A 24-year-old male presented with history of slowly growing right-sided scalp swelling noticed a few months back and left upper and lower limb weakness of 3 days duration. He also gave a history of abdominal pain and distension as well as intermittent leg pain. There was no history of fever or trauma and he had no other relevant medical history.
CT (computed tomography) and MRI (magnetic resonance imaging) of the skull (Fig 1a, 1b,2,3) revealed a large multiloculated lytic expansile lesion in the right parietal bone with smooth enhancing septations and fluid-fluid levels inside the locules. Marked thinning of the inner and outer cortices was seen, with a few areas of defects in the outer cortex. No obvious periosteal reaction, matrix mineralization, or extraosseous soft tissue component was seen. The fluid levels appeared slightly hyperdense on CT, hypointense on T2, and hyperintense on T1 weighted images, corresponding blooming on the susceptibility-weighted image (SWI), suggesting haemorrhage. Intensely enhancing eccentric solid components were seen along the walls of locules which showed facilitated diffusion. Mass effect was seen over the right frontoparietal lobes of the brain with a mild midline shift to the left. There was, however, no evidence of neuroparenchymal infiltration.
Background
Brown tumours (BT) are focal bony lesions caused by bone remodeling in primary (incidence 3%) or less commonly, in secondary hyperparathyroidism (incidence 1.5-7%) [1]. The excess parathyroid hormone stimulates osteoclastic activity, resulting in poor bony trabecular development. The growth of fibrovascular tissue into the marrow space causes microfractures and haemorrhage with hemosiderin deposition [2]. Prior case reports indicate that BT commonly develop in the mandible, pelvis, ribs, and long bones and are rarely seen in skull and para-nasal sinuses [1,3].
Clinical perspective
BT manifest clinically as palpable bony swelling, bone pain, or pathological fractures. Osteopenia, subperiosteal/subchondral/intracortical bone resorption, and acro-osteolysis are also common skeletal findings in PHPT (primary hyperparathyroidism). PHPT can have systemic manifestations such as recurrent renal stones, weight loss, polyuria, and gastrointestinal and neuromuscular symptoms [4].
Imaging perspective
BT often present as well-circumscribed lytic lesions with cortical thinning but rarely cause frank destruction [5]. Other less common presentations include ill-defined lesions, mixed lytic and sclerotic lesions, adjacent soft tissue involvement, etc.[6]. BT usually contain a mixture of solid, cystic, and hemorrhagic components, hence give inhomogeneous signals in MRI [7]. In T1, degraded blood products show hyperintense signal. Cystic areas may show fluid levels in T2 [3]. In our case, presence of multiple blood fluid levels brings aneurysmal bone cyst (ABC) and telangiectatic osteosarcoma as close differentials. In BT, the enhancing solid components represent fibrovascular tissue which exhibits facilitated diffusion, allowing it to be differentiated from telangiectatic osteosarcoma and metastasis where the solid components show restricted diffusion. In addition, matrix mineralization is seen in telangiectatic osteosarcoma. Primary ABC does not contain enhancing solid components. Giant cell tumours will have solid components, scattered cystic components, areas of T2 hypointensity and blooming with no matrix mineralization making it a close mimicker of brown tumours on imaging.
On nuclear bone scans, BT show focal high uptake [3].
Outcome
In this case, detection of multiple other lytic bone lesions in the CT abdomen study (Fig 4) taken for abdominal pain evaluation raised the suspicion of BT, and further biochemical workup showed an elevated serum calcium level. Ultrasonography neck was ordered which revealed an oval hypoechoic lesion in the inferior aspect of left thyroid lobe (Fig 5) suggestive of left parathyroid adenoma. It was then confirmed by nuclear 99mTc-Sestamibi scan (Fig 6). He was diagnosed as a case of primary hyperparathyroidism and started on bisphosphonates. For the scalp lesion, right frontotemporoparietal craniectomy with tumour excision was done. Histopathology showed multinucleated osteoclast-type giant cells in the background with spindle cells, hemorrhage, and hemosiderin deposition. Although histopathology is considered as the gold standard for definitive diagnosis, at times histology can be uncertain as it can resemble a few other giant cell lesions [8].
Excision of the parathyroid adenoma was done. Postoperatively, the patient developed hungry bone syndrome and was managed with calcium supplements.
Take home message
Radiological features of BT can be variable, and hence need a high index of suspicion for diagnosis. Detailed history, biochemical analysis correlated with a bone scan, and other associated imaging findings of PHPT help clinch the diagnosis.
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Brown tumour of right parietal bone secondary to primary hyperparathyroidism
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(1) Cranial CT: There is notable expansile bone destruction of the right parietotemporal cranial bone with thinning of the cortex but partial preservation of cortical integrity. Multiple low-density, septated, lytic lesions with relatively clear boundaries are visible in the lesion.
(2) MRI (Head): On T1-weighted images, some areas of the lesion appear hyperintense, suggesting possible breakdown products or hemorrhagic components; on T2-weighted images, multiple fluid-fluid levels are seen, indicating cystic or hemorrhagic components. After contrast administration, there is heterogeneous enhancement of soft tissue components.
(3) Imaging of Other Sites: Abdominal CT shows multiple lucent lesions in the bones, suggesting multiple lytic bone lesions.
(4) Neck Ultrasound: A well-defined, oval-shaped hypoechoic nodule located near the lower pole of the left thyroid lobe is noted, considered a possible parathyroid lesion. Subsequent 99mTc-Sestamibi scan indicates high uptake in the area.
Based on the above imaging findings (multiple lytic lesions, expansile bones with thinning cortex, fluid-fluid levels and hemorrhagic components), combined with hypercalcemia and a parathyroid nodule, the following differential diagnoses are considered:
(1) Brown Tumor: Due to primary or secondary hyperparathyroidism causing abnormal bone remodeling, characterized by multiple lytic lesions containing fibrous tissue, hemorrhage, and giant cells.
(2) Aneurysmal Bone Cyst (ABC): Typically presents as a multiloculated, blood-filled chamber with thin septations on imaging; fluid-fluid levels can be seen on MRI. However, it usually lacks fibrotic or solid enhancement components and is less commonly associated with hypercalcemia or parathyroid pathology.
(3) Giant Cell Tumor: Often occurs in the long bones or at the epiphyses, may show giant cells and hemorrhagic regions, can present with lytic changes, but there is no strong association with hyperparathyroidism, and it usually appears as a solitary lesion or in specific skeletal locations.
(4) Metastatic Lesions or Rare Malignant Bone Tumors: Must be ruled out, but the patient is young, lacks evidence of a primary malignancy, and the presence of elevated parathyroid hormone levels is more supportive of a Brown Tumor.
Considering the following:
• A young male patient with chronic bone pain and a prominent expansile lesion in the cranial bones,
• Laboratory findings indicating hypercalcemia,
• Neck ultrasound and 99mTc-Sestamibi scan revealing a parathyroid adenoma,
• Histopathology showing multinucleated giant cells within fibrous vascular tissue, hemorrhagic components, and hemosiderin deposits,
It is most likely a Brown Tumor caused by primary hyperparathyroidism.
(1) Treatment Strategy:
• Medical Therapy: After confirming primary hyperparathyroidism, bisphosphonates may be used to reduce bone turnover and correct hypercalcemia.
• Surgical Treatment: Surgical resection of the adenoma causing hyperparathyroidism may be considered. Surgical intervention for cranial or other Brown Tumors may be required if they cause significant symptoms or structural compromise. Some patients may experience “hungry bone syndrome” after surgery, requiring adequate supplementation with calcium and vitamin D.
• Supportive Care: Close monitoring of serum calcium, bone density, and renal function is essential to promptly address any electrolyte imbalances.
(2) Rehabilitation and Exercise Prescription:
Given the patient’s bone fragility and potential fluctuations in calcium and phosphate metabolism postoperatively, a safe, moderate, and individualized approach following the FITT-VP principle should be adopted.
• Frequency: 3–5 times per week, adjusted according to patient recovery and any comorbidities.
• Intensity: Begin with low-intensity, such as low-load resistance exercises or light-to-moderate aerobic activities (e.g., brisk walking on flat ground). Increase the load gradually as bone mass recovers and serum calcium levels stabilize, avoiding high-impact movements.
• Time: Start with 15–20 minutes per session and gradually extend to 30–45 minutes, monitoring for tolerance.
• Type: Choose activities that minimize joint stress, such as swimming, using an elliptical machine, lower-limb resistance training, and core stability exercises. Combine with physical therapy and range-of-motion exercises, avoiding excessive loading or twisting movements.
• Progression: Increase resistance or training intensity only if blood chemistry remains stable and the skeletal system can tolerate it. Monitor the patient’s pain, fatigue, and lab results, and revert to lower intensity if necessary.
Precautions: In the early postoperative phase, closely monitor serum calcium to prevent and manage “hungry bone syndrome.” If severe muscle weakness or symptoms of hypocalcemia occur, seek medical attention immediately to adjust calcium supplementation, vitamin D intake, and the exercise regimen.
Disclaimer: This report is a reference-based medical analysis based on existing information and does not replace an in-person clinical assessment or professional medical guidance. If there are any questions or changes in condition, please consult a qualified healthcare professional promptly.
Brown tumour of right parietal bone secondary to primary hyperparathyroidism
