Importance of increased urinary calcium excretion in the development of secondary hyperparathyroidism of patients under glucocorticoid therapy

Suzuki, Yasuo; Ichikawa, Yōichi; Saito, Eizo; Homma, Mitsuo

doi:10.1016/0026-0495(83)90221-4

Cited by 328 publications

(110 citation statements)

References 23 publications

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“…Increased bone resorption has been attributed to secondary hyperparathyroidism resulting from glucocorticoid inhibition of gastrointestinal calcium absorption (6)(7)(8) and increased urinary calcium loss (9). Other investigators (10,l I) have been unable to find an increase in serum immunoreactive parathyroid hormone (iPTH) and postulate that there may be increased bone sensitivity to iPTH.…”

mentioning

confidence: 99%

Relationship of glucocorticoid dosage to serum bone gla‐protein concentration in patients with rheumatologic disorders

Kotowicz

Hall

Hunder

et al. 1990

Arthritis & Rheumatism

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Serum bone Gla-protein (BGP) measurements in 50 rheumatic disease patients receiving long-term prednisone therapy revealed an inverse relationship (r = -0.71, P < 0.001) between serum BGP levels and prednisone dosage. Multiple regression analysis demonstrated significant relationships (R' = 0.72, P < 0.001) between serum BGP'" and prednisone dosage, dosage', serum creatinine, age, and an age-creatinine interaction. This model predicts the suppression of serum BGP with low dosages of steroids and 50% suppression with dosages of 20-25 mg/day.Osteoporosis is a serious complication of glucocorticoid therapy. During treatment, bone loss occurs principally in regions of the skeleton that have a high content of cancellous bone, such as the ribs and vertebrae, and this may result in fractures at these sites (1). In a prospective study of glucocorticoidtreated asthmatic patients, the incidence of vertebral or rib fractures was 45% (2). Based on measurements made at the distal radius by single-photon absorptiometry, the prevalence of osteopenia among steroidtreated patients attending rheumatology clinics was 38% (3).Microradiography of rib (4) and histomorphometric analysis of iliac crest bone ( 5 ) from patients with excess levels of glucocorticoids have demonstrated both increased bone resorption and decreased bone formation. Increased bone resorption has been attributed to secondary hyperparathyroidism resulting from glucocorticoid inhibition of gastrointestinal calcium absorption (6-8) and increased urinary calcium loss (9). Other investigators (10,l I) have been unable to find an increase in serum immunoreactive parathyroid hormone (iPTH) and postulate that there may be increased bone sensitivity to iPTH. However, inhibition of bone formation appears to be due to a direct effect of steroids on osteoblast function. Evidence supporting a direct effect of corticosteroids on bone synthesis includes decreased collagen synthesis (12-14), decreased alkaline phosphatase activity (14), decreased production of bone Gla-protein (BGP, or osteocalcin) (IS), and decreased incorporation of 3H-thymidine into DNA and of 3H-uridine into RNA (12,13) by bone cells in vitro, after treatment with glucocorticoids.Bone formation can be assessed indirectly by measurement of serum BGP levels. BGP, the most abundant of the noncollagenous bone proteins, is synthesized by osteoblasts (16,17). Circulating BGP levels have been shown to reflect bone formation, but not resorption, as determined by histomorphometric techniques, in patients with postmenopausal osteoporosis (18), primary hyperparathyroidism, or hyper-

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mentioning

confidence: 99%

Relationship of glucocorticoid dosage to serum bone gla‐protein concentration in patients with rheumatologic disorders

Kotowicz

Hall

Hunder

et al. 1990

Arthritis & Rheumatism

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“…Interventions aiming at restoring calcium [9,46,134]. In a recent meta-analysis, the efficacy of active vitamin D3 analogues in preserving bone and in decreasing the risk of vertebral fractures was shown to be significantly higher than no treatment, placebo and plain vitamin D3 with or without concomitant calcium [28].…”

Section: Calcium Vitamin D and Thiazide Diureticsmentioning

confidence: 99%

“…in combination with sodium restriction was shown to increase intestinal calcium absorption and to lower renal calcium excretion and thus to lower PTH levels [111,134]. However, the combination with vitamin D may lead to increased risk of hypercalcaemia and to worsening of the GC-induced hypokaliemia.…”

Section: Calcium Vitamin D and Thiazide Diureticsmentioning

confidence: 99%

Glucocorticosteroid-induced spinal osteoporosis: scientific update on pathophysiology and treatment

et al. 2006

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“…Potent bisphosphonates, such as zoledronic acid, suppress bone resorption with great efficacy, and therefore eliminate an effective compensatory mechanism to correct hypocalcaemia by releasing calcium from the skeleton. Secondly, high-dose glucocorticoids, used immediately post transplant or for the treatment of relapse myeloma, can further precipitate hypocalcaemia due to hypercalciuria 6 and intestinal calcium malabsorption. 7 As vitamin D deficiency is common among patients with chronic diseases, vitamin D status should be evaluated before bisphosphonate therapy.…”

mentioning

confidence: 99%

Hypocalcaemic cardiac failure post BMT secondary to unrecognized vitamin D deficiency

Lee

Milliken

2008

Bone Marrow Transplant

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Importance of increased urinary calcium excretion in the development of secondary hyperparathyroidism of patients under glucocorticoid therapy

Cited by 328 publications

References 23 publications

Relationship of glucocorticoid dosage to serum bone gla‐protein concentration in patients with rheumatologic disorders

Relationship of glucocorticoid dosage to serum bone gla‐protein concentration in patients with rheumatologic disorders

Glucocorticosteroid-induced spinal osteoporosis: scientific update on pathophysiology and treatment

Hypocalcaemic cardiac failure post BMT secondary to unrecognized vitamin D deficiency

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