Suchergebnisse

Purpose of the studyTo investigate the impact of ART, HIV viremia and immunosuppression on triglyceride (TG), total cholesterol (TC) and high density lipoprotein cholesterol (HDL‐C) levels.MethodsWe considered the cross‐sectional associations between TG, TC and HDL‐C (mmol/l; first available measurement on/after enrolment in the D:A:D study) and use of ART, HIV viral load (VL; copies/ml), and CD4 count (cells/mm3) measured at the same time. TG was log10 transformed to ensure normality. Analyses were performed using linear regression and adjusted for other factors known to impact lipid levels (table footnote). ART and VL status were combined (off ART&VL >100,000, off ART&VL <100,000, on ART&VL <500, on ART&VL >500), current and nadir CD4 count were categorised as <200, 200–349, 350–499 and >500.Summary of results44,322/49,734 participants in the D:A:D Study (89.1%) contributed a TG measurement (median; IQR 1.52; 1.00–2.45), 45,169 (90.8%) a TC measurement (4.80; 4.00–5.70) and 38,604 (77.6%) a HDL‐C measurement (1.12; 0.90–1.40). Most participants were male (74%), of white ethnicity (51%), without AIDS (78%), were not receiving lipid‐lowering drugs (4%) and were ART experienced (61%) with 47% previously exposed to PIs, 61% previously exposed to NRTIs and 29% previously exposed to NNRTIs. The median (IQR) age, current CD4 count and CD4 nadir were 38 (36–45) years, 400 (242–590) cells/µl and 240 (100–410) cells/µl respectively. Compared to those on ART with a suppressed VL, all lipids were lower for those off ART (Table); non‐suppressive ART was also associated with lower TC and HDL‐C levels (no impact on TG). A low current CD4 count was associated with lower lipid levels, whereas a low nadir CD4 count was associated with higher TC and TG levels. Prior AIDS diagnosis was associated with higher TG and TC, but lower HDL‐C levels.

Impact of ART, immunosuppression and viraemia, on TG, TC and HDL‐C (mmol/l)












Average impact on log10TG*†

Average inpact on TC*
Average impact on HDL‐C*




ART and VL


Off ART … VL≥100000
−0.09 (−0.10,−0.08)
<0.001
−0.55 (−0.60,−0.51)
<0.001
−0.14 (−0.16,−0.13)
<0.001


Off ART … VL<100000
−0.04 (−0.06,−0.03)
<0.001
−0.85 (−0.91,−0.78)
<0.001
−0.31 (−0.33,−0.29)
<0.001


On ART … VL<500
Ref

Ref

Ref



On ART … VL≥500
0.00 (−0.01, 0.00)
0.38
−0.40 (−0.44,−0.36)
<0.001
−0.16 (−0.17,−0.15)
<0.001


CD4 count


<200
−0.03 (−0.04,−0.02)
<0.001
−0.33 (−0.39,−0.28)
<0.001
−0.04 (−0.06,−0.02)
<0.001


200–349
−0.02 (−0.03,−0.01)
<0.001
−0.11 (−0.15,−0.06)
<0.001
0.00 (−0.01, 0.02)
0.72


350–499
Ref

Ref

Ref



500+
0.04 (0.03, 0.04)
<0.001
0.12 (0.08, 0.16)
<0.001
−0.02 (−0.03,−0.00)
0.02


Nadir CD4 Count


<200
0.07 (0.06, 0.08)
<0.001
0.19 (0.14, 0.24)
<0.001
−0.05 (−0.06,−0.03)
<0.001


200–349
0.02 (0.01, 0.03)
<0.001
0.01 (−0.03, 0.06)
0.57
−0.03 (−0.05,−0.02)
<0.001


350–499
Ref

Ref

Ref



500 +
0.00 (−0.02, 0.01)
0.33
0.03 (−0.02, 0.09)
0.23
0.04 (0.02, 0.06)
<0.001


Prior AIDS
0.05 (0.05, 0.06)
<0.001
0.11 (0.08, 0.15)
<0.001
−0.03 (−0.04,−0.01)
<0.001





estimates included are mutually adjusted for each other and for the following demographic variables: age; gender; mode of infection; ethnicity; body mass index; smoking; family history of CVD; diabetes; use of lipid lowering drugs; co‐infection with hepatitis C; participating cohort; and year of entry into study.
TG is log10 transformed. Thus, the results presented for TG reflect relative rather than absolute effects. For example, lipid levels for those off ART … VL ≥100000 are 9% lower than those on ART … VL < 500.

ConclusionAlthough specific drug classes were not considered, lipid levels are considerably higher in those on a suppressive ART regimen. The higher TC/TG and lower HDL‐C levels seen among those with low nadir CD4 count and with a prior AIDS diagnosis suggests severe immunosuppression may be associated with dyslipidaemia over the long‐term.

AbstractUp to 30% of European HIV‐positive patients tested for hepatitis C virus (HCV) are seropositive. All co‐infected patients with chronic HCV and ≥F2 fibrosis should be considered for HCV therapy given their increased risk of death from liver disease. Despite this the extent to which co‐infected patients initiate HCV treatment is not well described. The aims of this study were to determine the rate of HCV treatment uptake among co‐infected patients and to estimate the effect of treatment on all‐cause and liver‐related death. EuroSIDA patients positive for HCV antibody and HCV‐RNA were included in the study. Baseline was defined as the date of recruitment or HCV seroconversion, whichever occurred later. Poisson regression was used to identify temporal changes and regional differences in HCV treatment uptake (use of at least interferon‐α [peg‐IFN]± ribavirin) and to study the association between HCV treatment and progression to all‐cause and liver‐related death. 1947 patients were included, with a median follow‐up time of 107 months (IQR: 57–156). Overall 456 (23.4%) of HIV/HCV co‐infected patients have received HCV therapy so far. The incidence of HCV treatment rose from 0.29 (95% CI: 0.13–0.45) per 100 person‐years follow‐up in 1998 to 5.26 (95% CI: 3.87–65) in 2007, before falling to 3.73 (95% CI: 2.40–5.06) in 2009. There were considerable regional differences (Figure). In a multivariable model treatment incidence increased 11.0% (95% CI: 4.0–18.4; p=0.0016) per 2 calendar years. Patients with CD4 cell counts greater than 350 cell/mm3 (incidence rate ratio [IRR]: 1.75 [1.37–2.23; p < 0.0001]), HIV‐RNA less than 500 copies/ml (IRR: 1.58 [1.18–2.12; p=0.0023]), with HCV genotype 3 (IRR: 1.55 [1.21–1.98; p=0.0006]) compared to genotype 1) and those from south (IRR: 1.99 (1.45–2.72; p<0.0001) and east central Europe (IRR: 1.61 [1.11–2.34; p=0.011]) compared to west Europe, were more likely to initiate treatment. In a multivariable model treatment for HCV was not significantly associated with all‐cause death (355 deaths, IRR: 0.81 [95% CI: 0.54–1.19; p=0.28]) or liver‐related death (95 deaths, IRR: 1.0 [95% CI: 0.50–2.02; p=0.99]). The incidence of treatment for HCV among co‐infected patients increased from 1998 until 2007 and was common in those with higher CD4 cell counts and lower HIV‐RNA, consistent with HCV treatment guidelines. HCV treatment was not associated with all‐cause or liver‐related death in this population.
image

7‐11 November 2010, Tenth International Congress on Drug Therapy in HIV Infection, Glasgow, UK

Purpose of the studyTo describe long‐term incidence trends and median age at diagnosis for the three AIDS‐defining cancers (ADC) in HIV‐1‐ infected (HIV1+) patients compared to general population. To study the risk of ADC in HIV1+patients with good immune status (CD4≥500/mm3 for at least 2 years).MethodsIncident ADC (Kaposi's sarcoma [KS], non‐Hodgkin's lymphomas [NHL] and cervix uteri cancer [CUC]) were retrieved in HIV1+adults followed in the French hospital database on HIV (FHDH) cohort between 1992 and 2009. Cancer incidence rates (IR) in general population were calculated using data from the French cancer registries (Francim network). IR among the HIV1+and the general population were standardized using the 5 years age and sex groups structure of the HIV1+population (1997–2009) and standardized incidence ratios (SIR) were estimated in HIV1+ patients vs. general population in 4 calendar periods (1992–1996, 1997–2000, 2001–2004, and 2005–2009). Median age at diagnosis was estimated after adjusting for the difference in age structure between HIV1+and general population.Summary of results5,935 incident ADC were diagnosed among 100,536 HIV1+ patients followed between 1992 and 2009. All ADC IRs were significantly reduced between pre‐ and post‐cART eras and continue to decline in the cART period (p<10−4). SIR are presented in the table.Median age at diagnosis was significantly younger among HIV1+ patients than the general population for KS (40.4 vs. 42.5; p<10−4), NHL (41.4 vs. 52.5; p<10−4) and CUC (39.3 vs. 42.5; p<10−4). For HIV1+ patients under treatment who maintained controlled viral load (<500 copies/µL) and CD4 ≥500/mm3 for at least 2 years, the risk for KS, NHL and CUC were respectively SIR=71.6 (28.7–147.5), 2.4 (0.9–4.8) and 1.6 (0.3–4.7) vs. general population.ConclusionsThe incidence rates of KS, NHL and CUC continued to decline through 2009 but the risk remained elevated as compared to general population in the most recent cART period. Despite the great reduction when compared to general population, the risk is still very high for KS in HIV1+patients who maintained CD4 ≥500/mm3 for at least 2 years. The risk was not significant for CUC and NHL.















Pre‐cART (1992–1996)
Early‐cART (1997–2000)
Intermediate‐cART (2001–2004)
Lte‐cART (2005–2009)



O/E
SIR (95% CI)
O/E
SIR (95% CI)
O/E
SIR (95% CI)
O/E
SIR (95% CI)




Kaposi's sarcoma
2177/0.9
2299.7 (2204.1–2398.4)
462/0.4
1080.1 (983.87–1183.3)
403/0.4
1130.1 (1022.5–1246.1)
354/0.4
817.7 (734.8–907.52)


Non– Hodgkins's lymphoma
1111/4.0
278.7 (262.5–295.6)
515/6.2
83.8 (76.7–91.4)
370/8.8
42.1 (37.9–46.6)
372/14.8
25.1 (22.6–27.8)


Cervix uteri
38/3.2
12.0 (8.5–16.5)
48/5.3
9.1 (6.7–12.1)
37/7.0
5.3 (3.7–7.3)
48/10.4
4.6 (3.4–6.1)





O/E: Observed cases / Expected cases.

Publisher's version (útgefin grein) ; Objectives There are currently few data on the long‐term risk of cancer and death in individuals taking raltegravir (RAL). The aim of this analysis was to evaluate whether there is evidence for an association. Methods The EuroSIDA cohort was divided into three groups: those starting RAL‐based combination antiretroviral therapy (cART) on or after 21 December 2007 (RAL); a historical cohort (HIST) of individuals adding a new antiretroviral (ARV) drug (not RAL) to their cART between 1 January 2005 and 20 December 2007, and a concurrent cohort (CONC) of individuals adding a new ARV drug (not RAL) to their cART on or after 21 December 2007. Baseline characteristics were compared using logistic regression. The incidences of newly diagnosed malignancies and death were compared using Poisson regression. Results The RAL cohort included 1470 individuals [with 4058 person‐years of follow‐up (PYFU)] compared with 3787 (4472 PYFU) and 4467 (10 691 PYFU) in the HIST and CONC cohorts, respectively. The prevalence of non‐AIDS‐related malignancies prior to baseline tended to be higher in the RAL cohort vs. the HIST cohort [adjusted odds ratio (aOR) 1.31; 95% confidence interval (CI) 0.95–1.80] and vs. the CONC cohort (aOR 1.89; 95% CI 1.37–2.61). In intention‐to‐treat (ITT) analysis (events: RAL, 50; HIST, 45; CONC, 127), the incidence of all new malignancies was 1.11 (95% CI 0.84–1.46) per 100 PYFU in the RAL cohort vs. 1.20 (95% CI 0.90–1.61) and 0.83 (95% CI 0.70–0.99) in the HIST and CONC cohorts, respectively. After adjustment, there was no evidence for a difference in the risk of malignancies [adjusted rate ratio (RR) 0.73; 95% CI 0.47–1.14 for RALvs. HIST; RR 0.95; 95% CI 0.65–1.39 for RALvs. CONC] or mortality (adjusted RR 0.87; 95% CI 0.53–1.43 for RALvs. HIST; RR 1.14; 95% CI 0.76–1.72 for RALvs. CONC). Conclusions We found no evidence for an oncogenic risk or poorer survival associated with using RAL compared with control groups. ; EuroSIDA was supported by the European Union's Seventh Framework Programme for research, technological development and demonstration under EuroCoord grant agreement no. 260694. Current support includes unrestricted grants from Bristol‐Myers Squibb, Gilead, GlaxoSmithKline LLC, Janssen R&D, Merck and Co. Inc. and Pfizer Inc. The participation of centres from Switzerland was supported by The Swiss National Science Foundation (Grant 108787). The study is also supported by a grant (grant number DNRF126) from the Danish National Research Foundation. ; Peer Reviewed