Calcium Absorption in Corticoid Treated Subjects Effects of a Single Oral Dose of Calcitriol

Colette, C.; Monnier, L.; Herbute, N. Pares; Blotman, F; Mirouze, J

doi:10.1055/s-2007-1011815

Cited by 27 publications

(5 citation statements)

References 12 publications

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“…Colette et al . [70] reported similar increases in fractional calcium absorption in patients treated with GCs and in control subjects, although the peak absorption rate was slower than in the control subjects. There is some evidence that tubular reabsorption of calcium is decreased [71], but this may only occur at high doses of prednisolone (25 mg day −1 ), and the increase in urinary calcium may be explained by a greater filtered load resulting from an increase in mean serum calcium concentration [43].…”

Section: How Do Gcs Cause Osteoporosis?mentioning

confidence: 82%

A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update

Eastell

Reid

Compston

et al. 1998

Journal of Internal Medicine

290

159

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. Eastell R, Reid DM, Compston J, Cooper C, Fogelman I, Francis RM, Hosking DJ, Purdie DW, Ralston SH, Reeve J, Russell RGG, Stevenson JC, Torgerson DJ (University of Sheffield Medical School, Sheffield; University of Aberdeen, Aberdeen; University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge; Southampton General Hospital, Southampton; Guy's Hospital, London; Freeman Hospital, Newcastle upon Tyne; Nottingham City Hospital, Nottingham; Hull Royal Infirmary, Hull; Wynn Institute for Metabolic Research, London; and the University of York, York, UK). A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update (Review). J Intern Med 1998; 244: 271–292. In the UK, over 250 000 patients take continuous oral glucocorticoids (GCs), yet no more than 14% receive any therapy to prevent bone loss, a major complication of GC treatment. Bone loss is rapid, particularly in the first year, and fracture risk may double. This review, based wherever possible on clinical evidence, aims to provide easy‐to‐use guidance with wide applicability. A treatment algorithm is presented for adults receiving GC doses of 7.5 mg day−1 or more for 6 months or more. General measures, e.g. alternative GCs and routes of administration, and therapeutic interventions, e.g. cyclical etidronate and hormone replacement, are recommended.

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Section: How Do Gcs Cause Osteoporosis?mentioning

confidence: 82%

A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update

Eastell

Reid

Compston

et al. 1998

Journal of Internal Medicine

290

159

View full text Add to dashboard Cite

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“…Synthesis and clearance rates of 1,25-(OH) 2 D have shown to be normal in subjects receiving GCs [139] . Moreover, 1,25-(OH) 2 D improves calcium transport but does not restore it to normal in humans [140] . Therefore, the GC-induced reduction in the gastrointestinal calcium absorption appears to be vitamin Dindependent [141,142] .…”

Section: Vitamin D Metabolismmentioning

confidence: 95%

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Alesci

Martino

Ilias

et al. 2005

Neuroimmunomodulation

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Glucocorticoid (GC)-induced osteoporosis (GCOP) is the most common cause of osteoporosis in adults aged 20–45 years as well as the most common cause of iatrogenic osteoporosis. GC excess, either endogenous or exogenous, induces bone loss in 30–50% of cases. Indeed, bone loss leading to fractures is perhaps the most incapacitating, sometimes partially irreversible, complication of GC therapy. Nevertheless, GCOP is often underdiagnosed and left untreated. The following article provides an update on the cellular and molecular mechanisms implicated in the pathophysiology of GC-induced bone loss, as well as some guidelines on diagnostic, preventive and therapeutic strategies for this medical condition, in an effort to promote a better knowledge and greater awareness of GCOP by both the patient and the physician.

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“…It interferes with vitamin D action on intestinal calcium absorption [32, 33]and calcium renal reabsorption [34], leading to secondary hyperparathyroidism, which affects growth plate cartilage and the adjacent bone. Despite these changes, vitamin D levels and function remain mostly normal during GC therapy.…”

Section: Effects On Calcium Metabolismmentioning

confidence: 99%

“…Despite these changes, vitamin D levels and function remain mostly normal during GC therapy. Supplementation of vitamin D improves intestinal calcium absorption in GC-treated patients [32]. …”

Section: Effects On Calcium Metabolismmentioning

confidence: 99%

Mechanisms of Steroid Impairment of Growth

Hochberg

2002

Horm Res Paediatr

118

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With child growth being multifactorial and the glucocorticoids (GC) having many target physiological and biochemical mechanisms, growth and the GC collide in several meeting points. Indirectly, GC have a general anti-anabolic and catabolic influences that include bone, cartilage and muscle proteins. The GC interfere with the GH–IGF-1 axis at the hypothalamic, pituitary and target organ levels, affecting hormone release, receptor abundance, signal transduction, gene transcription, pre-mRNA splicing and mRNA translation. GC disturb normal calcium balance at the intestine and kidney. Direct effects at the growth plate include the suppression of multiple gene expression, chondrocyte proliferation and matrix proteoglycan synthesis, sulfation, release and mineralization as well as the augmentation of hypertrophic cell apoptosis. At the tissues adjacent to the growth plate, GC enhance osteoclast and suppress osteoblast recruitment and function, they reduce muscle strength and disrupt the normal control of vascular invasion at the cartilage–bone interface. Growth damage from GC is maximal during the initial months of treatment and prevention is more effective than post-factual therapy. To reduce these growth-retarding effects, the following measures, which are partly experimental, may be effective in a decreasing order: minimize GC dose and use an alternate-day treatment; utilize the oxazoline analog of prednisolone deflazacort, normalize calcium balance; employ hGH or IGF-1.

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Calcium Absorption in Corticoid Treated Subjects Effects of a Single Oral Dose of Calcitriol

Cited by 27 publications

References 12 publications

A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update

A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Mechanisms of Steroid Impairment of Growth

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