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Metabolic Bone Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Hyperparathyroidism may be primary, secondary or tertiary: Primary hyperparathyroidism: This is usually caused by a single benign parathyroid gland adenoma (85% of cases). Carcinoma of a single parathyroid gland is rare, as are familial forms such as MEN 1 and 2.Secondary hyperparathyroidism: This is a physiological response to hypocalcaemia (eg. in chronic renal failure and osteomalacia). It is reversible following correction of calcium and phosphate levels.Tertiary hyperparathyroidism: This occurs when the increased PTH release of secondary hyperparathyroidism becomes autonomous. Raised PTH levels then persist, despite correction of calcium and phosphate levels, leading to hypercalcaemia.
Surgical Management of Parathyroid Disorders
Published in Madan Laxman Kapre, Thyroid Surgery, 2020
Neeti Kapre Gupta, Gregory W. Randolph, Dipti Kamani
For secondary and tertiary hyperparathyroidism, the management is primarily medical. However, patients whose HPT is not controlled or who are symptomatic in spite of maximum medical management are surgical candidates. K/DOQI guidelines from the U.S. Kidney Foundation have proposed that parathyroidectomy should be recommended in patients with severe SHPT (persistent serum levels of intact PTH >800 pg/mL), associated with hypercalcemia or hyperphosphatemia, which is refractory to medical therapy. Both subtotal parathyroidectomy and total parathyroidectomy with auto-graft are recommended options (Table 23.4).
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Tertiary hyperparathyroidism occurs after prolonged secondary hyperparathyroidism. The parathyroid glands begin to act autonomously (insensitive to calcium levels) secreting large amounts of PTH and causing hypercalcaemia. The glands show hyperplasia or adenomatous change.
Toward an individualized determination of dialysis adequacy: a narrative review with special emphasis on incremental hemodialysis
Published in Expert Review of Molecular Diagnostics, 2021
Massimo Torreggiani, Antioco Fois, Linda Njandjo, Elisa Longhitano, Antoine Chatrenet, Ciro Esposito, Hafedh Fessi, Giorgina Barbara Piccoli
While long lists of uremic toxins have been compiled, only few have acquired a role in clinical practice [75,78]. One of them is the parathyroid hormone (PTH). This molecule, whose molecular weight is 9400 Da, is pivotal to metabolic bone disease in dialysis patients, and it is both a hormone and a uremic toxin. Serum PTH levels depend on multiple factors, including serum calcium and phosphate levels; although international guidelines suggest to keep PTH levels in the range of 2 to 9 times the upper limit of normality [79], in the presence of optimal medical therapy (vitamin D and calcium supplements, calcimimetics, phosphate binders, etc.) and in the absence of tertiary hyperparathyroidism, an increased PTH concentration may be an indicator of an inadequate dialysis. Indeed, the attitude toward hyperparathyroidism management in CKD is not uniform worldwide and the Japanese Society for Dialysis Therapy suggests to keep PTH levels between 60 and 240 pg/ml [80]. This suggestion may be of particular interest on the account of the experience of the Japanese Society with patients with long dialysis vintage. The metabolism of PTH is too complex to allow PTH levels to be used as a self-standing marker of dialysis efficiency; nonetheless, their evaluation could guide dialysis prescription and its intradialytic profile could help tailoring the dialysate calcium content [81–83].
Current treatment options for secondary hyperparathyroidism in patients with stage 3 to 4 chronic kidney disease and vitamin D deficiency
Published in Expert Opinion on Drug Safety, 2021
Andrea Galassi, Paola Ciceri, Giulia Porata, Rossella Iatrino, Giulia Boni Brivio, Eliana Fasulo, Lorenza Magagnoli, Andrea Stucchi, Michela Frittoli, Anila Cara, Mario Cozzolino
Reduction of nephron mass at early CKD stages is accompanied by lower renal excretion of P, leading to insensible positive P balance. Due to main extravascular distribution of P, circulating P represents almost 1% of the organic P pool [14]. This implies that circulating P levels commonly remain within normal ranges in CKD stages 1–3, despite progressive expansion of systemic P load. However, increased systemic P levels trigger adaptive response of FGF-23 and PTH, both capable to increase renal P excretion by inhibition of tubular P reabsorption (Figure 1) [15]. FGF-23 also inhibit 1-α-hydroxylase (CYP27B1) with consequent reduction of levels of 1–25(OH)2D, leading to lower intestinal P absorption [16]. However, reduced 1–25(OH)2D also implies lower intestinal absorption of Ca and reduced VDR activation in parathyroid glands, both leading to further increase in PTH synthesis. FGF-23 may finally close the adaptive cascade by inhibitory feedback on PTH transcription [17,18]. Expression of VDR, CaSR and FGFR is impaired in parathyroid glands of patients affected by SHPT, with consequent resistance to the inhibitory effects of Ca, calcitriol and FGF-23 [18]. Thus, progression of SHPT in the presence of uncontrolled positive P balance, FGF-23 increase and 1–25(OH)2D deficiency may lead to severe tertiary hyperparathyroidism unresponsive to more advanced medications as VDRA and calcimimetics [11], requiring parathyroidectomy in severe cases or in candidates to renal transplantation [1].
Calciphylaxis-as a drug induced adverse event
Published in Expert Opinion on Drug Safety, 2019
Ignacio Portales-Castillo, Daniela Kroshinsky, Cindy K. Malhotra, Roberta Culber-Costley, Mario Gennaro Cozzolino, Shelly Karparis, Charles L. Halasz, Jeremy Goverman, Harold J. Manley, Rajeev Malhotra, Sagar U. Nigwekar
Treatments of secondary and tertiary hyperparathyroidism include both medical and surgical options. Cinacalcet acts on the calcium sensory channel in the parathyroid gland to decrease the secretion of PTH [51]. In the EVOLVE (Evaluation of Cinacalcet Hydrochloride Therapy to Lower Cardiovascular Events) trial, cinacalcet use in hemodialysis patients with hyperparathyroidism was associated with a 69–75% reduction in the incidence of calciphylaxis compared to placebo (0.9% versus 0.3% p = 0.009) [52]. This benefit was observed over a very wide level of intact PTH values (71–4957 pg/ml) and it is hypothesized that some of the effects of cinacalcet might be independent of PTH reduction [53]. In contrast, another study reported cinacalcet use to be associated with an increased odds of calciphylaxis (OR: 4.21, 95% CI: 2.80–6.30 at doses <60 mg/d, and OR: 3.10, 95% CI: 1.52–6.33 at doses >60 mg d) [13]. These findings are not necessarily contradictory as the EVOLVE trial included only patients with advanced hyperparathyroidism, while studies analyzing risk factors did not account for this distinction. The association of cinacalcet use with increased risk of calciphylaxis in the epidemiologic study might be confounded by the fact that patients with more severe bone disease are more likely to be using this medication. Others have hypothesized that there might be an intermediate ‘protective’ level of PTH [24].