Relationship between Inflammatory Markers, Endothelial Activation Markers, and Carotid Intima‐Media Thickness in HIV‐Infected Patients Receiving Antiretroviral Therapy

Ross, Alistair; Rizk, Nesrine; O’Riordan, Mary Ann; Dogra, Vikram S.; El-Bejjani, Dalia; Storer, Norma; Harrill, Danielle; Tungsiripat, Marisa; Adell, Jerome; McComsey, Grace A.

doi:10.1086/605578

Cited by 219 publications

(192 citation statements)

References 45 publications

(50 reference statements)

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“…The reasons for this phenomenon are likely complex, although recent studies suggested that chronic inflammation and immune activation/senescence may contribute to the initiation and progression of atherosclerosis in HIV infection (37,(140)(141)(142). LPS represents an important source of inflammatory stimuli (143) and has been investigated in the setting of atherosclerosis (144).…”

Section: Microbial Translocation In Cardiovascular Diseasementioning

confidence: 99%

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

2013

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SUMMARYIn pathogenic simian immunodeficiency virus (SIV) and human immunodeficiency virus (HIV) infections, the translocation of microbial products from the gastrointestinal (GI) tract to portal and systemic circulation has been proposed as a major driver of the chronic immune activation that is associated with disease progression. Consistently, microbial translocation is not present in nonpathogenic SIV infections of natural host species.In vivostudies demonstrated that HIV/SIV-associated microbial translocation results from a series of immunopathological events occurring at the GI mucosa: (i) early and severe mucosal CD4+depletion, (ii) mucosal immune hyperactivation/persistent inflammation; (iii) damage to the integrity of the intestinal epithelium with enterocyte apoptosis and tight junction disruption; and (iv) subverted the gut microbiome, with a predominance of opportunistic bacteria. Directin situevidence of microbial translocation has been provided for SIV-infected rhesus macaques showing translocated microbial products in the intestinal lamina propria and distant sites. While the mechanisms by which microbial translocation causes immune activation remain controversial, a key pathogenic event appears to be innate immunity activation via Toll-like receptors and other pathogen recognition receptors. Accumulating clinical observations suggest that microbial translocation might affect HIV disease progression, response to therapy, and non-AIDS comorbidities. Given its detrimental effect on overall immunity, several interventions to prevent/block microbial translocation are currently under investigation as novel therapeutic agents for HIV/AIDS.

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Section: Microbial Translocation In Cardiovascular Diseasementioning

confidence: 99%

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

2013

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“…56 The risk of CHD is also likely to be higher in patients with chronic inflammation. 57 Carotid artery intima-media thickness (cIMT), a surrogate marker of artherosclerosis, has been associated with vascular inflammation in HIV-positive patients; 58,59 and HIV-positive patients are at increased risk for progression of cIMT compared with sex-and age-matched controls. 50,60 However, others have not shown an increased cIMT in HIV-positive patients compared with HIV-negative controls.…”

Section: Hiv Infectionmentioning

confidence: 99%

HIV infection, aging and cardiovascular disease: epidemiology and prevention

Petoumenos

Worm

2011

Sex. Health

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Abstract. In the developed world, HIV infection is now well managed with very effective and less toxic antiretroviral treatment. HIV-positive patients therefore are living longer, but are now faced by challenges associated with aging. Several non-AIDS associated morbidities are increased in this population, including cardiovascular disease (CVD). It is suggested that CVD occurs earlier among HIV-positive patients compared with HIV-negative patients, and at a higher rate. Several factors have been proposed to contribute to this. First, the traditional CVD risk factors are highly prevalent in this population. High rates of smoking, dyslipidaemia and a family history of CVD have been reported. This population is also aging, with estimates of more than 25% of HIV-positive patients in the developed world being over the age of 50. Antiretroviral treatment, both through its effect on lipids and through other, sometimes less well understood, mechanisms, has been linked to increased CVD risk. HIV infection, especially untreated, is a further contributing factor to increased CVD risk in HIV-positive patients. As the HIV-positive population continues to age, the risk of CVD will continue to increase. Guidelines for the management and prevention of CVD risk have been developed, and are largely modelled on those used in the general population. However, the data currently suggest that these interventions, such as the use of lipid-lowering medications and smoking cessation programs, remain quite low. A better understanding the mechanisms of CVD risk in this aging population and further efforts in improving uptake of prevention strategies will remain an important research area.

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“…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. However, chronic inflammation and immune activation produced by chronic HIV infection as well as many AIDS‐defining events (ADEs) are now recognized as significant drivers in the pathogenesis of non‐AIDS‐related deaths 14, 24, 25, 26, 27, 28.…”

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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Relationship between Inflammatory Markers, Endothelial Activation Markers, and Carotid Intima‐Media Thickness in HIV‐Infected Patients Receiving Antiretroviral Therapy

Cited by 219 publications

References 45 publications

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

Microbial Translocation in the Pathogenesis of HIV Infection and AIDS

HIV infection, aging and cardiovascular disease: epidemiology and prevention

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

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