Markers of Inflammation, Coagulation, and Renal Function Are Elevated in Adults with HIV Infection

Abstract

Background HIV replication and immune activation may increase inflammation and coagulation biomarkers. Limited data exist comparing such biomarkers for those with and without HIV infection. Methods For those aged 45–76, high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), D-dimer, and cystatin C were compared for 494 HIV-infected individuals in the Strategies for Management of Anti-Retroviral Therapy (SMART) study with 5,386 participants in the Multi-Ethnic Study of Atherosclerosis (MESA). For those aged 33–44, hsCRP and IL-6 were compared for 287 participants in SMART with 3,231 participants in the Coronary Artery Development in Young Adults (CARDIA) Study. Results hsCRP and IL-6 were 55% (p<0.001) and 62% (p<0.001) higher among HIV-infected participants compared to CARDIA. Compared to MESA, hsCRP, IL-6, D-dimer and cystatin C were 50%, 152%, 94%, and 27% higher (p<0.001 for each). For HIV-infected participants on ART with HIV-RNA levels ≤400 copies/mL, levels were higher (p<0.001) than the general population for all biomarkers (by 21% to 60%). Conclusions hsCRP, IL-6, D-dimer and cystatin C are elevated with HIV infection and remain so even after HIV-RNA levels are suppressed with ART. Further research is needed on the pathophysiology of HIV-induced activation of inflammatory and coagulation pathways in order to guide potential interventions.

Metabolic Effects of Darunavir/Ritonavir Versus Atazanavir/Ritonavir in Treatment-Naive, HIV Type 1-Infected Subjects over 48 Weeks

“…39 Subjects infected with HIV-1 have increased levels of hs-CRP, TNF alpha (TNF-a), IL-6, d-dimer, and other biomarkers compared with HIV-negative subjects. 2,[40][41][42] These elevations in biomarkers persist even after virologic suppression, likely due to HIV-induced activation of inflammation and coagulation pathways. 2 Levels of TNF-a, IL-6, hs-CRP, and other proinflammatory cytokines are associated with HIV-1 viral load and may predict disease progression, as well as correlate with a higher risk of CVD and all-cause mortality.…”

“…2,[40][41][42] These elevations in biomarkers persist even after virologic suppression, likely due to HIV-induced activation of inflammation and coagulation pathways. 2 Levels of TNF-a, IL-6, hs-CRP, and other proinflammatory cytokines are associated with HIV-1 viral load and may predict disease progression, as well as correlate with a higher risk of CVD and all-cause mortality. [42][43][44][45] Our findings corroborate another recent analysis, which reported that only d-dimer, and not IL-6 or hs-CRP, is reduced over the short term in those initiating ARV therapy.…”

HIV infection, aging and cardiovascular disease: epidemiology and prevention

“…[9][10][11][12] Lifestyle factors such as smoking and substance misuse are much higher in HIV-positive patients, 13,14 and HIV-positive patients are also more likely to experience dyslipidaemia and often have other chronic conditions that increase the risk of severe non-AIDS morbidity. 15 Furthermore, antiretroviral treatment (ART) increases the rates of dyslipidaemia, insulin resistance and diabetes. 16,17 Finally, HIV infection itself appears to be associated with age-related complications.…”

HIV pada Geriatri HIV in Geriatrics

“…Pengaruh terapi antiretroviral dalam mengatasi hal tersebut belum diketahui dan sulit untuk ditentukan karena dinilai memiliki efek toksik terhadap organ-organ tersebut. 22 Sebuah studi melaporkan bahwa angka kejadian osteopenia dan osteoporosis tiga kali lebih tinggi pada populasi HIV. Fraktur juga lebih sering dijumpai pada pasien HIV.…”