Parathyroid function in human vitamin D deficiency and vitamin D deficiency in primary hyperparathyroidism

Lumb, G. A.; Stanbury, Sarah

doi:10.1016/0002-9343(74)90812-2

Cited by 128 publications

(68 citation statements)

References 17 publications

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“…Vitamin D deficiency is also common in countries where primary hyperparathyroidism is a symptomatic disorder, an observation that fits with the proposal made years ago by Lumb and Stanbury that primary hyperparathyroidism is worse in the presence of vitamin D deficiency (28). Even in mild, asymptomatic primary hyperparathyroidism, it has been shown that low 25(OH)D levels are associated with increased indices of disease activity (29). In these patients with primary hyperparathyroidism, it seems reasonable to consider restoring vitamin D to sufficient levels.…”

Section: Vitamin D In Primary Hyperparathyroidismsupporting

confidence: 76%

Asymptomatic primary hyperparathyroidism

Bilezikian

Rubin

Silverberg

2006

Arq Bras Endocrinol Metab

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Primary hyperparathyroidism is a common disorder of mineral metabolism characterized by incompletely regulated, excessive secretion of parathyroid hormone from one or more of the parathyroid glands. In adults with the disease, a single, benign adenoma is seen approximately 80 percent of the time, with multiple gland involvement comprising most of the remaining patients. Very rarely, a parathyroid cancer is responsible but it is seen in less than 0.5 percent of patients with primary hyperparathyroidism. In this article, we will review important clinical and diagnostic features of asymptomatic primary hyperparathyroidism as well as considerations for surgical or medical management of the disease. O hiperparatiroidismo primário é uma distúrbio comum do metabolismo mineral, caracterizado por um excesso de secreção do hormônio das paratiróides, de uma ou mais glândulas paratiroidianas. Nos pacientes adultos portadores da doença, um adenoma único é responsável por aproximadamente 80% dos casos, e o envolvimento de múltiplas glân-dulas pelo restante dos casos. Muito raramente um câncer de paratiróide é a causa, sendo visto em menos de 0,5% dos pacientes com hiperparatiroidismo. Neste artigo, revisaremos as características clínicas e diagnósticas do hiperparatiroidismo primário assintomático, bem como o tratamento clínico e cirúrgico. DIAGNOSIS SINCE IN PRIMARY HYPERPARATHYROIDISM, parathyroid hormone (PTH) is oversecreted, a reliable immunoassay for PTH is essential. The currently available immunoradiometric assay (IRMA) has the requisite sensitivity and specificity, revealing PTH levels that are either frankly elevated or in the upper range of normal. Even though the PTH is sometimes technically in the upper normal range, it is abnormal considering the presence of hypercalcemia. Moreover, in malignancy, the other most common cause of hypercalcemia, the PTH level is classically suppressed even when the cause of the malignancy-related hypercalcemia is parathyroid hormone related protein (PTHrP). Despite the reliability of the IRMA for PTH in general

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Section: Vitamin D In Primary Hyperparathyroidismsupporting

confidence: 76%

Asymptomatic primary hyperparathyroidism

Bilezikian

Rubin

Silverberg

2006

Arq Bras Endocrinol Metab

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“…Such a mixed biochemical phenotype (i.e. coexistent primary and secondary hyperparathyroidism) has been previously proposed (9,10), but changes in bone mass upon resolution of secondary hyperparathyroidism were not previously reported. The annualized rates of BMD increase in these patients (6 -8%) were similar to that observed by us in the treatment of vitamin D-deficient patients without primary hyperparathyroidism (4).…”

Section: Discussionmentioning

confidence: 78%

“…Fifteen subjects (13 women and 2 men) had low 25OHD levels (10.3 Ϯ 0.6 ng/mL; range, [5][6][7][8][9][10][11][12][13][14] and consistently elevated iPTH levels (109.2 Ϯ 13.7 pg/mL; range, 69 -252). All patients were supplemented with 1000 mg elemental calcium (Os-Cal 500, SmithKline Beecham, Pittsburgh, PA) and oral vitamin D 2 (50,000 IU) was administered twice weekly for a 5-week period.…”

Section: Methodsmentioning

confidence: 99%

Bone Mineral Density Increases with Vitamin D Repletion in Patients with Coexistent Vitamin D Insufficiency and Primary Hyperparathyroidism

Kantorovich¹

2000

Journal of Clinical Endocrinology & Metabolism

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Two hundred and twenty-nine consecutive subjects, 202 women and 27 men, referred for evaluation of osteoporosis or low bone mineral density (BMD) had serum measurements of immunoreactive PTH (iPTH) and 25-hydroxyvitamin D (25OHD) performed. Fifteen individuals (mean age Ϯ SE, 75 Ϯ 2.4 yr) had depressed serum 25OHD (Ͻ15 pg/mL) and concomitantly elevated (Ͼ65 pg/mL) iPTH levels. After successful treatment of vitamin D insufficiency in all subjects, iPTH remained inappropriately high or frankly elevated in 5, describing a 2.2% prevalence rate of coexistent primary hyperparathy-

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“…Vitamin D deficiency is more common among patients with primary HPT than among controls. Some investigators have suggested that chronic vitamin D deficiency may accelerate parathyroid adenoma growth and PTH secretion (11)(12)(13). Others have recently shown that vitamin D deficiency increases PTH secretion activity without demonstrable effect on adenoma growth (14,15).…”

Section: Discussionmentioning

confidence: 99%

Association of parathyroid adenoma and familial hypocalciuric hypercalcaemia in a teenager

Brachet

Boros

Tenoutasse

et al. 2009

European Journal of Endocrinology

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Objective: Familial hypocalciuric hypercalcaemia (FHH) is clinically characterized by mild to moderate parathyroid hormone (PTH)-dependent hypercalcaemia, autosomal dominant pattern of inheritance, and normal to frankly reduced urinary calcium excretion in spite of a high serum calcium (clearance (Ca)/clearance (Cr)!0.01). FHH has a benign course and should be differentiated from primary hyperparathyroidism. It is usually caused by a heterozygous loss-of-function mutation in the calciumsensing receptor gene (CASR). Design: We report the case of a 16-year-old patient with hypercalcaemia and a mixed family history of parathyroid adenoma and mild hypercalcaemia. Serum calcium was 14 mg/dl with a serum iPTH of 253 pg/ml. Results: A neck 99m Tc-sesta MIBI tomoscintigraphy showed a definite hyperactivity in the left upper quadrant. A surgical four-gland exploration confirmed a single parathyroid adenoma. After surgical resection of a left superior parathyroid adenoma, the patient's hypercalcemia improved but did not normalize, returning to a level typical of FHH. An inactivating mutation in exon 4 of the CASR gene, predicting a p.Glu297Lys amino acid substitution was found. Conclusions: Thus, this 16-year old patient presented with the association of FHH and a single parathyroid adenoma. The young age of the patient and the association of parathyroid adenoma and FHH in his grandmother argue for a causal link between CASR mutation and parathyroid adenoma in this family. This case contributes to illustrate the expanding clinical spectrum of CASR loss-of-function mutations.

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Parathyroid function in human vitamin D deficiency and vitamin D deficiency in primary hyperparathyroidism

Cited by 128 publications

References 17 publications

Asymptomatic primary hyperparathyroidism

Asymptomatic primary hyperparathyroidism

Bone Mineral Density Increases with Vitamin D Repletion in Patients with Coexistent Vitamin D Insufficiency and Primary Hyperparathyroidism

Association of parathyroid adenoma and familial hypocalciuric hypercalcaemia in a teenager

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