Aciclovir/mycophenolate-mofetil/prednisone

Abstract

Aciclovir/mycophenolate-mofetil/prednisone Varicella zoster virus reactivation and associated complications: case reportA 38-year-old woman developed Varicella zoster virus reactivation due to rebound effect following dose reduction of prednisone. The reactivation of Varicella zoster virus infection was exacerbated to develop erythema multiforme and aseptic meningitis, secondary to rebound effect following withdrawal of aciclovir and mycophenolate mofetil [not all routes, times to reactions onsets and outcomes stated].The woman with dermatomyositis presented with a 3-day history of multiple painful grouped vesiculobullous lesions distributed along the left L2 and L3 dermatomes. She had received prednisone 20 mg/day and mycophenolate mofetil 1.5 g/day for 2 months. Following tapering of prednisone, she developed Herpes zoster. She started receiving oral famciclovir 30 mg/kg for 1 day following IV aciclovir 750 mg/day for 5 days. Consequently, the lesions started healing with crusting and postinflammatory pigmentation. She was discharged with on prednisone and mycophenolate mofetil. Two days after cessation of aciclovir, she developed severe intermittent headaches with fever, cervical rigidity, and multiple erythematous papules and plaques on the left thigh (day 17). She was treated with unspecified NSAID; however, the headaches did not improve. Lumbar puncture was performed to investigate the cause of the headache. Under suspicion of adverse effects, mycophenolate mofetil was discontinued; however, the clinical symptoms rapidly worsened. She had fever. CSF analysis revealed elevated WBC count and protein levels. Varicella zoster virus DNA was detected by PCR in the CSF viral panel. The Varicella zoster virus DNA load on day 17 was 1.9 × 10 2 copies/mL in saliva, 6.0 × 10 4 copies/mL in CSF and undetectable in blood. A diagnosis of aseptic meningitis due to Varicella zoster virus reactivation and Varicella zoster virus-induced erythema multiforme was made. Histology of a skin biopsy revealed perivascular lymphocytic infiltrates in the papillary dermis with few histiocytes. Varicella zoster virus immunostaining of the skin tissue was interpreted as positive, with glycoprotein E detected only at crusts formed in the upper epidermis. She was initiated on IV aciclovir 1500 mg/day along with prednisone 10 mg/day, and the headaches resolved completely. At a follow-up at 6 months after the episode of meningitis, she was noted to be completely free of any CNS symptoms. It was determined that she developed Varicella zoster virus reactivation due to rebound effect following dose reduction of aciclovir. The reactivation of Varicella zoster virus infection was exacerbated due to rebound effect following withdrawal of aciclovir and mycophenolate mofetil.