Growth hormone axis in patients with chronic kidney disease

Paschou, Stavroula Α.; Kanaka‐Gantenbein, Christina; Chrousos, George P.; Vryonidou, Andromachi

doi:10.1007/s42000-018-0066-9

Cited by 6 publications

(7 citation statements)

References 25 publications

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“…Growth hormone (GH) initiates and maintains the process of growth through the stimulation of insulin-like growth factor 1 (IGF1), a growth factor that leads to chondrocyte hypertrophy and the production of ECM. 14 , 15 Local factors in the perichondrium also affect bone growth, contributing to chondrocyte hypertrophy and osteoblast invasion. Bone morphogenetic proteins (BMPs), 16 fibroblast growth factors (FGFs), 17 and wingless/Int-1 (Wnt) signalling 18 are all involved in the communication between perichondral cells and cartilage chondrocytes.…”

Section: Humoral Control Of Physeal Growth and Fusionmentioning

confidence: 99%

“…Growth hormone supplementation has been advocated in constitutionally short stature and is not allowed in athletes because of its anabolic steroid effects. 15 …”

Section: Hormones and The Physismentioning

confidence: 99%

“… 45 Ciprofloxacin has also been shown to cause growth retardation in children, 46 although its effects may not be clinically significant. 47 Diabetes, 48 hypothyroidism, 49 and renal failure 15 have been investigated as acquired causes of growth retardation that impact growth through their effects on systemic hormones, ECM, and chondrocytes.…”

Section: Systemic Causes Of Growth Plate Disordersmentioning

confidence: 99%

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The growth plate: a physiologic overview

Ağırdil

2020

EFORT Open Reviews

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The growth plate is the cartilaginous portion of long bones where the longitudinal growth of the bone takes place. Its structure comprises chondrocytes suspended in a collagen matrix that go through several stages of maturation until they finally die, and are replaced by osteoblasts, osteoclasts, and lamellar bone. The process of endochondral ossification is coordinated by chondrocytes and a variety of humoral factors including growth hormone, parathyroid hormone, oestrogen, growth factors, cytokines, and various signalling pathways. Chondrocytes progress from a resting state to enter the phases of proliferation and hypertrophy. Under the influence of oestrogen, the proliferation of chondrocytes decreases as the resting chondrocytes are consumed. During the terminal phase of differentiation, cartilage is replaced by blood vessels and organized bone tissue, and once chondrocytes have died, the longitudinal growth of the bone ceases and the growth plate closes. The highly complex regulatory signals involved in this process are genetically determined, and genetic perturbations in any of the associated genes can result in abnormalities of bone growth. Hundreds of chondrodysplasias have been described, pointing to the complexity of the humoral control systems involved in endochondral ossification. While our knowledge of the mechanisms behind the various bone growth control systems is improving, a deeper understanding of the underlying processes could aid clinicians to better understand bone health and bone growth abnormalities. This review describes the current clinical research into the physiology of the growth plate. Cite this article: EFORT Open Rev 2020;5:498-507. DOI: 10.1302/2058-5241.5.190088

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Section: Humoral Control Of Physeal Growth and Fusionmentioning

confidence: 99%

“…Growth hormone supplementation has been advocated in constitutionally short stature and is not allowed in athletes because of its anabolic steroid effects. 15 …”

Section: Hormones and The Physismentioning

confidence: 99%

Section: Systemic Causes Of Growth Plate Disordersmentioning

confidence: 99%

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The growth plate: a physiologic overview

Ağırdil

2020

EFORT Open Reviews

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“…Indications for growth hormone treatment in other children after solid organ recipients vary but it is typically effective in enhancing statural growth and also improving bone density in these children 147‐150 . Adults with CKD may also demonstrate improved muscle strength and bone density with short courses of rGH therapy 151,152 …”

Section: Emerging Bone Anti‐resorptive and Anabolic Therapiesmentioning

confidence: 99%

Promoting bone health in children and adolescents following solid organ transplantation

Kusumi

Shaikhkhalil

Patel

et al. 2020

Pediatric Transplantation

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Solid organ transplantation in children and adolescents provides many benefits through improving critical organ function, including better growth, development, cardiovascular status, and quality of life. Unfortunately, bone status may be adversely affected even when overall status is improving, due to issues with pre-existing bone disease as well as medications and nutritional challenges inherent post-transplantation. For all children and adolescents, bone status entering adulthood is a critical determinant of bone health through adulthood. The overall health and bone status of transplant recipients benefits from attention to regular physical activity, good nutrition, adequate calcium, phosphorous, magnesium and vitamin D intake and avoidance/minimization of soda, extra sodium, and obesity. Many immunosuppressive agents, especially glucocorticoids, can adversely affect bone function and development. Minimizing exposure to "bone-toxic" medications is an important part of promoting bone health in children post-transplantation. Existing guidelines detail how regular monitoring of bone status and biochemical markers can help detect bone abnormalities early and facilitate valuable bone-directed interventions. Attention to calcium and vitamin D supplementation, as well as tapering and withdrawing glucocorticoids as early as possible after transplant, can provide best bone outcomes for these children. Dual-energy X-ray absorptiometry can be useful to detect abnormal bone mass and fracture risk in this population and newer bone assessment methods are being evaluated in children at risk for poor bone outcomes. Newer bone therapies being explored in adults with transplants, particularly bisphosphonates and the RANKL inhibitor denosumab, may offer promise for children with low bone mass post-transplantation.

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“…The oxidation and rise of FFAs play an additional intensifying role in insulin resistance [1]. GH promotes an increase in IGF-1 via the Janus kinase 2/ signal transducer and activator of transcription 5b (JAK2/ STAT5b) pathway [10,11]. Although with a lower affinity, due to its molecular similarity, IGF-1 can bind to insulin receptors [12], promoting insulin secretion as well [13].…”

Section: Pathophysiologymentioning

confidence: 99%

The Effect of Pituitary Gland Disorders on Glucose Metabolism: From Pathophysiology to Management

et al. 2020

Self Cite

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This review aims to explore, present, and discuss disorders of glucose metabolism implicated in pituitary gland diseases, the appropriate interventions, as well as the therapeutic challenges that may arise. Pituitary pathologies may dysregulate glucose homeostasis, as both the excess and deficiency of various pituitary hormones can affect glucose metabolism. Increased circulating levels of growth hormone, glucocorticoids or prolactin have been shown to mainly provoke hyperglycemic states, while hypopituitarism can be associated with both hyperglycemia and hypoglycemia. Addressing the primary cause of these disorders with the use of surgery, medical treatment or radiotherapy forms the cornerstone of current management strategies. Physicians should bear in mind that some such medications have an unfavorable effect on glucose metabolism too. When unsuccessful, or until the appropriate treatment of the underlying pituitary problem, the addition of established antidiabetic therapies might prove useful. Further studies aiming to discover more accurate and effective drug preparations in combination with optimal lifestyle management models will contribute to achieving a more successful glycemic control in these patients.

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Growth hormone axis in patients with chronic kidney disease

Cited by 6 publications

References 25 publications

The growth plate: a physiologic overview

The growth plate: a physiologic overview

Promoting bone health in children and adolescents following solid organ transplantation

The Effect of Pituitary Gland Disorders on Glucose Metabolism: From Pathophysiology to Management

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