Baril L, Idhammou A, Beucler I, Coutellier A, Valantin MA, Caumes E, Bruckert E, Katlama C, Bricaire F; Conference on Retroviruses and Opportunistic Infections.
Program Abstr 6th Conf Retrovir Oppor Infect Conf Retrovir Oppor Infect 6th 1999 Chic Ill. 1999 Jan 31-Feb 4; 6th: 192 (abstract no. 664).
Pitie-Salpetriere Hospital, Paris, France.
Objective: To evaluate the role of the lipolytic enzymes (lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL)) in HTG occurring in PI-treated patients. Methods: We selected 10 HIV1 men who had a HTG from 297 to 4500 mg/dl receiving antiretroviral therapy and seven non HIV-infected normolipidemic controls similar by age and sex. After a 12-hour overnight fast, subjects received heparin (100U/kg) and postheparin plasmas were collected 10 minutes after the injection in chilled EDTA tubes. LPL and HTGL activities were measured according to Nilson-Ehle method. Results: All 10 patients received at least 2 nucleosides: 9 received various PI and 1 patient 3 nucleosides. The TG median was 548.5 mg/dl (interquartile (IQ): 492-1421). The LPL activity median was 8.8 (IQ: 5.1-16.9) and the HTGL activity median was 13 (IQ: 4.9-18.8). Spearman correlation coefficient was significant at -0.63 (p < 0.04) between concentration of TG and LPL activity and it was at - 0.86 (p < 0.001) between concentration of TG and HTGL. Compared to the 7 controls, patients had a significant lower HTGL activity at p = 0.03 but no statistical difference was shown according to the LPL activity. The five patients that had the highest HTG (> 600 mg/dl) had the lowest activities of both LPL and HTGL. Conclusion: The mechanisms of HTG in PI-treated HIV1-infected patients remain heterogeneous and complex, a drastic decrease in both LPL and HTGL activities (< 50%) could be responsible for high HTG.
Publication Types:
Keywords:
- Heparin
- Humans
- Hypertriglyceridemia
- Hypokinesia
- Lipase
- Lipoprotein Lipase
- Male
- Thyroglobulin
- Triglycerides
Other ID:
UI: 102195429
From Meeting Abstracts