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Osteitis Fibrosa Cystica
Published in Charles Theisler, Adjuvant Medical Care, 2023
Osteitis fibrosa cystica (OFC), also known as Von Recklinghausen's disease, is a serious skeletal disorder and a complication of primary or secondary hyperparathyroidism. As a result, osteoclasts are activated to resorb bone. This results in fibrous tissue replacing calcified supporting structures. The loss of bone mass causes bone pain and susceptibility to fractures, especially in the arms, legs, or spine. Ultimately, sites of increased bone activity (i.e., phalanges, skull bones, ends of long bones, and trabecular bones of the vertebrae) are softened, weakened, and deformed.1 Advanced OFC results in lytic lesions due to defective remodeling called brown tumors, which are more severe in young adults. Persistent hypercalcemia and an elevated serum parathyroid hormone (PTH) level help confirm the diagnosis of primary hyperparathy-roidism. Whenever possible, the underlying cause of secondary hyperparathyroidism should be removed.
Bones and fractures
Published in Henry J. Woodford, Essential Geriatrics, 2022
PTH is secreted from the parathyroid glands. It has complex actions on bone but the net result is osteoclast-mediated increased bone resorption, which releases calcium and phosphate into the circulation. PTH also has an inhibitory effect on renal calcium excretion but conversely increases renal phosphate loss. The combined effect is to increase serum calcium and reduce serum phosphate concentrations. In addition, PTH has a major role in controlling the metabolism of vitamin D as it stimulates the conversion of 25OHD to 1,25(OH)2D, mainly in the kidney. PTH secretion is controlled by negative feedback of serum calcium on the parathyroid glands. Therefore, its secretion is reduced when serum calcium concentration is elevated. Primary hyperparathyroidism results from excess secretion from the parathyroid glands. Secondary hyperparathyroidism occurs in response to low serum calcium, which can be caused by low dietary calcium intake, low serum 1,25(OH)2D concentration and by a range of kidney, liver and bowel diseases.12
Muscle Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Kourosh Rezania, Peter Pytel, Betty Soliven
Secondary hyperparathyroidism (typically to renal disease): Partial parathyroidectomy.1, 25-dihydroxycholecalciferol.1-alpha tocopherol.
Parathyroid carcinoma in chronic renal disease – a case series of three patients and review of literature
Published in Acta Chirurgica Belgica, 2023
Vladan Zivaljevic, Rastko Zivic, Nikola Slijepcevic, Matija Buzejic, Dusko Dundjerovic, Jasna Trbojevic Stankovic, Dejan Stojakov, Milan Jovanovic, Ivan Paunovic
Secondary hyperparathyroidism accompanied with parathyroid hyperplasia is common in patients with chronic renal failure. On the other hand, parathyroid carcinoma is an extremely rare entity, even more so in patients with end-stage renal disease (ESRD). Approximately, 1000 cases of parathyroid carcinoma have been reported until now; of which 34 cases were diagnosed in patients with ESRD [1,2]. Seven patients with parathyroid carcinoma and primary hyperparathyroidism underwent surgery at our tertiary referral university hospital in a seven-year period. On the other hand, there were only three cases of parathyroid carcinoma in haemodialysis patients that underwent surgery at our clinic over a period of 19 years [3]. The diagnosis of parathyroid carcinoma is very difficult and relies on a combination of preoperative, intraoperative, and pathohistological findings. Usually in these patients, highly elevated parathyroid hormone (PTH) levels and hyperphosphataemia are accompanied with clinical signs and symptoms, such as bone pain and pruritus.
A single-center experience of parathyroidectomy in 1500 cases for secondary hyperparathyroidism: a retrospective study
Published in Renal Failure, 2022
Shasha Zhao, Wei Gan, Wenjia Xie, Jinlong Cao, Liang Zhang, Ping Wen, Junwei Yang, Mingxia Xiong
Secondary hyperparathyroidism, a common complication of chronic kidney disease, has gradually become important for the prolonged survival of patients with end-stage renal disease and has been accompanied by improvements in medical care [1]. There have been many subsequent studies on this disease since it was initially reported in 1934 [2]. To date, hyperphosphatemia, hypocalcemia, vitamin D deficiency, dysfunction of the fibroblast growth factor 23-klotho axis and other factors [3] are presumed to be associated with secondary hyperparathyroidism, which causes renal osteodystrophy, disorders of calcium and phosphorus metabolism, cardiovascular calcification, ectopic calcification, pruritus, anemia, myopathy, malnutrition and neuropathy [4]. In addition, it results in worse quality of life, increased cardiovascular and all-cause mortality [5]. Combined conservative therapy composed of appropriate diet, dialysis and medication is widely adopted. Nevertheless, diet control and adjustment of dialysis prescription contribute only slightly. Calcium-based phosphorus binders, active vitamin D and analogs may lead to hypercalcemia, which increases the risk of cardiovascular and ectopic calcification [6,7]; however, noncalcium-based phosphorus binders, vitamin D receptor agonists and calcimimetics have limited therapeutic effects on refractory secondary hyperparathyroidism, and they are costly.
Aluminum overload in the reverse osmosis dialysis era: does it exist?
Published in Renal Failure, 2022
Mei-Yin Chen, Shih-Hsiang Ou, Nai-Ching Chen, Chun-Hao Yin, Chien-Liang Chen
In patients with hyperparathyroidism, the parathyroid hormone can protect against aluminum deposition in the bone. PTX in patients with chronic renal failure is associated with increased aluminum deposition on the bone surface, possibly as a result of low bone formation [13]. The protection decreases in patients who have undergone PTX or anti-resorption therapy or during vitamin D treatment for hyperparathyroidism, as these treatments could decrease bone turnover, worsen lower turnover symptoms [32–34] and hypercalcemic osteomalacia [14]. Considering the current case of secondary hyperparathyroidism, necessary parathyroidectomy and possible anti-resorption therapy may lower bone turnover. Therefore, it is generally suggested that aluminum bone disease should be excluded before lowering bone turnover treatment, such as PTX and bone resorption therapy. Hence, early screening and diagnosis of aluminum overload are important before lowering bone turnover treatments.