Immunosuppressants
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West Nile virus encephalitis: 2 case reports In a case series, two women aged 56 years and 34 years were described, who developed West Nile virus (WNV) encephalitis during immunosuppressant drug therapy with mycophenolate, ciclosporin, mycophenolate mofetil, prednisone or tacrolimus [dosages, routes and times to reaction onsets not stated]. Case 1: The 56-year-old woman, who had past medical history of multiple sclerosis and chronic kidney disease status postrenal and pancreatic transplant 10 years prior, had been receiving immunosuppressant drug therapy with mycophenolate and ciclosporin. In September, she presented with worsening left lower extremity weakness. She was admitted. Subsequently, she developed fever of unknown origin with a sudden decline in mentation. Severe brainstem dysfunction was noted, requiring mechanical ventilation. Meningitis was suspected, and an empiric unspecified antibiotic therapy was started. Initial serum and CSF analysis findings were nonconclusive. Initial brain MRI scan exhibited nonspecific white matter changes. At one-week follow-up, CSF analysis showed increased WBC count with lymphocytic pleocytosis. A repeat brain MRI scan exhibited new symmetric T2-hyperintense signal in the bilateral thalami, with associated diffusion restriction and mild abnormal contrast enhancement. Based on the clinical picture, viral encephalitis with the possibility of deep cerebral venous thrombosis was suspected. However, a subsequent magnetic resonance venogram was negative. Eventually, one-week follow-up WNV serology resulted positive. Elevated IgM antibodies definitively established the diagnosis of WNV encephalitis. Eventually, her condition progressively deteriorated, and she was discharged home with hospice. Case 2: The 34-year-old woman, who had a medical history of hypertension and end stage renal disease status post renal transplantation, presented in late September due to light headedness, abdominal pain, weakness and fever. She was admitted. Her immunosuppressant drug regimen included mycophenolate mofetil, prednisone and tacrolimus along with concomitant administration of valganciclovir and cotrimoxazole [trimethoprim/sulfamethoxazole]. On admission day 5, rapid decline in her mental status with diminished alertness was noted along with increasing lethargy. Eventually, she required intubation for hypoxic respiratory failure. Initial CSF analysis was unremarkable. Neurological examination showed further deterioration as she became responsive to painful stimuli only and developed a left gaze palsy. After 8 days, a repeat CSF analysis showed an elevated cell count with lymphocytic pleocytosis, elevated protein, low-normal glucose and a negative viral panel. A brain MRI scan exhibited only chronic microvascular ischaemic changes. After 9 days, repeat imaging showed diffusion restriction and T2W and FLAIR hyperintense signal with expansile changes within the bilateral centrum semiovale, corona radiata, deep gray nuclei, deep white matter tracts, midbrain, bilateral superior cerebellar ped
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