Correction of 25-OH-vitamin D deficiency improves control of secondary hyperparathyroidism and reduces the inflammation in stable haemodialysis patients

López, Raquel Ojeda; Motta, Elvira Esquivias de; Carmona, Andrés; Montemayor, Victoria García; Berdud, Isabel; Malo, Alejandro Martín; García, Pedro Aljama

doi:10.1016/j.nefroe.2018.01.002

Cited by 7 publications

(3 citation statements)

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“…Resolving vitamin D deficiency has been associated with better secondary hyperparathyroidism control and an improvement in inflammatory status in patients receiving haemodialysis. 20 Serum parathyroid hormone levels have been reported to be independently correlated with inflammatory markers including C-reactive protein, platelet-to-lymphocyte ratios, red cell distribution width, and presence of chronic inflammation. 21,22 Interestingly, in a recent study involving postmenopausal women, a positive correlation was reported between serum parathyroid hormone levels and the pro-inflammatory cytokines tumour necrosis factor-α, interleukin (IL)-1β, and IL-6.…”

Section: Discussionmentioning

confidence: 99%

Biochemical changes associated with temporomandibular disorders

Demir

Ersöz

2018

J Int Med Res

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Objective To assess vitamin D, parathyroid hormone, calcitonin, calcium, phosphorus and magnesium levels in patients with versus without temporomandibular disorders (TMDs). Methods This prospective observational study included patients with TMDs and age-matched healthy controls. TMDs were diagnosed via physical and radiologic examination, and serum levels of 25 (OH) vitamin D, parathyroid hormone, calcitonin, calcium, magnesium, and phosphorus were determined. The impact of age, sex and seasonal variations in serum 25 (OH) vitamin D levels was controlled by the inclusion of age, sex and date-matched control patients. Results The study included 100 patients, comprising 50 patients with TMDs and 50 control patients. No statistically significant between-group differences were found regarding age or sex. No statistically significant between-group differences were found in terms of serum 25 (OH) vitamin D, calcitonin, calcium, magnesium or phosphorus levels. Parathyroid hormone levels were statistically significantly higher in patients with TMDs versus healthy control patients. Conclusion In patients with temporomandibular disorders, increased parathyroid hormone levels in response to vitamin D deficiency was significantly more prominent. These data suggest that, in patients with temporomandibular disorders, vitamin D deficiency should be assessed and corrected.

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Section: Discussionmentioning

confidence: 99%

Biochemical changes associated with temporomandibular disorders

Demir

Ersöz

2018

J Int Med Res

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“…Vitamin D deficiency can lead to insufficient calcium absorption and result in excessive PTH production, causing SHPT. Thus, vitamin D and its analogs treat SHPT by correcting the associated vitamin D deficiency ( 17 ). Commonly used medications include calcitriol, paricalcitol, and alfacalcidol.…”

Section: Treatment For Hptmentioning

confidence: 99%

Advances in the treatment of secondary and tertiary hyperparathyroidism

et al. 2022

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Secondary hyperparathyroidism (SHPT) and tertiary hyperparathyroidism (THPT) are common and complicated clinical endocrine diseases. The parathyroid glands maintain endocrine homeostasis by secreting parathyroid hormone to regulate blood calcium levels. However, structural alterations to multiple organs and systems occur throughout the body due to hyperactivity disorder in SHPT and THPT. This not only decreases the patients’ quality of life, but also affects mortality. Since current treatments for these diseases remains unclear, we aimed to develop a comprehensive review of advances in the treatment of SHPT and THPT according to the latest relevant researches.

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“…As reported, correction of 25(OH)D deficiency in patients on hemodialysis was associated with better SHPT control with lower doses of vitamin D analogues. 42 In addition,…”

mentioning

confidence: 99%

Does combination of paricalcitol with cinacalcet in secondary hyperparathyroidism in hemodialysis treatment make sense?

Zawierucha¹,

Małyszko²,

Małyszko³

et al. 2017

Polish Archives of Internal Medicine

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secondary hyperparathyroidism (SHPT), bone abnormalities, and vascular calcification in patients with chronic kidney disease (CKD) are the components of chronic kidney disease-mineral bone disorder (CKD -MBD).1-3 This systemic disorder significantly contributes to the morbidity and mortality of patients with CKD. [4][5][6] SHPT (intact parathyroid hormone [iPTH] level >300 pg/ml) is diagnosed in 30% to 49% of dialyzed patients in Europe and even in 54% of those in the United States and Canada). 7 The diagnosis IntroductIon With progressive renal impairment and worsening of renal excretory function, the disorders of calcium and phosphorus metabolism become more severe. The increasing reduction of glomerular filtration results in lower phosphate excretion and, consequently, hyperphosphatemia. Phosphorus anions bond serum calcium cations, which leads to a reduction of ionized calcium levels. At the same time, a sustained high phosphate level inhibits vitamin D 3 synthesis. AbstrActIntroductIon Secondary hyperparathyroidism (SHPT) is a common hormonal disorder associated with chronic kidney disease (CKD). The treatment of SHPT should lead to a reduction in parathormone concentrations by calcimimetics or active vitamin D administration and stabilization of calcium and phosphate metabolism. In the event of failure of conservative treatment, complete or partial parathyroid resection should be considered.

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Correction of 25-OH-vitamin D deficiency improves control of secondary hyperparathyroidism and reduces the inflammation in stable haemodialysis patients

Cited by 7 publications

References 20 publications

Biochemical changes associated with temporomandibular disorders

Biochemical changes associated with temporomandibular disorders

Advances in the treatment of secondary and tertiary hyperparathyroidism

Does combination of paricalcitol with cinacalcet in secondary hyperparathyroidism in hemodialysis treatment make sense?

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