Misdiagnosis of brown tumour caused by primary hyperparathyroidism: a case report with literature review.

BACKGROUND: Brown tumour is a rare tumour-like lesion of the bone, which is considered as an end-stage lesion of abnormal bone metabolism caused by persistently high parathyroid hormone (PTH) levels. Brown tumour can be found in any part of the skeleton; in some cases, it can occur in multiple bones and can be easily misdiagnosed as a metastatic tumour. CASE PRESENTATION: We report the case of a 44-year-old man who presented to the Department of Oncology in our hospital with a 2-month history of local pain in his left shoulder joint. The initial diagnosis was an aneurysmal bone cyst by biopsy, for which the patient underwent tumour resection surgery. The diagnosis of a malignant tumour was made again following postoperative pathological examination. The pathological sections and all clinical data were sent to the Department of Pathology of the First Affiliated Hospital of Sun Yat-sen University; the diagnosis made there was brown tumour. His blood PTH level was 577 pg/ml (15-65 pg/ml). Colour Doppler ultrasonography of the parathyroid gland suggested a parathyroid adenoma. For further treatment, the left parathyroid adenoma was removed by axillary endoscopic resection. Postoperatively, a pathologic examination was performed, and the diagnosis of a parathyroid adenoma was confirmed. One year after the surgery, the left humerus was completely healed, and the left shoulder joint had a good range of movement. CONCLUSIONS: In summary, histopathological diagnosis is not sufficient for the diagnosis of brown tumours. A comprehensive analysis combining clinical symptoms with findings of imaging and laboratory tests is also required. Generally, the treatment of brown tumour includes only partial or complete resection of the parathyroid glands. However, when the tumour is large, especially when it involves the joint, surgery is indispensable.

Coexistence of brown tumors due to secondary hyperparathyroidism and prostate cancer in a patient.

We present the case of a 65-year-old man with brown tumors due to secondary hyperparathyroidism. Magnetic resonance imaging of the pelvis showed multiple lesions with expansive bone appearance. Additionally, prostate cancer was diagnosed during this time. For this reason, differential diagnosis was performed through biopsy of the right iliac bone lesion. Brown tumors are caused by osteoclastic activity and fibroblast proliferation; the differential diagnosis of these bone lesions includes giant tumors, metastases, Paget's disease, and paraneoplastic syndrome with high levels of parathyroid hormone-related peptide (PTHrP). This case report describes the coexistence of two pathologies that could explain these images. In this report, we present a case of a 65-year-old man with brown tumors due to secondary hyperparathyroidism and prostate cancer. In this setting, histologic confirmation is recommended.

Primary hyperparathyroidism presenting as a brown tumor in the mandible: a case report.

BACKGROUND: Primary hyperparathyroidism is characterized by hypercalcemia and elevated or inappropriately normal serum levels of parathyroid hormone. Brown tumor of bone is a rare non-neoplastic lesion resulted from abnormal bone metabolism in hyperparathyroidism. However, nowadays, skeletal disease caused by primary hyperparathyroidism is uncommon. We report a case of brown tumor in the mandible as the initial exhibition of primary hyperparathyroidism associated with an atypical parathyroid adenoma. CASE PRESENTATION: The patient was a 49-year-old female, she had a pain mass on the right mandible a year ago and was treated with root canal therapy and marginal resection. After seven months, the mass recurred and enlarged. Enhanced CT scan, laboratory examination, Ultrasonography, 99mTc-MIBI SPECT-CT scintiscan and pathological examination were used to confirm the diagnosis of brown tumor. The patient's symptom improved after parathyroidectomy. CONCLUSIONS: 99mTc-MIBI SPECT/CT scintigraphy is a highly sensitive examination of the localization diagnosis of hyperparathyroidism. Brown tumors should be considered in the differential diagnosis of osteolytic lesions to avoid unnecessary and harmful interventions.

Severe hypercalcemia and a pelvic brown tumor in an adolescent with primary hyperparathyroidism: a case report.

BACKGROUND: Primary hyperparathyroidism may present in a myriad of manners, varying from an incidental asymptomatic biochemical finding to gastrointestinal, psychiatric, renal, and bone manifestations. While hyperparathyroidism remains a rare diagnosis in the pediatric population, the initial approach to diagnosis and management of hypercalcemia in children is imperative for the general pediatrician. Herein, we describe an adolescent who presented with a lytic bone lesion and severe, symptomatic hypercalcemia due to primary hyperparathyroidism. CASE PRESENTATION: A 14-year-old male presented with vomiting, constipation, abdominal pain, and lethargy. He had an elevated total corrected calcium of 4.3 mmol/L. He was found to have a large pelvic lytic tumor consistent with a brown tumor due to primary hyperparathyroidism. He received pharmacologic therapy for stabilization of his hypercalcemia, including intravenous saline, intravenous bisphosphonates, and calcitonin. He subsequently received definitive therapy via parathyroidectomy and his post-operative course was complicated by hungry bone syndrome. Long-term follow-up has found full resolution of the lytic lesion and restored calcium homeostasis. CONCLUSIONS: We present this case to highlight the possible presentations of hypercalcemia and hyperparathyroidism that are essential for a general pediatrician to recognize to ensure prompt diagnosis and management. Evaluation for hypercalcemia should be considered in patients with suggestive symptoms and physical exam findings. To our knowledge, this patient represents the first reported pediatric case of a pelvic brown tumor in an adolescent. While the multi-systemic complications of hyperparathyroidism may be quite severe, swift and appropriate management may mitigate these clinical outcomes.

[Disseminated osteolytic lesions in a 28-year-old refugee]. / Disseminierte osteolytische Läsionen bei einem 28-jährigen Flüchtling.

A 28-year-old Syrian refugee presented with right-sided knee pain and progressive deterioration of the general condition over the past months. Laboratory diagnostics revealed severe hypercalcemia due to primary hyperparathyroidism, and computed tomography (CT) scanning demonstrated disseminated osteolytic lesions throughout the skeleton. Histologically, these lesions were characterized by multinuclear giant cells (defining these lesions as so-called brown tumors). Finally, surgical removal of a jugular mass allowed the histopathologic diagnosis of a sporadic parathyroid carcinoma. In the patient, this condition was associated with a mutation in the HPRT2 gene locus.

Bone histomorphometry and indicators of bone and mineral metabolism in wait-listed dialysis patients.

AIMS: The aim of this study was to evaluate the associations between bone histomorphometry and bone volume measured by dual-energy X-ray absorptiometry (DXA) in wait-listed dialysis patients. Further, the circulating markers of mineral metabolism and bone turnover were compared. MATERIAL AND METHODS: Bone biopsies were performed on 61 wait-listed dialysis patients. Plasma samples were obtained for indicators of mineral metabolism and bone turnover. Bone mineral density (BMD) was determined by DXA and bone histomorphometry was performed. RESULTS: Bone histomorphometry could be determined in 52 patients (72% men, 54% on hemodialysis and median dialysis vintage 18 months). Adynamic bone disease was present in 21% of patients and 4% had osteomalacia. High turnover bone disease (mixed uremic osteodystrophy and osteitis fibrosa) was observed in 48% of patients (17% and 31%, respectively). 10% of patients had normal bone histomorphometry while 17% had mild osteitis fibrosa. Mineralization defect was found in 33% of patients. There was a strong correlation between femoral neck (FN) T-score and histologically measured cancellous bone volume (p = 0.004), FN T-score having a good negative predictive value for low cancellous bone volume. Plasma osteocalcin levels were significantly higher in the high-turnover group and lower in the mineralization defect group (p = 0.014 and p = 0.02, respectively). CONCLUSIONS: Our study confirms the high frequency of abnormal bone histology in wait-listed dialysis patients. Low bone turnover was less common than previously reported. Noninvasive markers had a limited value for assessing bone histology, whereas femoral BMD reflected bone volume well.

Giant cell tumor of bone in a patient with diagnosis of primary hyperparathyroidism: a challenge in differential diagnosis with brown tumor.

Giant cell lesions of bone share similar clinical, radiological, and histological features. The most challenging differential diagnosis is between giant cell tumor (GCT) and brown tumor (BT) secondary to hyperparathyroidism. Differential diagnosis is based on determining serum calcium concentration and other markers of calcium metabolism. The authors present the unusual case of a 37-year-old Caucasian woman affected by a GCT of the proximal left tibia and concomitant asymptomatic primary hyperparathyroidism (PHPT) due to a parathyroid adenoma. The presence of two concurrent diseases complicated diagnosis and relative treatment. The patient was first treated for the adenoma, then after 9 months, she underwent curettage of tibial GCT. Denosumab treatment was administered for 12 months to control a relapse occurring at 15 months post-curettage. At 32-month follow-up from primary tibial surgery, the patient was free from tumor disease. To our knowledge, this is the first case in the literature reporting the concomitant presence of asymptomatic PHPT and GCT. The possibility of concomitant finding these two diseases has to be considered during the decision-making process.

Computed tomography and magnetic resonance imaging of maxillofacial lesions in renal osteodystrophy.

PURPOSE: This study aims to describe the computed tomography (CT) and magnetic resonance (MR) imaging appearance of maxillofacial lesions in renal osteodystrophy. PATIENTS AND METHODS: We retrospectively reviewed the CT and MR imaging of maxillofacial region in 9 patients (6 females and 3 males with mean age of 31 yr) with renal osteodystrophy. They presented with facial swelling (n = 6), facial disfigurement (n = 2), and oral cavity mass (n = 1). They underwent CT and MR imaging of the maxillofacial region. RESULTS: Brown tumors (n = 6) were seen in the mandible (n = 4) and maxilla (n = 2). They appeared as mixed lytic and sclerotic (n = 4) and sclerotic (n = 2) lesions at CT. The lesions appeared as hypointense at T1-weighted images and of mixed signal intensity at T2-weighted images with intense contrast enhancement (n = 6). Uremic leontiasis ossea (n = 2) appeared at CT as diffuse hyperostosis with protruded maxilla and obliterated sinus. At MR imaging, there was expansion of the maxilla with obliteration of the maxillary sinuses and protrusion of the mandible. The lesion exhibited low signal intensity at T1-weighed images. At T2-weighted images, the lesion showed low signal intensity with small hyperintense lesions. Dystrophic calcification (n = 2) was seen in the parotid and the check. CONCLUSION: We concluded that CT and MR imaging are helpful for diagnosis and treatment planning of maxillofacial lesions of patients with renal osteodystrophy.

Parathyroid adenoma diagnosed on the basis of a giant cell tumor of parieto-occipital region and multifocal bone injuries.

Brown tumors are rare skeletal manifestations of hyperparathyroidism (HPT) that may mimic cancer metastases. Histopathologically, they are difficult to differentiate from other giant cell lesions. A case is presented of 41-year-old woman with giant cell tumor in parieto-occipital region with injury of external bone lamina, growing into the skull cavity. The mass was suspected of being neoplastic. Numerous osteolytic lesions in the skull skeleton and multifocal bone injuries were observed, also. Elevation in calcium (5.91 mEq/L) and parathormone (1188 ng/mL) concentrations and hypercalciuria (52 mEq/24 h) suggested the diagnosis of HPT initially manifesting as a brown tumor of the skull. Further exploration confirmed the existence of parathyroid adenoma as a cause of the disease. The key treatment for the condition was surgical excision of the adenoma followed by the normalization of parathyroid function and significant reduction in size of skull tumor and other lesions.

Clinical aspects of primary hyperparathyroidism: clinical manifestations, diagnosis, and therapy.

Primary hyperparathyroidism (PHPT) is the most common cause of hypercalcemia. An autonomous overproduction of parathyroid hormone leading to hypercalcemia, which is not downregulated by the calcium-sensing receptor, is the pathophysiological basis of the disease. The classical manifestations of PHPT include a generalized bone disease, kidney stones, and nephrocalcinosis, gastrointestinal, cardiovascular, neuromuscular and neuropsychiatric symptoms. Recently, the clinical presentation of PHPT, however, has changed in Western countries, it occurs oligo-asymptomatic in up to 80 %. Clinical examination, laboratory, and imaging techniques for the characterization of the disease and the localization include the diagnostic procedure. If possible, parathyroidectomy is the treatment of choice for clinically overt PHPT, for asymptomatic PHPT guidelines were developed in order to decide in individual cases between surgical and conservative approach; this consists of monitoring, adequate calcium and vitamin D intake, as well as hydration. Medical therapy includes bisphosphonates and calcimimetics.

Brown tumor of the cervical spine with primary hyperparathyroidism: A case report and literature review.

RATIONALE: Brown tumor (BT), an uncommon focal lytic bone tumor, is a non-neoplastic and reactive process caused by increased osteoclastic activity and fibroblastic proliferation in primary or secondary hyperparathyroidism. Vertebral tumor causing neural compression is relatively rare, especially in the cervical spine. PATIENT CONCERNS: A 29-year-old man developed neck pain and arm radicular pain 4 months ago, with the level of serum calcium significantly higher than normal. Computed tomography scan of the cervical spine revealed an expansile lytic lesion occupying the C6 body, left pedicle, and left lamina of C5-6. DIAGNOSES: Osteoclastoma according to imaging and histopathological results. INTERVENTIONS: A laminectomy of C5-6 was performed. OUTCOMES: One month later, he was re-hospitalized due to nausea and vomiting and the serum calcium, was still, kept at a high level. Additionally, the parathormone (PTH) was greatly higher than normal. BT with primary hyperparathyroidism due to the parathyroid tumor was considered. After the surgery of the right parathyroid gland was performed, serum calcium and PTH both decreased, and computed tomography showed good recovery. LESSONS: BTs might be misdiagnosed as other giant cell tumors, thus when giant cell tumors are considered, serum calcium and PTH examination may be needed to exclude BTs.

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.

Manifestations of hyperparathyroidism in the jaws: Concepts, mechanisms, and clinical aspects.

Hyperparathyroidism is one of the most common endocrine disorders worldwide. In countries where routine biochemical screening is not common, symptomatic hyperparathyroidism predominates. Its manifestations include skeletal alterations, calcification of soft tissues, kidney stones, and functional alterations in other systems. Notably, jaw alterations can be the first clinical sign of hyperparathyroidism, including brown tumor, renal osteodystrophy, osteitis fibrosa, and leontiasis ossea, and knowing such conditions is of core importance for the multidisciplinary diagnosis and management of hyperparathyroidism. We aimed to perform a concise review, systematizing the concepts and mechanisms underlying hyperparathyroidism and associated gnathic alterations. In addition, a detailed description of the clinical aspects of the jaw manifestations is presented.

[The case of late diagnosis of giant parathyroid adenoma in combination with fibrocystic osteitis and brown tumor of the upper jaw: a case report].

In this case report the authors inform about late diagnosis of giant adenoma of the parathyroid gland with primary hyperparathyroidism (PHPT) and the development of fibrocystic osteitis with a «brown¼ tumor of the upper jaw. The patient has been under the care endocrinologist with type 2 diabetes mellitus and multinodular goiter for 8 years.The last 5 years there was a clinical manifestation of PHPT, but the diagnosis was made by an oncologist after the detection of a «brown¼ tumor of the upper jaw. According to multispiral computed tomography and scintigraphy with 99mTc-MIBI, a focal lesion was found in the upper jaw on the right, lytic foci in the bones of the cranial vault, pelvis, lower extremities, ribs on the right, as well as a giant parathyroid adenoma on the right. According to the increased risk of the patient having a malignant neoplasm of the parathyroid gland, an extended surgical treatment of PHPT in the enblock volume was carried out with the achievement of remission of the PHPT. This clinical case illustrates a variant of the severe course of PHPT with the development of such a rare complication as fibrocystic osteitis and demonstrates the importance of timely diagnosis.

Missed brown tumors in a young adult with decreased bone density.

Brown tumors, a benign osteolytic process, are most commonly caused by hyperparathyroidism. Multiple bone involvement is relatively rare. There are many similarities in the radiologic and histological features of brown tumors and giant cell tumors (GCTs) of bone. Differentiation between the two lesions is dependent upon evaluation of serum biochemistry including serum calcium, phosphorous, and intact parathyroid hormone (I-PTH) levels. Herein, the case of a 32-year-old man with multiple osteolytic lesions of the left tibia and fibula as well as the fourth metacarpal bone of the left hand, previously misdiagnosed with multiple GCTs, is presented. Based on the radiographic findings and biochemistry results in a young adult patient, brown tumor was suspected and subsequently definitively diagnosed.

[Overlooked primary hyperparathyroidism presented with fractures: case report]. / Kiriklarla gelen atlanmis primer hiperparatiroidi olgusu: Olgu Sunumu.

In the present paper, we report a female patient with multiple cystic lesions of bone arising from the primary hyperparathyroidism and pathological femur and contralateral tibia fractures at the level of these cystic lesions (osteitis fibrosa cystica). The patient's history revealed that she was admitted to a medical center with vague symptoms such as sudden onset of dyspepsia, loss of appetite, myalgia, arthralgia, fatigue, and weight loss six years ago but no disease was diagnosed. Loss of appetite and loss of weight continued. She had been walking only by assisted ambulation for the last year. However, primary hyperparathyroidism was overlooked until our examination. The fractures were managed by interlocking nailing and grafting after confirming with biopsy that the fractures were due to osteitis fibrosa cystica. The fractures healed uneventfully. In conclusion, it is essential to evaluate patients with these vague symptoms with full biochemical screening and radiological examination for the early detection of the disease.