Short report: Bone density in asthmatic children treated with inhaled corticosteroids

Reilly, S.; Hambleton, G; Adams, Judith E.; Mughal, M. Zulf

doi:10.1136/adc.84.2.183

Cited by 36 publications

(13 citation statements)

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“…Our data suggest that BUD diminishes bone formation, both mineralization and collagen synthesis, at least transiently, even at a dose of 400 g/d, whereas FP seems to diminish only the later mineralization phase of bone formation, and only at 500 g/d doses. These results are consistent with the recent study of Reilly et al (28), who found that FP is less likely than BUD to affect trabecular bone mineral density. On the other hand, during CROM treatment, both markers of bone formation tended to increase, probably reflecting normal agedependent growth and increase in bone mass (29,30).…”

Section: Discussionsupporting

confidence: 93%

Biochemical Markers of Bone Metabolism in Relation to Adrenocortical and Growth Suppression During the Initiation Phase of Inhaled Steroid Therapy

Kannisto

2002

Pediatric Research

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Growth suppression is usually most evident during the first year of inhaled steroid therapy. Steroid-induced changes in bone metabolism may contribute to this growth suppression. The aim of the present study was to evaluate the changes in biochemical markers of bone metabolism in relation to adrenal and growth suppression during the initiation phase of inhaled steroid therapy. Seventy-five school-aged children with new asthma were enrolled into budesonide (BUD, n ϭ 30), fluticasone propionate (FP, n ϭ 30) or cromone (CROM, n ϭ 15) treatment groups. BUD dose was 800 g/d during the first two months and 400 g/d thereafter. The respective FP doses were 500 and 200 g/d. Biochemical markers of bone metabolism were measured before treatment and after 2 and 4 mo of therapy. In the control (CROM) group, the mean concentrations of serum osteocalcin (OC), carboxyterminal propeptide of type I procollagen (PICP) (formation markers) and type I collagen carboxyterminal telopeptide (ICTP) (degradation marker) tended to increase. In the BUD group, OC and PICP decreased during the 4 mo by a mean of 23% (p Ͻ 0.001) and 15% (p Ͻ 0.05), respectively, while ICTP did not change significantly. In the FP group, OC and ICTP decreased during the first 2 mo by a mean of 19% (p Ͻ 0.01) and 21% (p Ͻ 0.01), respectively, returning to the pretreatment level at 4 mo, while PICP tended to increase during the 4 mo (14%, p ϭ 0.12).In the steroid treated children whose height SD score decreased during the first 12 mo of therapy, both OC and PICP decreased during the first 4 mo by a mean of 20% (p Ͻ 0.01) and 21% (p Ͻ 0.001), respectively. In those children who had no growth suppression, the changes were not significant: Ϫ4% in OC and ϩ13% in PICP. Furthermore, in children who developed evidence of adrenocortical suppression (on the basis of a low-dose ACTH test), OC decreased more (23%, p Ͻ 0.01) than in those with normal adrenocortical function (10%, p ϭ 0.06). In conclusion, both inhaled BUD and FP caused dose-dependent effects on biochemical markers of bone metabolism. The children who developed growth or adrenocortical suppression were likely to have changes also in bone metabolism. Asthmatic children treated with inhaled steroids seem to attain normal adult height (1). Despite this, inhaled steroids may at least temporarily suppress adrenocortical function (2, 3), growth (4, 5), and bone metabolism (6, 7). Glucocorticoids affect calcium metabolism (8, 9), and they can reduce bone formation by impairing the function of osteoblasts (10). Therefore, long-term use of inhaled steroids can cause osteopenia, at least in adults (11,12). There is a difference in the doseresponse relation between efficacy and systemic adverse effects of inhaled steroids. A plateau in the efficacy is reached at relatively low doses (13), while a linear relation between the dose and the effects on the adrenocortical function and bone metabolism continues for much higher doses (14).OC, the most abundant noncollagenous protein in bone matrix, is produced mainly by osteoblas...

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Section: Discussionsupporting

confidence: 93%

Biochemical Markers of Bone Metabolism in Relation to Adrenocortical and Growth Suppression During the Initiation Phase of Inhaled Steroid Therapy

Kannisto

2002

Pediatric Research

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“…study of healthy skeletal development [1][2][3][4][5][6][7][8][9][10] and for the assessment of paediatric disorders associated with skeletal fragility [11][12][13][14][15][16][17][18][19][20][21]. pQCT is designed to measure peripheral skeletal sites such as the radius, tibia and femur.…”

mentioning

confidence: 99%

A reference database for the Stratec XCT-2000 peripheral quantitative computed tomography (pQCT) scanner in healthy children and young adults aged 6–19 years

et al. 2008

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“…Os estudos longitudinais e transversais não revelaram efeitos indesejáveis na mineralização óssea 13 . Por outro lado, os efeitos secundários locais não podem ser desprezados, como a sensação de sede (22%), disfonia (11%), candidíase oral (11%) 14 , estes dois últimos podendo ser significativamente reduzidos com bochechos e/ou escovação dos dentes após a inalação.…”

Section: Efeitos Colateraisunclassified

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Moura¹,

Camargos²,

Blic³

2002

J. Pediatr. (Rio J.)

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Short report: Bone density in asthmatic children treated with inhaled corticosteroids

Cited by 36 publications

References 3 publications

Biochemical Markers of Bone Metabolism in Relation to Adrenocortical and Growth Suppression During the Initiation Phase of Inhaled Steroid Therapy

Biochemical Markers of Bone Metabolism in Relation to Adrenocortical and Growth Suppression During the Initiation Phase of Inhaled Steroid Therapy

A reference database for the Stratec XCT-2000 peripheral quantitative computed tomography (pQCT) scanner in healthy children and young adults aged 6–19 years

Tratamento profilático da asma

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