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Acute Meningoencephalitis in Chronic HIV Infection: Clinical Resolution with Lopinavir-Ritonavir-Containing Therapy
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Clinical Infectious Diseases June 15, 2008;46:1938-1938
CORRESPONDENCE
Giuseppe Vittorio L. De Socio,1 Laura Martinelli,1 Maurizio Zazzi,2 and Franco Baldelli1
1Department of Infectious Diseases, "Santa Maria della Misericordia" Hospital, University of Perugia, Perugia, and 2Department of Molecular Biology, University of Siena, Siena, Italy
Reprints or correspondence: Dr. Giuseppe V. L. De Socio, Clinica di Malattie Infettive, Universita degli Studi di Perugia, Ospedale "Santa Maria della Misericordia," piazzale Menghini, 1-06129 Perugia, Italy
To the Editor-
We read with interest the article by Letendre et al. [1], which showed that lopinavir-ritonavir therapy reduced autonomous human immunodeficiency virus (HIV) RNA levels in CSF. We recently observed a case of symptomatic acute neurological syndrome in a patient with chronic HIV infection and exceedingly high CSF HIV levels; the neurological syndrome was successfully treated with antiretroviral therapy containing lopinavir-ritonavir.
To our knowledge, acute meningoencephalitis secondary to HIV infection has been described in 3 patients with chronic HIV infection [2], but neither high levels of HIV in CSF nor successful treatment with lopinavir-ritonavir was reported in any of these cases.
A 35-year-old African man was admitted to the hospital ("Santa Maria della Misericordia" Hospital; Perugia, Italy) with a 4-week history of severe headache, apathy, and impairment in cognitive function. At hospital admission, the patient presented with severe confusion, complete disorientation, neck stiffness, severe weakness of the limbs, urinary retention, molluscum contagiosum in the face, and oral thrush. Serological diagnosis of HIV infection was made by ELISA, followed by a fully reactive confirmatory recombinant immunoblot test for antibody to HIV. The patient's CD4+ T lymphocyte count was 35 cells/_L, and his plasma HIV RNA level was 159,000 copies/mL. An MRI of the brain showed increased T2-weighted signal diffusely scattered with confluent aspect. An electroencephalographic examination revealed diffuse abnormal findings.
A lumbar puncture yielded clear CSF with 22 mononuclear cells/_L, a protein level of 80 mg/dL, and a glucose level of 41 mg/dL. The results of routine laboratory tests were negative for bacterial, mycobacterial, fungal, and viral agents (including JC virus and herpesvirus). An extraordinarily high level of HIV RNA was detected in the patient's CSF (13,000,000 copies/mL). Parallel HIV genotype examination of isolates obtained from plasma and CSF samples showed identical subtype CRF02_AG sequences, without any drug resistance mutation.
Antiretroviral therapy was started with lopinavir-ritonavir, zidovudine, and lamivudine. Two weeks after initiation of antiretroviral therapy, the patient's headaches resolved, his mental status improved remarkably, his neck stiffness and urinary trouble disappeared, and his CSF cell counts and biochemical test results were normal. The clinical improvement was accompanied by a progressive decrease in levels of HIV in CSF that paralleled the time course of viremia (figure 1). At 6 months of follow-up, the patient was free of symptoms, his plasma HIV RNA level was <40 copies/mL, and his CSF HIV RNA level was 73 copies/mL. The patient's risk factor for HIV infection was identified as heterosexual activity with multiple sex partners 5-10 years before hospital admission. Taken together, the patient's past sexual exposure, his clinical status, the results of the HIV recombinant immunoblot test, and the patient's CD4+ cell count were all consistent with chronic HIV infection. Clinical presentation, MRI findings, and CSF abnormalities were highly suggestive of acute meningoencephalitis. The absence of cerebral atrophy and of JC virus DNA in 3 consecutive CSF samples could reliably exclude both AIDS dementia complex and progressive multifocal leukoencephalopathy. HIV RNA levels remained 2 logs higher in the patient's CSF samples, compared with plasma samples, throughout the entire follow-up period, which supports the hypothesis that the CSF HIV originated from CNS cells.
Although zidovudine and lamivudine penetrate into the CNS, the dramatic decrease of HIV replication could have not been obtained without a major contribution from lopinavir-ritonavir. Such a strong benefit of lopinavir-ritonavir therapy has not been previously reported in similar conditions and reinforces the role of lopinavir-ritonavir in the context of HIV-related neurological symptoms.
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