# Progressive Anterior Tibial Tumefaction: A Case of Unusual Bone Lesion

**Authors:** Catarina R Silva, João L Pereira, Nidia Oliveira, Elisa Veigas, Maria C Coelho

PMC · DOI: 10.7759/cureus.100248 · Cureus · 2025-12-28

## TL;DR

A rare case of a non-cancerous bone lesion caused by overactive parathyroid glands is described, highlighting the importance of accurate diagnosis to avoid unnecessary cancer treatments.

## Contribution

The paper presents a rare clinical case of a brown tumor caused by primary hyperparathyroidism, emphasizing diagnostic challenges and management.

## Key findings

- Brown tumors can mimic malignancy on imaging, leading to diagnostic uncertainty.
- Elevated PTH and calcium levels, along with imaging and biopsy, confirmed a parathyroid adenoma as the cause of the bone lesion.
- Successful parathyroidectomy resolved the condition, avoiding unnecessary oncologic interventions.

## Abstract

Brown tumors are rare, non-neoplastic bone lesions caused by excessive bone remodeling due to hyperparathyroidism. Their estimated prevalence is approximately 3-5% in primary hyperparathyroidism and about 1.5% in secondary forms. Prolonged elevation of parathyroid hormone (PTH) stimulates osteoclastic activity, leading to progressive bone resorption and cortical disruption. These lesions develop through replacement of normal bone marrow by highly vascularized fibrous tissue, often accompanied by repeated microfractures and hemorrhage, resulting in pain, skeletal deformity, structural weakness, and an increased risk of fractures. Their clinical and radiologic resemblance to malignancy often poses a diagnostic challenge.

We report the case of an 81-year-old male who presented with a progressively enlarging, painless tumefaction on the anterior aspect of the right tibia. Magnetic resonance imaging (MRI) of the lower limb revealed a large heterogeneous lesion with internal cystic areas, initially suggestive of a secondary bone process. Laboratory studies showed markedly elevated parathyroid hormone (PTH 705 pg/dL), hypercalcemia (11.5 mg/dL), increased alkaline phosphatase (ALP 416 U/L), and elevated prostate-specific antigen (PSA 11.88 ng/mL). Bone scintigraphy demonstrated diffuse uptake compatible with metabolic bone disease. Thoracoabdominal-pelvic computed tomography (TAP-CT) showed diffuse bone involvement, raising suspicion of metastatic disease, and a heterogeneous thyroid gland with small nodules in the right lobe. The possibility of primary thyroid neoplasia was ruled out after thyroid ultrasound and biopsy of the thyroid nodule were performed. Due to the elevated PSA, a PSMA-PET (prostate-specific membrane antigen positron emission tomography) was requested, which demonstrated diffuse bone involvement not compatible with metastasis from a primary prostate neoplasm. The free-to-total PSA ratio and digital rectal examination were consistent with benign prostatic hyperplasia. Due to elevated PTH and calcium levels, parathyroid scintigraphy was requested, which revealed a hyperfunctioning parathyroid nodule, compatible with a parathyroid adenoma. Biopsy of the tibial lesion confirmed a brown tumor, likely secondary to primary hyperparathyroidism caused by a parathyroid adenoma. The patient underwent a successful parathyroidectomy.

Although rare, brown tumors should be considered in the differential diagnosis of osteolytic bone lesions, especially in the presence of elevated PTH. Recognition of this entity is essential to prevent misdiagnosis and unnecessary oncologic treatments.

## Linked entities

- **Chemicals:** calcium (PubChem CID 5460341), alkaline phosphatase (PubChem CID 18985873)
- **Diseases:** hyperparathyroidism (MONDO:0001741), benign prostatic hyperplasia (MONDO:0010811)

## Full-text entities

- **Genes:** KLK3 (kallikrein related peptidase 3) [NCBI Gene 354] {aka APS, KLK2A1, PSA, hK3}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, FOLH1 (folate hydrolase 1) [NCBI Gene 2346] {aka FGCP, FOLH, GCP2, GCPII, NAALAD1, PSM}, ALPP (alkaline phosphatase, placental) [NCBI Gene 250] {aka ALP, PALP, PLAP, PLAP-1}
- **Diseases:** weakness (MESH:D018908), metastasis (MESH:D009362), Bone Lesion (MESH:D001847), prostate neoplasm (MESH:D011471), primary hyperparathyroidism (MESH:D049950), benign prostatic hyperplasia (MESH:D011470), pain (MESH:D010146), thyroid (MESH:D013966), fractures (MESH:D050723), metastatic disease (MESH:D000092182), hyperparathyroidism (MESH:D006961), Anterior Tibial Tumefaction (MESH:D000868), parathyroid adenoma (MESH:D010282), tibial lesion (MESH:D020429), skeletal deformity (MESH:D009140), Brown tumors (MESH:D009369), hypercalcemia (MESH:D006934), hemorrhage (MESH:D006470)
- **Chemicals:** calcium (MESH:D002118)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC12838763/full.md

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Source: https://tomesphere.com/paper/PMC12838763