Abnormal calcium metabolism in normocalcaemic sarcoidosis.

Reiner, Martin F.; Sigurðsson, Gunnar; Nunziata, V.; Malik, Masud; Poole, Graham; Joplin, G. F.

doi:10.1136/bmj.2.6050.1473

Cited by 31 publications

(10 citation statements)

References 29 publications

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“…Abnormal calcium metabolism in sarcoidosis is characterized by enhanced intestinal absorption of the ion and hypercalciuria with or without hypercalcemia, which may be associated with renal stones, nephrocalcinosis, and impaired renal function (1)(2)(3)(4)(5)(6)(7)(8). Patients with sarcoidosis exhibit increased sensitivity to small doses of vitamin D, which are ineffective in normal subjects (1,(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Evidence that Increased Circulating 1α,25-Dihydroxyvitamin D is the Probable Cause for Abnormal Calcium Metabolism in Sarcoidosis

et al. 1979

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A B S T R A C T Mean plasma 1,,25-dihydroxyvitamin D [1,,25(OH)2D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1,,25(OH)2D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D2 were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1a,,25(OH)2D and, in some studies, calcium balance were measured. Vitamin D2, 250 ,ug a day for 12 d, produced little, ifany, change in mean plasma 1a,25(OH)2D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D2 produced increases in plasma 10,,25(OH)2D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D2, 250 ,ug a day for 4 d, also increased plasma 1,,25(OH)2D abnormally from a normal value. There was a highly significant correlation between plasma 1,,25(OH)2D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degrada-

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Section: Introductionmentioning

confidence: 99%

Evidence that Increased Circulating 1α,25-Dihydroxyvitamin D is the Probable Cause for Abnormal Calcium Metabolism in Sarcoidosis

et al. 1979

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“…They proposed that bone resorption due to cumulative effects of calcitriol on osteoclasts and/or bone granuloma and of an osteoclast-activating factor produced by sarcoid granuloma may also have contributed. Reiner et al, 14 who performed calcium absorption and kinetic studies in 13 normocalcemic patients with untreated sarcoidosis, found evidence of calcium hyperabsorption from the gut and increased bone turnover. PTH did not seem to be responsible for increased bone turnover.…”

Section: Discussionmentioning

confidence: 97%

“…From low phosphate excretion index values in their patients, they inferred a reduced biological effect of PTH. 14 Physiologic requirements for calcium increase during normal pregnancy to meet the needs of growing fetus and to maintain maternal plasma and bone calcium concentrations. 11 Gertner et al 15 described pregnancy as a state of physiologic absorptive hypercalciuria.…”

Section: Discussionmentioning

confidence: 99%

Pregnancy and Sarcoidosis

Padmanabhan

Chinthalapalli

Krishnan

et al. 2004

Chest

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“…The most important protection in preventing the complications of vitamin D intoxication is to monitor serum calcium concentrations and urinary calcium excretion frequently. Hypercalcemia is found in about 17% of all patients with sarcoidosis and associated with increased intestinal absorption of calcium and increased calcium release from bone [22]. The pathogenesis of hypercalcemia in sarcoidosis is extrarenal [23].…”

Section: Metabolic Factorsmentioning

confidence: 99%

Calcium Nephrolithiasis

Brener

Winchester

Bergman

2011

Clinic Rev Bone Miner Metab

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Nephrolithiasis is a major cause of morbidity involving the urinary tract. The prevalence of this disease in the United States increased from 3.8% in the 1970s to 5.2% in the 1990s. There were nearly 2 million physician office visits for nephrolithiasis in 2000, and estimated annual costs totaled $2 billion. About 80% of stones are composed of calcium oxalate with variable amounts of calcium phosphate. New information has become available on the clinical presentation, epidemiologic risk factors, evaluative approach, and outcome of various therapeutic strategies. In this report, we will review the epidemiology and mechanisms of calcium kidney stones formation and outline management aimed at preventing recurrences. Improved awareness and education in both the general population and among health care providers about these modifiable risk factors has the potential to improve general health and decrease morbidity and mortality secondary to renal stone disease.

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Abnormal calcium metabolism in normocalcaemic sarcoidosis.

Cited by 31 publications

References 29 publications

Evidence that Increased Circulating 1α,25-Dihydroxyvitamin D is the Probable Cause for Abnormal Calcium Metabolism in Sarcoidosis

Evidence that Increased Circulating 1α,25-Dihydroxyvitamin D is the Probable Cause for Abnormal Calcium Metabolism in Sarcoidosis

Pregnancy and Sarcoidosis

Calcium Nephrolithiasis

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