Brown Tumors: The Hidden Face of Primary and Renal Hyperparathyroidism Amid Real-Life Settings.

Brown tumors, an exceptional bone complication of severe primary (PHP) or renal (secondary) hyperparathyroidism (RHP), are caused by long-standing, elevated parathormone (PTH)-induced osteoclast activation causing multinucleated giant cell conglomerates with hemosiderin deposits in addition to the local production of cytokines and growth factors. We aim to present an adult case series including two females displaying this complication as part of a multidisciplinary complex panel in high PTH-related ailments. The approach was different since they had distinct medical backgrounds and posed a wide area of challenges amid real-life settings, namely, a 38-year-old lady with PHP and long-term uncontrolled hypercalcemia (with a history of pregnancy-associated PHP, the removal of a cystic jaw tumor, as well as a family and personal positive diagnosis of polycystic kidney disease, probably a PHP-jaw tumor syndrome), as well as, a 26-year-old woman with congenital single kidney and chronic renal disease-associated RHP who was poorly controlled under dialysis and developed severe anemia and episodes of metabolic acidosis (including one presentation that required emergency hemodialysis and was complicated with convulsive seizures, followed by resuscitated respiratory arrest). Both subjects displayed a severe picture of PHP/RHP with PTH levels of >1000 pg/mL and >2000 pg/mL and elevated serum bone turnover markers. Additionally, they had multiple brown tumors at the level of the ribs and pelvis (asymptomatically) and the spine, skull, and pelvis (complicated with a spontaneous cervical fracture). As an endocrine approach, the control of the underlying parathyroid disease was provided via surgery in PHP (for the postparathyroidectomy hungry bone syndrome) via medical intervention (with vitamin D analogs) in RHP. Additionally, in this case, since the diagnosis was not clear, a multidisciplinary decision to perform a biopsy was taken (which proved inconclusive), and the resection of the skull tumor to confirm the histological traits. This series highlights the importance of addressing the entire multidisciplinary panel of co-morbidities for a better outcome in patients with PHP/RHP-related brown tumors. However, in the instance of real-life medicine, poor compliance and reduced adherence to recommendations might impair the overall health status. Thus, sometimes, a direct approach at the level of cystic lesion is taken into consideration; this stands for a narrow frame of decision, and it is a matter of personalized decision. As seen here, brown tumors represent the hidden face of PHP/RHP, primarily the complex and severe forms, and awareness is essential even in the modern era.

Management Modalities of Aggressive Brown Tumor of the Jaws-a Case Series.

Primary hyperparathyroidism is an endocrine disorder occurring due to increased secretion of parathormone resulting in clinical, anatomical, and biochemical alterations. On the other hand, excision of a parathyroid adenoma can normalize the metabolic status. Brown tumors represent the terminal stage of the remodeling processes during primary or secondary hyperparathyroidism. They are erosive bony lesions caused by rapid osteolysis and peritrabecular fibrosis, resulting in a local destructive phenomenon. Facial skeleton is involved in about 2% of all cases of which the mandible is frequently affected. We report a case series of four patients who presented with brown tumor of both maxilla and mandible. A complete assessment of the medical history, blood investigations and radiological findings combined with biopsy results is necessary for a correct diagnosis. The standard treatment of the Brown tumors is not a surgical resection, but the treatment of the cause of the tumor, which in this case is hyperparathyroidism. However in our case, the extent of the lesion and the non resolution after the parathyroidectomy necessitated a surgical approach in two of our patients however two responded well to medical management alone.

Brown tumors: Retrospective analysis of 26 cases.

INTRODUCTION: Brown tumors are reactive osteolytic lesions caused by hyperparathyroidism. These rare lesions are non-neoplastic processes that result from bone resorption. The purpose of this study was to retrospectively review a 34-year experience with brown tumors in our institution. MATERIALS AND METHODS: We retrospectively analyzed the records of 26 consecutive patients with brown tumor who were treated in our institution between May 1988 and October 2020, with a mean follow-up of 36,1 months. RESULTS: 17 male (65,4%) and 9 female (34,6%) patients with a mean age of 41,6 were included in the study. Localized bone pain was present in 13 cases (50,0%) as the first presenting symptom. 3 patients (11,5%) presented with diffuse bone pain. 7 patients (26,9%) were diagnosed with brown tumor while being investigated for pathological fractures. The other 3 patients (11,5%) were diagnosed while being evaluated for hypercalcemia symptoms. 7 patients (26,9%) had solitary lesions, while 19 patients (73,1%) had multiple lesions. Pelvis, femur, ribs, tibia, proximal humerus and mandible were the most common sites of localization. 23 patients (88,5%) were diagnosed with primary hyperparathyroidism, while the other 3 patients (11,5%) had secondary hyperparathyroidism. A total of the 65 lesions, 23 (35.4%) underwent orthopedic surgery, and 42 (64.6%) were followed up conservatively after parathyroidectomy. Orthopedic surgery was performed in 21 of 26 patients, the other 5 cases were followed up conservatively. Intralesional curettage was performed in 19 cases (82,6%). The resulting cavity was filled with bone cement in 11 cases (47,8%). Bone grafting was applied in 8 cases (34,8%). No recurrence was observed in any of the patients. CONCLUSION: The diagnosis of brown tumor begins with clinical suspicion. Endocrinology and general surgery consultation is important before surgery. Treatment of brown tumors requires a multidisciplinary approach.

Fragility Fractures Unveil the Hidden Dragon: A Case of Osteitis Fibrosa Cystica and Secondary Hyperparathyroidism in End-Stage Renal Disease Post-Trauma.

Secondary hyperparathyroidism is a prevalent complication of end-stage renal disease (ESRD), arising from chronic renal insufficiency leading to disturbed calcium metabolism. This disruption triggers hypersecretion of the parathyroid gland, characterizing the condition. Osteitis fibrosa cystica (OFC), a rare complication of untreated secondary hyperparathyroidism, results in benign resorptive bone lesions and the formation of cystic cavities within bones. Our case report describes a 46-year-old incarcerated Hispanic male with a 17-year history of end-stage renal disease and secondary hyperparathyroidism. The patient initially presented with a traumatic right elbow injury. Further diagnostic evaluation revealed an 8 cm destructive process involving the distal humerus, initially suspected as malignancy but confirmed as OFC through bone biopsy. Management involved orthopedic surgery performing an open reduction and internal fixation (ORIF) of the affected limb, with subsequent consideration for inpatient parathyroidectomy. Imaging studies, including magnetic resonance imaging (MRI) and computed tomography (CT) scans, elucidated a 6 × 5.5 cm soft tissue mass, further confirmed as a brown tumor. The case underscores the complexities of diagnosing OFC, often misinterpreted in radiologic studies, and highlights the multidisciplinary approach involving orthopedics, otolaryngology, and nephrology in managing this intricate scenario. The objective is to explore clinical manifestations and treatment challenges of OFC and secondary hyperparathyroidism triggered by trauma in end-stage renal disease, emphasizing the need for continued awareness and precise diagnostic strategies in resource-rich areas.

Brown Tumor From Secondary Hyperparathyroidism Mimicking Metastatic Renal Cell Carcinoma in a Patient With End-Stage Renal Disease.

Brown tumors (also known as osteitis fibrosa cystica) are rare complications of end-stage renal disease (ESRD) and secondary hyperparathyroidism (HPT), characterized by focal bone lesions that resemble neoplasms. They are often misdiagnosed as metastatic bone disease, especially in patients with a history of malignancy. We present a case of a 60-year-old man with a history of renal cell carcinoma (RCC), and ESRD on hemodialysis (HD), who developed diffuse bone lesions on imaging with osteolytic/osteoblastic appearance concerning metastases, but on further workup was found to have brown tumors. We discuss the treatment and outcome and briefly review the relevant medical literature.

Primary Hyperparathyroidism With Brown Tumor of the Mandible Misdiagnosed as a Giant Cell Tumor: A Case Report.

In this case study, we present an incidentally discovered giant cell granuloma, which, upon detailed investigation, led to an unexpected diagnosis. A 36-year-old woman exhibited a bone lesion in the right retromolar trigone area, initially suspected of being malignant. However, histopathological examination revealed a giant cell tumor of bone. Further biochemical profiling, including serum calcium, phosphorus, and parathyroid hormone (PTH) levels, showed elevated PTH and hypercalcemia, prompting consideration of primary hyperparathyroidism and the diagnosis of a brown tumor due to this condition. This case underscores the importance of considering brown tumors associated with primary hyperparathyroidism as a potential differential diagnosis in patients with lytic bone lesions.

Expect the unexpected: Brown tumor of the mandible as the first manifestation of primary hyperparathyroidism.

Hyperparathyroidism (HPT) is a condition in which one or more parathyroid glands produce increased levels of parathyroid hormone (PTH), causing disturbances in calcium homeostasis. Most commonly HPT presents with asymptomatic hypercalcemia but the clinical spectrum may include disturbances reflecting the combined effects of increased PTH secretion and hypercalcemia. Brown tumors are rare, benign, tumor-like bone lesions, occurring in 1.5% to 4.5% of patients with HPT, as a complication of an uncontrolled disease pathway, and are nowadays rarely seen in clinical practice. The tumor can appear either as a solitary or multifocal lesion and usually presents as an asymptomatic swelling or a painful exophytic mass. Furthermore, it can cause a pathological fracture or skeletal pain and be radiologically described as a lytic bone lesion. The diagnosis of a brown tumor in HPT is typically confirmed by assessing the levels of serum calcium, phosphorus, and PTH. Although when present, brown tumor is quite pathognomonic for HPT, the histologic finding often suggests a giant cell tumor, while clinical presentation might suggest other more frequent pathologies such as metastatic tumors. Treatment of brown tumors frequently focuses on managing the underlying HPT, which can often lead to regression and resolution of the lesion, without the need for surgical intervention. However, in refractory cases or when dealing with large symptomatic lesions, surgical treatment may be necessary.

Unusual body weight loss due to primary hyperparathyroidism: A case study with literature review.

Brown tumors (osteitis fibrosa cystica) are rare pathognomonic signs that occur in patients with primary hyperparathyroidism (PHPT). Brown tumors can exist in multiple bones and can easily be misdiagnosed as a metastatic tumor or multiple myeloma. It is also localized in the forearm, humerus, and leg. The symptoms of hypercalcemia, pathologic fracture, and bodyweight loss may increase the diagnostic difficulty of brown tumors because multiple myeloma and bone metastasis also show the same symptoms. We studied a 68-year-old woman who had experienced unusual bodyweight loss in the past 6 months (56kg-40kg) and bone pain. She went to the hospital after a fall with a complaint of bone pain. An X-ray revealed a left bubbly-like cystic change and multiple fractures at the left ulna midshaft. Upon investigation, the level of intact parathyroid hormone was ascertained to be 1800 (normal: 10-60) pg/ml. Microscopically, the tumor demonstrated a benign bone lesion and was compatible with osteitis fibrosa cystica due to PHPT. The parathyroid scan (Tc-99 m sestamibi) indicated right parathyroid hyperplasia, which was later confirmed by a parathyroidectomy. She was diagnosed with osteitis fibrosa cystica associated with PHPT due to a parathyroid adenoma. PHPT can be presented with multiple fractures, bone pain, and bodyweight loss. Therefore, if a patient presents these symptoms, PHPT should be considered.

Hyperparathyroidism Jaw Tumor Syndrome, an Unforeseen Diagnosis.

Asymptomatic primary hyperparathyroidism (PHPT) is often missed in developing nations due to limited formal healthcare exposure and biochemical screening programs. Many patients are thus only diagnosed once symptomatic. We present a 32-year-old female who developed bony protrusions in her jaw during pregnancy, resulting in a stillbirth. Three months later, during a dental consultation for worsening toothache, jaw abnormalities were detected. Radiological studies revealed bilateral mandibular radiolucent lesions, and bone biopsy confirmed histological features consistent with a brown tumor. These findings raised concerns about underlying PHPT, which was confirmed with a markedly elevated parathyroid hormone level in the presence of significant hypercalcemia. Further examination revealed impaired renal function, normal urine calcium excretion, and bilateral nephrocalcinosis. Low bone mineral density was measured with dual-energy X-ray absorptiometry, and conventional radiology identified additional low-density bony lesions in keeping with brown tumors. A parathyroid MIBI confirmed the presence of a singular parathyroid adenoma. A vague but possible family history, the patient's young age, and the severe renal and skeletal involvement prompted genetic testing. A cell division cycle 73 (CDC73) pathogenic variant, in keeping with primary hyperparathyroidism jaw tumor syndrome, was identified.

Gene Polymorphism Influencing Persistent Bone Resorption in Brown Tumor: A Case Series with Possible Pathogenesis and Potential Therapeutic Approach.

Brown tumor represents a terminal stage of bone remodeling process due to an imbalance between osteoclastic and osteoblastic activity. It represents a reparative cellular process, rather than a neoplastic process mostly associated with primary or secondary hyperparathyroidism. Although parathyroidectomy is the first treatment of choice for brown tumors, several cases don't resolve even after normalization of parathyroid hormone levels which leads to surgical intervention. Therefore, to avoid multiple bone surgeries in the same patient, it is crucial to have a conservative approach like targeted therapy which could block certain molecules involved in bone resorption. In this string, we have recognized and quantified three molecules namely sclerostin, MCP-1 and CD73 in brown tumors and correlated their expression with bone resorption pathogenesis and potential therapeutic approach.

A Rare Manifestation of Secondary Hyperparathyroidism Due to Brown Tumors: A Case Report.

Purpose: Brown tumors, also known as cystic fibrosa, are rare, benign, osteolytic, fibrotic lesions of the bones that occur secondary to hyperparathyroidism. They are caused by increased osteoclastic activity leading to an abnormal bone metabolism. Case Description: Here, we present the case of a 58-year-old male, who presented with painful bony lesions, initially attributed to metastatic disease. After biochemical workout, imaging and biopsy, the nature of the lesions was revealed. We discuss the differential diagnosis and clinical management of the disease. Conclusion: Patients with brown tumors should be assessed in the differential diagnosis of bony lesions and should always be tested for hyperparathyroidism. An early diagnosis is crucial for the successful treatment of such patients.

Multiple brown tumors: a bone complication due to long-term untreated pseudohypoparathyroidism.

Bone lytic lesions are a possible complication of pseudohypoparathyroidism type 1B, in undertreated adult patients. Whole body [18F] F-fluorocholine PET/CT is a useful imaging tool to assess brown tumor progression in this context. We describe the case of a 33-year-old woman, referred for the diagnostic evaluation of lytic bone lesions of the lower limbs, in the context of asymptomatic pseudohypoparathyroidism. She had been treated with alfacalcidol and calcium during her childhood. Treatment was discontinued at the age of 18 years old because of the lack of symptoms. A femur biopsy revealed a lesion rich in giant cells, without malignancy, consistent with a brown tumor. Laboratory tests showed a parathyroid level at 1387 pg/ml (14-50). Whole-body Fluorocholine PET/CT revealed hypermetabolism of bone lesions. The final diagnosis was brown tumors related to hyperparathyroidism complicating an untreated pseudohypoparathyroidism. Genetic testing confirmed PHP type 1B. Pseudohypoparathyroidism with radiographic evidence of hyperparathyroid bone disease, is a very rare condition due to parathyroid hormone resistance in target organs, i.e., kidney resistance, but with conserved bone cell sensitivity. It has been reported in only a few cases of pseudohypoparathyroidism type Ib. Long-term vitamin D treatment was required to correct bone hyperparathyroidism. With this rationale, the patient was treated with calcium, alfacalcidol, and cholecalciferol. One-year follow-up showed complete resolution of pain, improvement in serum calcium, and regression of bone lesions on [18F]F-fluorocholine PET/CT. This case illustrates the usefulness of [18F]F-fluorocholine PET/CT for the imaging of brown tumors in pseudohypoparathyroidism type 1B, and emphasizes the importance of calcium and vitamin D treatment in adult patients, to avoid the deleterious effects of high parathyroid hormone on skeletal integrity.

Mandibular Brown Tumor Revealing Hyperparathyroidism in a Patient With Neurofibromatosis Type I: Case Report.

The brown tumor is a non-neoplastic lesion resulting from an abnormality in bone metabolism in the context of primary, secondary, or tertiary hyperparathyroidism. They can affect any bone structure and be single or multiple. They are usually located on the long bones, pelvis, ribs, and collarbones. Facial localization is rare and is found in only 4.5% of brown tumors dominated by mandibular involvement. The treatment of a brown tumor depends on several elements: etiology, location, and symptomatology. It can regress or disappear after the treatment of hyperparathyroidism, thus avoiding surgical removal. Otherwise, excision of this mass is performed. We illustrate through this case a brown mandibular tumor revealing secondary hyperparathyroidism in a patient with a history of end-stage chronic renal failure on hemodialysis and associated neurofibromatosis type 1.

Brown tumor due to primary hyperparathyroidism in a familial case: a case report.

BACKGROUND: Primary hyperparathyroidism (PHPT) is an uncommon disorder characterised by hypercalcemia with an increased parathyroid hormone level. We reported a PHPT familial case with two subjects, a father and a daughter, and both of them had suffered from the brown tumor. CASE PRESENTATION: The proband, a 43-year-old patient, developed parathyroid adenomas at the age of 15; a histologically confirmed right parathyroid adenoma was removed by parathyroidectomy; and after six months follow-up, the serum calcium level was normalised. At the age of thirty-three, a CT scan of his head and neck revealed a mass in the right maxilla, as well as PHPT (i.e., left inferior parathyroid adenoma). Then, he underwent a biopsy of an exophytic lesion in the right maxilla and was diagnosed by pathology as a brown tumor, with the serum calcium and PTH levels at 2.78 mmol/L and 221 pg/mL, respectively. Subsequently, the patient took a left inferior parathyroid microwave ablation with ultrasound guidance. After three months of follow-up, the serum calcium and PTH levels returned to normal, and the brown tumor was resolved. After three years, it mineralised as revealed in a CT scan. By the time he was 43 years old, during the 28-year follow-up period, the serum calcium and PTH levels were still within the normal range, and there was no discomfort reported. He has consistently taken calcium supplements throughout the 28 years. Since the initial diagnosis, his blood indicators of kidney function have been normal, and ultrasound showed renal calculus in the right kidney and a normal left kidney. The proband's daughter, a 15-year-old girl, experienced left upper extremity pain for ten months. CT scan revealed a mass in the distal left radius, and a giant cell tumor was suspected. A surgical internal fixation was performed, and the pathology showed a brown tumor. Laboratory tests revealed a serum parathyroid hormone (PTH) level of 1554pg/mL, calcium level of 3.14 mmol/L, phosphorus level of 0.72 mmol/L, and alkaline phosphatase level of 1892 U/L. Given the osteitic changes and elevated levels of calcium and PTH, ultrasonography was performed, after which a mass was detected measuring 19 × 9 × 7 mm mixed with solid components and cystic fluid in the right thyroid gland. The results of 99mTc-MIBI scintigraphy confirmed the abnormal accumulation of 99mTc-MIBI in the right thyroid gland but not seen in the bilateral parathyroid glands. The patient underwent thyroidectomy, and the postoperative pathology report indicated an intra-thyroid ectopic parathyroid adenoma. The serum calcium and PTH levels became normal at 4 h after surgery. One to three months after operation, the serum calcium level was low, while the serum PTH level was high. Then, the patient was advised to take calcium supplements. Until the sixth month after the operation, the serum calcium level and serum PTH level returned to normal, and the bone pain was relieved. The patient's blood tests for kidney function remained normal. There was no evidence of bilateral kidney disease (such as nephrolithiasis or nephrocalcinosis) detected by ultrasound scan. There were several similarities in the state of illness between these two subjects. Both the father and the daughter developed parathyroid adenomas at the age of 15, and there was no lesion in other endocrine glands. And genetic testing revealed mutations in the CDC73 genes in both father and daughter. On the other hand, there were also a few differences. The father's first signs of brown tumor were in the right maxilla, while the daughter's appeared in the distal left radius. The father presented pathological changes in the left and right parathyroid glands, whereas the daughter presented with an ectopic parathyroid adenoma in the right thyroid gland. CONCLUSION: We report a familial case in which father and daughter were diagnosed to have brown tumors due to parathyroid adenoma and ectopic parathyroid adenoma, and genetic testing revealed CDC73 gene mutations in both. Therefore, in the diagnostic and differential process of young patients having bone disease, clinicians should not only focus on the clinical manifestations of the skeleton, but also implement a comprehensive analysis of systemic symptoms, considering the possibility that the patient has familial PHPT.

A Rare Case of Post-parathyroidectomy Calciphylaxis in a Young Patient With End-Stage Renal Disease: A Case Report and Literature Review.

Calciphylaxis is a serious complication in chronic kidney disease (CKD) patients and requires a multidisciplinary approach. Dialysis patients are the most affected, especially those who are obese and diabetic, have liver diseases and autoimmune diseases, or are on systemic glucocorticoids. Parathyroidectomy (PTx) is curative for secondary hyperparathyroidism (SHPT) and calciphylaxis in most cases. Calciphylaxis after parathyroidectomy is a rare presentation. We present a case of a young patient who developed calciphylaxis after parathyroidectomy, an uncommon presentation.

Brown tumor of the jaw as a rare manifestation of hyperparathyroidism: Two case reports and literature review.

INTRODUCTION AND IMPORTANCE: Brown tumor is a giant cell focal lesion of bone associated with hyperparathyroidism, even primary or secondary. Differential diagnosis of these lesions from others giant cell lesions of the jaw bone is mandatory for the correct treatment of the patient. CASE PRESENTATION: We present here two cases of brown tumor affecting the jaws by describing their clinical aspects and radiographic features, diagnostic criteria and treatment of this disease. CLINICAL DISCUSSION: Brown tumor is one of the lesions that develop in patients with hyperparathyroidism or renal failure. Skeletal bones including maxillo-facial ones can be the site of this lesion, also radiographic and histopathological exams of the jaw lesion are not sufficient to determine the diagnosis, which requires laboratory tests and radiographic examination. CONCLUSION: Dental surgeon should be aware of oral manifestations associated with systemic diseases, hence the importance of careful physical examination and thorough investigation for the diagnosis and treatment success. This article aims to illustrate the management strategy to aid clinicians in suspected cases of brown tumor.

The value of integration of bone scan and targeted SPECT/CT in diagnosis of primary hyperparathyroidism with multiple bone brown tumor.

Although parathyroid bone disease is rarely seen nowadays, skeletal manifestation can be the first sign of hyperparathyroidism (HPT) in some clinical practice. Nevertheless, the diagnosis of HPT is often overlooked. We describe three cases of multiple brown tumors (BT) in which bone pain and destruction were the first symptoms that masqueraded as a malignancy. However, according to the results of bone scan and targeted single-photon emission computed tomography/computed tomography (SPECT/CT), we considered BTs as the diagnosis in all of three cases. The final diagnoses were confirmed by laboratory tests and post-parathyroidectomy pathology. Parathyroid hormone (PTH) is significantly elevated in primary hyperparathyroidism (PHPT) as we know. However, such elevation is virtually never seen in malignancies. Diffuse or multiple foci of tracer uptakes in the bone scan were always seen in bone metastasis, multiple myeloma, and other bone neoplasm. When patients visited nuclear medicine for first consultation without biochemical results, radiological evidence from planar bone scan and targeted SPECT/CT can help in distinguishing the skeletal diseases. Lytic bone lesions with sclerosis, intra-focal or ectopic ossification and calcification, fluid-fluid level, and distribution of the lesions may be helpful in the differential diagnosis in these reported cases. In conclusion, when patients present with multiple foci of uptake on bone scan, targeted SPECT/CT is acquired for suspicious lesions, which can increase the diagnostic sensitivity and reduce unnecessary interventions and treatment. Moreover, BTs should be always kept in differential diagnosis of multiple lesions without a conclusive primary tumor.

A rare case of "Brown tumor" of the axis with parathyroid adenoma and tertiary hyperparathyroidism.

"Brown tumors (BTs)" of the spine are benign rare lesions, seen in about 5%-13% of all patients with chronic hyperparathyroidism (HPT). They are not true neoplasms and are also known as osteitis fibrosa cystica or occasionally osteoclastoma. Radiological presentations are often misleading and may mimic other common lesions such as metastasis. A strong clinical suspicion is therefore necessary, especially in the background of chronic kidney disease with HPT and parathyroid adenoma. Surgical spinal fixation in case of instability due to pathological fracture may be required along with excision of the parathyroid adenoma being the treatment of choice, that maybe usually curative and carries a good prognosis. We would like to report one such rare case of BT involving the axis, or C2 vertebra, presenting with neck pain and weakness that was treated surgically. Only a few cases of spinal BTs have been reported so far in the literature. Involvement of cervical vertebrae and in particular C2 is rarer still with the one in this report only being the fourth such case.

Multiple Brown Tumors in Primary Hyperparathyroidism Causing Pathological Fracture: A Case Report of a 21-Year-Old Adult Male.

Multiple brown tumors are more common in females and older age groups and an unlikely site is the long bones. We report a case of a 21-year-old male presenting with a pathological fracture at the left neck of the femur. Laboratory investigations showed elevated parathyroid hormone (PTH) and serum calcium levels (PTH-dependent hypercalcemia). A CT scan revealed multiple osteolytic lesions in the pelvis and femurs, and a Tc-99m sestamibi scan showed a solitary parathyroid adenoma. We demonstrate this rare case and illustrate the importance of the consideration of multiple brown tumors in young males presenting with multiple osteolytic lesions at the long bones in the differential diagnosis. Every physician needs to have a high clinical suspicion of primary hyperparathyroidism innovation, in those who present with osteolytic lesions, with respect to the patient's age and gender.

Spinal cord compression caused by a brown tumor secondary to primary hyperparathyroidism.

Background: Brown tumors (BTs) are rare non-neoplastic lesions that arise secondary to hyperparathyroidism largely involving mandible, ribs, pelvis, and large bones. Spinal involvement is extremely rare and may result in cord compression. Case Description: A 72-year-old female with the primary hyperparathyroidism developed a thoracic spine BT causing T3-T5 spinal cord compression warranting operative decompression. Conclusion: BTs should be included in the differential diagnosis in lytic-expansive lesions involving the spine. For those who develop neurological deficits, surgical decompression may be warranted followed by parathyroidectomy.