Many practical clinical questions regarding the management of human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) remain unanswered. We sought to identify and develop practical answers to key clinical questions in HAND management. Sixty-six specialists from 30 countries provided input into the program, which was overseen by a steering committee. Fourteen questions were rated as being of greatest clinical importance. Answers were drafted by an expert group based on a comprehensive literature review. Sixty-three experts convened to determine consensus and level of evidence for the answers. Consensus was reached on all answers. For instance, good practice suggests that all HIV patients should be screened for HAND early in disease using standardized tools. Follow-up frequency depends on whether HAND is already present or whether clinical data suggest risk for developing HAND. Worsening neurocognitive impairment may trigger consideration of antiretroviral modification when other causes have been excluded. The Mind Exchange program provides practical guidance in the diagnosis, monitoring, and treatment of HAND.
Neurocognitive impairments following central nervous system opportunistic infections and HIV-associated dementia (HAD) were common clinical features of HIV infection prior to anti-retroviral therapy. As HIV infection has evolved from an invariably fatal disease with a poor prognosis to a condition requiring long-term management, HIV-related neurocognitive disorders have been the subject of increasing research. This review will examine the recent changes in the understanding of the HIV-associated neurocognitive disorders (HAND) including the changing epidemiology, risk factors associated with its development, methods for screening for the disorders and evolving treatment options.
Objective: To characterize the clinical, laboratory and radiological characteristics of persons with HIV (PWH) presenting with cerebrospinal fluid (CSF) HIV RNA escape.Design: Retrospective case review of PWH presenting with symptomatic CSF HIV RNA escape at seven tertiary HIV clinical sites in the United Kingdom and Italy.Method: PWH with symptomatic CSF HIV RNA escape episodes were identified and data obtained from medical records. CSF HIV RNA escape was defined as quantifiable CSF HIV RNA in unquantifiable plasma HIV RNA or CSF HIV RNA greater than plasma HIV RNA in cases where plasma HIV RNA was quantifiable. The onset of clinical symptoms was classified as acute (<2 weeks-6 months), or chronic (>6 months) and differences in presentation in those with CSF HIV RNA below and above 1000 copies/ ml determined. Results:We identified 106 PWH with CSF HIV RNA escape (65 male); 68 (64%) PWH had acute presentations and 38 (36%) had chronic presentations. Cognitive decline (n ¼ 54; 50.9%), confusion (n ¼ 20; 18.9%) and headache (n ¼ 28; 26.4%) were the most common presentations, with cognitive decline being more common in PWH who presented chronically compared with PWH who presented acutely (73.7% vs. 35.3%, P ¼ 0.0002). Sixty PWH had CSF HIV RNA at least 1000 copies/ml and presented more frequently with confusion (n ¼ 15/60; 25.0%) compared with PWH with CSF HIV RNA less than 1000 copies/ml at presentation (n ¼ 5/46; 10.9%; P ¼ 0.03).
Purpose of Review Cognitive impairment leading to disability is increasingly seen in people living with human immunodeficiency virus (PLWH). Rehabilitation can alleviate the effects of cognitive impairment upon function. The aim of this paper is to discuss the strategies that have been used in cognitive and neurologic rehabilitation in PLWH. Recent Findings Studies examining pharmacological and non-pharmacological strategies were analysed. Medical management of HIV and co-morbidities should be optimised. Non-pharmacological strategies, including nerve stimulation techniques, exercise-based interventions, and paper and computer-based cognitive rehabilitation, have some evidence supporting their use in PLWH either as stand-alone interventions or as part of a multidisciplinary approach. Summary Both pharmacological and non-pharmacological rehabilitation strategies have been used with PLWH. More intervention trials are needed to assess cognitive and neurological rehabilitation strategies and further evaluate their potential benefit in PLWH.
The incidence of HIV-associated dementia has decreased significantly with the introduction of combination antiretroviral therapy; however, milder or more subtle forms of neurocognitive disorders associated with HIV appear to remain common. There is a lack of consensus on when to screen and on which methods are most appropriate for identifying patients at risk of neurocognitive impairment. Multiple factors (demographic, social, genetic, psychological and medical) can play a role in its aetiology and progression, including potential central nervous system toxicity of antiviral therapy. It is important to identify these factors in order to apply relevant management strategies. In this review, we discuss a series of case studies that address some of the challenges presented by the diagnosis and management of HIV-associated neurocognitive impairment in different patient types.
Using deep sequencing, human immunodeficiency virus (HIV) resistance-associated mutations were detected as minority species in the cerebrospinal fluid (CSF) of 4 patients with higher HIV type 1 RNA load in CSF than in plasma, but not in 2 patients with higher plasma viral load. Deep sequencing could help our understanding of viral escape in the central nervous system.
We report an individual who had HIV-associated dementia, but a good clinical response to antiretroviral therapy, with a rising CD4 count and undetectable viral load. A severe leukoencephalopathy was noted at postmortem; however, no HIV immunopositive cells were found in the brain, suggesting that this new severe leukoencephalopathy is associated with immune reconstitution.
Background Switching from boosted PIs to dolutegravir in people living with HIV (PLWH) with high cardiovascular risk improved plasma lipids at 48 weeks in the NEAT022 trial. Whether this strategy may have an impact on cardiovascular biomarkers is unknown. Methods We assessed 48 week changes in biomarkers associated with inflammation, endothelial dysfunction, monocyte immune activation, oxidation, insulin resistance, hypercoagulability, heart failure, myocardial injury, and glomerular and tubular kidney injury. Results Of 415 PLWH randomized in the NEAT022 study, 313 (75.4%) remained on allocated therapy and had paired samples available. Soluble CD14 (–11%, P < 0.001) and adiponectin (–11%, P < 0.001) significantly declined and high-sensitive C-reactive protein (–13%, P = 0.069) and oxidized LDL (–13%, P = 0.084) tended to decrease with dolutegravir. Switching to dolutegravir remained significantly associated with soluble CD14 and adiponectin reductions after adjustment for baseline variables. There were inverse correlations between soluble CD14 and CD4 count changes (P = 0.05), and between adiponectin and BMI changes (P < 0.001). Conclusions Switching from boosted PIs to dolutegravir in PLWH with high cardiovascular risk led to soluble CD14 and adiponectin reductions at 48 weeks. While decreasing soluble CD14 may entail favourable health effects in PLWH, adiponectin reduction may reflect less insulin sensitivity associated with weight gain.
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