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Published on: October 12, 2017
Abnormalities in plasma fatty acid composition in human immunodeficiency virus-infected children treated with
Luis Aldámiz-Echevarría1, Itziar Pocheville, Pablo Sanjurjo
1Division of Metabolism, Department of Paediatrics, Hospital de Cruces and Basque University School of Medicine, Baracaldo, Basque Country, Spain. kaldamiz@hcru.osakidetza.net
Insights
Protease inhibitor treatment in children with human immunodeficiency virus (HIV) is linked to metabolic syndrome and altered plasma fatty acid profiles. These changes correlate with insulin resistance and insulin-like growth factor 1 (IGF-1) levels.
Area of Science:
- Pediatric Endocrinology
- Infectious Diseases
- Metabolic Disorders
Background:
- Protease inhibitors (PIs) are crucial for managing human immunodeficiency virus (HIV) infection in children.
- Metabolic syndrome complications have been observed in HIV-infected individuals on antiretroviral therapy.
- Understanding the biochemical changes associated with PI therapy is vital for long-term patient management.
Purpose of the Study:
- To investigate plasma fatty acid composition in HIV-infected children receiving protease inhibitor therapy.
- To examine the relationship between altered fatty acid profiles and metabolic syndrome components in this pediatric population.
Main Methods:
- A cross-sectional study analyzed data from 17 HIV-infected children on protease inhibitors (ritonavir or nelfinavir) and 112 healthy controls.
- Plasma fatty acids were quantified using gas chromatography.
- Enzyme activities (Delta desaturases) were assessed, and correlations with metabolic parameters were evaluated.
Main Results:
- HIV-infected children on protease inhibitors showed elevated plasma cholesterol, triglycerides, and insulin-like growth factor 1 (IGF-1).
- Significant increases in omega-6 long-chain polyunsaturated fatty acids (22:4ω6, 22:5ω6) and altered desaturase activities (increased Δ6, Δ4; decreased Δ5) were observed.
- Plasma IGF-1 levels correlated significantly with triglycerides, plasminogen activator inhibitor-1 activity, and Δ6 desaturase activity.
Conclusions:
- HIV-infected children treated with protease inhibitors exhibit a metabolic syndrome associated with distinct plasma fatty acid alterations.
- These fatty acid changes resemble those seen in insulin resistance states.
- The observed metabolic shifts are linked to variations in plasma IGF-1 concentration.
Aim:
To study plasma fatty acid composition in human immunodeficiency virus-infected children treated with protease inhibitors and its relation with other components of the metabolic syndrome observed after this therapy.
Design:
Cross-sectional study from collected clinical database.
Subjects:
17 children with HIV infection treated with protease inhibitors. Nine patients received ritonavir (20-30 mg/kg/d) and the remaining eight received nelfinavir (60-90 mg/kg/d). Duration of protease inhibitors treatment was 711+/-208 d. As controls, we used 112 matched blood samples from apparently healthy children admitted for minor surgical procedures.
Methods:
Plasma fatty acids were determined using a Hewlett Packard GC 5890 gas chromatograph.
Results:
Plasma levels of cholesterol and triglycerides and insulin-like growth factor 1 (IGF-1) tended to be high in protease inhibitor-treated patients. Plasma content of omega6 long-chain polyunsaturated fatty acids and, in particular, of the highly unsaturated 22ratio4omega6 and 22ratio5omega6, was significantly increased. Also, infected children had increased Delta6 and Delta4 desaturase activities and decreased Delta5 desaturase activity. Significant correlations were present between plasma IGF-1 level and plasma triglycerides, plasminogen activator inhibitor-1 activity and Delta6 desaturase activity.
Conclusion:
HIV-infected, protease inhibitor-treated children exhibit a metabolic syndrome which is associated with significant changes in plasma fatty acid composition. These changes are similar to those observed in situations of insulin resistance and are linked to variations in plasma IGF-1 concentration.
