Secondary Hyperparthyroidism: Pathogenesis, Diagnosis, Preventive and Therapeutic Strategies

Portillo, Mariano Rodríguez; Rodríguez‐Ortiz, María E.

doi:10.1007/s11154-017-9421-4

Cited by 54 publications

(37 citation statements)

References 198 publications

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“…Phosphate retention, hyperphosphatemia, and the ensuing hypocalcemia are the other major factors contributing to the development of SHPT. In this altered mineral environment and progressively dysfunctional regulators, over time, the parathyroid glands develop diffuse polyclonal hyperplasia [12]. The latter can further undergo monoclonal nodular transformation, an entity associated with reduced expression of calcium-sensing receptors (CaSR) and VDR, rendering the parathyroid glands poorly responsive to treatment with calcimimetics or vitamin D. The consequences of untreated SHPT traditionally are bone disease, vascular calcifications, and abnormal biochemical parameters.…”

Section: Vitamin D In Ckd and The Development Of Shptmentioning

confidence: 99%

Active Vitamin D in Chronic Kidney Disease: Getting Right Back Where We Started from?

Negrea

2018

Kidney Dis

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Background: The vitamin D system is essential for optimal health in humans. Circulating calcitriol, a key metabolite in maintaining calcium and phosphorus homeostasis, is produced in the kidney. In kidney failure, calcitriol levels progressively decrease, contributing to the development of renal secondary hyperparathyroidism (SHPT). Summary: For years, SHPT had a central role in the disturbed mineral metabolism of renal patients. As calcitriol deficiency contributes to SHPT development, treatment with calcitriol or other compounds able to activate the vitamin D receptor (VDR) was one of the mainstays of therapy for renal patients in the last 40 years. In this review, we discuss how the treatment with VDR activators (VDRA) evolved during this time in the United States, as well as the main factors responsible for these changes. Key Messages: Management of SHPT with VDRA in renal patients has undergone a few paradigm shifts over the last 40 years. When treating SHPT, the newly developed therapies as well as VDRA need to be carefully considered and used appropriately. Nephrologists need to use an integrated approach that avoids excessive use of VDRA, ensures replenishment of vitamin D stores, and avoids hypercalcemia and hyperphosphatemia.

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Section: Vitamin D In Ckd and The Development Of Shptmentioning

confidence: 99%

Active Vitamin D in Chronic Kidney Disease: Getting Right Back Where We Started from?

Negrea

2018

Kidney Dis

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“…For asymptomatic patients, specific guidelines must be consulted. Secondary hyperPT, frequently derived from chronic kidney disease (CKD), and tertiary hyperPT, that follows long-standing secondary hyperPT with hypercalcaemia, are rarer parathyroid gland disorders presenting symptoms of bone, organic and metabolic disorders [10,11]. These forms are primarily pharmacologically treated and may occasionally require parathyroid surgery [10,12].…”

Section: Introductionmentioning

confidence: 99%

Epidemiology and management of parathyroid gland disorders in Spain over 15 years: A retrospective multicentre analysis

Darbà

Marsà²

2020

PLoS ONE

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Parathyroid gland disorders are rare conditions with an incidence that displays great variability among populations. Its direct influence in calcium homeostasis originates variable symptoms that affect bone remodelling among other processes. This study aimed to provide data on the epidemiology and characteristics of patients admitted with these disorders in Spain between 2003 and 2017, and to analyse disease management and direct medical costs. Medical records in which a disorder of the parathyroid gland was registered as the admission motive were extracted from a nationwide hospital-discharge database via the Spanish Ministry of Health. Records from 12,903 patients were obtained, with predominance of female patients (74.70%) and of admissions due to hyperparathyroidism (90.23%). The number of patients admitted per year increased over the study period along the incidence of these disorders. The year 2017 incidence of hyperparathyroidism was 2.95 per 10,000, 4.03 per 10,000 in females and 1.37 in males; the same year, the incidence of hypoparathyroidism was 0.17 per 10,000. Length of hospital stay was significantly extended in patients with hypoparathyroidism (7.16 days), admitted mostly due to emergencies. Heart failure was diagnosed in more than 20% of admissions in patients with secondary and tertiary hyperparathyroidism and hypoparathyroidism, while this last group displayed the highest levels of mineral metabolism disruption. Parathyroidectomy was performed in 78.95% of all admissions for primary hyperparathyroidism. The total annual direct medical cost parathyroid gland disorders has increased over the study period, due to the increase of the costs associated to hyperparathyroidism, whereas the cost per patient remained relatively stable, with an average of €3,748, €3,430 and €3,737 for patients with hyperparathyroidism, hypoparathyroidism and other disorders of the parathyroid gland, respectively. This study provides novel data to extend the scarce available knowledge on parathyroid gland disorders' epidemiology and management in Spain.

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“…Continuous overproduction of PTH also occurs due to secondary causes such as chronic renal disease and vitamin D deficiency. The skeletal manifestations of secondary hyperparathyroidism are also heterogeneous 8,9 . This condition is modeled in animals by feeding a low calcium diet 10 .…”

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confidence: 99%

PTH induces bone loss via microbial-dependent expansion of intestinal TNF+ T cells and Th17 cells

Tyagi

et al. 2020

Nat Commun

113

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Bone loss is a frequent but not universal complication of hyperparathyroidism. Using antibiotic-treated or germ-free mice, we show that parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was enriched by the Th17 cell-inducing taxa segmented filamentous bacteria (SFB). SFB + microbiota enabled PTH to expand intestinal TNF + T and Th17 cells and increase their S1P-receptor-1 mediated egress from the intestine and recruitment to the bone marrow (BM) that causes bone loss. CXCR3-mediated TNF + T cell homing to the BM upregulated the Th17 chemoattractant CCL20, which recruited Th17 cells to the BM. This study reveals mechanisms for microbiota-mediated gut-bone crosstalk in mice models of hyperparathyroidism that may help predict its clinical course. Targeting the gut microbiota or T cell migration may represent therapeutic strategies for hyperparathyroidism.

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Secondary Hyperparthyroidism: Pathogenesis, Diagnosis, Preventive and Therapeutic Strategies

Cited by 54 publications

References 198 publications

Active Vitamin D in Chronic Kidney Disease: Getting Right Back Where We Started from?

Active Vitamin D in Chronic Kidney Disease: Getting Right Back Where We Started from?

Epidemiology and management of parathyroid gland disorders in Spain over 15 years: A retrospective multicentre analysis

PTH induces bone loss via microbial-dependent expansion of intestinal TNF+ T cells and Th17 cells

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