Recombinant growth hormone therapy for cystic fibrosis in children and young adults

Thaker, Vidhu; Haagensen, Alexandra; Jagannath, Vanitha A; Fedorowicz, Zbys; Houston, Brian W

doi:10.1002/14651858.cd008901

Cited by 2 publications

(2 citation statements)

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“…Administration of recombinant growth hormone significantly increases height, growth velocity, and serum levels of IGF-1 and IGFBP-3, but not lung functions [ 285 ]. Meta-analyses show that growth hormone therapy improves the intermediate outcomes in height, weight, and lean tissue mass, but pulmonary function improvement is inconsistent [ 286 ]. No significant changes in quality of life, clinical status, or side-effects are observed [ 287 ].…”

Section: Igf-1 Signaling In Cystic Fibrosis (Cf)mentioning

confidence: 99%

Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases

Wang

Guo

et al. 2018

BioMed Research International

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Insulin-like growth factor-1 (IGF-1) was firstly identified as a hormone that mediates the biological effects of growth hormone. Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IGF-1 signaling modulates the development and differentiation of many types of lung cells, including airway basal cells, club cells, alveolar epithelial cells, and fibroblasts. IGF-1 signaling deficiency results in alveolar hyperplasia in humans and disrupted lung architecture in animal models. The components of IGF-1 signaling pathways are potentiated as biomarkers as they are dysregulated locally or systemically in lung diseases, whereas data may be inconsistent or even paradoxical among different studies. The usage of IGF-1-based therapeutic agents urges for more researches in developmental disorders and inflammatory lung diseases, as the majority of current data are collected from limited number of animal experiments and are generally less exuberant than those in lung cancer. Elucidation of these questions by further bench-to-bedside researches may provide us with rational clinical diagnostic approaches and agents concerning IGF-1 signaling in lung diseases.

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