Dataset Information

Incidence of AIDS-Defining Opportunistic Infections in a Multicohort Analysis of HIV-infected Persons in the United States and Canada, 2000-2010.

ABSTRACT:

Background

There are few recent data on the rates of AIDS-defining opportunistic infections (OIs) among human immunodeficiency virus (HIV)-infected patients in care in the United States and Canada.

Methods

We studied HIV-infected participants in 16 cohorts in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) during 2000-2010. After excluding 16 737 (21%) with any AIDS-defining clinical events documented before NA-ACCORD enrollment, we analyzed incident OIs among the remaining 63 541 persons, most of whom received antiretroviral therapy during the observation. We calculated incidence rates per 100 person-years of observation (hereafter, "person-years") with 95% confidence intervals (CIs) for the first occurrence of any OI and select individual OIs during 2000-2003, 2004-2007, and 2008-2010.

Results

A total of 63 541 persons contributed 261 573 person-years, of whom 5836 (9%) developed at least 1 OI. The incidence rate of any first OI decreased over the 3 observation periods, with 3.0 cases, 2.4 cases, and 1.5 cases per 100 person-years of observation during 2000-2003, 2004-2007, and 2008-2010, respectively (Ptrend<.001); the rates of most individual OIs decreased as well. During 2008-2010, the leading OIs included Pneumocystis jiroveci pneumonia, esophageal candidiasis, and disseminated Mycobacterium avium complex or Mycobacterium kansasii infection.

Conclusions

For HIV-infected persons in care during 2000-2010, rates of first OI were relatively low and generally declined over this time.

SUBMITTER: Buchacz K

PROVIDER: S-EPMC4996145 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

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Publications

Incidence of AIDS-Defining Opportunistic Infections in a Multicohort Analysis of HIV-infected Persons in the United States and Canada, 2000-2010.

Buchacz Kate K Lau Bryan B Jing Yuezhou Y Bosch Ronald R Abraham Alison G AG Gill M John MJ Silverberg Michael J MJ Goedert James J JJ Sterling Timothy R TR Althoff Keri N KN Martin Jeffrey N JN Burkholder Greer G Gandhi Neel N Samji Hasina H Patel Pragna P Rachlis Anita A Thorne Jennifer E JE Napravnik Sonia S Henry Keith K Mayor Angel A Gebo Kelly K Gange Stephen J SJ Moore Richard D RD Brooks John T JT

The Journal of infectious diseases 20160418 6

<h4>Background</h4>There are few recent data on the rates of AIDS-defining opportunistic infections (OIs) among human immunodeficiency virus (HIV)-infected patients in care in the United States and Canada.<h4>Methods</h4>We studied HIV-infected participants in 16 cohorts in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) during 2000-2010. After excluding 16 737 (21%) with any AIDS-defining clinical events documented before NA-ACCORD enrollment, we analyzed inciden ...[more]

PMID: 27559122

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Project description:Background and introduction Human immune deficiency virus (HIV) infection remains a major health problem since discovery of the virus in 1981. Globally, since introduction of antiretroviral therapy, AIDS-related mortality was reduced by 47% since 2010. Also, HIV-related opportunistic infections (OIs) became less common, especially with use of prophylaxis to prevent such infections. In this study, we aim to assess the incidence of HIV infection and related OIs in Qatar for 17-year period, and to assess the spectrum of these infections, risk factors and treatment outcomes. Methods This is a retrospective cohort study for all HIV infected patients registered in the state of Qatar from 2000 to 2016. Incidence of HIV infection and related opportunistic illness was calculated per 100,000 population. Demographic and Clinical characteristic were compared between two groups of patients with and without opportunistic illness. Results of 167 cases with HIV infection 54 (32.3%) had opportunistic illness. The average incidence rate of HIV infection over 17 years is 0.69 per 100,000 population, and the incidence rate for opportunistic illness is 0.27 per 100,000 population. The most common opportunistic illness is pneumocystis jirovecii pneumonia (PCP) which constituted 25% of cases, followed by cytomegalovirus (CMV) retinitis 7.2%, Tuberculosis 5.4%, Toxoplasmosis 4.2% and, less than 2% for each of Kaposi sarcoma, lymphoma and cryptococcal infection. The outcome of treatment of cases with opportunistic illness showed cure rates of 59.3%, one year relapse rates of 8.76% and overall, 90-day mortality of 3.7% however, 33.4% of patients left the country before completion of therapy. Most of our patients in both groups were of young age, majority males, and almost half of them were Qatari. The CD4 count, CD4%, CD4/CD8 ratio and viral load were statistically significant risk factors in cases with opportunistic illness with a p value < 0.05, however presence of comorbidities was lower in patients with opportunistic illness P value of 0.032. Conclusion Qatar has a low prevalence rate for HIV infection and related opportunistic illness. Early diagnosis and use of antiretroviral therapy are important measures to decrease the rate of opportunistic illness. Highlights • HIV is a widely spread infection with special interest to public health.• HIV-related morbidity is associated with a large burden to health systems.• It is associated with opportunistic infections that affect all body systems.• Population-based studies are essential for understanding its complications.

Project description:HIV-1 infection leads to chronic inflammation and to an increased risk of non-AIDS mortality. Our objective was to determine whether AIDS-defining events (ADEs) were associated with increased overall and cause-specific non-AIDS related mortality after antiretroviral therapy (ART) initiation. We included HIV treatment-naïve adults from the Antiretroviral Therapy Cohort Collaboration (ART-CC) who initiated ART from 1996 to 2014. Causes of death were assigned using the Coding Causes of Death in HIV (CoDe) protocol. The adjusted hazard ratio (aHR) for overall and cause-specific non-AIDS mortality among those with an ADE (all ADEs, tuberculosis (TB), Pneumocystis jiroveci pneumonia (PJP), and non-Hodgkin's lymphoma (NHL)) compared to those without an ADE was estimated using a marginal structural model. The adjusted hazard of overall non-AIDS mortality was higher among those with any ADE compared to those without any ADE (aHR 2.21, 95% confidence interval (CI) 2.00 to 2.43). The adjusted hazard of each of the cause-specific non-AIDS related deaths were higher among those with any ADE compared to those without, except metabolic deaths (malignancy aHR 2.59 (95% CI 2.13 to 3.14), accident/suicide/overdose aHR 1.37 (95% CI 1.05 to 1.79), cardiovascular aHR 1.95 (95% CI 1.54 to 2.48), infection aHR (95% CI 1.68 to 2.81), hepatic aHR 2.09 (95% CI 1.61 to 2.72), respiratory aHR 4.28 (95% CI 2.67 to 6.88), renal aHR 5.81 (95% CI 2.69 to 12.56) and central nervous aHR 1.53 (95% CI 1.18 to 5.44)). The risk of overall and cause-specific non-AIDS mortality differed depending on the specific ADE of interest (TB, PJP, NHL). In this large multi-centre cohort collaboration with standardized assignment of causes of death, non-AIDS mortality was twice as high among patients with an ADE compared to without an ADE. However, non-AIDS related mortality after an ADE depended on the ADE of interest. Although there may be unmeasured confounders, these findings suggest that a common pathway may be independently driving both ADEs and NADE mortality. While prevention of ADEs may reduce subsequent death due to NADEs following ART initiation, modification of risk factors for NADE mortality remains important after ADE survival.

Project description:BackgroundThe suppression of viremia among persons with HIV (PWH) using antiretroviral therapy has been hypothesized to reduce HIV incidence at the population level. We investigated the impact of state level viral suppression among PWH in the United States on estimated HIV incidence between 2010 and 2015.MethodsViral suppression data and HIV incidence estimates from the National HIV Surveillance System were available from 29 states and the District of Columbia. We assumed a one year delay for viral suppression to impact incidence. Poisson regression models were used to calculate the estimated annual percent change (EAPC) in incidence rate. We employed a multivariable mixed-effects Poisson regression model to assess the effects of state level race/ethnicity, socioeconomic status, percent men who have sex with men (MSM) and hepatitis C virus prevalence as a proxy for injection drug use on HIV incidence.FindingsFitted HIV incidence for 30 jurisdictions declined from 11.5 in 2010 to 10.0 per 100,000 population by 2015 corresponding with an EAPC of -2.67 (95% confidence interval [95%CI] -2.95, -2.38). Southern states experienced the highest estimated incidence by far throughout this period but upon adjustment for viral suppression and demographics there was a 36% lower incidence rate than Northeast states (adjusted rate ratio [aRR] 0.64; 95%CI 0.42, 0.99). For every 10 percentage point (pp) increase in viral suppression there was an adjusted 4% decline in HIV incidence rate in the subsequent year (aRR 0.96; 95%CI 0.93, 0.99). While controlling for viral suppression, HIV incidence rate increased by 42% (aRR 1.42 95%CI 1.31, 1.54) for every 5 pp increase in percent Black race and by 27% (aRR 1.27 95%CI 1.10, 1.48) for every 1 pp increase in percent MSM in states.InterpretationA decline in estimated HIV incidence from 2010 to 2015 was associated with increasing viral suppression in the United States. Race and sexual orientation were important HIV acquisition risk factors.

Project description:Background:Viral suppression is a primary marker of HIV treatment success. Persons with HIV are at increased risk for AIDS-defining cancer (ADC) and several types of non-AIDS-defining cancer (NADC), some of which are caused by oncogenic viruses. Objective:To determine whether viral suppression is associated with decreased cancer risk. Design:Prospective cohort. Setting:Department of Veterans Affairs. Participants:HIV-positive veterans (n = 42 441) and demographically matched uninfected veterans (n = 104 712) from 1999 to 2015. Measurements:Standardized cancer incidence rates and Poisson regression rate ratios (RRs; HIV-positive vs. uninfected persons) by viral suppression status (unsuppressed: person-time with HIV RNA levels ?500 copies/mL; early suppression: initial 2 years with HIV RNA levels <500 copies/mL; long-term suppression: person-time after early suppression with HIV RNA levels <500 copies/mL). Results:Cancer incidence for HIV-positive versus uninfected persons was highest for unsuppressed persons (RR, 2.35 [95% CI, 2.19 to 2.51]), lower among persons with early suppression (RR, 1.99 [CI, 1.87 to 2.12]), and lowest among persons with long-term suppression (RR, 1.52 [CI, 1.44 to 1.61]). This trend was strongest for ADC (unsuppressed: RR, 22.73 [CI, 19.01 to 27.19]; early suppression: RR, 9.48 [CI, 7.78 to 11.55]; long-term suppression: RR, 2.22 [CI, 1.69 to 2.93]), much weaker for NADC caused by viruses (unsuppressed: RR, 3.82 [CI, 3.24 to 4.49]; early suppression: RR, 3.42 [CI, 2.95 to 3.97]; long-term suppression: RR, 3.17 [CI, 2.78 to 3.62]), and absent for NADC not caused by viruses. Limitation:Lower viral suppression thresholds, duration of long-term suppression, and effects of CD4+ and CD8+ T-cell counts were not thoroughly evaluated. Conclusion:Antiretroviral therapy resulting in long-term viral suppression may contribute to cancer prevention, to a greater degree for ADC than for NADC. Patients with long-term viral suppression still had excess cancer risk. Primary Funding Source:National Cancer Institute and National Institute on Alcohol Abuse and Alcoholism of the National Institutes of Health.

Project description:BACKGROUND:The differential effects of commonly prescribed combined antiretroviral therapy (cART) regimens on AIDS-defining neurological conditions (neuroAIDS) remain unknown. SETTING:Prospective cohort studies of HIV-positive individuals from Europe and the Americas included in the HIV-CAUSAL Collaboration. METHODS:Individuals who initiated a first-line cART regimen in 2004 or later containing a nucleoside reverse transcriptase inhibitor backbone and either atazanavir, lopinavir, darunavir, or efavirenz were followed from cART initiation until death, lost to follow-up, pregnancy, the cohort-specific administrative end of follow-up, or the event of interest, whichever occurred earliest. We evaluated 4 neuroAIDS conditions: HIV dementia and the opportunistic infections toxoplasmosis, cryptococcal meningitis, and progressive multifocal leukoencephalopathy. For each outcome, we estimated hazard ratios for atazanavir, lopinavir, and darunavir compared with efavirenz via a pooled logistic model. Our models were adjusted for baseline demographic and clinical characteristics. RESULTS:Twenty six thousand one hundred seventy-two individuals initiated efavirenz, 5858 initiated atazanavir, 8479 initiated lopinavir, and 4799 initiated darunavir. Compared with efavirenz, the adjusted HIV dementia hazard ratios (95% confidence intervals) were 1.72 (1.00 to 2.96) for atazanavir, 2.21 (1.38 to 3.54) for lopinavir, and 1.41 (0.61 to 3.24) for darunavir. The respective hazard ratios (95% confidence intervals) for the combined end point were 1.18 (0.74 to 1.88) for atazanavir, 1.61 (1.14 to 2.27) for lopinavir, and 1.36 (0.74 to 2.48) for darunavir. The results varied in subsets defined by calendar year, nucleoside reverse transcriptase inhibitor backbone, and age. CONCLUSION:Our results are consistent with an increased risk of neuroAIDS after initiating lopinavir compared with efavirenz, but temporal changes in prescribing trends and confounding by indication could explain our findings.

Project description:BackgroundStudies have reported young ages at cancer diagnosis in HIV-infected persons and have suggested that HIV accelerates carcinogenesis. However, these comparisons did not account for differences in population age structures.ObjectiveTo compare ages at diagnosis for non-AIDS-defining types of cancer that occur in both the AIDS and general populations, after adjustment for differences in age and other demographic characteristics between these populations.DesignRegistry linkage study.Setting15 HIV/AIDS and cancer registry databases in the United States.Participants212 055 persons with AIDS enrolled in the U.S. HIV/AIDS Cancer Match Study from 1996 to 2007.MeasurementsComparison of age-at-diagnosis distributions for various types of cancer in both the AIDS and general populations, after adjustment for age and other demographic characteristics.ResultsThe proportion of person-time contributed by older persons (age ≥65 years) was far smaller in the AIDS population (1.5%) than in the general population (12.5%). Reflecting this difference, the ages at diagnosis for most types of cancer were approximately 20 years younger among persons with AIDS. However, after adjustment for differences in the populations at risk, the median ages at diagnosis in the AIDS and general populations did not differ for most types of cancer (for example, colon, prostate, or breast cancer; all P > 0.100). In contrast, ages at diagnosis of lung (median, 50 vs. 54 years) and anal cancer (median, 42 vs. 45 years) were significantly younger in persons with AIDS than expected in the general population (P < 0.001), and the age at diagnosis of Hodgkin lymphoma was significantly older (median, 42 vs. 40 years; P < 0.001).LimitationsInformation on other cancer risk factors, including cigarette smoking, was not available. Analysis was restricted to non-Hispanic white and black persons who had AIDS, which could limit the generalizability of the findings to other racial and ethnic groups or to persons with HIV but not AIDS.ConclusionFor most types of cancer, the age at diagnosis is similar in the AIDS and general populations, after adjustment for the ages of the populations at risk. Modest age differences remained for a few types of cancer, which may indicate either acceleration of carcinogenesis by HIV or earlier exposure to cancer risk factors.Primary funding sourceNational Cancer Institute.

Dataset Information

Incidence of AIDS-Defining Opportunistic Infections in a Multicohort Analysis of HIV-infected Persons in the United States and Canada, 2000-2010.

Background

Methods

Results

Conclusions

Publications

Incidence of AIDS-Defining Opportunistic Infections in a Multicohort Analysis of HIV-infected Persons in the United States and Canada, 2000-2010.

Similar Datasets

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