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Regulation of plasma PAI-1 concentrations in HAART-associated lipodystrophy during rosiglitazone therapy.
Arterioscler Thromb Vasc Biol 2003; 23(4):688-94AT

Abstract

OBJECTIVE

Patients with highly active antiretroviral therapy-associated lipodystrophy (HAART+LD+) have high plasminogen activator inhibitor-1 (PAI-1) concentrations for unknown reasons. We determined whether (1). plasma PAI-1 antigen concentrations are related to liver fat content (LFAT) independently of the size of other fat depots and (2) rosiglitazone decreases PAI-1 and LFAT in these patients.

METHODS AND RESULTS

In the cross-sectional study, 3 groups were investigated: 30 HIV-positive patients with HAART+LD+, 13 HIV-positive patients without lipodystrophy (HAART+LD-), and 15 HIV-negative subjects (HIV-). In the treatment study, the HAART+LD+ group received either rosiglitazone (8 mg, n=15) or placebo (n=15) for 24 weeks. Plasma PAI-1 was increased in HAART+LD+ (28+/-2 ng/mL) compared with the HAART+LD- (18+/-3, P<0.02) and HIV- (10+/-3, P<0.001) groups. LFAT was higher in HAART+LD+ (7.6+/-1.7%) than in the HAART+LD- (2.1+/-1.1%, P<0.001) and HIV- (3.6+/-1.2%, P<0.05) groups. Within the HAART+LD+ group, plasma PAI-1 was correlated with LFAT (r=0.49, P<0.01) but not with subcutaneous or intra-abdominal fat or serum insulin or triglycerides. In subcutaneous adipose tissue, PAI-1 mRNA was 2- to 3-fold higher in the HAART+LD+ group than in either the HAART+LD- or HIV- group. Rosiglitazone decreased LFAT, serum insulin, and plasma PAI-1 and increased serum triglycerides but had no effect on intra-abdominal or subcutaneous fat mass or PAI-1 mRNA.

CONCLUSIONS

Plasma PAI-1 concentrations are increased in direct proportion to LFAT in HAART+LD+ patients. Rosiglitazone decreases LFAT, serum insulin, and plasma PAI-1 without changing the size of other fat depots or PAI-1 mRNA in subcutaneous fat. These data suggest that liver fat contributes to plasma PAI-1 concentrations in these patients.

Authors+Show Affiliations

Department of Medicine, Helsinki University Central Hospital, PO Box 348, FIN-00029 HUS, Helsinki, Finland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12615670

Citation

Yki-Järvinen, Hannele, et al. "Regulation of Plasma PAI-1 Concentrations in HAART-associated Lipodystrophy During Rosiglitazone Therapy." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 23, no. 4, 2003, pp. 688-94.
Yki-Järvinen H, Sutinen J, Silveira A, et al. Regulation of plasma PAI-1 concentrations in HAART-associated lipodystrophy during rosiglitazone therapy. Arterioscler Thromb Vasc Biol. 2003;23(4):688-94.
Yki-Järvinen, H., Sutinen, J., Silveira, A., Korsheninnikova, E., Fisher, R. M., Kannisto, K., ... Hamsten, A. (2003). Regulation of plasma PAI-1 concentrations in HAART-associated lipodystrophy during rosiglitazone therapy. Arteriosclerosis, Thrombosis, and Vascular Biology, 23(4), pp. 688-94.
Yki-Järvinen H, et al. Regulation of Plasma PAI-1 Concentrations in HAART-associated Lipodystrophy During Rosiglitazone Therapy. Arterioscler Thromb Vasc Biol. 2003 Apr 1;23(4):688-94. PubMed PMID: 12615670.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of plasma PAI-1 concentrations in HAART-associated lipodystrophy during rosiglitazone therapy. AU - Yki-Järvinen,Hannele, AU - Sutinen,Jussi, AU - Silveira,Angela, AU - Korsheninnikova,Elena, AU - Fisher,Rachel M, AU - Kannisto,Katja, AU - Ehrenborg,Ewa, AU - Eriksson,Per, AU - Hamsten,Anders, Y1 - 2003/02/20/ PY - 2003/3/5/pubmed PY - 2004/1/16/medline PY - 2003/3/5/entrez SP - 688 EP - 94 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler. Thromb. Vasc. Biol. VL - 23 IS - 4 N2 - OBJECTIVE: Patients with highly active antiretroviral therapy-associated lipodystrophy (HAART+LD+) have high plasminogen activator inhibitor-1 (PAI-1) concentrations for unknown reasons. We determined whether (1). plasma PAI-1 antigen concentrations are related to liver fat content (LFAT) independently of the size of other fat depots and (2) rosiglitazone decreases PAI-1 and LFAT in these patients. METHODS AND RESULTS: In the cross-sectional study, 3 groups were investigated: 30 HIV-positive patients with HAART+LD+, 13 HIV-positive patients without lipodystrophy (HAART+LD-), and 15 HIV-negative subjects (HIV-). In the treatment study, the HAART+LD+ group received either rosiglitazone (8 mg, n=15) or placebo (n=15) for 24 weeks. Plasma PAI-1 was increased in HAART+LD+ (28+/-2 ng/mL) compared with the HAART+LD- (18+/-3, P<0.02) and HIV- (10+/-3, P<0.001) groups. LFAT was higher in HAART+LD+ (7.6+/-1.7%) than in the HAART+LD- (2.1+/-1.1%, P<0.001) and HIV- (3.6+/-1.2%, P<0.05) groups. Within the HAART+LD+ group, plasma PAI-1 was correlated with LFAT (r=0.49, P<0.01) but not with subcutaneous or intra-abdominal fat or serum insulin or triglycerides. In subcutaneous adipose tissue, PAI-1 mRNA was 2- to 3-fold higher in the HAART+LD+ group than in either the HAART+LD- or HIV- group. Rosiglitazone decreased LFAT, serum insulin, and plasma PAI-1 and increased serum triglycerides but had no effect on intra-abdominal or subcutaneous fat mass or PAI-1 mRNA. CONCLUSIONS: Plasma PAI-1 concentrations are increased in direct proportion to LFAT in HAART+LD+ patients. Rosiglitazone decreases LFAT, serum insulin, and plasma PAI-1 without changing the size of other fat depots or PAI-1 mRNA in subcutaneous fat. These data suggest that liver fat contributes to plasma PAI-1 concentrations in these patients. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/12615670/Regulation_of_plasma_PAI_1_concentrations_in_HAART_associated_lipodystrophy_during_rosiglitazone_therapy_ L2 - http://www.ahajournals.org/doi/full/10.1161/01.ATV.0000062885.61917.A5?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -