Startseite Role of Insulin-like Growth Factor Monitoring in Optimizing Growth Hormone Therapy
Artikel
Lizenziert
Nicht lizenziert Erfordert eine Authentifizierung

Role of Insulin-like Growth Factor Monitoring in Optimizing Growth Hormone Therapy

Division of Endocrinology, Department of Pediatrics, Mattel’s Children’s Hospital at UCLA, Los Angeles, California, USA
  • Lawrence Wetterau und Pinchas Cohen
Veröffentlicht/Copyright: 22. Juli 2014

ABSTRACT

Much has been learned over the past two decades regarding the management of growth hormone (GH) deficiency in children and adolescents. Current GH therapy under ideal circumstances enables children to attain a final height within the normal range and close to their target height However, such a successful outcome is not always achieved and the necessity to individualize treatment according to the specific needs of each GH-deficient child is now well recognized. Consensus does not currently exist as to how to formulate individualized treatment plans. Nonetheless, a clear role for a biochemical, as well as an auxological, monitoring approach has been established. Accurate determinations of height velocity and interval height increase (expressed as the change in height Z-score) continue to be the most important parameters in monitoring the response to treatment. The importance of routinely monitoring serum levels of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 is an emerging paradigm. Firm roles have been established for this approach in the assurance of compliance and safety (particularly to avoid long-term theoretical risks). IGF monitoring also has important potential utility as a tool to assess and optimize the response to GH therapy through dose adjustments. In years to come, we expect the development of multiple GH treatment optimization strategies, including approaches such as prediction modeling, as well as serum IGF monitoring and dose adjustments, to evolve and improve.

Published Online: 2014-07-22
Published in Print: 2000-12-01

© 2014 by Walter de Gruyter Berlin/Boston

Artikel in diesem Heft

  1. Titelei
  2. TABLE OF CONTENTS
  3. Foreword
  4. What Happens When Growth Hormone is Discontinued at Completion of Growth? Metabolic Aspects
  5. Growth Hormone Deficiency and Peak Bone Mass
  6. Optimal Strategy for Management of Pituitary Disease in the Growth Hormone-Deficient Teenager
  7. Ethical Dilemmas in Pediatric Endocrinology: Growth Hormone for Short Normal Children
  8. Evidence-Based Approach to Growth Hormone Replacement Therapy in Adults, with Special Emphasis on Body Composition
  9. Evidence-Based Growth Hormone Therapy Prediction Models
  10. New Paradigms for Growth Hormone Treatment in the 21st Century: Prediction Models
  11. Role of Insulin-like Growth Factor Monitoring in Optimizing Growth Hormone Therapy
  12. Knockout Mice Challenge Our Concepts of Glucose Homeostasis and the Pathogenesis of Diabetes Mellitus
  13. Type 2 Diabetes Mellitus in Children: Pathophysiology and Risk Factors
  14. Emergence of Type 2 Diabetes Mellitus in Children: Epidemiological Evidence
  15. Treatment of Type 2 Diabetes Mellitus in Children and Adolescents
  16. Diagnosis of Maturity-Onset Diabetes of the Young in the Pediatric Diabetes Clinic
  17. Thrifty Genotypes and Phenotypes in the Pathogenesis of Type 2 Diabetes Mellitus
  18. Estradiol: A Protective Factor in the Adult Brain
  19. Estrogen Treatment and Estrogen Suppression: Metabolic Effects in Adolescence
  20. Estrogen, Bone, Growth and Sex: A Sea Change in Conventional Wisdom
  21. Route-Dependent Endocrine and Metabolic Effects of Estrogen Replacement Therapy
  22. Telomerase and the Cellular Lifespan: Implications for the Aging Process
  23. Human Aging and Progeria
  24. A Role for the Somatotropic Axis in Neural Development, Injury and Disease
  25. Hypothalamic Growth Hormone-Insulin-like Growth Factor-I Axis across the Human Life Span
  26. The Lost Voice: A History of the Castrato
  27. SELECTED POSTER ABSTRACTS
  28. GROWTH. FETAL GROWTH. SGA
  29. SYNDROMES: TURNER. PRADER-WILLI. NOONAN. PHP. OTHERS
  30. GHD. HYPOPITUITARISM. KIGS
  31. METABOLIC. GENETIC. ADULT. ACROMEGALY
  32. GH. IGF. IGFBPs
  33. GROWTH IN SYSTEMIC DISEASE. CRI. RICKETS. STEROIDS
Heruntergeladen am 12.10.2025 von https://www.degruyterbrill.com/document/doi/10.1515/jpem-2000-s610/html?lang=de
Button zum nach oben scrollen