Antivirals
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Acquired drug resistance and drug toxicity: case report A 65-year-old man developed drug resistance following treatment with ganciclovir and valganciclovir for cytomegalovirus (CMV) viraemia and CMV ventriculitis. Subsequently, he developed drug toxicity during treatment with foscarnet [outcome not stated; not all routes and dosages stated]. The man, who had AIDS, was observed unconscious at his home in September 2017. He had been diagnosed with HIV, but he was not on active treatment. Following further investigations, CMV viraemia with CNS involvement presented as CMV ventriculitis was diagnosed. He started receiving IV ganciclovir in September 2017 with concurrent administration of anti-retroviral therapy with emtricitabine, dolutegravir and tenofovir. He was discharged on oral valganciclovir with improvement. Six months later, he was again hospitalised with worsening cognition. He was adherent to his therapies. CD4 was 60 cells/mm3, suggesting poor immune recovery. On 13 April 2018, his plasma CMV viral load remained undetectable, but CMV viral load in CSF 4.2 × 104 IU/mL on readmission. Genotypic analysis of the UL54 and UL97 genes showed the presence of the A594V mutation in the UL97 gene, which was known to confer ganciclovir and valganciclovir resistance. Additionally, analysis of the UL54 sequence showed the presence of the accessory mutation del524, which showed ganciclovir and valganciclovir resistance and pre-existing cidofovir resistance. Due to the drug resistance, the man’s valganciclovir therapy was changed to IV foscarnet. CMV DNA remained undetectable in his blood during foscarnet therapy; however, CMV DNA were detectable in the CSF. Mini-Mental State Examination demonstrated continued deterioration of the cognitive scoring. He developed drug toxicity while receiving foscarnet. Due to insignificant improvement, oral off label monotherapy with letermovir 480mg once a day was started for drug-resistant CMV ventriculitis in July 2018. Eventually, a one-hundred-fold decrease in CMV viral load was noted after 4 weeks of letermovir. However, in October 2018, he was transferred to the ICU with a hospital-acquired pneumonia. At that time, a repeat CSF CMV viral load was elevated to 2.4 × 103 IU/mL. An analysis of his specimens for evidence of developing letermovir resistance mutations was performed, which did not show resistance to letermovir. The reason for the sudden increase in CMV viral load during letermovir remained unclear. Subsequently, he died [immediate cause of death not stated]. Bosworth A, et al. Letermovir salvage therapy in the management of a case of cytomegalovirus ventriculitis complicated by drug resistance. Clinical Infection in Practice 7: 803498640 Oct 2020. Available from: URL: http://doi.org/10.1016/j.clinpr.2020.100039
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Reactions 29 Aug 2020 No. 1819
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