Growth Hormone in Glucocorticoid-Induced Osteoporosis

Manelli, Filippo; Carpinteri, R.; Bossoni, Simonetta; Burattin, Anna; Bonadonna, Stefania; Rosei, E. Agabiti; Giustina, Andrea

doi:10.1159/000061083

Cited by 26 publications

(16 citation statements)

References 37 publications

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“…Interestingly, GH suppression has been seen also in patients administered inhaled corticosteroids (25), suggesting the even topical use of glucocorticoids could have undesired skeletal consequences (26). GH and IGF-I administration has been proposed to revert some of the negative effects of chronic glucocorticoid treatment on bone (27)(28)(29)(30)(31)(32)(33). An increase in serum osteocalcin, carboxy-terminal propeptide of type I procollagen and carboxy-terminal telopeptide of type I collagen was observed following shortterm recombinant human (rh)GH treatment in a selected population of patients receiving chronic corticosteroid treatment for non-endocrine diseases (27).…”

Section: Extraskeletal Effects Of Glucocorticoids On Bone Metabolismmentioning

confidence: 99%

“…GH and IGF-I administration has been proposed to revert some of the negative effects of chronic glucocorticoid treatment on bone (27)(28)(29)(30)(31)(32)(33). An increase in serum osteocalcin, carboxy-terminal propeptide of type I procollagen and carboxy-terminal telopeptide of type I collagen was observed following shortterm recombinant human (rh)GH treatment in a selected population of patients receiving chronic corticosteroid treatment for non-endocrine diseases (27). Moreover, combined therapy of rhGH and rhIGF-I counteracted selected negative effects of glucocorticoids on bone in healthy volunteers who received short-term glucocorticoid therapy (29).…”

Section: Extraskeletal Effects Of Glucocorticoids On Bone Metabolismmentioning

confidence: 99%

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Glucocorticoid-Induced osteoporosis: clinical and therapeutic aspects

Mazziotti¹,

Giustina²,

Canalis³

et al. 2007

Arq Bras Endocrinol Metab

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Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Fractures tend to occur at higher BMD levels than in women with postmenopausal osteoporosis. Glucocorticoids have direct and indirect effects on the skeleton. They impair the replication, differentiation, and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO. Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are the most effective of the various therapies that have been assessed for the management of GIO. Anabolic therapeutic strategies are under investigation. Teriparatide seems to be also efficacious for the treatment of patients with GIO. RESUMO Osteoporose Induzida por Glicocorticóides: Aspectos Clínicos e Terapêuticos.A osteoporose induzida por glicocorticóides (OIG) é a forma mais comum de osteoporose secundária. Fraturas, que são freqüentemente assintomáticas, podem ocorrer em até 30-50% dos pacientes recebendo terapia glicocorticóide crônica. Fraturas vertebrais ocorrem logo após exposição aos glicocorticóides, ocasião em que a densidade mineral óssea (DMO) diminui rapidamente. As fraturas tendem a ocorrer mais com níveis elevados de DMO do que em mulheres com osteoporose da pós-menopausa. Os glicocorticóides têm efeitos diretos e indiretos sobre o esqueleto: eles impedem a replicação, a diferenciação e a função dos osteoblastos e induzem apoptose dos osteoblastos maduros e osteócitos. Esses efeitos levam à supressão da formação óssea, uma manifestação central da patogênese da OIG. Os glicocorticóides também favorecem a osteoclastogênese e, como conseqüência, aumentam a reabsorção óssea. Os bisfosfonatos são a mais efetiva das várias terapias que têm sido avaliadas para o manuseio da OIG. Estratégias terapêuticas com anabolizantes estão sendo investigadas. O teriparatídeo parece também ser eficaz no tratamento de pacientes com OIG. (Arq Bras Endocrinol Metab 2007;51/8

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Section: Extraskeletal Effects Of Glucocorticoids On Bone Metabolismmentioning

confidence: 99%

Section: Extraskeletal Effects Of Glucocorticoids On Bone Metabolismmentioning

confidence: 99%

Glucocorticoid-Induced osteoporosis: clinical and therapeutic aspects

Mazziotti¹,

Giustina²,

Canalis³

et al. 2007

Arq Bras Endocrinol Metab

View full text Add to dashboard Cite

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“…Novos dados com uso de terapias anabólicas (PTH e GH) na osteoporose induzida pelos GC são encorajadores, mas precisam se melhor normatizados 38,63,64 .…”

Section: Puberdadeunclassified

Effects of glucocorticoids on growth and bone mineralization

Donatti¹,

Koch²,

Takayama³

et al. 2011

J Pediatr (Rio J)

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Objective: To review the various mechanisms of glucocorticoid action and the ability of these agents to induce osteoporosis and growth deficits. Sources:A review of the scientific literature was conducted on the basis of a MEDLINE search using the keywords and descriptors "glucocorticoids," "bone mineralization," "growth," and "side effects" and limited to articles published in the last decade. The references cited by these articles were used to identify relevant older publications, with an emphasis on landmark studies essential to an understanding of the topic. Summary of the findings:Emphasis was placed on the actions of glucocorticoids on the hormones and cytokines that modulate linear growth. The end effects of glucocorticoids on the skeletal system are the result of systemic effects on bone metabolism and of direct actions on bone cells, which alter bone cell counts and predispose to bone loss. The mechanisms underlying catch-up growth and bone mass recovery after discontinuation of glucocorticoid treatment are discussed, followed by a review of diagnostic methods available for assessment of bone metabolism and mineralization and of measures for prevention and management of glucocorticoid-induced bone changes. Conclusion:Patient monitoring on a case-by-case basis plays an essential role in detection and, potentially, reversal of the damage associated with chronic glucocorticoid therapy. J Pediatr (Rio J). 2011;87(1):4-12:Glucocorticoids, steroids, growth, bone mineralization, growth retardation, child growth, children, adolescents, densitometry, bone mineral density, bone mineralization markers, bone. ResumoObjetivo: Revisar os mecanismos de ações dos glicocorticoides e sua capacidade de induzir osteoporose e déficits de crescimento. Fontes dos dados:A revisão bibliográfica de artigos científicos foi realizada na base de dados MEDLINE e utilizou as palavras-chave agrupadas nas sintaxes "glicocorticoides", "mineralização óssea", "crescimento" e "efeitos colaterais", nos últimos 10 anos, e das referências destes nos reportamos para as publicações mais antigas, mas com os estudos fundamentais para a compreensão do assunto. Síntese dos dados:Destacam-se ações dos glicocorticoides sobre hormônios e citocinas responsáveis pelo crescimento longitudinal. Os efeitos finais dos glicocorticoides sobre o esqueleto são determinados por ações sistêmicas no metabolismo ósseo e por ações diretas desses esteroides nas células ósseas, levando a mudanças no número e função das mesmas e favorecendo a perda óssea. Discutem-se os mecanismos indutores da recuperação dos canais de crescimento e recuperação da massa óssea após a descontinuação dos glicocorticoides; os métodos diagnósticos do metabolismo e mineralização óssea; assim como medidas terapêuticas e preventivas das alterações óssea induzidas pelos glicocorticoides.Conclusão: A monitorização de cada paciente é essencial para identificação e potencial reversão dos danos associados ao uso crônico de glicocorticoides. J Pediatr (Rio J). 2011;87(1):4-12:Glicocorticoide...

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“…38,63,64 Specific measures: the role of bisphosphonates Some studies have reported that bisphosphonates are safe, effective, and well-tolerated for the prevention 65 and treatment 66 of GC-induced osteopenia and osteoporosis in children and adolescents. However, bisphosphonate therapy in the pediatric setting remains controversial, as data on long-term effects is lacking; hence, many experts recommend that use of these agents be limited to children with recurrent extremity fractures, symptomatic vertebral collapse, and significantly reduced bone mass, particularly when associated with aggravating factors such as immobility.…”

Section: Pubertymentioning

confidence: 99%