeared hyperintense, while on T1-weighted imaging appeared hypointense lesions and devoid of contrast enhancement. Based on the CSF findings, she was diagnosed with cryptococcal meningitis. The woman’s therapy with infliximab and methotrexate were discontinued. Subsequently, she started receving treatment with amphotericin B along with flucytosine. Six weeks later, fluconazole was started. Three weeks after the initiation of antifungal therapy, PCR targeting the John Cunningham (JC) virus large T gene in CSF showed the presence of JC virus-DNA with 479 copies/mL. The JC virus genome in the CSF revealed a mutation characteristic of the progressive multifocal leukoencephalopathy-type virus identified in the non-coding control region using multiplex real-time PCR. Based on PCR test results and MRI findings for JC virus in CSF, she was diagnosed with progressive multifocal leukoencephalopathy. She continued receiving anti-fungal treatment without re-initiating infliximab and methotrexate. Her clinical symptoms improved gradually without recurrence of rheumatoid arthritis. One month after the re-hospitalisation, follow-up MRI revealed appearance of new lesions and enlargement of some lesions. Diffuse-weighted imaging revealed a partial low signal on the apparent diffusion coefficient map and slight hyperintensities of the lesions. Due to the lack of neurological symptoms, she was monitored without any treatment, other than anti-fungal therapy. Eight weeks after the re-hospitalisation, she was discharged with improvement in double vision. Her Revised Hasegawa’s 1