Correlation between the components of the insulin-like growth factor I system, nutritional status and visceral

Claudia M C Gomes1, Daniel Giannella-Neto, Monica E A Gama

  • 1Department of Pathology, University of Sao Paulo Medical School, Avenida Dr. Arnaldo, 455 - sala 1209, CEP 01246-903 São Paulo, SP, Brazil. gomescla@usp.br

Insights

Visceral leishmaniasis (VL) in children significantly reduces insulin-like growth factor I (IGF-I) and IGF binding-protein 3 (IGFBP3) levels. Growth retardation in active VL is primarily due to disease factors, not IGF-I deficiency.

Area of Science:

  • Endocrinology
  • Infectious Diseases
  • Pediatrics

Background:

  • The insulin-like growth factor I (IGF-I) system plays a crucial role in growth and development.
  • Visceral leishmaniasis (VL) is an endemic parasitic disease affecting children, potentially impacting growth.
  • Nutritional status is a known determinant of growth in pediatric populations.

Purpose of the Study:

  • To investigate the relationship between the IGF-I system, nutritional status, and visceral leishmaniasis in Brazilian children.
  • To determine if IGF-I system alterations or nutritional deficits are primary drivers of growth retardation in active VL.

Main Methods:

  • Serum concentrations of growth hormone (GH), total and free IGF-I, and IGF binding-protein 3 (IGFBP3) were measured in 241 children using radioimmunoassay.
  • Nutritional status was assessed through anthropometric indicators (weight-for-age Z, height-for-age Z scores) and biochemical markers (albumin).
  • Statistical analyses, including multiple discriminant analysis, were employed to identify predictors of active and oligosymptomatic VL.

Main Results:

  • Children with active VL exhibited significantly reduced serum concentrations of total and free IGF-I and IGFBP3 compared to uninfected children.
  • Height-for-age Z scores, weight-for-age Z scores, and albumin levels were significantly lower in the active VL group.
  • Albumin and height-for-age Z scores were identified as significant predictors for active and oligosymptomatic VL.

Conclusions:

  • Active VL is associated with significant reductions in the IGF-I system components and nutritional status indicators.
  • Growth retardation in children with active VL appears to be primarily driven by intrinsic factors of the disease, which may secondarily affect the GH/IGF axis.
  • The study suggests that VL itself, rather than isolated IGF-I or IGFBP3 deficiency, is the main cause of impaired growth in affected children.