Management of hypovitaminosis D in patients with primary hyperparathyroidism

Rathi, Manjusha; González, Susana; Wright, Dianne; Ellis, N. R.; Peacey, Steven R.

doi:10.1007/s40618-014-0056-y

Cited by 12 publications

(20 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Схеми можуть бути різні -по 20 000 МО 1 раз на тиждень ергокальциферолу або по 3000 МО щоденно, 1600 МО 1 раз на день холекальциферолу. Принципової різниці не виявлено між застосуванням ергокальциферолу та холекальциферолу щодо компен-сації недостатності вітаміну D. Необхідно зазначити, що навіть високі дози вітаміну D безпечно підвищують рівень сироваткового вітаміну D(25(ОН)D 3 і знижують рівень ПГ та зменшують резорбцію кісток у хворих на ПГПТ [6][7][8]. Призначення активних метаболітів віта-міну D недоцільне, оскільки вони не мають здатно-сті до кумулювання в печінці та жировій клітковині та мають короткий термін напіввиведення (4 доби), що для ергокальциферолу становить 14 днів.…”

Section: вступunclassified

Диференціальна Діагностика Первинного Та Вторинного Гіперпаратиреозу, Спричиненого Дефіцитом Вітаміну D

Черенько¹,

Bandura²

2021

Mìžnarodnij endokrinologìčnij žurnal

View full text Add to dashboard Cite

19№ 5(69) • 2015 УДК 616. 447-008.61:612.015.6:577.161 ВступПервинний гіперпаратиреоз (ПГПТ) належить до однієї з найбільш поширених хвороб ендокринної системи з частотою в популяції 3-5 на 1000 населен-ня (та до 3-5 % серед жінок віком понад 60 років). Сутністю захворювання є первинна гіперпродукція однією чи кількома прищитоподібними залозами (ПЩЗ) (найчастіше уражених доброякісною пухли-ною -аденомою) специфічного паратиреоїдного гормона (ПГ) із відповідним збільшенням концен-трації позаклітинного кальцію. Єдиним радикальним способом лікування захворювання є хірургічне вида-лення однієї чи кількох ПЩЗ, патологічно змінених внаслідок пухлини або гіперплазії. Кількість нових випадків ПГПТ у розвинутих країнах світу, таких як США, Франція, Японія, обчисляється десятками-со-тнями тисяч, тоді як у країнах, що розвиваються, ви-являють переважно запущені форми з частотою 1-2 на 100 тисяч населення.Зростання частоти виявлення випадків захво-рювання на ПГПТ безпосередньо залежить від Адреса для листування з авторами: Бандура Г.В.

show abstract

Section: вступunclassified

Диференціальна Діагностика Первинного Та Вторинного Гіперпаратиреозу, Спричиненого Дефіцитом Вітаміну D

Черенько¹,

Bandura²

2021

Mìžnarodnij endokrinologìčnij žurnal

View full text Add to dashboard Cite

show abstract

“…Second, Rolighed et al [12] have recently demonstrated that daily supplementation with 2800 IU of vitamin D safely improves vitamin D status and decreases PTH. Finally, Rathi et al [13] in this issue of the Journal report on normalizing vitamin D nutritional status with significant reductions in serum PTH levels without any safety concerns.…”

mentioning

confidence: 99%

“…The conclusion of Rathi and co-workers [13] is that high oral doses of cholecalciferol normalise vitamin D levels without worsening underlying hypercalcemia in patients with primary hyperparathyroidism. Admittedly, further studies of longer duration are needed to better define the amount and modalities of refilling body stores with vitamin D. In the meantime, it seems prudent to suggest targeting vitamin D threshold (Endocrine Society, IOM), because this reduces the severity of the disease with no safety concerns.…”

mentioning

confidence: 99%

“…There are now at least three papers favouring the correction of hypovitaminosis D [4,12,13]. First, in a meta-analysis of ten studies comprising of 340 patients, Shah et al In all the studies performed thus far, other aspects of vitamin D treatment have not been uniform; inconsistencies have been noted concerning, for example, the changes of bone numeral density and biochemical markers of bone turnover [14][15][16].…”

mentioning

confidence: 99%

“…There are now at least three papers favouring the correction of hypovitaminosis D [4,12,13]. First, in a meta-analysis of ten studies comprising of 340 patients, Shah et al [4] concluded that vitamin D replacement in patients with primary hyperparathyroidism and coexistent vitamin D deficiency increases 25(OH)D levels and significantly reduces PTH values without causing hypercalcemia and hypercalciuria.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Hypovitaminosis D in primary hyperparathyroidism: to treat or not to treat? That is the question

Minisola

Romagnoli

Scillitani

et al. 2014

J Endocrinol Invest

View full text Add to dashboard Cite

A number of epidemiological studies have shown a high prevalence of hypovitaminosis D in the world, independent of the threshold used to define insufficiency or deficiency [1]. Somewhat counterintuitively, hypovitaminosis D appears to be more prevalent in patients with primary hyperparathyroidism [2][3][4][5]. The reasons for this finding may be multiple and not mutually exclusive. For example, parathyroid hormone (PTH) stimulates the renal 1a-hydroxylase causing an increased conversion of 25(OH)D to 1,25(OH) 2 D, leading to ''conditional'' vitamin D depletion [6]. The resulting increase in 1,25(OH) 2 D has a negative feedback on PTH production and secretion, in addition to accelerated inactivation of 25(OH)D by 24-hydroxylase [7]. Other reasons for the common finding of low calcidiol levels may include an enhanced hepatic inactivation of 25(OH)D [8] or avoidance of vitamin D supplementation in a person with hypercalcemia for fear of further increasing serum calcium level. However, a number of investigations have shown that hypovitaminosis D in patients with primary hyperparathyroidism is associated with higher preoperative PTH levels, larger adenomas, more compromised skeletal health, and increased incidence of hungry bone syndrome after parathyroidectomy compared with vitamin D repleted or vitamin D sufficient patients [9][10][11].Despite these rather convincing aspects on the prevalence and pathogenesis of hypovitaminosis D in patients with primary hyperparathyroidism, there is still a pervasive uncertainty whether we should treat or not to treat vitamin D depletion in patients with PHPT. There are now at least three papers favouring the correction of hypovitaminosis D [4,12,13]. First, in a meta-analysis of ten studies comprising of 340 patients, Shah et al. In all the studies performed thus far, other aspects of vitamin D treatment have not been uniform; inconsistencies have been noted concerning, for example, the changes of bone numeral density and biochemical markers of bone turnover [14][15][16]. However, these discrepancies are clearly related to the site for bone mineral density assessment (lumbar vs proximal femur) or the biomarker employed. It is well known, for example, that changes of markers of bone formation lag behind those of bone resorption [17,18]; therefore, the length of observation is another important parameter.

show abstract

Low 25‐Hydroxyvitamin D in Primary Hyperparathyroidism: Enhanced Conversion Into 1,25‐Hydroxyvitamin D May Not Be “True” Deficiency

Kabadi

2020

JBMR Plus

View full text Add to dashboard Cite

Vitamin D deficiency is reported in individuals with primary hyperparathyroidism (PHP). However, decreased 25OHD may be attributed to enhanced conversion into 1,25-hydroxyvitamin D [1,25(OH)D]. To examine vitamin D metabolism in individuals with PHP, serum calcium, PTH, 25OHD, and 1,25(OH)D levels were determined in 210 adults: 102 with PHP, 40 with normal 25OHD, and 68 with vitamin D deficiency. Concentrations were redetermined in 37 individuals with PHP following vitamin D supplementation and 43 patients postsurgery. Comparisons were conducted by Student's t test and ANOVA. Correlations were assessed between PTH and 25OHD, 1,25(OH)D, and 1,25(OH)D/25OHD in individuals with PHP. Calcium, PTH, and 1,25(OH)D were higher (p < 0.001) in individuals with PHP (11.4 AE 0.4, 116 AE 21, 79 AE 6) than in individuals with normal 25OHD (9.6 AE 0.2, 49 AE 5, 57 AE 6) and vitamin D deficiency (9.3 AE 0.2, 62 AE 6, 32 AE 4). Compared with individuals with normal 25OHD (47 AE 5), 25OHD was lower (18 AE 3), but not different from subjects with vitamin D deficiency (15 AE 2). In individuals with PHP, vitamin D2 supplementation induced rises in 1,25(OH)D and calcium without lowering PTH, whereas postsurgery, calcium, PTH, 25OHD, and 1,25(OH)D normalized. Finally, in individuals with PHP, significant correlations (p < 0.01) were documented between PTH and calcium (r = 0.74), 25OHD (r = −0.43), 1,25 (OH)D (r = 0.52), and 1,25(OH)D/25OHD (r = 0.46); and between 1,25(OH)D/25OHD and calcium (r = 0.47). Subnormal 25OHD in most individuals with PHP may be attributed to enhanced conversion to 1,25(OH)D-not "true" vitamin D deficiency-although in some patients, both PHP and vitamin D deficiency coexisted. Moreover, vitamin D supplementation exaggerated hypercalcemia in individuals with PHP.

show abstract

Management of hypovitaminosis D in patients with primary hyperparathyroidism

Abstract: High doses of oral cholecalciferol normalised vitamin D levels without worsening underlying hypercalcaemia in individuals with PHPT.

Cited by 12 publications

References 17 publications

Диференціальна Діагностика Первинного Та Вторинного Гіперпаратиреозу, Спричиненого Дефіцитом Вітаміну D

Диференціальна Діагностика Первинного Та Вторинного Гіперпаратиреозу, Спричиненого Дефіцитом Вітаміну D

Hypovitaminosis D in primary hyperparathyroidism: to treat or not to treat? That is the question

Low 25‐Hydroxyvitamin D in Primary Hyperparathyroidism: Enhanced Conversion Into 1,25‐Hydroxyvitamin D May Not Be “True” Deficiency

Contact Info

Product

Resources

About