Related Experiment Videos

GH therapy in juvenile chronic arthritis: results of a two-year controlled study on growth and bone

S Bechtold1, P Ripperger, D Mühlbayer

  • 1Endocrine Division University Children's Hospital, D-80337 Munich, Germany. susanne.bechtold@kk-i.med.uni-muenchen.de

The Journal of Clinical Endocrinology and Metabolism
|December 12, 2001
PubMed

Insights

Human growth hormone (hGH) treatment improved growth velocity and height in prepubertal children with juvenile chronic arthritis (JCA). GH therapy may counteract glucocorticoid side effects, but long-term studies are needed.

Area of Science:

  • Pediatric Endocrinology
  • Rheumatology
  • Growth Hormone Therapy

Background:

  • Juvenile chronic arthritis (JCA) frequently causes growth disturbances in children.
  • Reduced final height is a permanent consequence of growth impairment in JCA.
  • Glucocorticoid therapy, often used for JCA, can also impede growth.

Purpose of the Study:

  • To evaluate the efficacy and safety of human growth hormone (hGH) in growth-retarded prepubertal children with JCA.
  • To assess the impact of hGH on growth velocity and height parameters.
  • To investigate the potential of hGH to mitigate adverse effects of glucocorticoids.

Main Methods:

  • Thirty-five prepubertal children with JCA were assessed for GH deficiency (GHD).
  • Children were randomized into a study group (hGH treatment) and an untreated control group.
  • The study group received 1 IU/kg BW/wk of hGH, and the GHD group received 0.5 IU for 2 years.

Main Results:

  • hGH treatment led to significant increases in growth velocity and height standard deviation (SD) scores compared to baseline.
  • Both treated groups showed marked growth velocity increases, with some increase also observed in the control group.
  • Insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 levels increased with GH treatment.

Conclusions:

  • hGH therapy shows potential utility in treating growth impairment associated with JCA.
  • GH may counteract growth-inhibiting effects of glucocorticoids in JCA patients.
  • Further long-term controlled studies are necessary to establish definitive risks and benefits of GH therapy in JCA.

Related Concept Videos

Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...