The impact of corticosteroids on growth and bone health

Mushtaq, Talat

doi:10.1136/adc.87.2.93

Cited by 146 publications

(107 citation statements)

References 60 publications

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“…In children, maintenance of growth is a complex process that is affected by a number of distinct mechanisms, such as alterations in growth hormone (GH) secretion and in GH/insulin-like growth factor 1 (IGF-1) sensitivity (3,13). Although compensatory growth often follows the cessation of GC therapy, children with systemic chronic inflammatory diseases subjected to long-term GC treatment may have reduced final height (14,15).…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone reduces ATDC5 chondrocyte cell viability by inducing autophagy

Zhao

Zuo

Huo

et al. 2014

Molecular Medicine Reports

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Abstract. Prolonged use of glucocorticoids (GCs) for the treatment of chronic inflammatory and autoimmune diseases commonly exerts various side-effects, including impairment of skeletal development. However, the effect of GCs on chondrocytes, which play a key role in skeletal development, has been rarely reported. In the present study, autophagy was induced in the ATDC5 chondrocyte cell line following treatment with dexamethasone (Dex) at doses of 1-100 µM, and that this effect can be inhibited by RU486, a GC antagonist. Autophagy induced by the highest Dex dose (100 µM) was associated with a reduction in ATDC5 cell viability. We conclude that high doses of GC can reduce ATDC5 chondrocyte cell viability by inducing autophagy.

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Section: Discussionmentioning

confidence: 99%

Dexamethasone reduces ATDC5 chondrocyte cell viability by inducing autophagy

Zhao

Zuo

Huo

et al. 2014

Molecular Medicine Reports

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“…Bone loss is dependent on the type and dose of GC and occurs most prominently in the first 6 months of treatment [19,25,30]. GCs have a suppressive effect on osteoblastogenesis in the bone marrow and promote the apoptosis of osteoblasts and osteocytes, thus leading to decreased bone formation [31].…”

Section: Discussionmentioning

confidence: 99%

Bone mineral density and serum bone turnover markers in survivors of childhood acute lymphoblastic leukemia: Comparison of megadose methylprednisolone and conventional‐dose prednisolone treatments

et al. 2005

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During recent decades, the survival rate after childhood acute lymphoblastic leukemia (ALL) has improved substantially; consequently, the long-term side effects of ALL and its treatment have gained attention, of which osteoporosis is one of the most important. The purpose of the present study was to compare the influence of different treatment protocols that include high-dose methylprednisolone (HDMP) versus conventional-dose prednisolone (CDP) for remission-induction therapy on bone mineral density (BMD) and serum bone turnover markers in survivors of childhood ALL after cessation of chemotherapy. Thirty-six boy and 23 girl survivors, treated for ALL, were cross-sectionally studied, at a mean age of 11.7 years (range 6-19). Group 1 (n = 30) received CDP therapy (prednisolone, 2 mg/kg/day, orally) and group 2 (n = 29) received HDMP therapy (prednol-L, 900-600 mg/m 2 , orally). All other therapies were similar in both groups. Cranial irradiation was added for high-risk patients as soon as possible after consolidation therapy. We found that mean lumbar spine BMD z score value was -1.75 (0.83) SDS in group 1 and -1.66 (1.21) SDS in group 2. There is no difference between both groups (P = 0.736). The mean BMD z scores of prepubertal and pubertal patients were not significantly different in both groups. Comparison of serum bone turnover parameters of the patients revealed no difference between the two groups. Stepwise regression analysis revealed that lumbar spine BMD z scores was predicted by height SDS and the time past since cessation of therapy, but not age at diagnosis, BMI SDS, cranial radiotherapy, and puberty. Our study results showed that HDMP treatment did not deteriorate the bone mass any more than CDP treatment. These results proved that high-dose steroid therapy over a short period of time in remission-induction treatment would not affect the bone mass any more adversely than would conventional doses approximately 3 years after cessation of chemotherapy. Am.

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“…The growthsuppressing effects of GCs can be mediated through both systemic and local mechanisms. GCs suppress the GH/IGF1 axis through inhibiting GH secretion (Mushtaq 2002) and downregulating GH receptors in the liver, thereby inhibiting IGF1 production and activity (Kritsch et al 2002). The effect of GCs on pubertal development has also been studied but the results vary and are still debated (Kinouchi et al 2012).…”

Section: Impact Of Inflammation On Bone Growthmentioning

confidence: 99%

RECENT RESEARCH ON THE GROWTH PLATE: Impact of inflammatory cytokines on longitudinal bone growth

Sederquist¹,

Fernandez-Vojvodich²,

Zaman³

et al. 2014

Journal of Molecular Endocrinology

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Children with inflammatory diseases usually display abnormal growth patterns as well as delayed puberty. This is a result of several factors related to the disease itself, such as malnutrition, hypercortisolism, and elevated levels of pro-inflammatory cytokines. These factors in combination with glucocorticoid treatment contribute to growth retardation during chronic inflammation by systemically affecting the major regulator of growth, the GH/IGF1 axis. However, recent studies have also shown evidence of a direct effect of these factors at the growth plate level. In conditions of chronic inflammation, pro-inflammatory cytokines are upregulated and released into the circulation. The most abundant of these, tumor necrosis factor a, interleukin 1b (IL1b), and IL6, are all known to directly act on growth plate cartilage to induce apoptosis and thereby suppress bone growth. Both clinical and experimental studies have shown that growth retardation can partly be rescued when these cytokines are blocked. Therefore, therapy modulating the local actions of these cytokines may be effective for preventing growth failure in patients with chronic inflammatory disorders. In this review, we report the current knowledge of inflammatory cytokines and their role in regulating bone growth.

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The impact of corticosteroids on growth and bone health

Cited by 146 publications

References 60 publications

Dexamethasone reduces ATDC5 chondrocyte cell viability by inducing autophagy

Dexamethasone reduces ATDC5 chondrocyte cell viability by inducing autophagy

Bone mineral density and serum bone turnover markers in survivors of childhood acute lymphoblastic leukemia: Comparison of megadose methylprednisolone and conventional‐dose prednisolone treatments

RECENT RESEARCH ON THE GROWTH PLATE: Impact of inflammatory cytokines on longitudinal bone growth

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