Effects of recombinant human growth hormone (GH) on bone and intermediary metabolism in patients receiving chronic glucocorticoid treatment with suppressed endogenous GH response to GH-releasing hormone.

Giustina, Andrea; Bussi, Anna Rosa; Jacobello, C; Wehrenberg, W B

doi:10.1210/jcem.80.1.7829600

Cited by 33 publications

(14 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In patients with SH, the GH reserve seems to recover shortly after the normalization of cortisol levels (66), but if these patients are conservatively managed, the GH deficit may persist for many years. Thus, theoretically, GH treatment could be an option in patients with SH-induced osteoporosis (102). However, this therapy has potential drawbacks as both recombinant GH and cortisol excess may induce insulin resistance that may potentially result in glucose intolerance (103).…”

Section: Therapymentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Endogenous subclinical hypercortisolism and bone: a clinical review

Chiodini

Vainicher

Morelli

et al. 2016

European Journal of Endocrinology

View full text Add to dashboard Cite

In recent years, the condition of subclinical hypercortisolism (SH) has become a topic of growing interest. This is due to the fact that SH prevalence is not negligible (0.8-2% in the general population) and that, although asymptomatic, this subtle cortisol excess is not harmless, being associated with an increased risk of complications, in particular of osteoporosis and fragility fractures. As specific symptoms of hypercortisolism are absent in SH, the SH diagnosis relies only on biochemical tests and it is a challenge for physicians. As a consequence, even the indications for the evaluation of bone involvement in SH patients are debatable and guidelines are not available. Finally, the relative importance of bone density, bone quality and glucocorticoid sensitivity in SH is a recent field of research. On the other hand, SH prevalence seems to be increased in osteoporotic patients, in whom a vertebral fracture may be the presenting symptom of an otherwise asymptomatic cortisol excess. Therefore, the issue of who and how to screen for SH among the osteoporotic patients is widely debated. The present review will summarize the available data regarding the bone turnover, bone mineral density, bone quality and risk of fracture in patients with endogenous SH. In addition, the role of the individual glucocorticoid sensitivity in SH-related bone damage and the problem of diagnosing and managing the bone consequences of SH will be reviewed. Finally, the issue of suspecting and screening for SH patients with apparent primary osteoporosis will be addressed.

show abstract

Section: Therapymentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Endogenous subclinical hypercortisolism and bone: a clinical review

Chiodini

Vainicher

Morelli

et al. 2016

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…GH secretion is blunted by glucocorticoids mainly by increasing somatostatin tone in the hypothalamus (24,25), causing a state of "functional GH deficiency". 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).…”

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

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

show abstract

“…This finding would suggest that anabolic effects of GH may protect the skeleton from the deleterious effects of subtle glucocorticoid excess. Indeed, short-term rGH treatment was shown to be effective in reverting the negative effects of glucocorticoids on bone turnover (33,34). Moreover, rGH treatment may decrease the tissue exposure to glucocorticoids inhibiting the transformation of cortisone into cortisol (35,36).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid replacement therapy and vertebral fractures in hypopituitary adult males with GH deficiency

Mazziotti

Porcelli

Bianchi

et al. 2010

European Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

Objective: GH deficiency (GHD) and glucocorticoid excess are associated with increased risk of fragility fractures. We aimed to evaluate whether the prevalence of vertebral fractures may be influenced by glucocorticoid over-replacement in hypopituitary males with GHD. Design: Cross-sectional study. Methods: Fifty-one adult hypopituitary patients (all males; mean age 55 years, range: 23-81) with severe adult-onset GHD (replaced in 21 patients and untreated in 30 patients) and glucocorticoid deficiency on replacement treatment were studied for vertebral fractures using a radiological and morphometric approach. Results: Vertebral fractures were observed in 31 patients (60.8%) in correlation with untreated GHD, urinary cortisol values, and cortisone doses. Patients were stratified according to treatment of GHD, and current and cumulative cortisone doses. In untreated GHD, vertebral fractures occurred more frequently in patients who had received higher (greater than median) cumulative and current doses of cortisone compared with patients who had received lower (less than median) drug doses (95.2 vs 50.0%, PZ0.009 and 90.5 vs 55.6%, PZ0.04 respectively). In untreated GHD, fractured patients had significantly higher urinary cortisol values compared with patients without vertebral fractures (84 mg/24 h, range: 24-135 vs 49 mg/24 h, range: 30-96; PZ0.04). In treated GHD patients, by contrast, the prevalence of vertebral fractures was not influenced by cumulative and current cortisone doses and urinary cortisol values. Conclusions: Glucocorticoid over-replacement may increase the prevalence of vertebral fractures in patients with untreated GHD. However, treatment of GHD seems to protect the skeleton from the deleterious effects of glucocorticoid overtreatment in hypopituitary patients.

show abstract

Effects of recombinant human growth hormone (GH) on bone and intermediary metabolism in patients receiving chronic glucocorticoid treatment with suppressed endogenous GH response to GH-releasing hormone.

Cited by 33 publications

References 38 publications

MECHANISMS IN ENDOCRINOLOGY: Endogenous subclinical hypercortisolism and bone: a clinical review

MECHANISMS IN ENDOCRINOLOGY: Endogenous subclinical hypercortisolism and bone: a clinical review

Glucocorticoid-Induced osteoporosis: clinical and therapeutic aspects

Glucocorticoid replacement therapy and vertebral fractures in hypopituitary adult males with GH deficiency

Contact Info

Product

Resources

About