Academic literature on the topic 'Osteitis fibrosa. Osteitis Fibrosa Cystica'

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Journal articles on the topic "Osteitis fibrosa. Osteitis Fibrosa Cystica"

1

Gavrić, Nikola. "Osteitis fibrosa cystica generalisata." Scripta Medica 37, no. 2 (2006): 101–3. http://dx.doi.org/10.5937/scrimed0602101g.

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Agstam, Sourabh. "Osteitis fibrosa cystica." Indian Journal of Nephrology 30, no. 6 (2020): 433. http://dx.doi.org/10.4103/ijn.ijn_292_19.

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Ramon, Andre, and Pierre-Emmanuel Berthod. "Osteitis Fibrosa Cystica." New England Journal of Medicine 382, no. 11 (March 12, 2020): e15. http://dx.doi.org/10.1056/nejmicm1907828.

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Cherian, E. T., and K. B. Guttenberg. "Osteitis fibrosa cystica." QJM: An International Journal of Medicine 111, no. 7 (February 5, 2018): 487. http://dx.doi.org/10.1093/qjmed/hcy019.

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Arbault, Anaïs, Paul Ornetti, Davy Laroche, and Pierre Pottecher. "Osteitis fibrosa cystica." Joint Bone Spine 84, no. 2 (March 2017): 229. http://dx.doi.org/10.1016/j.jbspin.2016.02.027.

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Maanaoui, Mehdi, Aghiles Hamroun, Céline Lebas, Rémi Lenain, and Arnaud Lionet. "Osteitis fibrosa cystica von Recklinghausen." Journal of Nephrology 34, no. 3 (February 8, 2021): 925–26. http://dx.doi.org/10.1007/s40620-020-00961-4.

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7

Seo, D., and Y. Rhee. "Osteitis fibrosa cystica in primary hyperparathyroidism." QJM 108, no. 12 (August 9, 2015): 991. http://dx.doi.org/10.1093/qjmed/hcv144.

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8

Rodríguez-Gutiérrez, René, and José Miguel Hinojosa-Amaya. "Brown Tumors: Severe Osteitis Fibrosa Cystica." Mayo Clinic Proceedings 90, no. 5 (May 2015): 699–700. http://dx.doi.org/10.1016/j.mayocp.2014.08.025.

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9

Lee, Ja Hyun, Sung Min Chung, and Han Su Kim. "Osteitis Fibrosa Cystica Mistaken for Malignant Disease." Clinical and Experimental Otorhinolaryngology 6, no. 2 (2013): 110. http://dx.doi.org/10.3342/ceo.2013.6.2.110.

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10

Spaulding, CM, and G. Young. "Osteitis fibrosa cystica and chronic renal failure." Journal of the American Podiatric Medical Association 87, no. 5 (May 1, 1997): 238–40. http://dx.doi.org/10.7547/87507315-87-5-238.

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Books on the topic "Osteitis fibrosa. Osteitis Fibrosa Cystica"

1

German Society for Osteology. Conference. Generalized bone diseases: Osteoporosis, osteomalacia, ostitis fibrosa. Berlin: Springer-Verlag, 1987.

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2

Kuhlencordt, F., P. Dietsch, and E. Keck. Generalized Bone Diseases: Osteoporosis, Osteomalacia, Ostitis Fibrosa. Springer, 1988.

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Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.
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4

Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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Book chapters on the topic "Osteitis fibrosa. Osteitis Fibrosa Cystica"

1

"Osteitis fibrosa cystica." In Dermatology Therapy, 432. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1990.

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2

"Osteitis fibrosa disseminata." In Dermatology Therapy, 432. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1991.

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3

Silverberg, Shonni J., and John P. Bilezikian. "Primary hyperparathyroidism." In Oxford Textbook of Endocrinology and Diabetes, 653–64. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0419.

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Primary hyperparathyroidism is no longer the severe disorder of ‘stones, bones, and groans’ described by Fuller Albright and others in the 1930s (1,2). Osteitis fibrosa cystica, with its brown tumours of the long bones, subperiosteal bone resorption, distal tapering of the clavicles and phalanges, and ‘salt-and-pepper’ appearance of erosions of the skull on radiograph is rare, and kidney stones are seen in only 20% of patients. Asymptomatic disease is the rule in the vast majority of patients, with the diagnosis commonly following the finding of hypercalcaemia on routine serum chemistry analysis (Table 4.3.1) (3–5). Primary hyperparathyroidism is due to a solitary parathyroid adenoma in 80% of patients (5). Most cases are sporadic, although some are associated with a history of neck irradiation, or prolonged use of lithium therapy for bipolar disease (6, 7). Multiple parathyroid adenomas have been reported in 2 to 4% of cases (8). Parathyroid adenomas can be discovered in many unexpected anatomic locations, including within the thyroid gland, the superior mediastinum, and within the thymus. Occasionally, the adenoma may ultimately be identified in the retroesophageal space, the pharynx, the lateral neck, and even the alimentary submucosa of the oesophagus (9). In approximately 15% of patients with primary hyperparathyroidism, all four parathyroid glands are involved. There are no clinical features that differentiate single versus multiglandular disease. In nearly one-half of cases, four-gland disease is associated with a familial hereditary syndrome, such as multiple endocrine neoplasia 1 (MEN 1) or MEN 2a.
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4

Bardin, Thomas, and Tilman Drüeke. "Renal osteodystrophy." In Oxford Textbook of Rheumatology, 1274–82. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149_update_001.

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Abstract:
Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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5

Drüeke, Tilman, and Thomas Bardin. "Renal osteodystrophy." In Oxford Textbook of Rheumatology, 1274–82. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149_update_002.

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Abstract:
Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. Its main clinical expression is an increased propensity for fractures. It has been divided into several pathological entities based on histomorphometry criteria of bone turnover, mineralization and volume. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and α‎-klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can be schematically divided into three main types by histology: (1) osteitis fibrosa reflecting secondary hyperparathyroidism (sHP) is a high bone turnover disease which can develop early in CKD; (2) adynamic bone disease (ABD), at present the predominant type of ROD in dialysis patients, which is mainly the result of PTH resistance or excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone-specific alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus increases only in advanced CKD (stages G4-G5). Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage renal disease is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol, and in addition calcimimetics in dialysis patients, can be used to halt its progression.
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