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Fibromyalgia Syndrome: Canadian Clinical Working Case Definition, Diagnostic and Treatment Protocols–A Consensus Document
Published in I. Jon Russell, The Fibromyalgia Syndrome: A Clinical Case Definition for Practitioners, 2020
Anil Kumar Jain, Bruce M. Carruthers, Maijorie I. van de Sande, Stephen R. Barron, C. C. Stuart Donaldson, James V. Dunne, Emerson Gingrich, Dan S. Heffez, Y.-K. Frances Leung, Daniel G. Malone, Thomas J. Romano, I. Jon Russell, David Saul, Donald G. Seibel
Growth hormone treatment: It is of great interest that administration of growth hormone to people with FMS reduces many of the symptoms associated with this disorder (354). It appears that response to human growth hormone [HGH] takes time since the treated subjects did not exhibit significant improvement until about three months of continuous therapy. Withdrawal of the drug usually resulted in recurrence of the symptoms. The dosage must be carefully monitored by measuring the insulin-like growth hormone-1 [IGF1] levels to avoid the development of gigantism and other potentially serious side effects. Regular injection therapy with this hormone is not universally appealing to FMS patients although it is remarkable how well they adapted to its use in the research study. To date, the cost of such therapy is too expensive [approximately US $ 1,000.00/month] to allow its widespread clinical use despite the fact that a HGH and IGF1 deficiency is demonstrable and administration of HGH is effective against at least some of the FMS symptoms.
An Overview of the Biological Actions and Neuroendocrine Regulation of Growth Hormone
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
As implied by its name, growth hormone has potent effects on growth including an increase in nitrogen retention, lean body mass, body length, body weight, and width of the epiphyseal cartilage plate. Classically, the tibia test is used as a bioassay for the effects of growth hormone.85,86 This test compares the width of the epiphyseal plate after hypophysectomy and treatment with or without growth hormone. Comparisons are subsequently made in the width of the plate. The effects of growth hormone on body growth are supported by studies demonstrating that genetic dwarfs grow in response to growth hormone,87,88 passive immunization with growth hormone antiserum decreases growth,89–91 and transgenic animals expressing high levels of growth hormone exhibit increased body growth.92,93
Genetics
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Jane A. Hurst, Richard H. Scott
Monitoring and supportive management of development, growth and feeding is provided and endocrinology referral for management of growth retardation. Growth hormone therapy is beneficial in some cases, even in the absence of deficiency. Orthopaedic referral is provided in cases with marked leg length discrepancy.
Emerging therapeutic targets for anorexia nervosa
Published in Expert Opinion on Therapeutic Targets, 2023
Growth hormone is produced in the pituitary gland and involved in numerous physiological functions such as regulation of body weight, body composition and glucose homeostasis. Since a growth hormone resistance associated with reduced downstream insulin-like growth factor-1 levels has been described in young patients with anorexia nervosa [92] likely contributing to delayed puberty onset and reduced body height, growth hormone was put into the spotlight also as a possible treatment target. One study investigated the effects of supraphysiological levels of recombinant growth hormone in patients with anorexia nervosa for 12 weeks. This treatment did not induce an increase in circulating insulin-like growth factor-1 levels but decreased fat mass without effect on body weight [93]. In adolescents with anorexia nervosa treatment with recombinant growth hormone induced an increase of insulin-like growth factor-1 and led to a stimulation of height velocity [94]. Data from this pilot study should be followed up in a larger and controlled manner.
Advances in non-surgical treatment for pediatric patients with short bowel syndrome
Published in Expert Opinion on Orphan Drugs, 2020
Danielle Wendel, Beatrice E. Ho, Tanyaporn Kaenkumchorn, Simon P. Horslen
With the production of numerous hormones to regulate all aspects of GI function, the GI tract is the largest endocrinologic organ in the human body [106]. With the discovery of the many trophic and motility effects hormones have on the GI tract, they have become a prime target for SBS therapies. The first hormone therapy for SBS involved a long-acting somatostatin analogue Octreotide. While improvements were seen with fluid and electrolyte absorption, it is only recommended for short-term therapy for patients with high ostomy output secondary to the potential side effects related to fluid retention and inhibitory effects on other hormones [107]. Growth hormone was the next to be studied in conjunction with the amino acid glutamine with some response seen at high doses in wet weight absorption but variable effects on energy absorption. With the global effects of growth hormone and potential side effects, especially at higher doses, a Cochrane review questioned the utility of the treatment [108]. Glutamine alone has effects on enterocyte energy consumption but did not show significant clinical benefit in human SBS studies [109,110]. Oral insulin has also been studied as it is a factor present in human milk that has effects on intestinal maturation and enzyme expression [111]. While there were promising results from animal studies and preliminary pilot studies in infants, larger studies are needed to determine the efficacy of oral insulin [112,113].
Acquired neuro-secretory defect in growth hormone secretion due to Imatinib mesylate and the efficacy of growth hormone therapy in children with chronic myeloid leukemia
Published in Pediatric Hematology and Oncology, 2020
Rama Walia, Anuradha Aggarwal, Anil Bhansali, Anshita Aggarwal, Neelam Varma, Naresh Sachdeva, Niranjan Khandelwal, Deepak Bansal
Chronic myeloid leukemia (CML) is rare, accounting for 2–3% of all leukemias in childhood.1–3 Imatinib or second-generation tyrosine kinase inhibitors (TKIs) (Dasatinib or nilotinib) are the standard of care for children and adults with CML. TKIs are associated with several adverse effects. Growth impairment is one of the major concerns of long-term treatment with Imatinib in children with CML.4,5 The mechanism remains elusive. Several studies in adults have suggested that inhibition of c-kit, c-fms, and platelet-derived growth factor (PDGF) receptors results in the modulation of bone metabolism. Several reports, including our preliminary study, showed a disturbance of the growth hormone (GH) axis as a mechanism for growth impairment.6 Additional endocrine related-adverse effects of TKI include alterations in thyroid function, gonadal function, glucose metabolism and adrenal function.7