The effect of vitamin D status on the severity of bone disease and on the other features of primary hyperparathyroidism (pHPT) in a vitamin D deficient region

Raef, Hussein; Ingemansson, Stig; Sobhi, Saif Al; Sultan, Abdul H.; Ahmed, Mohammed; Chaudhry, M. Ahmad

doi:10.1007/bf03346273

Cited by 47 publications

(46 citation statements)

References 19 publications

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“…Bone density in a large population of postmenopausal women with osteoporosis correlated inversely with vitamin D levels 24. It has also been shown that lower vitamin D levels may contribute to the frequently encountered, severe bone manifestations, seen with primary hyperparathyroidism in Saudi Arabia and other countries with widespread vitamin D deficiency 25. Vitamin D deficiency should therefore be suspected and adequately treated in all patients with osteopenia and osteoporosis in our region.…”

Section: The Role Of Vitamin D Deficiencymentioning

confidence: 88%

Updated Recommendations for the Diagnosis and Management of Osteoporosis: A Local Perspective

Raef

Al-Bugami

Balharith

et al. 2011

Annals of Saudi Medicine

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Postmenopausal osteoporosis and osteoporosis in elderly men are major health problems, with a significant medical and economic burden. Although osteopenia and osteoporosis are more common locally than in the West, fracture rates are generally less than in Western countries. Vitamin D deficiency is common in the region and contributes adversely to bone health. Vitamin D deficiency should be suspected and treated in all subjects with ostopenia or osteoporosis. The use of risk factors to determine fracture risk has been adopted by the World Health Organization and many international societies. Absolute fracture risk methodology improves the use of resources by targeting subjects at higher risk of fractures for screening and management. The King Faisal Specialist Hospital Osteoporosis Working Group recommends screening for women 65 years and older and for men 70 years and older. Younger subjects with clinical risk factors and persons with clinical evidence of osteoporosis or diseases leading to osteoporosis should also be screened. These guidelines provide recommendations for treatment for postmenopausal women and men older than 50 years presenting with osteoporotic fractures for persons having osteoporosis—after excluding secondary causes—or for persons having low bone mass and a high risk for fracture. The Working Group has suggested an algorithm to use at King Faisal Specialist Hospital that is based on the availability, cost, and level of evidence of various therapeutic modalities. Adequate calcium and vitamin D supplement are recommended for all. Weekly alendronate (in the absence of contraindications) is recommended as first-line therapy. Alternatives to alendronate are raloxifene or strontium ranelate. Second-line therapies are zoledronic acid intravenously once yearly, when oral therapy is not feasible or complicated by side effects, or teriparatide in established osteoporosis with fractures.

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Section: The Role Of Vitamin D Deficiencymentioning

confidence: 88%

Updated Recommendations for the Diagnosis and Management of Osteoporosis: A Local Perspective

Raef

Al-Bugami

Balharith

et al. 2011

Annals of Saudi Medicine

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“…It has been suggested that preoperative serum alkaline phosphatase concentrations may predict the degree and duration of hypocalcaemia after successful parathyroidectomy (46). Other risk factors for the development of HBS include evidence of bone disease, such as osteitis fibrosa cystica, subperiostal bone erosions or bone cysts (4,15,16,17,26,27,31,39) and the volume and weight of the removed hyperactive parathyroid gland(s) (1, 3).…”

Section: Discussionmentioning

confidence: 99%

“…Radiological bone disease before surgery Radiological evidence of PHPT-related bone disease has been reported to be an important risk factor for the development of HBS (4,16,17,26,27,31,39). Fourteen of 18 case reports on HBS indeed report skeletal abnormalities, such as subperiostal erosions, lytic lesions, brown tumours and multiple fractures …”

Section: Risk Factors For the Development Of Hbsmentioning

confidence: 99%

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THERAPY OF ENDOCRINE DISEASE: Hungry bone syndrome: still a challenge in the post-operative management of primary hyperparathyroidism: a systematic review of the literature

Witteveen

Thiel

Romijn

et al. 2013

European Journal of Endocrinology

285

220

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Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcaemia associated with hypophosphataemia and hypomagnesaemia, and is exacerbated by suppressed parathyroid hormone (PTH) levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism (PHPT) and preoperative high bone turnover. It is a relatively uncommon, but serious adverse effect of parathyroidectomy. We conducted a literature search of all available studies reporting a 'hungry bone syndrome' in patients who had a parathyroidectomy for PHPT, to identify patients at risk and address the pitfalls in their management. The severe hypocalcaemia is believed to be due to increased influx of calcium into bone, due to the sudden removal of the effect of high circulating levels of PTH on osteoclastic resorption, leading to a decrease in the activation frequency of new remodelling sites and to a decrease in remodelling space, although there is no good documentation for this. Various risk factors have been suggested for the development of HBS, including older age, weight/volume of the resected parathyroid glands, radiological evidence of bone disease and vitamin D deficiency. The syndrome is reported in 25-90% of patients with radiological evidence of hyperparathyroid bone disease vs only 0-6% of patients without skeletal involvement. There is insufficient data-based evidence on the best means to treat, minimise or prevent this severe complication of parathyroidectomy. Treatment is aimed at replenishing the severe calcium deficit by using high doses of calcium supplemented by high doses of active metabolites of vitamin D. Adequate correction of magnesium deficiency and normalisation of bone turnover are required for resolution of the hypocalcaemia which may last for a number of months after successful surgery. Preoperative treatment with bisphosphonates has been suggested to reduce post-operative hypocalcaemia, but there are to date no prospective studies addressing this issue. European Journal of Endocrinology 168 R45-R53

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“…The pathophysiological mechanisms responsible for the low serum 25(OH)D level in PHPT are not completely clarified. The data obtained from several studies suggest that vitamin D status might influence the clinical and biological expression of PHTP [1,2,[4][5][6][7][8][9][10][11][12][13][14][15] and even recovery after surgical treatment [11,16,17], although some authors have not found such an association [18,19].…”

Section: Introductionmentioning

confidence: 99%

Biochemical effects of calcifediol supplementation in mild, asymptomatic, hyperparathyroidism with concomitant vitamin D deficiency

Isidro

Ruano

2009

Endocr

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It has been proposed to cautiously supplement with vitamin D to any patient with asymptomatic primary hyperparathyroidism (PHTP) and a plasma 25-hydroxyvitamin D [25(OH)D] concentration <50 nmol/l. Evidence about the safeness of this intervention is limited to two studies. Our aim was to prospectively assess the biochemical effects of one-year 25(OH)D supplementation in this context. Twenty-seven patients were included in this study. Calcifediol was started at a dose of 480-960 IU/24 h (8-16 microg/24 h) and adjusted up to a maximum of 960 IU/24 h (16 microg/24 h). Basal calcium, phosphate, albumin, total alkaline phosphatase (ALP), creatinine, 24 h calcium urinary excretion, intact PTH (iPTH) and 25(OH)D were measured before and during vitamin D supplementation. The mean basal 25(OH)D was 28.7 +/- 8.0 nmol/l, and at 12 months was 71.5 +/- 32.5 nmol/l (P = 0.00 vs. baseline). After 3, 6 and 12 months iPTH levels were 141.7 +/- 108.4 ng/l (P = 0.00 vs. baseline), 131.1 +/- 95.7 ng/l (P = 0.03 vs. baseline) and 162.2 +/- 139.3 ng/l (P = ns vs. baseline). Mean calcium did not change. Mean urinary calcium excretion increased significantly (basal: 5.7 +/- 2.9 mmol/24 h, 12 months: 7.9 +/- 4.9 mmol/24 h, P = 0.02). Cautious calcifediol supplementation significantly increased mean 25(OH)D and temporarily reduced mean iPTH. It did not change mean serum calcium, but urinary calcium excretion increased significantly. We suggest that serum calcium and 24 h calciuria be measured at regular intervals in patients with PHTP, while on calcifediol supplementation.

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The effect of vitamin D status on the severity of bone disease and on the other features of primary hyperparathyroidism (pHPT) in a vitamin D deficient region

Cited by 47 publications

References 19 publications

Updated Recommendations for the Diagnosis and Management of Osteoporosis: A Local Perspective

Updated Recommendations for the Diagnosis and Management of Osteoporosis: A Local Perspective

THERAPY OF ENDOCRINE DISEASE: Hungry bone syndrome: still a challenge in the post-operative management of primary hyperparathyroidism: a systematic review of the literature

Biochemical effects of calcifediol supplementation in mild, asymptomatic, hyperparathyroidism with concomitant vitamin D deficiency

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