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Determine if cocaine use impacts gut permeability, promotes microbial translocation and immune activation in people living with HIV (PLWH) using effective antiretroviral therapy (ART). Cross-sectional analysis of 100 PLWH (ART ≥6 months, HIV-RNA <200 copies/mL) from the Miami Adult Studies on HIV (MASH) cohort. Cocaine use was assessed by self-report, urine screen, and blood benzoylecgonine (BE). Blood samples were collected to assess gut permeability (intestinal fatty acid-binding protein, I-FABP), microbial translocation (lipopolysaccharide, LPS), immune activation (sCD14, sCD27, and sCD163) and markers of inflammation (hs-CRP, TNF-α and IL-6). Multiple linear regression models were used to analyze the relationships of cocaine use. A total of 37 cocaine users and 63 cocaine non-users were evaluated. Cocaine users had higher levels of I-FABP (7.92±0.35 vs. 7.69±0.56 pg/mL, P = 0.029) and LPS (0.76±0.24 vs. 0.54±0.27 EU/mL, P<0.001) than cocaine non-users. Cocaine use was also associated with the levels of LPS (P<0.001), I-FABP (P = 0.033), and sCD163 (P = 0.010) after adjusting for covariates. Cocaine users had 5.15 times higher odds to exhibit higher LPS levels than non-users (OR: 5.15 95% CI: 1.89-13.9; P<0.001). Blood levels of BE were directly correlated with LPS (rho = 0.276, P = 0.028), sCD14 (rho = 0.274, P = 0.031), and sCD163 (rho = 0.250, P = 0.049). Cocaine use was associated with markers of gut permeability, microbial translocation, and immune activation in virally suppressed PLWH. Mitigation of cocaine use may prevent further gastrointestinal damage and immune activation in PLWH.

The HIV/AIDS epidemic remains a major public health concern since the 1980s; untreated HIV infection has numerous consequences on quality of life. To optimize patients’ health outcomes and to reduce HIV transmission, this study focused on vulnerable populations of people living with HIV (PLWH) and compared different predictive strategies for viral suppression using longitudinal or repeated measures. The four methods of predicting viral suppression are (1) including the repeated measures of each feature as predictors, (2) utilizing only the initial (baseline) value of the feature as predictor, (3) using the last observed value as the predictors and (4) using a growth curve estimated from the features to create individual-specific prediction of growth curves as features. This study suggested the individual-specific prediction of the growth curve performed the best in terms of lowest error rate on an independent set of test data.

Our objective was to assess whether human immunodeficiency virus (HIV)-infection directly or indirectly promotes the progression of clinical characteristics of coronary artery disease (CAD). 300 African Americans with asymptomatic CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV-infected) who underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years) were randomly selected from 1429 participants of a prospective epidemiological study between May 2004 and August 2015. We calculated Agatston-scores, number of coronary plaques and segment stenosis score (SSS). Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use on CAD. There was no significant difference in annual progression rates between HIV-infected and—uninfected regarding Agatston-scores (10.8 ± 25.1/year vs. 7.2 ± 17.8/year, p  = 0.17), the number of plaques (0.2 ± 0.3/year vs. 0.3 ± 0.5/year, p  = 0.11) or SSS (0.5 ± 0.8/year vs. 0.5 ± 1.3/year, p  = 0.96). Multivariately, HIV-infection was not associated with Agatston-scores (8.3, CI: [− 37.2–53.7], p  = 0.72), the number of coronary plaques (− 0.1, CI: [− 0.5–0.4], p  = 0.73) or SSS (− 0.1, CI: [− 1.0–0.8], p  = 0.84). ASCVD risk scores and years of cocaine-use significantly increased all CAD outcomes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-medications were associated with any of the CAD outcomes. HIV-infection is not directly associated with CAD and therefore HIV-infected are not destined to have worse CAD profiles. However, HIV-infection may indirectly promote CAD progression as risk factors may have a more prominent role in the acceleration of CAD in these patients.

Background There is growing public health concern around the potential impact of the opioid crisis on efforts to eradicate HIV. This secondary analysis seeks to determine if those who report opioids as their primary problem drug compared to those who report other drugs and/or alcohol differ in engagement in HIV primary care among a sample of hospitalized people with HIV (PWH) who use drugs and/or alcohol, a traditionally marginalized and difficult to engage population key to ending the HIV epidemic. Setting and participants A total of 801 participants (67% male; 75% Black, non-Hispanic; mean age 44.2) with uncontrolled HIV and reported drug and/or alcohol use were recruited from 11 hospitals around the U.S. in cities with high HIV prevalence from 2012 to 2014 for a multisite clinical trial to improve HIV viral suppression. Methods A generalized linear model compared those who reported opioids as their primary problem drug to those who reported other problem drugs and/or alcohol on their previous engagement in HIV primary care, controlling for age, sex, race, education, income, any previous drug and/or alcohol treatment, length of time since diagnosis, and study site. Results A total of 95 (11.9%) participants reported opioids as their primary problem drug. In adjusted models, those who reported opioids were significantly less likely to have ever engaged in HIV primary care than those who reported no problem drug use (adjusted risk ratio, ARR  = 0.84, 95% Confidence Interval, CI 0.73, 0.98), stimulants ( ARR  = 0.84, 95% CI 0.74, 0.95), and polydrug use but no alcohol ( ARR  = 0.79, 95% CI 0.68, 0.93). While not statistically significant, the trend in the estimates of the remaining drug and/or alcohol categories (alcohol, cannabis, polydrug use with alcohol, and [but excluding the estimate for] other), point to a similar phenomena—those who identify opioids as their primary problem drug are engaging in HIV primary care less. Conclusions These findings suggest that for hospitalized PWH who use drugs and/or alcohol, tailored and expanded efforts are especially needed to link those who report problem opioid use to HIV primary care. Trial registration This study was funded by National Institutes of Health (NIH) grant: U10-DA01372011 ( Project HOPE — Hospital Visit as Opportunity for Prevention and Engagement for HIV - Infected Drug Users ; Metsch); which is also a registered clinical trial under the Clinical Trials Network (CTN-0049). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Objectives To develop a general framework to assess temporal changes in lesion morphology on radiological images beyond volumetric changes and to test whether cocaine abstinence changes coronary plaque structure on serial coronary CT angiography (CTA). Methods Chronic cocaine users with human immunodeficiency virus (HIV) infection were prospectively enrolled to undergo cash-based contingency management to achieve cocaine abstinence. Participants underwent coronary CTA at baseline and 6 and 12 months following recruitment. We segmented all coronary plaques and extracted 1103 radiomic features. We implemented weighted correlation network analysis to derive consensus eigen radiomic features (named as different colors) and used linear mixed models and mediation analysis to assess whether cocaine abstinence affects plaque morphology correcting for clinical variables and plaque volumes and whether serum biomarkers causally mediate these changes. Furthermore, we used Bayesian hidden Markov network changepoint analysis to assess the potential rewiring of the radiomic network. Results Sixty-nine PLWH (median age 55 IQR: 52–59 years, 19% female) completed the study, of whom 26 achieved total abstinence. Twenty consensus eigen radiomic features were derived. Cocaine abstinence significantly affected the pink and cyan eigen features (−0.04 CI: [−0.06; −0.02], p = 0.0009; 0.03 CI: [0.001; 0.04], p = 0.0017, respectively). These effects were mediated through changes in endothelin-1 levels. In abstinent individuals, we observed significant rewiring of the latent radiomic signature network. Conclusions Using our proposed framework, we found 1 year of cocaine abstinence to significantly change specific latent coronary plaque morphological features and rewire the latent morphologic network above and beyond changes in plaque volumes and clinical characteristics. Key Points • We propose a general methodology to decompose the latent morphology of lesions on radiological images using a radiomics-based systems biology approach. • As a proof-of-principle, we show that 1 year of cocaine abstinence results in significant changes in specific latent coronary plaque morphologic features and rewiring of the latent morphologic network above and beyond changes in plaque volumes and clinical characteristics. • We found endothelin-1 levels to mediate these structural changes providing potential pathological pathways warranting further investigation.

Determine if cocaine use impacts gut permeability, promotes microbial translocation and immune activation in people living with HIV (PLWH) using effective antiretroviral therapy (ART). Cross-sectional analysis of 100 PLWH (ART [greater than or equal to]6 months, HIV-RNA <200 copies/mL) from the Miami Adult Studies on HIV (MASH) cohort. Cocaine use was assessed by self-report, urine screen, and blood benzoylecgonine (BE). Blood samples were collected to assess gut permeability (intestinal fatty acid-binding protein, I-FABP), microbial translocation (lipopolysaccharide, LPS), immune activation (sCD14, sCD27, and sCD163) and markers of inflammation (hs-CRP, TNF-[alpha] and IL-6). Multiple linear regression models were used to analyze the relationships of cocaine use. A total of 37 cocaine users and 63 cocaine non-users were evaluated. Cocaine users had higher levels of I-FABP (7.92±0.35 vs. 7.69±0.56 pg/mL, P = 0.029) and LPS (0.76±0.24 vs. 0.54±0.27 EU/mL, P<0.001) than cocaine non-users. Cocaine use was also associated with the levels of LPS (P<0.001), I-FABP (P = 0.033), and sCD163 (P = 0.010) after adjusting for covariates. Cocaine users had 5.15 times higher odds to exhibit higher LPS levels than non-users (OR: 5.15 95% CI: 1.89-13.9; P<0.001). Blood levels of BE were directly correlated with LPS (rho = 0.276, P = 0.028), sCD14 (rho = 0.274, P = 0.031), and sCD163 (rho = 0.250, P = 0.049). Cocaine use was associated with markers of gut permeability, microbial translocation, and immune activation in virally suppressed PLWH. Mitigation of cocaine use may prevent further gastrointestinal damage and immune activation in PLWH.

Objectives To assess whether HIV infection directly or indirectly promotes coronary artery disease (CAD) volume progression in a longitudinal study of African Americans. Methods We randomly selected 300 individuals with subclinical CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV infected, 174 cocaine users) from 1429 cardiovascularly asymptomatic participants of a prospective epidemiological study between May 2004 and August 2015. Individuals underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years). We quantified noncalcified (NCP: −100–350HU), low-attenuation noncalcified (LA-NCP: −100-30HU), and calcified (CP: ≥ 351 HU) plaque volumes. Linear mixed models were used to assess the effects of HIV infection, atherosclerotic cardiovascular disease (ASCVD) risk, and years of cocaine use on plaque volumes. Results There was no significant difference in annual progression rates between HIV-infected and HIV-uninfected regarding NCP (8.7 [IQR: 3.0–19.4] mm 3 /year vs. 4.9 [IQR: 1.5–18.3] mm 3 /year, p = 0.14), LA-NCP (0.2 [IQR: 0.0–1.6] mm 3 /year vs. 0.2 [IQR: 0.0–0.9] mm 3 /year, p = 0.07) or CP volumes (0.3 [IQR: 0.0–3.4] mm 3 /year vs. 0.1 [IQR: 0.0–3.2] mm 3 /year, p = 0.30). Multivariately, HIV infection was not associated with NCP (−6.9mm 3 , CI: [−32.8–19.0], p = 0.60), LA-NCP (−0.1mm 3 , CI: [−2.6–2.4], p = 0.92), or CP volumes (−0.3mm 3 , CI: [−9.3–8.6], p = 0.96). However, each percentage of ASCVD and each year of cocaine use significantly increased total, NCP, and CP volumes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-associated medications had any effect on plaque volumes ( p > 0.05 for all). Conclusions The more profound adverse effect of risk factors in HIV-infected individuals may explain the accelerated progression of CAD in these people, as HIV infection was not independently associated with any coronary plaque volume. Key Points • Human immunodeficiency virus–infected individuals may have similar subclinical coronary artery disease, as the infection is not independently associated with coronary plaque volumes. • However, cardiovascular risk factors and illicit drug use may have a more profound effect on atherosclerosis progression in those with human immunodeficiency virus infection, which may explain the accelerated progression of CAD in these people. • Nevertheless, through rigorous prevention and abstinence from illicit drugs, these individuals may experience similar cardiovascular outcomes as -uninfected individuals.

Objectives. We examined the effectiveness of risk reduction counseling and the role of on-site HIV testing in drug treatment. Methods. Between January and May 2009, we randomized 1281 HIV-negative (or status unknown) adults who reported no past-year HIV testing to (1) referral for off-site HIV testing, (2) HIV risk-reduction counseling with on-site rapid HIV testing, or (3) verbal information about testing only with on-site rapid HIV testing. Results. We defined 2 primary self-reported outcomes a priori: receipt of HIV test results and unprotected anal or vaginal intercourse episodes at 6-month follow-up. The combined on-site rapid testing participants received more HIV test results than off-site testing referral participants (P < .001; Mantel-Haenszel risk ratio = 4.52; 97.5% confidence interval [CI] = 3.57, 5.72). At 6 months, there were no significant differences in unprotected intercourse episodes between the combined on-site testing arms and the referral arm (P = .39; incidence rate ratio [IRR] = 1.04; 97.5% CI = 0.95, 1.14) or the 2 on-site testing arms (P = .81; IRR = 1.03; 97.5% CI = 0.84, 1.26). Conclusions. This study demonstrated on-site rapid HIV testing’s value in drug treatment centers and found no additional benefit from HIV sexual risk-reduction counseling.

Using baseline data from the NIDA Clinical Trials Network 0049 study (Project HOPE), we performed latent class analyses (LCA) to identify discrete classes, or clusters, of people living with HIV (PLWH) based on their past year substance use behaviors and lifetime arrest history. We also performed multinomial logistic regressions to identify key characteristics associated with class membership. We identified 5 classes of substance users (minimal drug users, cocaine users, substantial cocaine/hazardous alcohol users, problem polysubstance users, substantial cocaine/heroin users) and 3 classes of arrest history (minimal arrests, non-drug arrests, drug-related arrests). While several demographic variables such as age and being Black or Hispanic were associated with class membership for some of the latent classes, participation in substance use treatment was the only covariate that was significantly associated with membership in all classes in both substance use and arrest history LCA models. Our analyses reveal complex patterns of behaviors among substance using PLWH and suggest that HIV intervention strategies may need to take into consideration such nuanced differences to better inform future studies and program implementation.

Increasing rates of HIV testing within substance use disorder (SUD) treatment clients is an important public health strategy for reducing HIV transmission rates. The present study examined uptake of HIV testing among 1,224 clients in five SUD treatment units that offered on-site testing in Florida, New York, and California. Nearly one-third (30 %) of the participants, who had not previously tested positive, reported not having been tested for HIV within the past 12 months. Women, African Americans, and injection drug users had a higher likelihood of having been tested within the past 12 months. The SUD treatment program was the most frequently identified location of participants’ last HIV test. Despite the availability of free, on-site testing, a substantial proportion of clients were not tested, suggesting that strategies to increase uptake of testing should include addressing barriers not limited to location and cost.