PubMed · 11203153
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
S Logan, H Bedford, D Elliman. 2000. Consider absolute risks in SIDS prevention.. https://doi.org/10.1136/adc.83.5.456d
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Growth in humans is a complex process, controlled at numerous levels and by a myriad of factors. These factors may act centrally or peripherally and may be hormones, receptors, or transcription factors. Many of these probably are still unknown. The factors that are discussed here include those that act on the developing pituitary gland (transcription factors including LHX3, HESX1, PROP1, and PIT-1); those that regulate the normal activity of the pituitary (hypothalamic hormones such as GHRH, Ghrelin [growth hormone secretagoguel and somatostatin); those factors coming from the pituitary (essentially growth hormone [GH]); and the downstream modulators, transducers, and effectors of GH (including the GH receptor/GH binding protein, insulin-like growth factor-I and -II, their receptors, and their binding factors). What is becoming increasingly clear is the role of genetics in determining stature. This review discusses the most clinically relevant factors, with an emphasis on ontogeny, genetic inheritance, and clinical presentation.
Growth hormone (GH) secretion from anterior pituitary is regulated by the hypothalamus and the mediators of GH actions. Major regulatory factors include GH releasing hormone (GHRH), somatostatin (SRIF), GH releasing peptide (ghrerin) and insulin-like growth factor (IGF-I). The principal physiological regulation mechanisms of GH secretion are neural endogenous rhythm, sleep, stress, exercise, and nutritional and metabolic signals. GH deficiency results from various hereditary or acquired causes, which may be isolated or combined with other pituitary hormone deficiencies. GH deficiency can be treated with recombinant human GH, which results in accelerating growth in children and normalization of intermediary metabolism in adults. GH hypersecretion mostly results from a pituitary tumor and causes acromegaly or gigantism. Hypersecretion of GH can be treated by transshenoidal surgery. Medical treatment with octreotide and analogs is also effective to reduce GH secretion in combination with or without the surgery.
Renal failure is associated with dramatic changes in the growth hormone/insulin-like growth factor (GH/IGF) axis. In children, this results in growth retardation, which is treated with injections of recombinant human GH (rhGH). Given the many recent advances in the knowledge of the components of the GH/IGF axis, it is timely to review the role of GH in renal failure and to discuss likely new treatments for growth failure. Renal failure is not a state of GH deficiency but a state of GH and IGF resistance, making other approaches to manipulating the GH axis more logical than treatment with rhGH alone. Although in children rhGH is safe, in critically ill adults it can be lethal. As the mechanisms of these lethal actions of rhGH are unknown, caution is advised when using rhGH outside approved indications. In renal failure, an optimal balance between safety and efficacy for growth may be achieved with the use of the combination of rhGH and rhIGF-I, as animal studies have shown synergistic growth responses. However, inhibition of the GH axis, with the use of GH antagonists, is likely to be tested clinically given the beneficial effects of GH antagonists on renal function in animal models of renal disease. Manipulating IGF-I by either administering rhIGF-1 or its binding proteins or increasing IGF-I bioavailability with the use of IGF displacers could prove to be a safer and more effective alternative to the use of rhGH in renal failure. In the future, both rhGH and rhIGF-1 likely will be included in growth-promoting hormone cocktails tailored to correct specific growth disorders.