Trends in Causes of Death among Persons with Acquired Immunodeficiency Syndrome in the Era of Highly Active Antiretroviral Therapy, San Francisco, 1994–1998

Louie, Janice K.; Hsu, Ling; Osmond, Dennis; Katz, Mitchell H.; Schwarcz, Sandra

doi:10.1086/343862

Cited by 176 publications

(119 citation statements)

References 12 publications

(9 reference statements)

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“…With this, there has been a shift in distribution of causes of death toward non‐AIDS‐defining events (NADEs) 8, 9, 10, 11, 12. Factors contributing to non‐AIDS mortality include immunodeficiency 13, 14, ART toxicity 15, 16, increasing age 17, 18, 19, 20, 21, 22, and lifestyle factors such as tobacco use and obesity 18, 21, 23.…”

Section: Introductionmentioning

confidence: 99%

Increased non‐AIDS mortality among persons with AIDS‐defining events after antiretroviral therapy initiation

et al. 2018

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Introduction 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.MethodsWe 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.ResultsThe 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).ConclusionsIn 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.

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Section: Introductionmentioning

confidence: 99%

Increased non‐AIDS mortality among persons with AIDS‐defining events after antiretroviral therapy initiation

et al. 2018

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“…Respiratory symptoms are common in the HIV-infected population, particularly in HIV-infected persons who smoke, and obstructive lung disease is an increasing cause of morbidity and mortality in the HIV-infected population. Almost 4% of deaths among HIV-infected persons in 1998 were due to obstructive airway disease, representing a 3-fold increase from the preantiretroviral therapy era (3). Rates of hospitalization for asthma, bronchitis, and COPD have also increased since the early 1990s (4).…”

mentioning

confidence: 99%

HIV and Chronic Obstructive Pulmonary Disease: Is It Worse and Why?

Morris¹,

George²,

Crothers³

et al. 2011

Proceedings of the American Thoracic Society

110

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“…Despite advances in treatment strategies and the introduction of antiretroviral therapy (ART), pulmonary diseases remain a leading cause of morbidity and mortality in HIV-infected patients (34). Both emphysema and chronic obstructive pulmonary disease (COPD) have been reported at an increased frequency in HIV-infected patients (7,15) and, unlike many AIDS-associated opportunistic infections, HIV-associated COPD may be increasing due to the prolonged life expectancy of the HIV ϩ population with ART and the high smoking rate in this population (5,24).…”

mentioning

confidence: 99%

Relationship of Pneumocystis jiroveci Humoral Immunity to Prevention of Colonization and Chronic Obstructive Pulmonary Disease in a Primate Model of HIV Infection

Kling

Shipley²,

Patil³

et al. 2010

Infect Immun

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Pulmonary colonization by the opportunistic pathogen Pneumocystis jiroveci is common in HIV؉ subjects and has been associated with development of chronic obstructive pulmonary disease (COPD). Host and environmental factors associated with colonization susceptibility are undefined. Using a simian-human immunodeficiency virus (SHIV) model of HIV infection, the immunologic parameters associated with natural Pneumocystis jiroveci transmission were evaluated. SHIV-infected macaques were exposed to P. jiroveci by cohousing with immunosuppressed, P. jiroveci-colonized macaques in two independent experiments. Serial plasma and bronchoalveolar lavage (BAL) fluid samples were examined for changes in antibody titers to recombinant Pneumocystis-kexin protein (KEX1) and evidence of Pneumocystis colonization by nested PCR of BAL fluid. In experiment 1, 10 of 14 monkeys became Pneumocystis colonized (Pc ؉ ) by 8 weeks post-SHIV infection, while 4 animals remained Pneumocystis colonization negative (Pc ؊ ) throughout the study. In experiment 2, 11 of 17 animals became Pneumocystis colonized by 16 weeks post-SHIV infection, while 6 monkeys remained Pc ؊ . Baseline plasma KEX1-IgG titers were significantly higher in monkeys that remained Pc ؊ , compared to Pc ؉ monkeys, in experiments 1 (P ‫؍‬ 0.013) and 2 (P ‫؍‬ 0.022). Pc ؊ monkeys had greater percentages of Pneumocystis-specific memory B cells after SHIV infection compared to Pc ؉ monkeys (P ‫؍‬ 0.037). After SHIV infection, Pc ؉ monkeys developed progressive obstructive pulmonary disease, whereas Pc ؊ monkeys maintained normal lung function throughout the study. These results demonstrate a correlation between the KEX1 humoral response and the prevention of Pneumocystis colonization and obstructive lung disease in the SHIV model. In addition, these results indicate that an effective Pneumocystis-specific memory B-cell response is maintained despite progressive loss of CD4 ؉ T cells during SHIV infection.

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Trends in Causes of Death among Persons with Acquired Immunodeficiency Syndrome in the Era of Highly Active Antiretroviral Therapy, San Francisco, 1994–1998

Cited by 176 publications

References 12 publications

Increased non‐AIDS mortality among persons with AIDS‐defining events after antiretroviral therapy initiation

Increased non‐AIDS mortality among persons with AIDS‐defining events after antiretroviral therapy initiation

HIV and Chronic Obstructive Pulmonary Disease: Is It Worse and Why?

Relationship of Pneumocystis jiroveci Humoral Immunity to Prevention of Colonization and Chronic Obstructive Pulmonary Disease in a Primate Model of HIV Infection

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