CROI 2016 Abstract eBook
Abstract Listing
Poster Abstracts
Results: Of 553 subjects, 158 (28.6%) were female, 536 (96.9%) were black, 490 (88.6%) had HCV, and 129 (23.3%) had HIV. The median total study interval was 16 yrs (IQR 15, 17), which included baseline to first TE (11 yrs [11, 12]) and first TE to most recent (5 yrs [4, 5]). At first TE, 337 (65.8%) participants had minimal liver stiffness (<8kPa), 103 (20.1%) had intermediate levels of liver stiffness (8-12.2 kPa), and 72 (14.1%) had evidence of cirrhosis (≥12.3 kPa). As previously published, liver stiffness was associated (p<0.001) with age, HIV, HCV RNA, BMI, and HBV. Interestingly, the initial IGF-1 level taken a median of 11 yrs earlier was inversely associated with liver stiffness (OR -11.6; 95% CI -22.0, -1.1; p=0.03), after adjusting for age, even though IGF-1 levels were also strongly and independently associated with age (p<0.0001). Declines in IGF-1 were also noted: at a rate of -1.84 pg/mL-yr in HCV mono-infected persons and at a rate of -1.47 pg/mL-yr in HIV/HCV co-infected persons (p<0.0001 for both compared to baseline). However, there was little evidence that IGF-1 levels (at baseline, the time of the TE, or the rate of change) altered associations of age and HIV with liver stiffness by GEE. Conclusions: Although IGF-1 levels were strongly associated with age and liver stiffness, we found no support that IGF-1 contributes to how HIV-1 accelerates liver aging. 713 HLA-B57.01 Promotes Significantly Better Periodontal Health in HIV-Positive Patients Gundolf Schuettfort 1 ; Kyu Hyun Park 2 ; Christoph Stephan 3 ;TimoWolf 4 ; Annette Haberl 4 ; Eva Herrmann 1 ; Hans-Reinhard Brodt 4 ; Philipp de Leuw 1 1 Univ Hosp Frankfurt, Frankfurt amMain, Germany; 2 Dental Office, Schöner Mund Oberursel, Oberursel, Germany; 3 Goethe Univ Hosp Frankfurt, Frankfurt, Germany; 4 JW Goethe Univ of Frankfurt, Frankfurt, Germany Background: In HIV-negative subjects with chronic periodontitis a relationship between the individual HLA system (human leukocyte antigen) and the incidence of chronic periodontitis was observed. The presented study is the first that investigates the incidence of chronic periodontitis in HIV-positive patients in connection with the HLA system and in particular with the HLA-B57.01 status. This study hereby evaluates associations among periodontitis, the HLA system and additional risk factors in HIV-positive patients in multivariate analyses. Methods: A group of 100 HIV-positive patients was enrolled in the study program. 45 patients were treatment naïve, whereas 55 patients were treated with combined antiretroviral therapy (cART). 19 patients presented a positive HLA-B57.01 status.The patients which received cART were treated with cART for at least 12 months. The periodontal testing included PSI-Score (Periodontal Screening Index), GI (Gingivalindex), Bleeding on Probing Index (BOP) and the DMF-T Score (decayed, missing, filled teeth). The testing was performed with a standardized periodontal probe by an experienced dentist. Results: HIV-positive patients who were carriers of HLA-B57.01 had significantly lower PSI- (p=< 0,001), GI- (p=< 0,001) and BOP-Scores (p=< 0,001) in comparison to naïve HIV-positive Patients as well as HIV-positive patients receiving cART, who were both not carriers of HLA-B57.01. A lower value of PSI-, GI- and BOP-Score equals a better periodontal health. The adjusted odds ratio (OR) of periodontitis was decreased in patients who were carriers of HLA-B57.01 by measurement of PSI-Score (OR = 0.006, 95% confidence interval (CI) = 0.001 to 0.026), GI-Score (OR = 0.018, 95% confidence interval (CI) = 0.003 to 0.104) and BOP-Score (OR = 0.003, 95% confidence interval (CI) =< 0.001 to 0.011). The DMF-T score showed no significant difference (p = 0.516) between the HIV-positive patients with and without cART, regardless of their HLA-B57.01 status. Conclusions: HLA-B57.01 was identified as an independent resistance indicator for generalized periodontitis in HIV-positive patients with respect to established cofactors for periodontitis. The underlying biological mechanisms for this finding have to be investigated in the future, especially the questions if there are periodontitis-specific bacterial peptides that are expressed by HLA-B57.01 and if HLA-B57.01 molecules are able to influence the immune response against periodontopathogens.
Poster Abstracts
Fig.1: Periodontal Screening Index (PSI) Median
714 Association of Depressive Symptoms With Biomarkers in Veterans With andWithout HIV
Jessica R. White 1 ; Kaku So-Armah 2 ; Jesse Stewart 3 ; Samir Gupta 4 ; Adeel A. Butt 5 ; Cynthia Gibert 6 ; Maria Rodriguez-Barradas 7 ; Roger Bedimo 8 ; Amy C. Justice 9 ; Matthew S. Freiberg 10 1 Maricopa County Dept of PH, Phoenix, AZ, USA; 2 Boston Univ Sch of Med, Boston, MA, USA; 3 Indiana Univ Purdue Univ Indianapolis, Indianapolis, IN, USA; 4 Indiana Univ Sch of Med, Indianapolis, IN, USA; 5 Hamad Hlthcare Quality Inst, Doha, Qatar; 6 VA Med Cntr, Washington, DC, USA; 7 Michael E. DeBakey VA Med Cntr and Baylor Coll of Med, Houston, TX, USA; 8 Dallas VA Med Cntr, Dallas, TX, USA; 9 Yale Univ, New Haven, CT, USA; 10 Vanderbilt Univ Sch of Med, Nashville, TN, USA Background: HIV infection is associated with increased cardiovascular disease risk. Recently, we found that HIV+ veterans with a diagnosis of clinical depression have higher risk of heart failure compared to HIV+ veterans without depression. To explain the physiological mechanism underlying this finding, we compared biomarkers of inflammation (IL-6), monocyte activation (sCD14) and altered coagulation (D-dimer) between HIV+ and HIV- veterans with and without depressive symptoms. Prior studies have separately linked higher IL-6 and D-dimer with HIV and depression. However, no study has examined these biomarkers in a cohort of HIV+ and HIV- people with and without depression. We hypothesize that HIV+ people with depression will have higher IL-6, sCD14 and D-dimer than people with one or neither of these conditions. Methods: Participants in this study were from the Veterans Aging Cohort Study-Biomarker Cohort, a prospective cohort study of HIV+ and HIV- veterans who provided blood specimens for research. Depression was assessed using the Patient Health Questionnaire-9 (PHQ-9), with scores ≥ 10 indicative of clinically significant symptoms of major depressive disorder in the last two weeks. We used linear regression to assess the associations between depression and biomarker levels, adjusting for age, race/ethnicity, hypertension, obesity, smoking, hepatitis C infection, antidepressant medication, and HIV infection. Results: In this sample of 2224 participants, 573 (24%) participants reported clinically significant depressive symptoms. PHQ-9 scores ≥ 10 were not associated with significant differences in IL-6, sCD14 or D-dimer in adjusted models (Table). Given a significant interaction between HIV and PHQ-9 in IL-6 models (P=0.07), we stratified this analysis by HIV status. PHQ-9≥10 was associated with higher IL-6 among HIV– veterans [β (95% CI): 0.11 (-0.02, -0.25)] but not among HIV infected participants with HIV-1 RNA< or ≥500 copies/ mL [0.00 (-0.12, 0.12) and -0.07 (-0.23, 0.09) respectively; p>0.05 for all]. Conclusions: We did not observe associations between depressive symptoms and IL-6, sCD14 or D-dimer. These findings suggest that the physiological pathways mediating depression and heart failure risk may not be captured by IL-6, sCD14, or D-dimer in HIV infected people. Future research is needed to elucidate the mechanisms driving depression- associated heart failure risk in HIV infected people.
296
CROI 2016
Made with FlippingBook - Online catalogs