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Relevant bibliographies by topics / Osteitis Fibrosa Cystica

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Academic literature on the topic 'Osteitis Fibrosa Cystica'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 March 2023

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Journal articles on the topic "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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3

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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4

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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5

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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6

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

Maanaoui, Mehdi, Aghiles Hamroun, Céline Lebas, Rémi Lenain, and Arnaud Lionet. "Correction to: Osteitis fibrosa cystica von Recklinghausen." Journal of Nephrology 34, no. 3 (March 27, 2021): 959. http://dx.doi.org/10.1007/s40620-021-01038-6.

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10

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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Books on the topic "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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3

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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Book chapters on the topic "Osteitis Fibrosa Cystica"

1

Sakr, Mahmoud F. "Osteitis Fibrosa Cystica." In Parathyroid Gland Disorders, 149–71. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07418-9_8.

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2

Theisler, Charles. "Osteitis Fibrosa Cystica." In Adjuvant Medical Care, 245–46. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-253.

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3

"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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4

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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