Osteoid Mineralization Defect in Primary Hyperparathyroidism

Bordier, P; Woodhouse, Nicholas; Sigurðsson, Gunnar; Joplin, G. F.

doi:10.1111/j.1365-2265.1973.tb01724.x

Cited by 21 publications

(5 citation statements)

References 16 publications

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“…An association between primary HPT and vit D deficiency was first suggested in 1971 [101. Two patients, each with a single adenoma, had severe "parathyroid" bone disease which healed during the administration of vit D. Subsequently, 4 additional patients were given small doses of vit D2, 500 units per day for 2-4 weeks: as previously noted, intestinal calcium absorption increased, but, in addition, bone mineralization was significantly improved as judged using a quantitative histological technique [8]. At that time, it was postulated that PTH might be responsible for inducing the vit D deficient state.…”

Section: Discussionmentioning

confidence: 83%

“…It seems likely that patients with HPT who start with low vit D stores are more prone to develop particularly severe parathyroid bone disease with the concomitant development of secondary hyperparathyroidism. That the osteomalacia component of the disease can heal with the administration of vit D alone had previously been shown [8]. The preoperative use of vit D might prevent postoperative bone hunger in patients who are vit D deficient and have combined secondary and primary HPT at presentation.…”

Section: Discussionmentioning

confidence: 93%

“…Additional findings were also reported and consisted of a coarsening of the trabecular pattern, intracortical resorption clefts, loss of corticomedullary differentiation, and cyst formation [6,7]. Osteomalacia or rickets were diagnosed if: (a) Looser's nodes !were seen, (b) the epiphyses were splayed or poorly mineralized with or without deformity of the long bones, or (c) the pelvi s was deformed in the presence of Looser's nodes in the healing phase after parathyroidectomy [8].…”

Section: Radiographymentioning

confidence: 99%

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Vitamin D deficiency and hyperparathyroidism with severe bone disease

1988

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Circulating 25‐hydroxycholecalciferol (25OHD3) levels are low in Saudi Arabia due to a lack of sunlight exposure and a low dietary intake of vitamin D (vit D). Recent studies in animals and man indicate that the half‐life of 25OHD3 is reduced in states of hyperparathyroidism. We, therefore, reviewed the charts of 43 patients with primary hyperparathyroidism (HPT) to establish whether there was coexisting vit D deficiency and osteomalacia. In the 22 patients studied, 25OHD3 levels were below normal in 14 and in the low normal range in 7, and the 1,25‐dihydroxycholecalciferol [1,25(OH)2D3] levels were inappropriately low in 8 of the 9 studied. Three of the 13 patients with classical “parathyroid” bone disease had evidence of osteomalacia with Looser's nodes or rickets. We conclude that patients with primary HPT are likely to develop vit D deficiency in countries in which 25OHD3, stores are low. In selected cases, preoperative treatment with vit D might diminish subsequent bone hunger.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 93%

Section: Radiographymentioning

confidence: 99%

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Vitamin D deficiency and hyperparathyroidism with severe bone disease

1988

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“…Bone turnover in primary HPT is faster than in postmenopausal osteoporosis. The increased numbers of bone-forming sites (Bordier et al, 1973;Byers and Smith, 1971;Meunier et al, 1972) lead to increased osteoid volume without increased osteoid seam width ( Fig. 20; Melsen and Mosekilde, 1980).…”

Section: With Locally Variable Sigma Periods: Primary Hyperparathyroimentioning

confidence: 99%

Errors in bone remodeling: Toward a unified theory of metabolic bone disease

1989

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Recent evidence suggests that skeletal adaptation is organized by a functional unit that includes cells of diverse origin working in coordination. Genetic and metabolic factors control and regulate the processes of modeling and remodeling, only rarely acting on the isolated individual functions of specific cell lines. Errors in the genetic or metabolic regulation of the functional unit affect the entire process of skeletal adaptation rather than specific elements of it. Viewed in this way, some metabolic bone diseases can be understood as relatively simple errors in factors that control the coordinated activities of the entire functional unit. This paper reviews the modeling and remodeling processes and demonstrates how abnormal morphological characteristics of bone tissue can be viewed as products of specific errors in the adaptive process.

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“…While osteoid mineralization defects have been observed in primary hyperparathyroidism (36), the combination of a presumed low level of DHCC (18)(19)(20) and the presumed accelerated bone formation due to his osteitis fibrosa cystica may have accentuated this defect in our patient.…”

Section: Discussionmentioning

confidence: 64%

Renal-Resistant Hormonoplethoric Hypoparathyroidism with Evidence for a Defective Response to cAMP*

Duck

Rosenberg

Ratzan

et al. 1978

The Journal of Clinical Endocrinology & Metabolism

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A 15.5-yr-old black male is reported with hypocalcemia, hyperphosphatemia, and severe osteitis fibrosa cystica. While hypocalcemic and hyperphosphatemic, the circulating parathyroid hormone (PTH) level and urinary cAMP excretion were increased. An infusion of exogenous PTH produced a normal maximal excretion of urinary cAMP but failed to increase phosphate excretion. Correction of the hypocalcemia by administration of 200,000 U vitamin D daily lowered the endogenous PTH level and basal excretion of cAMP to normal; at that time, infusion of PTH produced both a normal rise in urinary cAMP and a normal phosphaturic response. This pattern of response suggests pseudohypoparathyroidism with a calcium-sensitive defect in renal phosphate transport distal to the PTH receptor adenyl cyclase mechanism, producing hyperphosphatemia, hypocalcemia, and secondary hyperparathyroidism. The osteitis fibrosa cystica was presumably due to the increased PTH, suggesting that resistance to PTH was present in kidney but not bone.

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Osteoid Mineralization Defect in Primary Hyperparathyroidism

Abstract: serum. Journal of CZinical Investigation, 50,21. vitamin D on bone and phosphate metabolism in osteomalacia. Calcified Tissue Research, 4,78. vitamin D deficiency following gastric surgery. Histological evidence in bone. Lancet, i, 437.

Cited by 21 publications

References 16 publications

Vitamin D deficiency and hyperparathyroidism with severe bone disease

Vitamin D deficiency and hyperparathyroidism with severe bone disease

Errors in bone remodeling: Toward a unified theory of metabolic bone disease

Renal-Resistant Hormonoplethoric Hypoparathyroidism with Evidence for a Defective Response to cAMP*

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