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Journal articles on the topic 'Osteitis fibrosa'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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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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2

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

Shin, Sug Kyun, Do Hun Kim, Heung Su Kim, Kyu Tae Shin, Kyung Ae Ma, Sung Jung Kim, Youn Sik Kwak, Seung Kyu Ha, and Donald J. Sherrard. "Renal Osteodystrophy in Pre-Dialysis Patients: Ethnic Difference?" Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 19, no. 2_suppl (February 1999): 402–7. http://dx.doi.org/10.1177/089686089901902s65.

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The purpose of the present study is to investigate whether an ethnic difference exists in the incidence of renal osteodystrophy between Asian and Western countries in end-stage renal disease (ESRD) patients. We evaluated bone histology in 58 pre-dialysis patients (28 male, 30 female; mean age: 47.7 years). All patients had bone biopsies with quantitative histomorphometry and sero-logical parameters such as intact PTH, osteocalcin, total alkaline phosphatase, and basal and deferoxamine-stimulated serum aluminum levels. We observed that 91.4% of all evaluated patients showed renal osteodystrophy before the start of dialytic therapy. Mild osteitis fibrosa were observed in 21 patients (36.2%), severe osteitis fibrosa in 5 patients (8.6%), mixed lesions in 7 patients (12.1 %), osteomalacia in 6 patients (10.3%), aplastic bone disease in 14 patients (24.1%), and normal bone in 5 patients (8.6%). Among the bone histomorphometric parameters, fibrosis area rate (%) showed the best correlation with intact PTH, and osteocalcin and osteoid area rate (%) with total alkaline phosphatase. Aluminum-related bone disease was not observed. Among patients with aplastic bone disease, only 14.3% showed aluminum deposition of any significance (5% < stainable bone surface aluminum < 25%). In the diabetic patients, aplastic bone disease was most common, but no case was related to aluminum intoxication. In conclusion, the distribution of renal osteodystrophy in our study was different from that of Western countries in pre-dialysis patients. Our patients tended to have more mild-form osteitis fibrosa and normal findings, and less severe-form osteitis fibrosa and aplastic bone disease. Aluminum-related bone disease was not observed.
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8

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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9

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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10

Phitayakorn, Roy, and Christopher R. McHenry. "Jaw Tumor: An Uncommon Presenting Manifestation of Primary Hyperparathyroidism." World Journal of Endocrine Surgery 2, no. 1 (2010): 45–50. http://dx.doi.org/10.5005/jp-journals-10002-1021.

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ABSTRACT Introduction To report two unusual cases of primary hyperparathyroidism (HPT) that initially manifested with a “ jaw tumor” and to discuss the clinical implications of a giant cell granuloma vs an ossifying fibroma of the jaw. Material and methods The history, physical examination, laboratory values and the imaging and pathologic findings are described in two patients who presented with a “jaw tumor” and were subsequently diagnosed with primary HPT. The diagnosis and management of osteitis fibrosa cystica and HPT-jaw tumor syndrome are reviewed. Results Patient #1 was a 70-year-old male who presented with hypercalcemia, severe jaw pain, and an enlarging mass in his mandible. Biopsy of the mass revealed a giant cell tumor and he was subsequently diagnosed with primary HPT. A sestamibi scan demonstrated a single focus of abnormal radiotracer accumulation, corresponding to a 13,470 mg parathyroid adenoma, which was resected. Postoperatively, the serum calcium normalized and the giant cell granuloma regressed spontaneously. Patient #2 was a 36-year-old male with four incidentally discovered tumors of the mandible and maxilla, who was diagnosed with normocalcemic HPT and vitamin D deficiency. Biopsy of one of the tumors revealed an ossifying fibroma. Bilateral neck exploration revealed a 2480 mg right inferior parathyroid adenoma, which was resected. Postoperative genetic testing revealed an HRPT2 gene mutation. He subsequently underwent resection of an enlarging ossifying fibroma of the mandible with secondary reconstruction. Conclusions A “jaw tumor” in a patient with primary HPT may be a manifestation of osteitis fibrosa cystica or HPT-jaw tumor syndrome underscoring the importance of biopsy and genetic testing for management and follow-up.
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11

Duarte, Maria Eugênia Leite, Ana Lúcia Passos Peixoto, Andréa da Silva Pacheco, Angela Vieira Peixoto, Rodrigo Dezerto Rodriguez, Jocemir Ronaldo Lugon, and Elisa Albuquerque Sampaio da Cruz. "The spectrum of bone disease in 200 chronic hemodialysis patients: a correlation between clinical, biochemical and histological findings." Sao Paulo Medical Journal 116, no. 5 (September 1998): 1790–97. http://dx.doi.org/10.1590/s1516-31801998000500002.

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INTRODUCTION: Renal osteodystrophy includes the complete range of mineral metabolism disorders that affect the skeleton in patients with chronic renal failure. PATIENTS AND METHODS: 200 patients with end-stage renal disease and on dialysis were investigated regarding the clinical, biochemical and histological findings of bone disease. RESULTS: The spectrum of renal osteodystrophy consisted mainly of high turnover bone lesions (74.5%), including osteitis fibrosa in 57.5%. Patients with mild bone disease were on dialysis for shorter periods of time and were mostly asymptomatic. Patients with aluminum-related bone disease (16.5%) had the greatest aluminum exposure, either orally or parenterally, and together with patients with high turnover mixed disease, were the most symptomatic. Although on a non-regular basis, the vast majority of the patients (82.5%) had been receiving vitamin D. The incidence of adynamic bone disease was high (n=8) among parathyroidectomized patients (n=12). Significantly higher serum levels of alkaline phosphatase were observed in osteitis fibrosa. CONCLUSIONS: The use of calcitriol and phosphate-binding agents on a non-regular basis seems to be the reason for the apparent reduced response to the treatment of secondary hyperparathyroidism. Alkaline phosphatase has been shown to be a fair marker for bone turnover in patients with osteitis fibrosa. The severity of the clinical manifestations of bone disease correlates with the histological features of bone lesion and to the time spent on dialysis.
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12

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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13

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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14

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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15

ARLIEN-SØBORG, ULLA. "Generalized Osteitis Fibrosa Cystica of Uncertain Aetiology." Acta Medica Scandinavica 152, no. 1 (April 24, 2009): 9–12. http://dx.doi.org/10.1111/j.0954-6820.1955.tb05635.x.

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16

Andress, DL. "Calcitriol in the treatment of osteitis fibrosa." Biomedicine & Pharmacotherapy 44, no. 3 (January 1990): 191. http://dx.doi.org/10.1016/0753-3322(90)90010-7.

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17

Thorwarth, M., S. Rupprecht, A. Schlegel, D. Neureiter, and P. Kessler. "Riesenzellgranulom und Osteitis fibrosa cystica bei Hyperparathyreoidismus." Mund-, Kiefer- und Gesichtschirurgie 8, no. 5 (July 29, 2004): 316–21. http://dx.doi.org/10.1007/s10006-004-0556-6.

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18

Andrade, Gabriel Silva, Abrahão Cavalcante Gomes de Souza Carvalho, Tibério Gomes Magalhães, Edson Luiz Cetira Filho, Roberta Barroso Cavalcante, and Renato Luiz Maia Nogueira. "Expansive renal osteitis fibrosa: a case report." Oral and Maxillofacial Surgery 22, no. 3 (May 4, 2018): 323–27. http://dx.doi.org/10.1007/s10006-018-0697-7.

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19

Watson, Carolyn W., Pamela Unger, Mamoru Kaneko, and Jacques L. Gabrilove. "Fine needle aspiration of osteitis fibrosa cystica." Diagnostic Cytopathology 1, no. 2 (April 1985): 157–60. http://dx.doi.org/10.1002/dc.2840010212.

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20

Gerber, Fabienne A., Niels J. Rupp, Quirin Döbelin, Bernd Stadlinger, and Silvio Valdec. "Der braune Tumor bei unbehandeltem Hyperparathyreoidismus." SWISS DENTAL JOURNAL SSO – Science and Clinical Topics 132, no. 3 (March 7, 2022): 190–91. http://dx.doi.org/10.61872/sdj-2022-03-03.

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Der braune Tumor (Osteitis fibrosa cystica) ist eine seltene, nicht neoplastische, expansiv wachsende, riesenzellhaltige Läsion. Ein Hyperparathyreoidismus (Nebenschilddrüsenüberfunktion [HPT]) führt in 2 bis 3 Prozent der Fälle zur Entwicklung eines braunen Tumors. Dieser kann sich in jedem Teil des Skeletts manifestieren.
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21

Shrestha, Sundar K., and A. Tayal. "Generalised osteitis fibrosa cystica due to secondary hyperparathyroidism in chronic kidney disease." Journal of College of Medical Sciences-Nepal 9, no. 1 (January 20, 2014): 60–66. http://dx.doi.org/10.3126/jcmsn.v9i1.9676.

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Secondary hyperparathyroidism is a frequent complication of patients with chronic kidney disease and is characterized by excessive serum parathyroid hormone levels and an imbalance in calcium and phosphorus metabolism. Secondary hyperparathyroidism is the leading cause of renal osteodystrophy and bone disease. Osteitis fibrosa cystica, the classic and former most common osteodystrophy, is mainly caused by high bone turnover secondary to high levels of circulating PTH. Its pathophysiology is mainly due to hyperphosphatemia and vitamin D deficiency and resistance. This condition has a high impact on the mortality and morbidity of dialysis patients Hyperparathyroidism develops early in the course of CKD and becomes more prominent as kidney function declines. However recently, with the technical development of imaging and laboratory screening methods, hypercalcemia due to primary or secondary hyperparathyroidism can often be detected early; as a result the frequency of osteitis fibrosa cystica has declined. Journal of College of Medical Sciences-Nepal, 2013, Vol-9, No-1, 60-66 DOI: http://dx.doi.org/10.3126/jcmsn.v9i1.9676
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22

Duarte, M. E. L., E. F. Carvalho, E. A. S. Cruz, S. B. G. Lucena, and D. L. Andress. "Cytokine accumulation in osteitis fibrosa of renal osteodystrophy." Brazilian Journal of Medical and Biological Research 35, no. 1 (January 2002): 25–29. http://dx.doi.org/10.1590/s0100-879x2002000100004.

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23

Rickes, Steffen. "osteitis fibrosa cystica misdiagnosed as lytic bone metastases." Acta Endocrinologica (Bucharest) 6, no. 2 (2010): 264. http://dx.doi.org/10.4183/aeb.2010.264.

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24

Leite-Filho, Ronaldo V., Marcele B. Bandinelli, Gabriela Fredo, Matheus V. Bianchi, Alessandra van der lan Fonini, Marcelo M. Alievi, David Driemeier, Saulo P. Pavarini, and Luciana Sonne. "Osteitis fibrosa cystica in a domestic young cat." Journal of Feline Medicine and Surgery Open Reports 1, no. 2 (July 2015): 205511691560755. http://dx.doi.org/10.1177/2055116915607555.

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25

Sleiman, I., D. Godi, V. Villanacci, G. Pelizzari, and G. P. Balestrieri. "Osteitis fibrosa cystica, coeliac disease and Turner syndrome." Digestive and Liver Disease 36, no. 7 (July 2004): 486–88. http://dx.doi.org/10.1016/j.dld.2004.03.004.

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26

Gupta, Anju, Mark C. Horattas, Ali Reza Moattari, and Scott D. Shorten. "Disseminated Brown Tumors from Hyperparathyroidism Masquerading as Metastatic Cancer: A Complication of Parathyroid Carcinoma." American Surgeon 67, no. 10 (October 2001): 951–55. http://dx.doi.org/10.1177/000313480106701009.

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Osteitis fibrosa cystica (brown tumors) can be a skeletal manifestation of advanced hyperparathyroidism, including parathyroid cancer. Severe osteitis fibrosa cystica can mimic metastatic bone diseases especially in patients with a history of cancer. Because the treatment and prognosis of these two problems differ greatly considering hyperparathyroidism in the differential diagnosis of patients found to have osteolytic lesions is critical for the appropriate management of these patients. In this case report we describe a patient with a history of renal cell cancer and presumed osteolytic bone metastases. During prophylactic intramedullary rodding to prevent pathologic fracture of her femur she was found to have a benign lesion related to her previously undiagnosed hyperparathyroidism caused by an underlying parathyroid cancer. A detailed review of this disease and the associated bone changes is also included to underscore the importance of an adequate differential diagnosis as well as optimal management. Patients with hypercalcemia or bony lesions should not automatically be treated palliatively for metastatic disease just because of a past medical history of cancer. Hyperparathyroidism is a readily curable problem if properly diagnosed.
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Maina, Anthony M., and Harry Kraus. "Successful Treatment of Osteitis Fibrosa Cystica from Primary Hyperparathyroidism." Case Reports in Orthopedics 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/145760.

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Osteitis Fibrosa Cystica (OFC) is defined as the classic skeletal manifestation of advanced primary hyperparathyroidism. With the increased detection by means of routine calcium screening, the clinical profile of primary hyperparathyroidism in Western countries has shifted from symptomatic disease to one with subtle or no specific symptoms (“asymptomatic” primary hyperparathyroidism). The authors describe a classical feature of advanced primary hyperparathyroidism due to a parathyroid adenoma and its successful treatment.
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28

Pierrard, Patricia Luengo, Laura M. Tortolero Giamate, Belén Porrero Guerrero, Joaquín Gómez Ramírez, and Jordi Nuñez Nuñez. "Osteitis Fibrosa Cystica A Rare Presentation of Primary Hyperparathyroidism." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A207—A208. http://dx.doi.org/10.1210/jendso/bvab048.422.

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Abstract Introduction: Osteitis fibrosa cystica (OFC) is the most serious bone involvement of primary hyperparathyroidism (PHPT), it is characterized by subperiosteal resorption, lytic lesions and the appearance of brown tumors; this is why, in some cases, this condition can easily be mistaken for a malignant neoplasm. Its prevalence in developed countries is only 5%. Clinical Case: We present a 58-year-old woman, with no relevant personal history, who came to the emergency room with pain in her right shoulder after an accidental fall on the bus. The humerus radiograph shows a pathological fracture of the right humerus, with significant osteopenia. In the emergency analysis, serum Calcium 13.3 mg / d), Ionic Calcium 7.03 mg / dL, Phosphorus 2.4 mg / dL, Alkaline Phosphatase 248 U / L and normal kidney function stand out. With a diagnosis of severe hypercalcemia, treatment was started in the emergency room with serum therapy (1000 ml of 0.9% physiological saline in 4 hours) and intravenous diuretic treatment (furosemide 40mg) with a decrease in calcemia to 12.8mg / dL. Later, she was admitted to the Internal Medicine hospital ward to perform a differential diagnosis of hypercalcemia secondary to a primary tumor, Multiple Myeloma or Primary Hyperparathyroidism. The study findings are: Calcium metabolism: PTH 660 pg / ml (12 - 65), 25 Hydroxyvitamin D: 14.00. Thyroid ultrasound: Posterocaudal to right thyroid lobe, an area of ​​echogenicity slightly lower than the thyroid is identified, of dimensions not estimated by endothoracic component, which could correspond to a parathyroid adenoma. Body CT: Neck: Heterogeneous nodule dependent on the posterior region of the right thyroid nodule with endothoracic extension. Skeleton: Lytic lesions with a tumor aspect in the humerus, right scapula and bilateral seventh rib and right pubic branch. Skull: Diffuse increase in bone density of the calvaria, showing multiple punctate lytic lesions with a permeative appearance. Bone densitometry: Femur neck: - &lt;1.5, Lumbar spine: - &lt;3.0 With the diagnosis of PHPT causing osteitis fibrosa cystica, surgical intervention was decided. Under general anesthesia, a selective right approach was performed, finding a large parathyroid adenoma weighing 17 grams. PTH fell to 36 pg / ml after surgery. At 9 months after surgery, the patient presented calcium levels of 9 mg / dl and PTH 146 pg / ml with clear radiological improvement. Discussion: Osteitis fibrosa cystica is rare in our environment, it is often confused with other neoplasms. After parathyroidectomy, patients with PHPT have a marked and sustained recovery from OFC, although in some cases this recovery can only be achieved after several years. We consider this case of interest, since it illustrates the importance of evaluating the study of phospho-calcium metabolism and parathyroid function in all patients with bone lesions to rule out Primary Hyperparathyroidism with OFC.
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Rivas-Prado, Luis, Alejandro Morales-Ortega, Sonia Allodi-de la Hoz, and David Bernal-Bello. "Hyperparathyroidism shows its hand: findings of osteitis fibrosa cystica." Lancet 397, no. 10288 (May 2021): 1914. http://dx.doi.org/10.1016/s0140-6736(21)00796-0.

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30

Swarnkar, Manish. "Osteitis Fibrosa Cystica: A Forgotten Entity of Primary Hyperparathyroidism." World Journal of Endocrine Surgery 12, no. 2 (2020): 98–100. http://dx.doi.org/10.5005/jp-journals-10002-1290.

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31

Bains, Margaret A., Linda E. Pardoe, and Claudius E. Rudin. "Osteitis fibrosa cystica and secondary hyperparathyroidism in multiple myeloma." British Journal of Haematology 136, no. 2 (January 2007): 179. http://dx.doi.org/10.1111/j.1365-2141.2006.06315.x.

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32

Bassler, Thomas, Edward T. Wong, and Russell K. Brynes. "Osteitis Fibrosa Cystica Simulating Metastatic Tumor:An Almost-Forgotten Relationship." American Journal of Clinical Pathology 100, no. 6 (December 1, 1993): 697–700. http://dx.doi.org/10.1093/ajcp/100.6.697.

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33

Carsote, Mara, Anda Dumitrascu, Claudiu Tupea, Ana Valea, Marian Romeo Smarandache, Marioara Cristina Corneci, Dumitru Ioachim, and Monica Livia Gheorghiu. "Primary hyperparathyroidism - related osteitis fibrosa cystica: Exceptional finding nowadays." Bone Reports 13 (October 2020): 100619. http://dx.doi.org/10.1016/j.bonr.2020.100619.

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34

Gibbs, C. J., J. G. Millar, and J. Smith. "Spontaneous healing of osteitis fibrosa cystica in primary hyperparathyroidism." Postgraduate Medical Journal 72, no. 854 (December 1, 1996): 754–57. http://dx.doi.org/10.1136/pgmj.72.854.754.

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35

Luzuriaga, Maria Gracia, Elsie Diez-Cardona, and Violet S. Lagari-Libhaber. "Osteitis Fibrosa Cystica: An Unusual but Still Prevalent Manifestation of Uncontrolled Secondary Hyperparathyroidism." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A208—A209. http://dx.doi.org/10.1210/jendso/bvab048.423.

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Abstract Background: Osteitis fibrosa cystica is an uncommon complication of untreated secondary hyperparathyroidism in patients with end-stage renal disease. The characteristic bony lesions that are seen in this condition very rarely can regress after medical treatment or parathyroidectomy. Clinical Case: A 65-year-old male with PMH of Systemic Lupus Erythematous (SLE) resulting in End-Stage Renal Disease (ESRD) on peritoneal dialysis (PD) and HTN, presented to his primary care physician for evaluation of a painful, enlarging lesion in his left forearm. The patient reported no history of trauma and denied having systemic symptoms. An X-Ray of his left forearm showed a lytic lesion within the proximal neck of the ulna, with erosion of the adjacent cortex. CT of the forearm showed a very vascular soft tissue mass causing significant erosive changes of the anterior cortex in the proximal ulna. Due to the characteristics of the lesion, an underlying malignancy was suspected as a possible diagnosis. The patient had a whole-body PET CT which showed multiple scattered hypermetabolic lytic osseous lesions throughout the axial and appendicular skeleton, including a large left proximal ulnar lesion. The patient had a bone biopsy from the lesion in his left ulna which showed a giant cell proliferation in a background of fibrosis and hemosiderin, suggestive of Osteitis Fibrosa Cystica (brown tumor of hyperparathyroidism). His laboratory workup around the time of the symptoms showed a normal serum calcium (9 mg/dl), associated with a high serum phosphorus (6.2 mg/dl), low vitamin D (20 ng/ml), and an elevated PTH (900 pg/ml). The patient was started on Cinacalcet, an increased dose of phosphate binders, as well as Calcitriol and the lesions and pain disappeared. Follow up lab work showed a normal Vitamin D (34 mg/dl), normal Phosphorus (4 mg/dl), and a PTH of 199 mg/dl, with a normal serum Calcium. A surveillance PET was performed 6 months after the initial one when the lesions clinically had disappeared and it showed again the presence of the bony lesions described prior, including the one in the left ulna, but with decreased FDG uptake, as well as new lesions in the spine. To date, the patient is asymptomatic and has not noted any new painful lesions. Conclusions: Osteitis fibrosa cystica remains a rare manifestation of secondary hyperparathyroidism, which may lead to an initial impression of malignancy. This patient exhibited clinical resolution of the painful symptoms associated with osteitis fibrosa cystica following medical management, though the lytic lesions involving the axial and appendicular skeleton persisted on surveillance imaging. This case serves as a reminder of the severe manifestations of a skeletal disease that has become rare given advances in early detection of and appropriate medical management of hyperparathyroidism.
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36

Wolf, G., and G. Lehmann. "Knochenhistologie bei renaler Osteodystrophie." Osteologie 17, no. 03 (2008): 107–11. http://dx.doi.org/10.1055/s-0037-1619855.

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ZusammenfassungChronische Nierenfunktionseinschränkungen führen am Knochen zu Stoffwechsel- und Strukturschäden, deren differenzierte Beurteilung vor allem durch die histologische Aufarbeitung von Knochenbioptaten möglich ist. Die internationale Klassifikation unterscheidet vier Formen der renalen Osteodystrophie (ROD). Dabei wird zwischen renalem Hyperparathyreoidismus (Osteitis fibrosa), Osteomalazie, gemischter urämischer Osteodystrophie und adynamer renaler Knochenerkrankung unterschieden. In der Arbeit werden die Methoden der Knochenentnahme und -bearbeitung, typische histologische Befunde sowie die Indikationen zur osteologischen Beckenkammbiopsie dargestellt.
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37

Maturi, Ramesh, Hemanth Makineni, and Sri Santhosh Keerthi Marri. "A Unique Case of Osteitis Fibrosa Cystica with Postoperative Hungry Bone Syndrome and Hypocalcemic Cardiac Failure." World Journal of Endocrine Surgery 7, no. 1 (2015): 10–13. http://dx.doi.org/10.5005/jp-journals-10002-1157.

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ABSTRACT Osteitis fibrosa cystica, a manifestation of severe hyperparathyroidism presenting with crippling bone deformities is a rare presentation these days. We report a case of 40-year-old male patient who presented with generalized aches and pains and bony deformities. Radiographs showed diffuse osteopenia, brown tumors and pathological fractures of phalanges but common manifestations associated with hyperparathyroidism like pancreatic calcifications and nephrolithiasis were absent. Serum calcium and parathyroid hormone levels were elevated while ultrasound imaging of neck showed the presence of a left lower parathyroid adenoma and was confirmed by Tc99- sestamibi scan. Large parathyroid lesion along with high calcium levels and severely elevated PTH puts this patient in high-risk category for postoperative hungry bone syndrome leading to severe hypocalcemia postoperatively. Hypocalcemia usually results in neuromuscular irritability manifesting as paresthesia, Chvostek and Trousseau sign, carpopedal spasm and even convulsions in severe cases. However, our patient had none of the common manifestations, but developed hypocalcemic cardiac failure postoperatively. Case history and management of case is presented. How to cite this article Maturi R, Makineni H, Marri SSK. A Unique Case of Osteitis Fibrosa Cystica with Postoperative Hungry Bone Syndrome and Hypocalcemic Cardiac Failure. World J Endoc Surg 2015;7(1):10-13.
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38

Lih, Anna, Mridula Lewis, and John Carter. "A rare case of primary hyperparathyroidism and osteitis fibrosa cystica." Medical Journal of Australia 193, no. 7 (October 2010): 416. http://dx.doi.org/10.5694/j.1326-5377.2010.tb03973.x.

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ASK-UPMARK, E. "A Study on the Parathyroid Enlargement by Osteitis Fibrosa Generalisata." Acta Medica Scandinavica 74, no. 3 (April 24, 2009): 284–323. http://dx.doi.org/10.1111/j.0954-6820.1930.tb08294.x.

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40

Ellis, Hewett A. "Persistence of Bone Resorptions Following Treatment of Renal Osteitis Fibrosa." American Journal of Surgical Pathology 12, no. 4 (April 1988): 325. http://dx.doi.org/10.1097/00000478-198804000-00011.

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41

Misiorowski, Waldemar, Izabela Czajka-Oraniec, Magdalena Kochman, Wojciech Zgliczyński, and John P. Bilezikian. "Osteitis fibrosa cystica—a forgotten radiological feature of primary hyperparathyroidism." Endocrine 58, no. 2 (September 12, 2017): 380–85. http://dx.doi.org/10.1007/s12020-017-1414-2.

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42

Spicher, Rüdiger, Thomas Patzelt, and Hans-Joachim Bauer. "Osteitis fibrosa cystica an der Hand: eine seltene, aber wichtige Differentialdiagnose." Handchirurgie · Mikrochirurgie · Plastische Chirurgie 50, no. 01 (February 2018): 46–47. http://dx.doi.org/10.1055/a-0576-7505.

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EinleitungDer primäre Hyperparathyreodismus ist die zweithäufigste Knochenstoffwechselerkrankung (25–28 auf 100 000/Jahr) nach der Osteoporose 1. In ca. 80 % der Fälle liegt ursächlich ein Nebenschilddrüsenadenom zugrunde. Erhöhte Parathormon-Titer führen durch Osteoklastenaktivierung zu Hypercalci- und Hypophosphatämie 2. Undiagnostiziert und unbehandelt kann es neben vielfältigen anderen Symptomen (z. B. Nierensteine, Magenulcera) zu überschießenden Knochenresorptionen mit Ausbildung von Knochentumoren (sog. „braune Tumoren“) kommen. Diese betreffen gerade auch die Hand und können die Stabilität gefährden. Für die Erkrankung existieren verschiedene Synonyme, so u. a. „Osteodystrophia fibrosa“ oder im englischen Sprachraum „von-Recklinghausen`s disease of bone“.
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Wada, Michihito, Hiromi Ishii, Yoshihiro Furuya, John Fox, Edward F. Nemeth, and Nobuo Nagano. "NPS R-568 halts or reverses osteitis fibrosa in uremic rats." Kidney International 53, no. 2 (February 1998): 448–53. http://dx.doi.org/10.1046/j.1523-1755.1998.00782.x.

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Mellouli, Nour, Raouaa Belkacem Chebil, Marwa Darej, Yosra Hasni, Lamia Oualha, and Nabiha Douki. "Mandibular Osteitis Fibrosa Cystica as First Sign of Vitamin D Deficiency." Case Reports in Dentistry 2018 (2018): 1–5. http://dx.doi.org/10.1155/2018/6814803.

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Introduction. Brown tumors of hyperparathyroidism are locally destructive bone lesions. They are the late clinical consequence of the disease. They can occur in primary, secondary, and rarely tertiary forms. They affect usually long bones and less frequently those of the maxilla. Case Report. Our 45-year-old female patient presented with a mandibular tumor next to the first right lower molar. At first, we have chosen tooth extraction and tumor excision. When the histological report showed the giant cell tumor we suspected a metabolic bone disorder. Biochemical tests screened hyperparathyroidism and severe vitamin D deficiency, and parathyroid scintiscan revealed parathyroid adenoma. Discussion. The association of hyperparathyroidism and vitamin D deficiency leads to diagnostic uncertainty. First, secondary hyperparathyroidism can be due vitamin D deficiency. Second, data available show that vitamin D deficiency is more prevalent in patients with primary hyperparathyroidism than in general population. Hyperparathyroidism management is based on correct and precise diagnosis. Furthermore, the resolution of brown tumors depends on the cure of hyperparathyroidism. In fact, bone lesions should regress after biological tests’ normalization. Conclusion. Clinicians should be aware of such rare and complicated presentation. They must consider the diagnosis of the brown tumor to avoid extensive surgical excision and teeth extractions.
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WILTON, AKE. "ON THE GENESIS OF »OSTEITIS FIBROSA GENERALISATA« (ENGEL-RECKLING-HAUSEN DISEASE)." Acta Pathologica Microbiologica Scandinavica 23, no. 1 (August 17, 2009): 1–51. http://dx.doi.org/10.1111/j.1699-0463.1946.tb00519.x.

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Kulak, C. A. M. "Marked Improvement in Bone Mass after Parathyroidectomy in Osteitis Fibrosa Cystica." Journal of Clinical Endocrinology & Metabolism 83, no. 3 (March 1, 1998): 732–35. http://dx.doi.org/10.1210/jc.83.3.732.

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Kulak, Carolina A. Moreira, Cristina Bandeira, Dora Voss, Sylwester M. Sobieszczyk, Shonni J. Silverberg, Francisco Bandeira, and John P. Bilezikian. "Marked Improvement in Bone Mass after Parathyroidectomy in Osteitis Fibrosa Cystica1." Journal of Clinical Endocrinology & Metabolism 83, no. 3 (March 1998): 732–35. http://dx.doi.org/10.1210/jcem.83.3.4655.

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Rubin, Mishaela R., Virginia A. LiVolsi, Francisco Bandeira, Gustavo Caldas, and John P. Bilezikian. "Tc99m-Sestamibi Uptake in Osteitis Fibrosa Cystica Simulating Metastatic Bone Disease." Journal of Clinical Endocrinology & Metabolism 86, no. 11 (November 2001): 5138–41. http://dx.doi.org/10.1210/jcem.86.11.7994.

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Opelami, Oluwaseun, Tinatin Narsia, and Andrei Brateanu. "226: Generalized Osteitis Fibrosa Mimicking Metastatic Bone Disease: A Case Report." American Journal of Kidney Diseases 55, no. 4 (April 2010): B88. http://dx.doi.org/10.1053/j.ajkd.2010.02.233.

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Parra Ramírez, Paola Andrea, Beatriz Lecumberri Santamaría, Cristina Álvarez Escolá, and Luís Felipe Pallardo Sánchez. "Primary hyperparathyroidism with osteitis fibrosa cystica mimicking a malignant bone tumor." Endocrinología y Nutrición (English Edition) 60, no. 2 (February 2013): 96–98. http://dx.doi.org/10.1016/j.endoen.2012.02.007.

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