Brown tumor of the pelvis

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Brown tumor of the pelvis

A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.

On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:

  • Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
  • Calcium 2.32 mmol/L (1.15–1.32)
  • Phosphate 3.26 mmol/L (0.8–1.45).

Figure 1. Axial computed tomography of the pelvis (top) showed an exophytic calcified lesion of the pubis (arrow) with multiple cystic spaces and fluid-fluid levels. A coronal view (bottom) showed the same lesion and fracture of the left inferior pubic ramus (arrow).

Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.

Figure 2. Histologic study showed clusters of osteoclast-type giant cells (arrows) on a background of spindle cells and fibrous stroma (hematoxylin and eosin, x 100).

The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).1

BROWN TUMOR

Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.

Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.5 Clinical symptoms are nonspecific and depend on the size and location of the lesion.

Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.

References
  1. Davies AM, Evans N, Mangham DC, Grimer RJ. MR imaging of brown tumour with fluid-fluid levels: a report of three cases. Eur Radiol 2001; 11:1445–1449.
  2. Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81:2036–2040.
  3. Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986; 81:545–547.
  4. Demay MB, Rosenthal DI, Deshpande V. Case records of the Massachusetts General Hospital. Case 16-2008. A 46-year-old woman with bone pain. N Engl J Med 2008; 358:2266–2274.
  5. Perlman JS, Pletcher SD, Schmidt BL, Eisele DW. Pathology quiz case 2. Giant cell lesion (brown tumor) of the mandible, associated with primary hyperparathyroidism (HPT). Arch Otolaryngol Head Neck Surg 2004; 130:793–794.
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Tetiana Glushko, MD
Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Shorooq S.A. Banjar, MD
Teaching Assistant, Department of Internal Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia

Ayoub Nahal, MD
Associate Professor, Department of Pathology, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Inés Colmegna, MD
Assistant Professor, Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Address: Inés Colmegna, MD, Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, 1001 Decarie Boulevard, Montreal, QC H4A 3J1, Canada; e-mail: [email protected]

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Cleveland Clinic Journal of Medicine - 82(12)
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brown tumor, hyperparathyroidism, osteitis fibrosa cystica, Tetiana Glushko, Shorooq Banjar, Ayoub Nahal, Ines Colmegna
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Tetiana Glushko, MD
Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Shorooq S.A. Banjar, MD
Teaching Assistant, Department of Internal Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia

Ayoub Nahal, MD
Associate Professor, Department of Pathology, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Inés Colmegna, MD
Assistant Professor, Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Address: Inés Colmegna, MD, Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, 1001 Decarie Boulevard, Montreal, QC H4A 3J1, Canada; e-mail: [email protected]

Author and Disclosure Information

Tetiana Glushko, MD
Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Shorooq S.A. Banjar, MD
Teaching Assistant, Department of Internal Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia

Ayoub Nahal, MD
Associate Professor, Department of Pathology, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Inés Colmegna, MD
Assistant Professor, Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, Montreal, QC, Canada

Address: Inés Colmegna, MD, Division of Rheumatology, Department of Medicine, McGill University Health Center, Royal Victoria Hospital, 1001 Decarie Boulevard, Montreal, QC H4A 3J1, Canada; e-mail: [email protected]

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A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.

On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:

  • Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
  • Calcium 2.32 mmol/L (1.15–1.32)
  • Phosphate 3.26 mmol/L (0.8–1.45).

Figure 1. Axial computed tomography of the pelvis (top) showed an exophytic calcified lesion of the pubis (arrow) with multiple cystic spaces and fluid-fluid levels. A coronal view (bottom) showed the same lesion and fracture of the left inferior pubic ramus (arrow).

Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.

Figure 2. Histologic study showed clusters of osteoclast-type giant cells (arrows) on a background of spindle cells and fibrous stroma (hematoxylin and eosin, x 100).

The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).1

BROWN TUMOR

Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.

Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.5 Clinical symptoms are nonspecific and depend on the size and location of the lesion.

Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.

A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.

On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:

  • Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
  • Calcium 2.32 mmol/L (1.15–1.32)
  • Phosphate 3.26 mmol/L (0.8–1.45).

Figure 1. Axial computed tomography of the pelvis (top) showed an exophytic calcified lesion of the pubis (arrow) with multiple cystic spaces and fluid-fluid levels. A coronal view (bottom) showed the same lesion and fracture of the left inferior pubic ramus (arrow).

Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.

Figure 2. Histologic study showed clusters of osteoclast-type giant cells (arrows) on a background of spindle cells and fibrous stroma (hematoxylin and eosin, x 100).

The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).1

BROWN TUMOR

Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.

Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.5 Clinical symptoms are nonspecific and depend on the size and location of the lesion.

Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.

References
  1. Davies AM, Evans N, Mangham DC, Grimer RJ. MR imaging of brown tumour with fluid-fluid levels: a report of three cases. Eur Radiol 2001; 11:1445–1449.
  2. Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81:2036–2040.
  3. Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986; 81:545–547.
  4. Demay MB, Rosenthal DI, Deshpande V. Case records of the Massachusetts General Hospital. Case 16-2008. A 46-year-old woman with bone pain. N Engl J Med 2008; 358:2266–2274.
  5. Perlman JS, Pletcher SD, Schmidt BL, Eisele DW. Pathology quiz case 2. Giant cell lesion (brown tumor) of the mandible, associated with primary hyperparathyroidism (HPT). Arch Otolaryngol Head Neck Surg 2004; 130:793–794.
References
  1. Davies AM, Evans N, Mangham DC, Grimer RJ. MR imaging of brown tumour with fluid-fluid levels: a report of three cases. Eur Radiol 2001; 11:1445–1449.
  2. Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81:2036–2040.
  3. Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986; 81:545–547.
  4. Demay MB, Rosenthal DI, Deshpande V. Case records of the Massachusetts General Hospital. Case 16-2008. A 46-year-old woman with bone pain. N Engl J Med 2008; 358:2266–2274.
  5. Perlman JS, Pletcher SD, Schmidt BL, Eisele DW. Pathology quiz case 2. Giant cell lesion (brown tumor) of the mandible, associated with primary hyperparathyroidism (HPT). Arch Otolaryngol Head Neck Surg 2004; 130:793–794.
Issue
Cleveland Clinic Journal of Medicine - 82(12)
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Cleveland Clinic Journal of Medicine - 82(12)
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799-800
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799-800
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Brown tumor of the pelvis
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Brown tumor of the pelvis
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brown tumor, hyperparathyroidism, osteitis fibrosa cystica, Tetiana Glushko, Shorooq Banjar, Ayoub Nahal, Ines Colmegna
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brown tumor, hyperparathyroidism, osteitis fibrosa cystica, Tetiana Glushko, Shorooq Banjar, Ayoub Nahal, Ines Colmegna
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