Mizoribine/prednisolone

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Mizoribine/prednisolone Zoster sine herpete-related acute myelitis: case report

A 79-year-old man developed Zoster sine herpete (ZSH)-related acute myelitis following immunosuppressive treatment with mizoribine and prednisolone for systemic lupus erythematosus (SLE) and lupus nephropathy. The man, who had a medical history of herpes zoster on face, SLE and lupus nephropathy, presented due to lower limb muscle weakness, dysuria and difficulty defecating. Since he was not able to walk without assistance, he was brought to the hospital in ambulance and was admitted. One week prior to this presentation, he had started to experience prickly pain from the right precordia to the back without skin lesion and eruption. He had been receiving oral mizoribine 150mg and prednisolone 3mg for lupus conditions. On admission, his vitals were as follows: body temperature 37°C, BP 170/116mm Hg, pulse rate 116 /min and oxygen saturation 97% on room air. Neurological motor examinations revealed marked muscle weakness in both upper limbs and lower limbs, spastic paraplegia and increased tendon reflex of the lower limb. The Babinski sign was bilateral positive. Neurological sensory examination showed pain from the right precordial region to the back, low temperature pain sensation from the lower abdomen to both lower limbs and low vibration sensation of the lateral malleolus of both legs. Blood tests revealed renal dysfunction, increased blood glucose level and slight inflammatory response. Antinuclear antibody (homogeneous type) was elevated indicating history of SLE, while anti-aquaporin 4 antibody, anti-DNA antibody, anti-SS-A antibody and anti-SS-B antibody were negative. Urinalysis showed no abnormality. A CSF analysis following results: high number of cells, protein 107.40 mg/dL, glucose 58 mg/dL and decreased CSF glycaemic ratio. A CSF bacterial culture was negative, and PCR yielded negative results for Herpes simplex-DNA and Varicella zoster virus (VZV)-DNA in the CSF. The antibody titre for VZV showed following results: IgM 0, IgG 37.3 and VZV-IgG index 89.8. This elevated VZV-IgG antibody titre in the blood and CSF indicated towards antibody production against VZV infection. A trunk CT scan revealed bladder dilatation and bilateral hydronephrosis. An MRI of the head and whole spinal cord revealed no abnormal findings. In the lower limb somatosensory evoked potential by right posterior tibial nerve stimulation, the peripheral component had a normal latency, but central sensory conduction time was abnormally prolonged and cortical latency of P38 was delayed. Based on these findings, ZSH-associated acute myelitis was suspected [duration of treatments to reaction onset not stated]. The man was treated with methylprednisolone pulse therapy for 3 days and reduced dose of aciclovir for 7 days due renal dysfunction. His muscle strength and sensory impairment showed gradual improvement. He was able to sit on day 6 of illness, and his rectal and bladder disorders resolved on day 8 of illness. On day 10 of illness, the results of re

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