38-year-old man with chronic renal disease on haemodialysis. He presented cutaneous lesions compatible with calciphylaxis and severe musculoskeletal complaints, especially on the left hip. Laboratory results demonstrated elevated parathyroid hormone levels as well as hyperphosphataemia.
The pelvic and leg radiographs requested as a first line examination to assess the hip symptoms demonstrated diffuse reduction of bone mineralisation, compatible with moderate/severe osteopenia. Additionally, a relatively well-defined eccentric bubbly lytic lesion with sclerotic borders was depicted on the medial side of the left femoral diaphysis. On the radiograph there were also severe vascular calcifications related to the known renal dysfunction.
The abdominopelvic and lower limb computed tomography (CT) revealed a heterogeneous pattern of bone mineralisation, with significant loss of the normal bone trabeculation in the femoral shafts and also a “rugger-jersey” pattern in the spine, with an important subendplate sclerosis. In addition, CT confirmed the presence of an expansile soft tissue lesion in the left femoral diaphysis, with well-defined sclerotic borders, causing mild subperiosteal scalloping, but no periosteal reaction associated.
9mTc-sestamibi study depicted an increased uptake on the anatomical site of the right parathyroid gland.
Brown tumours (BT) are one of the rare skeletal manifestations of primary or secondary hyperparathyroidism, occurring in the setting of prolonged disease [1, 2, 4], more often in women. In fact, BT are not true malignant neoplasms, but rather result from a reparative process, known as osteitis fibrosa cystica, caused by abnormally high osteoclast activity, in which normal bone matrix is substituted for granulation and fibrotic tissue. There is also evidence of haemosiderin deposits within them, leading to its brownish coloration. [2, 4]. Primary hyperparathyroidism is frequently associated with lesions in the parathyroid, like adenomas, hyperplasia or malignant lesions. Secondary hyperparathyroidism is related to systemic resistance to the parathyroid hormone action, normally in the setting of chronic renal disease, vitamin D deficiency [3], with persisting high levels of parathyroid hormone, hypercalcaemia and hyperphosphataemia.
BT can occur in the jaw, skull, mandible, clavicles, pelvis, ribs, spine and extremities (femur).
At imaging, they often present as a well-defined, single or multiple lytic lesion, with non-sclerotic borders, sometimes with cortex thinning, but with no clear aggressive features. Other presentations include an expansible behaviour, bone deformity, multilobular cystic changes, generalised demineralisation and subperiosteal scalloping [1, 2], all as part of the high turnover bone disease. Fractures, compressive syndromes, face deformation and difficulties in eating or breathing can be one of the presentations of this lesions, due to their growing potential [4]. The imaging findings of BT can overlap those of giant-cell tumours, metastases, bone cysts or osteosarcoma [1]. Scintigraphy is helpful for detecting hyperparathyroidism-related bone disease, although conditions like metastatic disease, multiple myeloma, infection, trauma and other metabolic disease can present as “false-positives” [1]. Biopsy is the gold standard approach for the final diagnosis. Occasionally, biopsy can be inconclusive, as BT can histologically resemble other lesions. Having said that, biopsy is not usually performed in the setting of typical imaging features in a patient with known chronic kidney disease. Therefore, a high rate of suspicion, clinical history and laboratory results are all key features for an accurate diagnosis, without the need of an invasive procedure [2].
In this case, the clinical history (haemodialysis) and the additional musculoskeletal manifestations (rugger-jersey spine) were key findings that allowed the radiologist to put BT on the differential diagnosis list. This suspicion led to further examinations, including parathyroid gland ultrasound and scintigraphic assessment, which were both positive.
Partial or complete surgical removal of the parathyroid gland can be considered as treatment when medical approach fails [2]. Upon favourable response, BT can then regress or appear as an area of increased bone sclerosis [2].
In conclusion, the high rate of suspicion of BT tumours can improve patient management.
Written patient consent for this case was waived by the Editorial Board. Patient data may have been modified to ensure patient anonymity.
Brown tumour on a patient with chronic renal disease
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
1. X-ray and CT Imaging of the Pelvis and Both Hip Joints: A relatively well-defined round osteolytic lesion is observed in the left hip region and proximal femur, accompanied by localized cortical thinning and decreased bone density. No obvious sclerotic margin or erosive destructive changes are noted.
2. In the corresponding region of the femoral shaft, focal lytic changes with an expansile appearance are observed, accompanied by localized cortical thinning.
3. CT scans of the lumbar and thoracic spine show the “rugger-jersey” sign, characterized by thickened and sclerotic endplates with relatively radiolucent bone in the center, suggesting bone changes related to secondary hyperparathyroidism.
4. Concurrent nuclear medicine scans indicate elevated bone metabolism in multiple sites, consistent with high-turnover bone disease.
Based on the patient’s long-term chronic kidney disease (under dialysis), elevated parathyroid hormone (PTH) levels, and imaging findings (osteolytic lesions and “rugger-jersey” spine), the following diagnoses should be considered:
1. Brown Tumor: Caused by secondary or primary hyperparathyroidism. It manifests as osteolytic lesions with possible fibrous proliferation and hemosiderin deposition, giving it a brown appearance.
2. Giant Cell Tumor: Can also present as an expansile osteolytic lesion, most commonly near the epiphysis adjacent to the joint, and typically not associated with hyperparathyroidism or chronic kidney disease.
3. Metastatic Tumor: Osteolytic metastases may cause multifocal bone destruction. However, the patient’s history of kidney disease and the “rugger-jersey” sign lean more toward a metabolic bone disease; moreover, there is no confirmed history of malignancy.
4. Bone Cyst or Other Benign Lesions: May appear as well-defined cystic lesions, but the patient’s abnormal laboratory findings and other skeletal changes do not support a simple bone cyst diagnosis.
Considering the patient’s age, clinical presentation (long-term hemodialysis, likely disturbances in calcium-phosphorus metabolism), laboratory results (elevated parathyroid hormone and phosphate levels), and imaging findings (osteolytic lesions, characteristic spinal changes), the most probable diagnosis is: Brown Tumor caused by Secondary Hyperparathyroidism.
If diagnostic uncertainty remains, a biopsy of the lesion could be considered for histological confirmation; however, when clinical and imaging findings are strongly concordant, a biopsy is not always the first choice.
1. Medical and Surgical Interventions:
(1) Control Secondary Hyperparathyroidism: This includes correcting hyperphosphatemia, maintaining calcium balance, appropriately supplementing active vitamin D, and using medications that inhibit PTH secretion (such as calcimimetics).
(2) If medical therapy and calcium-phosphorus regulation fail to control PTH levels, partial or total parathyroidectomy may be considered. After surgical intervention, Brown Tumors may gradually diminish in size or show improved bone density.
(3) For severe bone pain or high risk of pathological fracture, targeted pain management, bracing, or prophylactic internal fixation may be needed.
2. Rehabilitation and Exercise Prescription:
Given the patient’s fragile bones and chronic kidney disease, an individualized and gradually progressive exercise program is imperative. Refer to the FITT-VP principle:
• Frequency: 2-3 sessions of aerobic training per week, and 1-2 sessions of light resistance training.
• Intensity: Begin with low intensity, aiming for moderate intensity (subjective exercise intensity rating of 3-4 on a 10-point RPE scale), adjusting according to tolerance.
• Time: Start with 15-20 minutes per aerobic session and gradually increase to 30 minutes; each resistance training session may last about 20 minutes.
• Type: Prioritize low-impact exercises (e.g., seated stationary cycling, walking with attention to hip support). Incorporate light resistance bands or low-weight dumbbells for muscle strengthening.
• Progression: If the patient experiences no bone pain or other discomfort, gradually increase exercise duration or intensity after 3-4 weeks, closely monitoring bone pain, joint stability, and cardiopulmonary tolerance.
• Volume & Individualization: Total exercise volume should be adjusted based on dialysis schedule, physical capacity, and bone health status. Reduce exercise intensity appropriately after dialysis or during periods of fatigue, ensuring adequate rest.
During rehabilitation, pay close attention to fracture risk and avoid intense, high-impact activities or those prone to falls. If severe pain, deformity, or functional decline occur, seek medical reevaluation promptly.
Disclaimer: The above report and recommendations are for medical reference only and do not replace a face-to-face diagnosis or individualized guidance from a healthcare professional. If you have any questions or if your condition changes, please consult a specialized medical institution or specialist promptly.
Brown tumour on a patient with chronic renal disease
