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The role of Rapid Intraoperative Parathyroid Hormone (ioPTH) assay in determining outcome of parathyroidectomy in primary hyperparathyroidism: A systematic review and meta-analysis.
Medas, F, Cappellacci, F, Canu, GL, Noordzij, JP, Erdas, E, Calò, PG
International journal of surgery (London, England). 2021;:106042
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Abstract
BACKGROUND Primary hyperparathyroidism (PHPT) is a common endocrine disorder. In the last few decades, the introduction of Rapid Intraoperative Parathyroid Hormone (ioPTH) monitoring has allowed to ensurance of the excision of all hyperfunctioning parathyroid tissues, reducing the risks of persistent and recurrent PHPT. However, the use of ioPTH is still debated among endocrine surgeons. MATERIAL AND METHODS The objective of this systematic review and meta-analysis was to assess if ioPTH monitoring is able to reduce the incidence of persistent or recurrent PHPT. A systematic literature search was performed using PubMed, Scopus, ISI-Web of Science and Cochrane Library Database. Prospective and retrospective studies addressing the efficacy of ioPTH monitoring were included in the systematic review and meta-analysis. The random-effects model was assumed to account for different sources of variation among studies. The overall effect size was computed through the inverse variance method. Heterogeneity across studies, possible outlier studies, and publication bias were evaluated. RESULTS A total of 28 studies with 13,323 patients were included in the quantitative analysis. The incidence of operative failure was 3.2% in the case group and 5.8% in the control group. After excluding three outlier studies, the quantitative analysis revealed that ioPTH reduced significantly the incidence of postoperative persistent or recurrent PHPT. (Risk Difference = -0.02; CI = -0.03, -0.01; p < 0.001). There was no evidence of heterogeneity among the studies (Q = 19.92, p = 0.70; I2 = 0%). The analysis of several continuous moderators revealed that the effectiveness of ioPTH was larger in studies with lower preoperative serum calcium values and higher incidences of multiple gland disease. CONCLUSION ioPTH monitoring is effective in reducing the incidence of persistent and recurrent PHPT. Its routine use should be suggested in the next guidelines regarding management of PHPT.
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Normocalcemic and Normohormonal Primary Hyperparathyroidism: Laboratory Values and End-Organ Effects.
Hollowoa, BR, Spencer, HJ, Stack, BC
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery. 2021;(3):387-397
Abstract
OBJECTIVE Variants of primary hyperparathyroidism (pHPT), described as normocalcemic (NC) and normohormonal (NH), can confuse the diagnosis of classic pHPT. DATA SOURCES A MEDLINE search was performed for variants of pHPT using the PubMed database (last queried October 2019). REVIEW METHODS The search was restricted to articles published after 1960 that were specific to humans. Studies were included in our analysis if laboratory values and incidence of end-organ involvement were reported for NCpHPT and NHpHPT variants. The search returned 189 articles; 27 additional studies were identified and included for a total of 216. Non-English-language studies were excluded. Abstracts were screened, full-text articles were then assessed, and 82 articles were excluded. Data were pooled using a random-effects model in studies that compared NC or NH pHPT to classic pHPT. Comparative laboratory values are presented. CONCLUSION This analysis compares NCpHPT and NHpHPT to classic pHPT. Nephrolithiasis was 21.7% (NCpHPT), 15.9% (classic pHPT), and 25.4% (NHpHPT). Decreased bone mineral density was 49.7% (NCpHPT), 39.7% (classic pHPT), and 40.3% (NHpHPT). Fractures in the NCpHPT group were not significantly different from the classic pHPT. Hypertension in the NCpHPT group was significantly less than classic pHPT (odds ratio, 0.59; 95% CI, 0.40-0.88). IMPLICATIONS FOR CLINICAL PRACTICE This information may serve to inform clinicians of the laboratory subtleties of these variants that are being seen with greater frequency in contemporary practice.
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Parathyroid Hormone-Related Changes of Bone Structure.
Kužma, M, Jackuliak, P, Killinger, Z, Payer, J
Physiological research. 2021;(Suppl 1):S3-S11
Abstract
Parathyroid hormone (PTH) increases the release of serum calcium through osteoclasts, which leads to bone resorption. Primary, PTH stimulates osteoblasts leading to increase RANKL (receptor activator for nuclear factor kappa-B ligand) expression and thus differentiation of osteoclasts. In kidneys, PTH increases calcium and decrease phosphate reabsorption. In kidneys, PTH stimulates 1alpha-hydroxylase to synthesize active vitamin D. Primary hyperparathyroidism (PHPT) is characterized by skeletal or renal complications. Nowadays, the classical form of PHPT is less seen and asymptomatic or subclinical (oligo symptomatic) forms are more frequent. Previously, it was thought that cortical bone is preferably affected by PHPT and that predispose bones to fracture at sites with a higher amount of cortical bone. However, an increased risk of vertebral fractures has been found by most of the studies showing that also trabecular bone is affected. Bone Mass measurement (BMD) at all skeletal sites is advised, but another specific tool for fracture assessment is needed. Trabecular bone score (TBS), an indirect measure of trabecular bone, maybe a useful method to estimate fracture risk. TBS is associated with vertebral fractures in PHPT regardless of BMD, age, BMI and gender. Furthermore, there is an association between TBS and high resolution peripheral quantitative computed tomography (HR-pQCT) parameters in the trabecular and cortical compartment. However, studies considering the effect of PHPT treatment on TBS are more conflicting. Secondary hyperparathyroidism caused by vitamin D deficiency was associated with impaired bone microarchitecture in all age categories, as measured by TBS and Hr-pQCT with further improvement after treatment with vitamin D.
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PTH and cardiovascular risk.
Gruson, D
Annales d'endocrinologie. 2021;(3-4):149-150
Abstract
Cardiovascular diseases remain the leading cause of non-communicable chronic diseases, are related to high morbidity and mortality and are associated to a huge impact on healthcare budgets. Biomarkers play an important role for the diagnosis and prognosis of cardiovascular diseases and are recognized tools for value-based care. Parathyroid hormone (PTH) is a major systemic calcium-regulating hormone and an important regulator of bone and mineral homeostasis. PTH 1-84, the biologically active hormone produced by the parathyroid glands and secreted into the systemic circulation, exerts its biological effects through the interaction of its first 34 amino acids with PTH receptors. PTH levels are raised in several cardio-renal disorders and hyperparathyroidism have detrimental effects on the heart and cardiac cells such as cardiac hypertrophy, remodeling and arrhythmias. High circulating PTH levels, through an increase in intracellular calcium, contribute also to the impairment of mitochondrial function and ATP production and to oxidative stress as well as inflammation states and, at the end, to cardiomyocytes necrosis. The interplay between PTH, fibroblast growth factor 23 and aldosterone is also detrimental for cardiovascular system and participate to endothelial dysfunction. Measurement of PTH levels could be therefore relevant in high risk individuals and could provide added value to established cardiac biomarkers for the sub-phenotyping of patients and treatment selection.
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Fibrosis in Chronic Kidney Disease: Pathogenesis and Consequences.
Panizo, S, Martínez-Arias, L, Alonso-Montes, C, Cannata, P, Martín-Carro, B, Fernández-Martín, JL, Naves-Díaz, M, Carrillo-López, N, Cannata-Andía, JB
International journal of molecular sciences. 2021;(1)
Abstract
Fibrosis is a process characterized by an excessive accumulation of the extracellular matrix as a response to different types of tissue injuries, which leads to organ dysfunction. The process can be initiated by multiple and different stimuli and pathogenic factors which trigger the cascade of reparation converging in molecular signals responsible of initiating and driving fibrosis. Though fibrosis can play a defensive role, in several circumstances at a certain stage, it can progressively become an uncontrolled irreversible and self-maintained process, named pathological fibrosis. Several systems, molecules and responses involved in the pathogenesis of the pathological fibrosis of chronic kidney disease (CKD) will be discussed in this review, putting special attention on inflammation, renin-angiotensin system (RAS), parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), Klotho, microRNAs (miRs), and the vitamin D hormonal system. All of them are key factors of the core and regulatory pathways which drive fibrosis, having a great negative kidney and cardiac impact in CKD.
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Calcium and Phosphate Hormones: Vitamin D, Parathyroid Hormone, and Fibroblast Growth Factor 23.
Underland, L, Markowitz, M, Gensure, R
Pediatrics in review. 2020;(1):3-11
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Parathyroid Hormone: A Uremic Toxin.
Duque, EJ, Elias, RM, Moysés, RMA
Toxins. 2020;(3)
Abstract
Parathyroid hormone (PTH) has an important role in the maintenance of serum calcium levels. It activates renal 1α-hydroxylase and increases the synthesis of the active form of vitamin D (1,25[OH]2D3). PTH promotes calcium release from the bone and enhances tubular calcium resorption through direct action on these sites. Hallmarks of secondary hyperparathyroidism associated with chronic kidney disease (CKD) include increase in serum fibroblast growth factor 23 (FGF-23), reduction in renal 1,25[OH]2D3 production with a decline in its serum levels, decrease in intestinal calcium absorption, and, at later stages, hyperphosphatemia and high levels of PTH. In this paper, we aim to critically discuss severe CKD-related hyperparathyroidism, in which PTH, through calcium-dependent and -independent mechanisms, leads to harmful effects and manifestations of the uremic syndrome, such as bone loss, skin and soft tissue calcification, cardiomyopathy, immunodeficiency, impairment of erythropoiesis, increase of energy expenditure, and muscle weakness.
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Vitamin D in chronic kidney disease: is there a role outside of PTH control?
Brogan, M, Astor, BC, Melamed, ML
Current opinion in nephrology and hypertension. 2020;(2):243-247
Abstract
PURPOSE OF REVIEW Vitamin D deficiency is common in patients with kidney disease and many patients receive vitamin D supplementation. Several large, well-designed clinical trials have been published in the last few years evaluating the effects of vitamin D supplementation on important outcomes for patients with kidney disease including effects on cardiovascular disease, secondary hyperparathyroidism, and kidney disease progression. RECENT FINDINGS Several negative trials have been published showing no effect of cholecalciferol supplementation on cardiovascular events, kidney disease progression, and albuminuria. Long-term supplementation does not appear to be associated with kidney stone disease. Vitamin D supplementation decreases parathyroid hormone (PTH) levels and high levels of 25-hydroxyvitamin D may be required for maximal suppression. SUMMARY There appear to be no effects of vitamin D supplementation on noncalcemic outcomes including progression of kidney disease, albuminuria, or cardiovascular disease. The primary reason to use vitamin D in kidney disease remains to lower PTH levels.
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Investigation and management of hypocalcaemia.
Nadar, R, Shaw, N
Archives of disease in childhood. 2020;(4):399-405
Abstract
Hypocalcaemia is a common clinical scenario in children with a range of aetiological causes. It will often present with common symptoms but may occasionally be identified in an asymptomatic child. An understanding of the physiological regulation of plasma calcium is important in understanding the potential cause of hypocalcaemia and its appropriate management. The age of presentation will influence the likely differential diagnosis. We have presented a stepwise approach to the investigation of hypocalcaemia dependent on the circulating serum parathyroid hormone level at the time of presentation. The acute and long-term management of the underlying condition is also reviewed.
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Calciotropic and phosphotropic hormones in fetal and neonatal bone development.
Ryan, BA, Kovacs, CS
Seminars in fetal & neonatal medicine. 2020;(1):101062
Abstract
There are remarkable differences in bone and mineral metabolism between the fetus and adult. The fetal mineral supply is from active transport across the placenta. Calcium, phosphorus, and magnesium circulate at higher levels in the fetus compared to the mother. These high concentrations enable the skeleton to accrete required minerals before birth. Known key regulators in the adult include parathyroid hormone (PTH), calcitriol, fibroblast growth factor-23, calcitonin, and the sex steroids. But during fetal life, PTH plays a lesser role while the others appear to be unimportant. Instead, PTH-related protein (PTHrP) plays a critical role. After birth, serum calcium falls and phosphorus rises, which trigger an increase in PTH and a subsequent rise in calcitriol. The intestines become the main source of mineral supply while the kidneys reabsorb filtered minerals. This striking developmental switch is triggered by loss of the placenta, onset of breathing, and the drop in serum calcium.