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.

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.

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.

Primary Hyperparathyroidism Mimicking Skeletal Metastasis - A Diagnostic Dilemma.

Introduction: Primary hyperparathyroidism (PHPT) is an intrinsic abnormality of the parathyroid glands in which there is an inappropriate secretion of parathormone (PTH), resulting in skeletal resorption and bone loss. The characteristic bony changes of fibrotic cystic lesions are called Brown's tumors. Clinical dilemmas exist due to the varied clinical presentation of hypercalcemia with multiple lytic lesions mimicking metastatic bone disease. The 99 mTc sestamibi scanning is the imaging modality of choice used for the preoperative localization of parathyroid adenomas. Surgery provides a definitive treatment, and the bony lesions resolve completely over a period of time. Case Report: We present four cases of PHPT where they presented with multiple lytic lesions and were evaluated for metastatic deposits. The diagnosis was confirmed with a biopsy. They were successfully treated by excision of the parathyroid gland. A high index of suspicion will avoid misdiagnosis and inappropriate treatment. Conclusion: PHPT must be considered as a differential diagnosis for multiple osteolytic bone lesions. Diagnosis can be aided by a thorough clinical examination, including an assessment for neck swelling, and laboratory testing of serum calcium levels and PTH levels. Surgical excision of the hyperactive gland serves as the definitive treatment for this condition, with bony lesions regressing gradually over time.

Brown Tumors of the Jaws: A Retrospective Study.

Objectives: (1) Describe the clinical spectrum, imaging features, management, and outcome of brown tumors (BT) of the jaws. (2) Determine via a literature review the facts and controversies around the characteristics and management of this lesion. Materials and methods: Our study was approved by the institutional committee of Sahloul University Hospital in accordance with the ethical standards of the Declaration of Helsinki. Sixteen patients with BT in the context of a primary, secondary, and tertiary hyperparathyroidism were treated and followed up during their recovery. Results: This study reports 16 patients with a mean age of 48 years old. Brown tumor lesions were associated with primary hyperparathyroidism in 6 cases (38%), secondary hyperparathyroidism to chronic kidney failure in 5 cases (31%), and tertiary hyperparathyroidism in the context of a long lasting CRI in 5 cases. Their location was maxillary in 7 cases, mandibular in 5 cases, and bimaxillary in 4 cases. The treatment consisted of parathyroidectomy in 13 patients, maxillary resection in 3 cases, and vitamin D treatment in 2 cases. Favorable outcomes, characterized by tumor regression, were reported in 9 cases, whereas unfavorable evolution was observed among 7 patients. Conclusion: Parathyroidectomy is the gold standard treatment for primary hyperparathyroidism. It resulted in a total regression in all our cases. Regarding secondary hyperparathyroidism, blood screening and chronic renal insufficiency follow-up are critically valuable to detect this condition at an early stage, hence increasing the success rate of brown tumor regression. Our secondary and tertiary hyperparathyroidism results were miscellaneous; although it is important to emphasize the importance of the chronic renal insufficiency management to ensure a success. Clinical relevance: Brown tumors should be included in the differential diagnosis of giant cell lesions. Parathyroidectomy is usually sufficient to induce the total regression of the lesion in primary hyperparathyroidism cases. A more delicate approach is needed regarding secondary hyperparathyroidism. Meticulous control of chronic renal insufficiency is mandatory in addition to parathyroidectomy.

Widespread presentation of brown tumors mimicking multiple myeloma.

Brown tumors or osteitis fibrosa cystica has become a rare presentation of primary hyperparathyroidism in up-to-date clinical practice. Here, we describe a case of longstanding untreated hyperparathyroidism presenting itself with brown tumors in a 65-year-old patient. During the diagnostic work-up of this patient, bone SPECT/CT and 18F-FDG-PET/CT revealed multiple widespread osteolytic lesions. Differentiating from other bone tumors such as multiple myeloma is challenging. In this case, the final diagnosis was made by integrating the medical history, biochemical diagnosis of primary hyperparathyroidism, pathological findings and medical imaging.

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.

Large parathyroid adenomas: Potential mechanisms to reconcile adenoma size and disease phenotype.

Parathyroid adenomas weighing more than 3.5 g are reported variously as "atypical", "large" or "giant" parathyroid adenomas. All such adenomas are rare variants accounting for no more than 1.5% of all parathyroid adenomas. Large parathyroid adenomas are often associated with more severe form of the disease, including osteitis fibrosa cystica (OFC) and share many biochemical, histological, and molecular features of both benign and malignant parathyroid neoplasms, and are considered a distinct clinical entity. However, the pathogenesis of oversized parathyroid adenomas and the often-associated skeletal phenotype remains unclear. We present 5 cases of primary hyperparathyroidism (PHPT) with OFC, an uncommon manifestation of contemporary PHPT, associated with larger parathyroid adenomas, seen in the Bone and Mineral Disorders Clinic of the Henry Ford Health in the last 30 years to illustrate the critical role of vitamin D nutrition in the pathogenesis of both the OFC and adenoma size. The estimated prevalence of OFC was very low 0.2%, 5 of the >3000 surgically confirmed cases of PHPT seen during this time. The mean ± SD values were: age: 36.8 ± 22.1 years (4 of the 5 <36years), serum calcium 11.6 ± 1.1 mg/dl, alkaline phosphatase 799 ± 487 IU/L, PTH 1440 ± 477 pg/ml, 25-hydroxyvitamin D 13.0 ± 8.9 ng/ml, 1,25-dihyroxyvitamin D 26.5 ± 13.7 pg/ml, urine calcium 562 ± 274 mg/day, and parathyroid adenoma weight 4.53 ± 2.2 g. Parathyroidectomy led to the resolution of both the biochemical indices and OFC in each patient without recurrence over >10 years of follow-up. Because OFC is a very rare in the West, but very common areas of endemic vitamin D deficiency, we also examined the relationship between vitamin D nutrition, as assessed by serum 25-hydroxyvitamin D level, and parathyroid adenoma weight as well as prevalence of OFC in two large secularly diverse cohorts of patients with PHPT (Detroit, USA and Chandigarh, India). Based on this relationship and the relative prevalence of OFC in these two large cohorts, we propose that vitamin D nutrition (and perhaps calcium nutrition) best explains both the adenoma size and prevalence of OFC.

Secondary Hyperparathyroidism Presenting as a Brown Tumor: A Case Report and Review of the Literature.

Severe secondary hyperparathyroidism in advanced stages of chronic kidney disease (CKD) is associated with CKD-related mineral and bone disease (CKD-MBD). A 70-year-old woman was admitted at the Hospital for generalized bone pain and peripheral edema. Initial laboratory tests revealed normocytic anemia and severe renal dysfunction, and further tests evidenced severe secondary hyperparathyroidism. Full-body computerized tomography showed an osteolytic lesion in the right iliac wing. The iliac bone lesion was biopsied and histological examination was consistent with the diagnosis of a brown tumor of hyperparathyroidism. Brown tumors are a rare variant of osteitis fibrosa cystica that results from sustained high levels of parathyroid hormone in CKD. This case sheds light on rare complications that are experienced today in CKD. The clinical and biochemical setting, as well as the clinical suspicion, are essential to the diagnosis.

Occult Pulmonary Neuroendocrine Tumor Causing Severe Hyperparathyroidism: Diagnostic Challenges and Clinical Outcomes.

Background/Objective: Ectopic tumoral production of parathyroid hormone (PTH) is rare. The incidence of hyperparathyroidism and osteitis fibrosa cystica (OFC) secondary to ectopic PTH secretion has only been reported in case reports, although infrequent. Case Report: We report a case of a well-differentiated pulmonary neuroendocrine tumor (NET) producing PTH that presented with severe hypercalcemia and OFC. Surgical removal of the pulmonary tumor resulted in resolution of hypercalcemia. Immunocytochemical analysis of the tumor tissue revealed PTH-positive staining. Recovery was complicated by severe hypocalcemia due to hungry bone syndrome. Discussion: To the best of our knowledge, this is the first documented case of a pulmonary NET causing OFC via PTH. We further describe the successful identification and resection of a rare NET and restoration of calcium homeostasis with aggressive calcium and vitamin D repletion. Conclusion: Although a rare cause of severe hypercalcemia and OFC, ectopic tumoral production of PTH must be considered in the differential diagnosis. Furthermore, resection of these tumors secreting PTH can lead to a protracted and severe high risk of hungry bone syndrome, which requires aggressive treatment to maintain calcium homeostasis.

Osteitis Fibrosa Cystica; A Forgotten Manifestation of Secondary Hyperparathyroidism Due to End-Stage Renal Disease: A Case Report.

Introduction: Osteitis fibrosa cystica is a rare complication of secondary hyperparathyroidism. Even though it is thought to be a disease of the past, it still continues to be seen in this modern era in the setting of undiagnosed or untreated chronic kidney disease. Case Presentation: A 26-year-old married Ethiopian women presented with 4 year history of progressive proximal weakness of extremities and diffuse bone pain. Physical examination revealed diffuse bone tenderness and features consistent with myopathy. Blood work up showed raised creatinine, markedly elevated PTH, borderline low calcium, and vitamin D in severe deficiency range. X-Ray findings were consistent with classical skeletal lesion of severe secondary hyperparathyroidism. Conclusion: Osteitis fibrosa cystica is a rare but still frequent complication of secondary hyperparathyroidism, which may be the initial presentation of chronic kidney disease. This case report emphasizes the importance of considering secondary hyperparathyroidism in patients presenting with weakness and bone pain to allow for early diagnosis, treatment, and improvement of overall prognosis.

Brown tumor of hyperparathyroidism with multiple lesions.

Brown tumors are rare focal giant-cell lesions that arise as a direct result of the effect of parathyroid hormone (PTH) on bone tissue in some patients with hyperparathyroidism. Browns tumor is a syndrome associated with an increase in PTH levels by parathyroid glands resulting in hypercalcemia. In the present case report, a 44-year-old female patient presented with a rare case of brown tumor with multiple lesions in the head-and-neck region. The recent advance in various diagnostic and biochemical tests helps in early diagnosis of hyperparathyroidism cases. The dentist should be aware of oral manifestations associated with this type of systemic disease.

A patient with femoral osteitis fibrosa cystica mimicking bone neoplasm: a case report.

BACKGROUND: Osteitis fibrosa cystica is a rare, benign and osteolytic lesion attributed to hyperparathyroidism. The high level of parathyroid hormone cause rapid bone loss. CASE PRESENTATION: The patient is a 50-year-old male complaining of severe and persistent pain in the right knee joint. Imaging studies were suspicious for a benign tumor in the right distal femur. Biopsy under CT guidance showed numerous osteoclast aggregation and hemosiderin deposition around the bone trabeculae. Blood tests disclosed significantly elevated parathyroid hormone, serum calcium, serum alkaline phosphatase. Parathyroid ultrasonography and CT scan showed a solid mass in front of the trachea at the thoracic entrance plane. After resection of the mass, the clinical symptoms were relieved and the radiological results were significantly improved, which further confirmed the diagnosis. CONCLUSIONS: Metabolic diseases-associated bone lesions require a comprehensive diagnosis of multiple inspection items. An interprofessional team approach to the diagnosis and treatment of osteitis fibrosa cystica will provide the best outcome.

Revisiting the Case of Sarah Newbury's Death from Mollities Ossium.

Multiple myeloma and its precursor and variant types represent some of the most common hematologic malignancies in adults. These plasma cell dyscrasias are well-known in modern medicine. There are well-established clinical, laboratory, and pathologic criteria for diagnosis and staging. There is debate about the diagnosis of some of the earliest cases of myeloma described in the literature. We present a critical review of one such case.

Primary hyperparathyroidism misdiagnosed as metastatic disease, with trans-oral endoscopic surgical management.

Primary hyperparathyroidism is not so uncommon a disease. In high-income countries, with the introduction of routine biochemical testing in 1980s, it is diagnosed early, and the majority are seen as asymptomatic disease. However, in India, a severe symptomatic form is still seen, and many times patients are undiagnosed, thus continuing to suffer debilitating disease. Here, we report such a patient who was being treated as having bony metastases from an unknown primary source, when in fact he had osteitis fibrosa cystica due to primary hyperparathyroidism and was cured after surgery.

Sporadic Primary Hyperparathyroidism.

Sporadic primary hyperparathyroidism is a common endocrinopathy, particularly afflicting postmenopausal women and both African American men and women. Although classic signs and symptoms of the disease are well appreciated and described, because of the ease and availability and low threshold for screening, the disorder often is diagnosed in patients who are minimally symptomatic or asymptomatic. Surgery conducted by experienced endocrine surgeons has a high cure rate, particularly if guided by concordant imaging. In patients who cannot safely undergo surgery or who fail to be cured, medical therapy with the oral calcimimetic cinacalcet is a validated option for controlling serum calcium levels.

Brown Tumor With Spine Involvement at Multiple Levels in a Hemodialysis Patient.

Brown tumor of the bone or osteitis fibrosa cystica is a rare manifestation of hyperparathyroidism, most seen nowadays in association with secondary and tertiary hyperparathyroidism. Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are the major culprits of secondary hyperparathyroidism (sHPTH). CKD is known to cause phosphate retention and a decrease in 1,25-dihydroxyvitamin D and ionized calcium levels, which in turn trigger the PTH secretion. Brown tumor can affect the jawbones, femur, sternum, ribs, and rarely the spine. We present the case of a 60-year-old male with ESRD on hemodialysis who was found to have lytic bone lesions in the thoracic and lumbar spine. Initially, malignancy was suspected. Blood work revealed markedly elevated PTH at 3,563 pg/mL, hypocalcemia, and hyperphosphatemia. Biopsy of the L5-S1 lesion was consistent with reactive changes due to sHPTH. Once a diagnosis of the brown tumor was confirmed, the patient was started on cinacalcet and was referred for parathyroidectomy.

Multiple brown tumors-Forgotten pathology in times of calcimimetics: A case report and literature review.

Multiple brown tumors represent a rare variant of osteitis fibrosa cystica. Brown tumors are associated with primary, secondary, or tertiary hyperparathyroidism. Brown tumors have been reported in patients with chronic kidney disease resulting in mineral and bone disorders. Chronic kidney disease resulting in mineral and bone disorder is a result of increased osteoclast activity and excessive production of parathormone due to parathyroid gland hyperactivity. Brown tumors are frequently overlooked in patients with end-stage renal disease since calcimimetics and vitamin D analogs were introduced as pharmacological therapy for secondary hyperparathyroidism. We present a case of a 79 year-old pre-dialysis woman, with multiple brown tumors secondary to a parathyroid adenoma despite being treated with cinacalcet for secondary hyperparathyroidism. In addition, we review the corresponding literature.

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.