Endocrinologic and immunologic factors associated with recovery of growth in children with human immunodeficiency virus type 1 infection treated with protease inhibitors

Pediatr Infect Dis J. 2003 Jan;22(1):70-6. doi: 10.1097/00006454-200301000-00017.

Abstract

Introduction: Growth failure is a common presenting sign in children with HIV disease and is a sensitive indicator of disease progression in children with AIDS. Highly active antiretroviral therapy (HAART) is associated with a significant decrease in viral load and a subsequent rise in CD4+ T cell counts in HIV-1-infected children and also with increased height and weight. The underlying mechanisms of catch-up growth during HAART are yet unknown.

Methods: Height and weight measurements, blood sample analyses for HIV-1 RNA and peripheral blood CD4+ T cell counts were obtained twice within 1 month before the start of HAART and after 12, 24, 36 and 48 weeks of treatment. Serum concentrations of insulin-like growth factor I (IGF-1), IGFs complexed to specific, structurally homologous binding proteins (IGFBP-3), cortisol, free thyroxine and tumor necrosis factor alpha (TNF-alpha) were measured before the start of therapy and after 24 weeks. In addition serum IGF-1 and IGFBP-3 values were determined after 48 weeks.

Results: Twenty-seven HIV-1-infected children with a median age of 5.5 years (range, 0.3 to 14.9 years) were included. Overall no significant changes in height and body mass index (BMI) z scores were observed. The median baseline plasma viral load of 68,800 copies/ml decreased to less than the detection limit of 500 copies/ml in 80% of the children after 48 weeks. TNF-alpha values were elevated (44 pg/ml) at baseline and decreased significantly to 37 pg/ml after 24 weeks. At baseline elevated TNF-alpha was observed in 78%, which decreased to 55% after 24 weeks. Baseline free thyroxine and cortisol values were normal and did not change during therapy. Baseline serum of IGF-1 and IGFBP-3 concentrations were normal, but IGF-1 tended to be lower than IGFBP-3. Both values increased significantly after the initiation of therapy. IGFBP-3 decreased after 48 weeks whereas IGF-1 stabilized. The increase in IGF-1 was significantly higher in children in whom the BMI and length (after correction for age and sex) increased the most.

Conclusion: Hypothyroidism and adrenal axis abnormalities are not associated with restoration of growth after the initiation of antiretroviral therapy in HIV-1-infected children. The combination of relatively high serum IGFBP-3 concentration and relatively lower serum IGF-1 suggests the presence of a growth hormone-resistant state. During treatment with a protease inhibitor-containing regimen, decreased serum IGFBP-3 and stabilization of IGF-1 after a significant initial increase suggest restoration of normal sensitivity to growth hormone and recovery to an anabolic condition.

Publication types

  • Clinical Trial
  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiretroviral Therapy, Highly Active*
  • Body Height
  • Body Mass Index
  • CD4 Lymphocyte Count
  • Child, Preschool
  • Female
  • Growth / drug effects*
  • HIV Infections / diagnosis
  • HIV Infections / drug therapy*
  • HIV Protease Inhibitors / administration & dosage
  • HIV Protease Inhibitors / therapeutic use*
  • HIV-1* / genetics
  • HIV-1* / isolation & purification
  • Humans
  • Hydrocortisone / analysis
  • Infant
  • Insulin-Like Growth Factor Binding Protein 3 / analysis
  • Insulin-Like Growth Factor Binding Protein 3 / immunology
  • Insulin-Like Growth Factor I / analysis
  • Insulin-Like Growth Factor I / immunology
  • Male
  • Nelfinavir / administration & dosage
  • Nelfinavir / blood
  • Nelfinavir / therapeutic use
  • Serum Albumin / analysis
  • Thyroxine / analysis
  • Time Factors
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / analysis
  • Viral Load

Substances

  • HIV Protease Inhibitors
  • Insulin-Like Growth Factor Binding Protein 3
  • Serum Albumin
  • Tumor Necrosis Factor-alpha
  • Insulin-Like Growth Factor I
  • Nelfinavir
  • Thyroxine
  • Hydrocortisone