VIIth and VIIIth cranial nerve palsies due to parathyroid adenoma with associated osteitis fibrosa cystica

1975 ◽  
Vol 89 (7) ◽  
pp. 761-766 ◽  
Author(s):  
J. R. Page ◽  
D. K. Jash ◽  
J. B. Patel
Orthopedics ◽  
2001 ◽  
Vol 24 (10) ◽  
pp. 1000-1002
Author(s):  
Treyce S Knee ◽  
Almond J Drake ◽  
David Turton ◽  
K M Mohamed Shakir

2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Anthony M. Maina ◽  
Harry Kraus

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.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A207-A208
Author(s):  
Patricia Luengo Pierrard ◽  
Laura M Tortolero Giamate ◽  
Belén Porrero Guerrero ◽  
Joaquín Gómez Ramírez ◽  
Jordi Nuñez Nuñez

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: - <1.5, Lumbar spine: - <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.


2010 ◽  
Vol 2 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Roy Phitayakorn ◽  
Christopher R McHenry

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.


2013 ◽  
Vol 31 (1) ◽  
pp. 26
Author(s):  
W.Y.M. Abeysekera ◽  
P.M.C. Udaya Kumara ◽  
A.A.W.K. Amarasinghe ◽  
D.M.H. Fernando ◽  
A.B.S. Ananda Perera

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Thaís Borguezan Nunes ◽  
Sheyla Batista Bologna ◽  
Andréa Lusvarghi Witzel ◽  
Marcello Menta Simonsen Nico ◽  
Silvia Vanessa Lourenço

Objective.The brown tumour of hyperparathyroidism is a result of a metabolic disorder caused by primary hyperparathyroidism.Report. We described a case of a 37-year-old female patient presenting bimaxillary intraoral lesions and swelling in the neck. Incisional biopsy of the oral lesion was performed and histopathological examination revealed a central giant cell lesion composed by intense haemorrhagic exudate, abundant presence of giant cells, and areas with hemosiderin pigment. The patient also presented high levels of serum calcium and parathyroid hormone, hyperfunctioning parathyroid tissue, bilateral parenchymal nephropathy, and densitometry lower than expected, showing an advanced stage ofosteitis fibrosa cystica. Synchronous parathyroid adenoma and papillary thyroid carcinoma were confirmed by imaging exams and histopathologically.Conclusion.The composition of all the clinical, pathological, and imaging findings led to the final diagnosis of brown tumour of hyperparathyroidism. The occurrence of parathyroid adenoma, papillary thyroid carcinoma, and brown tumours of hyperparathyroidism in their late stage (osteitis fibrosa cystica) associated with oral brown tumours involving the mandible and maxilla is extremely rare.


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