Abstract Book Vol. 2 [International Conference on AIDS (14th: 2002: Barcelona, Spain)]

420 Abstracts ThPeB7343-ThPeB7346

XIV International AIDS Conference

35); TG 4.42mmol/L (1.1-7.6); chol 5.71mmol/L (3.4-7.9); LDL 2.88mmol/L (1.4 -4.7); HDL 0.9mmol/L (0.6-1.3); CD4 528 (20-1540); duration HIV 108 mos (34 -308); duration ART 72 mos (1-132); kcal intakel952 (1035-3195); fat 33% kcal
(20-47). There were no differences between the n3/placebo groups except more
women were in the n3 group (17% vs 3%). Four wks after diet counseling TG decreased 7%, HDL increased 6%, LDL decreased 6%, chol decreased 4%. BMI,
kcal and fat intake did not change. From wk 4 to 12 (n3 protocol) there were no
significant differences between the n3 vs placebo group for SL, BMI, kcal or fat
intake. However, there was a favorable trend for TG. From wk 0 to 12, TG decreased 13% (n3) vs 6% (placebo) and from wk 4 to 12, TG decreased 10% (n3)
vs increased 3% (placebo).
Conclusion: Diet counseling had a favorable effect on SL and n3 supplementation resulted in decreased TG. These results suggest a therapeutic role for n3
in hypertriglyceridemia, especially in conjunction with diet counseling. The small
number of subjects may account for lack of statistical significance. Further larger
controlled study is warranted.
Presenting author: Diana Peabody, Oak Tree Clinic, Children's and Women's
Health Centre of British Columbia, 4500 Oak Street, Vancouver, British Colombia, V6H3N1, Canada, Tel.: [phone], Fax: [phone], E-mail:
[email protected]
ThPeB7343 IDifferences in endothelial function in HIV-infected
patients with or without HIV protease inhibitor
regimens and in HIV-negative controls
B.R. Cotter1, O.L. Kwan1, J.S. Currier2, A.N. DeMarial, F.J. Torrianil.
I University of California San Diego, division of cardiovascular medicine, ucsd
medical center, hillcrest, 200 west arbor drive, san diego, ca 92103-8411, United
States; 2University of California Los Angeles, Los Angeles, United States
Background: Protease inhibitor (PI) use may predispose HIV patients (HIV) to
accelerated atherosclerosis. Endothelial dysfunction (ED) may be an early event
in atherogenesis and is associated with coronary artery disease (CAD). Impaired
flow-mediated dilation (FMD) of the brachial artery (BA) in HIV on PI-containing,
but not on PI-sparing regimens was recently reported. We studied endothelial
function (EF) in males with HIV on PI >2 years (HIVPI), HIV PI-sparing (HIVnoPI),
and in HIV-negative (HIV-). Methods: EF was done on BA using a 12.5MHz
transducer and an ATL HDI 5000 ultrasound system. FMD was measured as
a difference in arterial diameter and blood flow at rest, 4.5 minutes after blood
pressure cuff inflation and after 4001tg of sub-lingual nitroglycerine (NTGMD).
Smoking status, lipids and other CAD risk factors (RF), antiretroviral therapy
(ARV) duration, CD4 and HIV RNA levels were assessed at baseline. Values
are in mean~SD. Results: 19 males with few CAD RF (no diabetes, hypertension, or family history of CAD) were studied: 8 HIVPI, 6 HIVnoPI, and 7 HIV-.
2/8 HIVPI and 1/6 HIVnoPI were smokers. Length of ARV was 4.2+1.3 years
in HIVPI, 0.8~0.4 years in HIVnoPI (p<0.001). CD4 counts were 626~229 and
495~354 cells/mm3. HIV RNA was <50 copies/ml in 6/8 and in 6/6, respectively. Total cholesterol was 230+56, 196~35 and 174~38 mg/dl; triglycerides
258~217, 146~104 and 139~70 in HIVPI, HIVnoPI and HIV-; comparisons non
significant. FMD was 8.2~3.0% in HIVPI, 13.7~5.9% in HIVnoPI, and 13.2+4.9%
in HIV-. FMD HIVPI vs. HIV-, P = 0.04; HIVPI vs. HIVnoPI, P = 0.07; HIVnoPI vs.
HIV- (P = NS).
Conclusions: These data suggest that FMD is reduced in patients on long-term
PI, but the values do not suggest marked impairment. The absence of CAD RF
may explain why ED was not observed even in HIV on chronic PI.
Presenting author: bruno cotter, division of cardiovascular medicine, ucsd medical center, hillcrest, 200 west arbor drive, san diego, ca 92103-8411, United
States, Tel.: [phone], Fax: [phone], E-mail: [email protected]
ThPeB7344 The heparin-releasable lipoprotein and hepatic
lipase activity in relation to the protease inhibitor
plasma level in HIV-infected patients with
lipodystrophy/dyslipidemia
T. Buhk, O. Degen, J. van Lunzen, H.J. Stellbrink, U. Beisiegel. University
Universitat Hamburg - UKE, Medizinische Klinik, Martinistr. 52, 20246 Hamburg,
Germany
Background: Lipodystrophy has been described since 1996 in HIV-infected patients treated with
HAART and is frequently associated with progressive peripheral and facial subcutaneous fat wasting, increases in truncal grith and lipid metabolism abnormalities.
The cause of this disorder is unknown. In this subanalysis we focused the possible connection between the current proteinase inhibitor medication level and its
influence on the activities of the heparin-releasable lipoprotein- (LPL) and hepatic
lipase (HL).
Methods: 28 patients of our collective received a divergent antiretroviral therapy
with one or two PI. The mean duration of the current antiretroviral therapy was

12.6 (min 1.2 - max 41.6) months.
When treated with 2 PI we considerated the 1 with the higher plasma level (Cmax)
for the statistics (SPSS). The distribution to the different PI: Nelfinavir: n=8 (25 -9007 - mean 4250; Cmin = 1000, Cmax = 3000 ng/ml), Saquinavir n=5 (3-2741
- mean 783; Cmin = 216, Cmax = 2181 ng/ml), Ritonavir n=8 (539-7763 - mean
2903; Cmin = 3700, Cmax = 11200 ng/ml), Indinavir n=7 (130-8782 - mean 2098;
Cmin = 179, Cmax = 7700 ng/ml).

Results: Valid n=28. The medication level of NEL is highly associated with a decrease of the LPL- (KI=0.49) and the HL-activity (KI=0.8). For IND high levels
have the same effect, but the correlation is weaker (0.26, 0.16). SAQ and RIT levels in the plasma each shows no correlation for the LPL-activity, but a correlation
for the HL-activity (SAQ:0.42; RIT: 0.3).
Conclusion: In this study we could find, especially for the hepatic lipase an inhibitory effect on its activity through the four proteinase inhibitors. The lipoproteinlipase activity is reduced in this analysis through higher levels of NEL and IND,
but not by SAQ and RIT. We hypothesise that the protease inhibitors reduce directly the heparin-releasable LPL and HL activity. This is considered to contribute
to hypertriglyceridaemia and -cholesterol levels in these patients.
Presenting author: Thomas Buhk, Universitat Hamburg - UKE, Medizinische
Klinik, Martinistr. 52, 20246 Hamburg, Germany, Tel.: [phone], Fax: [phone], E-mail: [email protected]
ThPeB7345 Effect of highly active antiretroviral therapy
(HAART) on body composition, energy
expenditure, caloric intake and its relation to
changes in viral load in patients with AIDS-related
wasting syndrome
L.Z.L. L6pez Zaragoza JL1, S.E.B. Salgado-Enriquez BL2,
T.H.J. Tovar-Hirashima j2, M.G.P. Milke-Garcfa MP3, S.R.L. Soto-Ramirez LE4,
C.M.J. Calva-Mercado J4, P.R.S. Ponce de Le6n-Rosales S5,
S.M.J. Sierra-Madero J4. 1lnternal Medicine Department, INCMNSZ, Instituto
Nacional de Ciencias M6dicas y Nutricidn SZ (Direccidn Mddica), Vasco de
Quiroga #15, Seccidn 16, Tlalpan, Dto. Federal, Mexico; 2Internal Medicine
Department, INCMNSZ, Mexico City, Mexico; 3Gastroenterology
Department, INCMNSZ, Mexico City, Mexico; 4AIDS-Clinic, INCMNSZ, Mdxico
City, Mexico; 5Clinical Epidemiology Unit, INCMNSZ, Mdxico City, Mexico
Background: Changes in body composition (BC), resting energy expenditure
(REE) and caloric intake (CI) that occur with HAART in AIDS patients with wasting
are not well characterized.
Objective: To evaluate the effect of HAART on these variables.
Patients: Fifteen adults with AIDS-related wasting, protease inhibitor (PI) naive
and plasma viral load (PVL) >30,000 c/ml.
Methods: Patients treated with different HAART regimens containing a PI and
2 nucleosides, were evaluated for changes in body weight (BW), BC by DEXASCAN, REE by indirect calorimetry and CI. PVL was measured every 4 weeks
and serum sTNFRo-p75 at 12 week intervals. Statistical analysis was done with
non-parametric tests.
Results: The median increase in BW was 6 kg [CI 95%, 4.37 to 9.98] (11.5%
of median weight at baseline) (P<0.01). The increase in fat and lean mass was
2.49 kg [1.40 to 3.84] and 1.66 kg [0.573 to 3.82] (P<0.01) respectively. REE and
adjusted REE for lean mass at the end of the study was not significantly different
from baseline. Median Cl increased 310.9 kcal/day [22.78 to 775.39] (P=0.02). At
24 weeks 11 of 15 patients had PVL <400 c/ml. A significant negative correlation
was found between changes in the PVL during the first eight weeks and the BW
gained during the follow up period (r= -.518 P=0.048). Changes in sTNFRo-p75
were significantly related with the decrease in PVL (r = 0.571 P=0.020) and with
the BW (r= -.586 P= 0.02).
Conclusions: The increase in BW observed with HAART in patients with wasting
is given mainly by an increase in fat mass. Weight gain could be associated with
a higher caloric intake instead of changes in REE. A direct role of HIV replication
might also be determinant in weight changes, probably mediated trough TNF-o
production.
Presenting author: Jose Luis L6pez Zaragoza, Instituto Nacional de Ciencias
Medicas y Nutrici6n SZ (Direcci6n Medica), Vasco de Quiroga #15, Secci6n 16,
Tialpan, Dto. Federal, Mexico, Tel.: [phone], Fax: [phone], Email: [email protected]
ThPeB7346 A randomized, double-blind, placebo-controlled,
comparative study on the effects of metformin or
gemfibrozil on markers of fibrinolysis and
increased cardiovascular risk in HIV-infected
patients with lipodystrophy
P. Domingo1, E. Martinez2, J.B. Perez Cuevas2, J.A. Arroyo1, A. Milinkovic2,
I. Conget2, M.A. Sambeat1, M. Borrell1, J. Fontcuberta1, J.M. Gatell2. 1Hospital
St. Pau, Barcelona, Spain; 2Hospital Clinic, Barcelona, Spain
Background: Plasminogen activator inhibitor-1 (PAl-i), tissue-type plasminogen
activator (t-PA), t-PA-PAI-1 complexes, factor VII, and thrombin activable fibrinolysis inhibitor (TAFI) antigen levels are known to be associated with cardiovascular
risk.
Aim of the study: to investigate the effects of metformin and gemfibrozil on the
levels of markers of fibrinolysis.

Patients and methods: 48 HIV lipodystrophic patients enrolled in a double-blind,
placebo controlled treatment study of metformin 500 mg twice daily or gemfibrozil
900 mg daily had PAl-1, t-PA, factor VII and TAFI antigen levels measured before
starting therapy and after 12 months. PAl-1 and tPA-PAI complexes were determined by ELISA methods (Biopool), t-PA and factor VII antigen by ELISA (Roche),
and TAFI antigen by ELISA (BioMed). Statistical analyses were performed with
the StatView 4.5TM statistical package.