Antiretrovirals
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Progressive multifocal leukoencephalopathy: case report A 47-year-old man developed progressive multifocal leukoencephalopathy (PML) during treatment with emtricitabine/tenofovir disoproxil fumarate, raltegravir, lamivudine/abacavir and maraviroc for HIV infection [routes, dosages and duration of treatment to reaction onset not stated]. The man, who had been diagnosed with HIV-1/hepatitis C (HCV) co-infection, was hospitalised with a 2-month history of progressive hemiparesis in February 2017. He was on emtricitabine/tenofovir disoproxil fumarate and raltegravir. He had preexisting HCV and alcoholic-related cirrhosis since 2011. At the time of admission, he had right hemiparesis with no facial palsy. Brain MRI revealed left-frontoparietal hyperintensity of the white matter on T2-weighted sequences without enhancement after gadolinium injection and without mass effect. Involvement of the grey matter was not observed. His cerebrospinal fluid (CSF) was unremarkable with undetectable HIV viral load. PCR for John Cunningham (JC) virus was positive at the limit of detection. Further, stereotactic brain biopsy was performed, and histological examination revealed rare oligodendrocyte nuclei with positive immunostaining for JC virus. His antiretroviral treatment was switched to abacavir/lamivudine, raltegravir and maraviroc. Laboratory findings showed a CD4 T cell count of 330 /mm3 and undetectable HIV-1 RNA viral load. The CD4/CD8 ratio was 0.49. The HCV RNA load was 1730000 IU/mL. An abdominal CT scan showed a dysmorphic liver, splenomegaly and portal hypertension. Liver stiffness was 20kPA (success rate of 80%; IQR of 3.3). Based on the clinical picture and these findings, PML was diagnosed, which was possibly related to HIV infection, HCV infection, cirrhosis or the anti-retroviral therapies. Standard immunological studies were normal. No monoclonal peak was noted. Analysis of the CD4 and CD8 T-cell subpopulations revealed a decrease in na¨ıve CD4 cells (CD45RA+CCR7+CD27+ CD4+ T cells - 23% CD4 cells, i.e. 75/mm3) and NK lymphopenia (CD3-CD16+ and/or CD56+; 5% lymphocytes, i.e. 58/mm3) without CD8 quantitative abnormality. His NK cell phenotype was highly abnormal with decreased expression of natural cytotoxicity receptors (NCR) NKp30 and NKp46 (26% and 22%) and elevated activation marker CD69 (91%). His neurological condition worsened. On a second CSF control performed 2 months later, JC viral load was 2210 copies/mL. The man was treated with elbasvir/grazoprevir for HCV infection for 12 weeks with sustained viral response. Immunological studies were performed 12 months after the completion of HCV treatment, which showed a CD4 T cell count of 516/mm3 and a CD4/CD8 ratio of 0.44. Analysis of the lymphocyte subpopulations revealed persistent NK lymphopenia (CD3- CD16+ and/or CD56+; 3.9% cells, i.e. 68/mm3) with improved activation status (%CD69 from 91 to 30%) and restoration of NCR expression: NKp30 70% and NKp46 44%. The na¨ıve CD4 T-cell count had increased slightly, and the effector memory CD4 T cell count had d
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