East African HIV care: depression and HIV outcomes.

IMPORTANCE: Depression is a common co-morbidity for people living with HIV (PLWH) and is associated with elevated plasma HIV RNA levels. While depression correlates with deficits in antiretroviral (ARV) adherence, little data exist to inform the relationship between depression and HIV vial load more broadly. OBJECTIVE: To examine the relationship between depression and viral load in the African Cohort Study (AFRICOS) independently of ARV adherence. DESIGN: PLWH in Kenya, Uganda and Tanzania underwent screening for depression using the Center for Epidemiologic Studies Depression Scale (CESD) upon enrollment at AFRICOS HIV care sites. SETTING: AFRICOS is an ongoing prospective longitudinal cohort study enrolling HIV-infected adults at HIV care centers including sites in Kenya, Tanzania and Uganda. These sites are administered by President's Emergency Plan For AIDS Relief programs. PARTICIPANTS: HIV+ individuals were eligible if they were at least 18 years old, receiving HIV care at the enrolling clinic and consented to data and specimen collection. MAIN OUTCOME MEASURE: CESD. RESULTS: Among 2307 participants, 18-25% met the CESD threshold for depression. Depression was associated with decreased ARV adherence (OR 0.59, p =  0.01). Higher scores on three CESD items were significantly associated with 209-282% higher viral load, independently of ARV adherence among participants on ARVs ⩾6 months. CONCLUSIONS: PLWH had high prevalence of depression on the CESD. Diverse depression symptoms were independently associated with increases in viral load, underscoring the need for comprehensive treatment of depression.

HIV DNA and cognition in a Thai longitudinal HAART initiation cohort: the SEARCH 001 Cohort Study.

OBJECTIVES: The extent to which highly active antiretroviral therapy (HAART) era cognitive disorders are due to active processes, incomplete clearance of reservoirs, or comorbidities is controversial. This study aimed to determine if immunologic and virologic factors influence cognition after first-time HAART in Thai individuals with HIV-associated dementia (HAD) and Thai individuals without HAD (non-HAD). METHODS: Variables were captured longitudinally to determine factors predictive of degree of cognitive recovery after first-time HAART. Neuropsychological data were compared to those of 230 HIV-negative Thai controls. RESULTS: HIV RNA and CD4 lymphocyte counts were not predictive of HAD cross-sectionally or degree of cognitive improvement longitudinally. In contrast, baseline and longitudinal HIV DNA isolated from monocytes correlated to cognitive performance irrespective of plasma HIV RNA and CD4 lymphocyte counts pre-HAART (p < 0.001) and at 48 weeks post HAART (p < 0.001). Levels exceeding 3.5 log(10) copies HIV DNA/10(6) monocyte at baseline distinguished all HAD and non-HAD cases (p < 0.001). At 48 weeks, monocyte HIV DNA was below the level of detection of our assay (10 copies/10(6) cells) in 15/15 non-HAD compared to only 4/12 HAD cases, despite undetectable plasma HIV RNA in 26/27 cases. Baseline monocyte HIV DNA predicted 48-week cognitive performance on a composite score, independently of concurrent monocyte HIV DNA and CD4 count (p < 0.001). CONCLUSIONS: Monocyte HIV DNA level correlates to cognitive performance before highly active antiretroviral therapy (HAART) and 48 weeks after HAART in this cohort and baseline monocyte HIV DNA may predict 48-week cognitive performance. These findings raise the possibility that short-term incomplete cognitive recovery with HAART may represent an active process related to this peripheral reservoir.

Neuropsychological abnormalities in patients with dementia in CRF 01_AE HIV-1 infection.

HIV-associated dementia (HAD) is not firmly established in patients with circulating recombinant form (CRF) 01_AE HIV-1. In this study, we compared neuropsychological performance among 15 Thai individuals with HAD, 15 Thai individuals without HAD, and 30 HIV-negative control subjects. HIV-1 participants were highly active anti-retroviral therapy naive and matched by age, education, and CD4 count. Neuropsychological testing abnormalities were identified in most cognitive domains among HAD vs HIV-negative participants, confirming the presence of HAD in CRF01_AE.

Symptomatic distal sensory polyneuropathy in HIV after age 50.

OBJECTIVE: To determine if aging changes the frequency, severity, or manifestations of symptomatic distal sensory polyneuropathy (SxDSPN) in patients with HIV-1. METHODS: Prospective observations of 70 older (age < or = 50) and 56 younger (age 20 to 40) patients with HIV, and a control group of 48 older non-HIV patients, were conducted utilizing neurologic examination, neuropsychological testing, lumbar puncture, laboratory, and medical history. RESULTS: The frequency of SxDSPN among older HIV patients was 50.4%, compared to 19.6% among younger HIV patients (p < 0.001). SxDSPN among control patients occurred in 4.2%, similar to the general population. Older compared to younger HIV patients demonstrated more severe symptoms (p = 0.02) and greater deficits for vibration (p < 0.01). Increasing numbers of neuropathic comorbidities among older compared to younger HIV patients were associated with increasing severity of deficits to pinprick (p = 0.003). Dementia and SxDSPN coexisted in 36% of the older HIV patients and in none of the younger HIV patients (p = 0.021). Older HIV patients with nadir CD4 < or =200 cells/mL were 4.23 times as likely to have SxDSPN than older patients with nadir CD4 >200 cells/mL (p = 0.007). Vibratory deficits excessive to pinprick deficits predicted SxDSPN among older (OR 2.83) but not younger seropositive patients (p = 0.036). CONCLUSIONS: Age > or = 50 increases the frequency of SxDSPN, and is associated with both vibratory loss as the predominant sensory deficit and increased severity of pinprick loss among symptomatic patients with neuropathic comorbidities. SxDSPN is associated with both dementia and low nadir CD4 in HIV-positive patients aged 50 and greater.

The detection of dementia in the primary care setting.

BACKGROUND: Recognition and medical record documentation of dementia in the primary care setting are thought to be poor. To our knowledge, previous studies have not examined these issues in private practice office settings within the United States. OBJECTIVE: To determine the rate of unrecognized and undocumented dementia in a primary care internal medicine private practice. METHODS: This was a cross-sectional study of 297 ambulatory persons aged 65 years and older attending an internal medicine private group practice within an Asian American community of Honolulu, Hawaii. Of the subjects, 95% had been with their current primary care physician for at least 1 year. Each subject's primary care physician noted the presence or absence of dementia by questionnaire at the time of an office visit. An investigating physician (V.G.V.) subsequently assessed cognitive function using the Cognitive Abilities Screening Instrument, and confirmed the presence of dementia and its severity, if present, using Benson and Cummings' criteria and the Clinical Dementia Rating Scale, respectively. A trained research assistant completed telephone interviews to proxy informants for collateral information concerning cognition, behavior, and occupational or social function. Subjects' outpatient medical records were reviewed for documentation of problems with cognition. RESULTS: Twenty-six cases of dementia were identified. Of these 26, 17 (65%) (95% confidence interval, 44.3-82.8) were not documented in outpatient medical records; of 18 patients, 12 (67%) (95% confidence interval, 40.9-86.7) were not thought to have dementia by their physicians at the time of the office visit. Recognition and documentation rates increased with advancing stage of disease. CONCLUSION: Dementia is often unrecognized and undocumented in private practice settings. Arch Intern Med. 2000;160:2964-2968