Primary hyperparathyroidism

Zahrani, Ali Al; Levine, Michael A.

doi:10.1016/s0140-6736(96)06176-4

Cited by 116 publications

(72 citation statements)

References 48 publications

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“…Elle est la troisième de point de vue fréquence après le diabète et l'hyperthyroïdie [1]. Elle peut survenir à tout âge avec une nette prédominance entre 44 et 62 ans [1,2].…”

Section: Discussionunclassified

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Traitement Chirurgical De L\'hyperparathyroidie Primaire : Techniques Et Resultats

Dhouib¹,

Hammami²,

Thabet³

et al. 2008

Journal Tunisien d'ORL Et De Chirurgie Cervico-Faciale

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“…Elle est la troisième de point de vue fréquence après le diabète et l'hyperthyroïdie [1]. Elle peut survenir à tout âge avec une nette prédominance entre 44 et 62 ans [1,2].…”

Section: Discussionunclassified

“…Elle est la troisième de point de vue fréquence après le diabète et l'hyperthyroïdie [1]. Elle peut survenir à tout âge avec une nette prédominance entre 44 et 62 ans [1,2]. Toutes les études sont unanimes sur la prédominance féminine de cette pathologie [1,2].…”

Section: Discussionunclassified

Traitement Chirurgical De L\'hyperparathyroidie Primaire : Techniques Et Resultats

Dhouib¹,

Hammami²,

Thabet³

et al. 2008

Journal Tunisien d'ORL Et De Chirurgie Cervico-Faciale

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“…mutations of the calcium sensor) or clinical characteristics (e.g. jaw tumours) (Zahrani & Levine 1997). Familial isolated HP due to parathyroid adenoma may be difficult to distinguish from incipient MEN1 syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…With an estimated incidence of 25-30/10 6 per year (Zahrani & Levine 1997), primary HP is among the most common endocrine disorders in Western countries, but only a minority of primary HP occurs in association with the MEN1 syndrome. The vast majority of patients with primary HP do not have a positive family history or concomitant endocrine neoplasia, and are thus considered sporadic cases.…”

Section: Introductionmentioning

confidence: 99%

Multiple endocrine neoplasia type 1 (MEN1) gene mutations in a subset of patients with sporadic and familial primary hyperparathyroidism target the coding sequence but spare the promoter region

Karges

Jostarndt²,

Maier³

et al. 2000

Journal of Endocrinology

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Germ line mutations of the multiple endocrine neoplasia type 1 (MEN1) tumour suppressor gene cause MEN1, a rare familial tumour syndrome associated with parathyroid hyperplasia, adenoma and hyperparathyroidism (HP). Here we investigated the role of the MEN1 gene in isolated sporadic and familial HP. Using RT-PCR singlestrand conformational polymorphism screening, somatic (but not germ line) mutations of the MEN1 coding sequence were identified in 6 of 31 (19·3%) adenomas from patients with sporadic primary HP, but none in patients (n=16) with secondary HP due to chronic renal failure. MEN1 mutations were accompanied by a loss of heterozygosity (LOH) for the MEN1 locus on chromosome 11q13 in the adenomas as detected by microsatellite analysis. No DNA sequence divergence within the 5 region of the MEN1 gene, containing the putative MEN1 promoter, was detectable in HP adenomas. Clinical characteristics were not different in HP patients with or without MEN1 mutation. Heterozygous MEN1 gene polymorphisms were identified in 9·6% and 25% of patients with primary and secondary HP respectively. In a large kindred with familial isolated familial HP, MEN1 germ line mutation 249 del4 and LOH was associated with the HP phenotype and a predisposition to non-endocrine malignancies. We suggest that the bi-allelic somatic loss of MEN1 wild-type gene expression is involved in the pathogenesis of a clinically yet undefined subset of sporadic primary HP adenomas. MEN1 genotyping may further help define the familial hyperparathyroidism-MEN1 disease complex, but it seems dispensable in sporadic primary HP.

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“…Whereas vitamin D repletion is routinely recommended for patients with hypovitaminosis D, there has been reluctance to restore serum 25-OHD levels to normal in PHPT due to concerns of potentially greater hypercalcaemia and hypercalciuria (3,14). In 1997, Zahrani et al indicated that until more data are available, patients with PHPT should moderate their intake of dietary calcium and avoid any calcium or vitamin D supplements (15 …”

Section: Introductionmentioning

confidence: 99%

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

Tucci

2009

European Journal of Endocrinology

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Objective: To determine whether vitamin D repletion of patients with primary hyperparathyroidism (PHPT) and vitamin D deficiency or insufficiency (hypovitaminosis D) has deleterious clinical and/or biochemical effects. Design: Prospective audit of the effect of vitamin D repletion on biochemical data in 56 patients with PHPT. Patients were treated with 50 000 units of vitamin D 2 weekly for 8 weeks with biochemical measurements at 5 and 10 weeks, and subsequently after 12 weeks on 800 units of vitamin D 3 daily, and in those with hypovitaminosis D after 12 weeks of up to 100 000 units of vitamin D 2 monthly. Methods: Serum calcium, albumin, phosphorus, 25-OHD, intact parathyroid hormone (PTH) and urine calcium/creatinine (Ca/Cr) ratios were measured before and during vitamin D therapy. Results: Patients treated with 50 000 units of vitamin D 2 weekly for 8 weeks resulted in a significant increase in serum 25-OHD levels from 36.4 to 89.4 nmol/l at 5 weeks (P!0.0001) and 88.6 nmol/l at 10 weeks (P!0.0001). There were no significant changes in serum calcium. At 10 weeks, there was a non-significant decrease in serum PTH and in urine Ca/Cr ratios. None of the patients developed any calcium-related adverse events. Subsequently, patients with subnormal 25-OHD levels on 800 units of vitamin D daily were treated for the next 12 weeks with up to 100 000 units of vitamin D 2 monthly with normalization of serum 25-OHD in all but 4 patients. Conclusion:These data fail to demonstrate any adverse effects of vitamin D repletion in PHPT.

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Primary hyperparathyroidism

Cited by 116 publications

References 48 publications

Traitement Chirurgical De L\'hyperparathyroidie Primaire : Techniques Et Resultats

Traitement Chirurgical De L\'hyperparathyroidie Primaire : Techniques Et Resultats

Multiple endocrine neoplasia type 1 (MEN1) gene mutations in a subset of patients with sporadic and familial primary hyperparathyroidism target the coding sequence but spare the promoter region

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

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