Brown Tumor of Lower Right Limb in Patients With Primary Hyperparathyroidism: A Case Report

Background.Brown tumor of Hyperparathyroidism is a metabolic disorder that can affect the entire skeleton and reactive process due to bone resorption caused by primary or secondary hyperparathyroidism (HPT). Brown tumors can occur as solitary or multiple lesions in any bone, most often in the pelvis, ribs, clavicle, mandibula, and extremities. Here, we report the Brown tumor in the lower right limb in patients with primary HPT, and the literature is reviewed. Case presentation. Patients was women 30 years old had married and come with main complains of difficulty walking. This condition has been experienced by patients since diagnosis with lunb of tibia last 8 months and caused pain from hip to lower leg. On laboratory results, it showed elevated PTH 1.249 (normal 15-65) pg/dL, elevated phosphatase alkali 1156 (normal 40-150) u/dL, elevated Ca 10,8 (n:8,6 -10,3) mg/dL, phosphor 2,1 (3–4,5) mg/dL. Histology examination of tibia lump was a benign lesion of bone (Brown Tumor). Ultrasonography transabdominal result revealed kidney stones with bilateral renal pelvis dilation, nephrolithiasis non-obstructive was found with size 1 cm & left kidney cyst with size 0.6 cm. On Neck USG showed giant cyst lesion on parathyroid glands. Radiologist pelvic examination results showed bone metastasis disease. Head CT Scan examination concluded as suspect metastatic bone. Body bone scans examination showed pathological bone metastatic process. Conclusion. Brown tumor in right lower limb caused by primary HPT

Primary Hyperparathyroidism in the Common Orthopaedic Practice

An extensive review of the publications on primary hyperparathyroidism (pHPT) is presented in this report. It has strongly been emphasized in the literature that patients with pHPT may present either with the classical symptomatology or with asymptomatic disease, emerged due to biochemical screening. The clinical and epidemiological presentation of pHPT in western countries has changed profoundly during the past few decades, and bone disease is nowadays a distinct rarity. The introduction of serum calcium screening for osteoporosis and the technological advances in the laboratory assessment of parathyroid hormone have played important roles in early diagnosis. Subsequently, the disease is increasingly being detected as asymptomatic hypercalcaemia without guiding signs or symptoms. A third type of disease, the normocalcaemic variant, has been recently described in the literature. However, the potential diagnosis of pHPT should always be on the orthopaedics’ list of differential diagnoses in female or elderly patients with vertebral fractures and nephrolithiasis, either symptomatic or asymptomatic, as well as when solitary or multiple osteolytic lesions are encountered on the radiographs. Additionally, a middle aged woman with parathyroid adenoma and subsequent brown tumors detected on the pelvic radiographs is reported. Her initial laboratory findings indicated a minimal increase of the serum calcium, a mild increase of the erythrocyte sedimentation rate, and a significant increase in total serum alkaline phosphatase. Finally, the detection of elevated parathyroid hormone levels indicated the diagnosis of pHPT and necessitated imaging studies of the parathyroid glands, which indicated a parathyroid adenoma. Following successful excision of the parathyroid adenoma, the patient suffered from the hungry bone syndrome. After a follow-up of 20 years, the patient had normal calcium, vitamin D, and parathyroid hormone serum levels, while a pelvic radiograph indicated no significant changes in the appearance of the brown tumors.

Metabolic and functional imaging employment in the differentiation of brown tumors from bone metastases in a case of primary papillary thyroid cancer and parathyroid adenoma: case report

Background Brown tumors are benign osteoclastic bone lesions encountered in patients with hyperparathyroidism. These tumors may demonstrate aggressive, destructive features in the skeleton and imitate metastatic bone lesions, particularly in patients with known primary neoplasm. In this case report of recurrent papillary thyroid cancer and ectopic parathyroid adenoma, we shed light on the importance of combining different nuclear medicine imaging modalities to differentiate brown tumors from metastatic bone lesions. Case presentation We present a 39-year-old woman with a known history of papillary thyroid carcinoma classic type stage pT1N1b post-total thyroidectomy and radioactive iodine (I-131) therapy (RAI) presented with upper limb weakness and pain. An expansile lytic lesion involving the 6th cervical vertebra was seen in cervical spine MRI, which was suspicious for metastatic deposit. Therapeutic and diagnostic I-131 whole-body scans were negative for any I-13-avid lesions. Laboratory results revealed high calcium, parathyroid hormone, and alkaline phosphatase. A Technetium-99m-sestamibi (Tc-99m MIBI) scan was done with the standard protocol of spot views to the neck and upper chest area to localize any suspicious parathyroid adenoma. The scan demonstrated right supraclavicular and mediastinal Tc-99m MIBI-avid lesions suspicious for being ectopic parathyroid adenomas. Whole-body fluorine-18-2-fluoro-2-deoxy-d-glucose (18F-FDG), positron emission tomography/computed tomography (PET/CT) (18F-FDG PET/CT) was performed for further evaluation. It demonstrated multiple focal lytic skeletal lesions of abnormal increased FDG uptake as well as right supraclavicular FDG-avid lymph nodes. However, the superior mediastinal lesion was non-FDG-avid, suggesting the existence of two different entities: ectopic parathyroid adenoma with multiple brown tumors and metastatic right supraclavicular lymph nodes. The patient underwent right neck dissection and superior mediastinal mass excision. An intra-operative fresh serum parathyroid sample was sent, which dropped down to 100ng/ml from 863.7ng/ml. Later, histopathological results revealed that the right supraclavicular lymph nodes were metastatic papillary thyroid carcinoma. At the same time, the superior mediastinal mass proved to be parathyroid adenoma by histopathology, confirming the 18F-FDG PET/CT findings. Conclusions In the case of papillary thyroid carcinoma, metastatic lymph nodes with hyperparathyroidism, and evidence of lytic bone lesions, careful interpretation of the different metabolic and functional imaging modalities are needed to exclude the concurrent parathyroid adenoma and facilitate the differentiation of brown tumors from bone metastases, leading to appropriate surgical and medical treatment plans.

A RARE CASE OF MAXILLARY BROWN TUMOUR AS PRIMARY PRESENTATION OF THE PARATHYROID CARCINOMA.

Background: Brown tumours are expansile osteolytic lesions of bone, occurring in Hyperparathyroidism. Brown tumours occur most commonly in ribs, clavicle, long bones and pelvis and are uncommon in other facial bones except mandible. Other facial bones are rarely affected. Brown tumors are due to the direct effect of the parathyroid hormone. Brown tumors occur more with primary hyperparathyroidism than secondary. However, they are reported more in secondary hyperparathyroidism. In primary hyperparathyroidism, a parathyroid adenoma is a cause in 81% while other causes include hyperplasia in 15% and parathyroid carcinoma only in 4%. We present a case report of maxillary Brown tumor due to parathyroid carcinoma in an elderly male patient. Case Report: A 67-year-old male presented with right maxillary swelling increasing in size for the last few months associated with ipsilateral nasal block and right eye epiphora. The contrast CT scan of paranasal sinuses and neck revealed a large expansile right maxillary tumor aggressively eroding maxillary wall with extension into the orbital oor, ethmoid, sphenoid sinuses, nasal cavity, and oral cavity with the erosion of hard palate and soft tissue extension to subcutaneous Plane. A three cm sized soft tissue density lesion was also noted posterior to the right thyroid lobe in CT sections of the neck. Blood prole was normal except extremely high serum parathormone and calcium as well as mildly elevated serum creatinine (S. PTH 3437 pg./ml. S. Ca. 19 mg%. S. Creatinine 1.77mg%.) Ultrasonography of the abdomen also revealed calcication in the renal medulla. Right lower parathyroidectomy was done with the frozen section as well as the Intraoperative Rapid PTH assay. The PTH level was reduced by 90 percent of the original value. The nal histopathology was suggestive of parathyroid carcinoma. Summary: The patient was under regular surveillance, as the maxillary tumor was under remittance after the resection of parathyroid carcinoma. Parathyroid carcinoma is a very rare tumor and involvement of maxillary bone due to primary hyperparathyroidism due to parathyroid carcinoma is also uncommon.

Molecular Imaging with 18F-FDG PET/CT and 99mTc-MIBI SPECT/CT in Osteitis Fibrosa Cystica Generalisata

Benign so-called “brown tumors” secondary to hyperparathyroidism are a rare diagnostic pitfall due to their impressively malignant-like character in various imaging modalities. We present the case of a 65-year-old male patient with multiple unclear osteolytic lesions on prior imaging suspicious for metastatic malignant disease. Eventually, findings of 18F-FDG PET/CT staging and 99mTc-MIBI scintigraphy resulted in revision of the initially suspected malignant diagnosis. This case illustrates how molecular imaging findings non-invasively corroborate the correct diagnosis of osteitis fibrosa cystica generalisata with the formation of multiple benign brown tumors.

Maxillary Brown Tumor as a Rare Complication of Hyperparathyroidism

Secondary hyperparathyroidism is a common complication of end stage renal disease (ESRD). The inherent impaired phosphorus and calcium metabolism result in altered bone metabolism, which rarely may manifest as osteitis fibrosa cystica with approximately 2% presenting as brown tumors. Brown tumors are areas of excessive bone resorption replaced by giant cells and fibrovascular tissue. Maxillofacial brown tumors are rare and result in increased patient morbidity due to associated nasal bleeding, diffuse pain and focal deformities. Nonetheless, these tumors are treatable and may regress following reduced parathyroid hormone (PTH) levels. Case of a 64-years-old Hispanic male with history of ESRD on hemodialysis for more than 20 years, secondary hyperparathyroidism with fragility fractures of femur status post parathyroidectomy on years 1999 and 2010, coronary artery disease and hypertension, who was consulted to our service for evaluation of a bleeding nasal septum mass suspected of a brown tumor. The patient presented to the emergency room with a massive spontaneous nasal bleeding which was subsequently controlled and evaluated by imaging. Maxillofacial CT scan without contrast showed an expansile soft tissue mass at the right maxillary sinus measuring 3.4 x 3.5 x 3.7 cm with innumerable, similar lesions distributed throughout the cranial, cervical and visualized portions of the shoulder girdle bones. Biochemical evaluation was remarkable for PTH levels 1,229 pg/ml (nl, 18.5 – 88.0 pg/ml), corrected serum calcium 9.0 mg/dl (nl, 8.3 – 10.6 mg/dl), alkaline phosphate levels 391 U/L (nl, 46 – 116 U/L), serum phosphoros 5.5 mg/dl (nl, 2.5 – 4.5 mg/dl), calciferol levels 32.2 ng/ml (nl, 30 – 100 ng/ml) and an estimated glomerular filtration rate at 21 ml/min/1.73 m2 (nl, > 60 ml/min/1.73 m2). An excisional tissue biopsy showed osteoclastic-like multinucleated cells consistent with a brown tumor. These findings are consistent with secondary hyperparathyroidism complicated with osteitis fibrosa cystica. Following histologic diagnosis, a 99mTc-Sestamibi parathyroid scan showed two focal lesions of increased radiotracer uptake in the lower poles of the thyroid confirming parathyroid hyperplasia. Patient’s medical therapy was optimized by increasing cinacalcet dose and adding calcitriol, while continuing Sevelamer. Serum calcium, PTH, and phosphorous levels were closely monitored. Finally, patient was referred for parathyroidectomy. Patients with ESRD are at high risk of developing secondary hyperparathyroidism. Even with prior parathyroidectomy, these patients can develop disease recurrence. Early recognition and management of secondary hyperparathyroidism is crucial to decrease disease complications such as Brown tumors.

A Unique Case of Primary Hyperparathyroidism

Background: Primary hyperparathyroidism is the most common cause of hypercalcemia. It is more commonly seen in postmenopausal women, but can develop in younger individuals. Brown Tumors are an uncommon finding that can be seen in sever hyperparathyroidism. These bone findings are most often seen in the maxilla or mandible, though can affect any bone. Bone changes are reversible after parathyroidectomy. Clinical Case: An 18 year old male with a PMH of nephrolithiasis presented with a two day history of flank pain and hematuria. Endocrinology was consulted for hypercalcemia and elevated PTH. He had a family history of nephrolithiasis in his maternal uncle and grandfather, but no known family history of hypercalcemia or thyroid cancer. He was not on any medications or supplements. His initial labs were significant for a calcium of 15.0, PTH of 644, and a Vitamin D 25 of 11.7. He had no known history of hypercalcemia. He was treated with aggressive hydration, 4mg of zometa, 30mg of sensipar and two doses of 200mg calcitonin, with improvement in his calcium levels. Imaging of the abdomen and pelvis revealed multifocal solid-cystic lesions in the right superior pubic ramus and the distal femur, with smaller enhancing lesions in the left subtrochanteric, consistent with Brown Tumors. SpectCT was obtained and significant for a 2.1 by 1.4cm lesion in the anterior superior mediastinum. His overall presentation was consistent with primary hyperparathyroidism secondary to an ectopic parathyroid adenoma. Due to his relative young age at presentation and degree of primary hyperparathyroidism, there was concern for MEN1 or possible parathyroid carcinoma. MRI of the pituitary was obtained and showed a 4mm microadenoma in the right side of the pituitary. Prolactin, thyroid hormones, IGF-1, plasma metanephrines and calcitonin were all within normal limits. CDC73, a genetic marker for parathyroid carcinoma, was negative. Genetic work up for MEN1 was also negative. Endocrine surgery was consulted and he underwent a resection of the ectopic parathyroid adenoma. Discusion: Though most patients with primary hyperparathyroidism are asymptomatic, nephrolithiasis and Brown Tumors can be seen with more severe cases. It is important to rule out possible genetic causes for primary hyperthyroidism in patients with abnormal presentations, as it will change the overall long term management.