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 Table of Contents  
CASE REPORTS
Year : 2021  |  Volume : 4  |  Issue : 2  |  Page : 203-213

Brown tumor causing thoracic compressive myelopathy: A case report and review of literature


Spine Care Centre, Manipal Hospital, Bengaluru, Karnataka, India

Date of Submission09-Jun-2020
Date of Decision15-Jul-2020
Date of Acceptance19-Sep-2020
Date of Web Publication24-May-2021

Correspondence Address:
Thomas Joseph Kishen
Spine Care Center, Manipal Hospital, 98, HAL-Airport Road, Bengaluru– 560017ig, Karnataka.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/isj.isj_48_20

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  Abstract 

Brown tumors are nonneoplastic bony lesions resulting from primary, secondary or tertiary hyperparathyroidism. Primary hyperparathyroidism is caused by parathyroid adenomas or parathyroid hyperplasia while chronic renal failure is a common cause of secondary hyperparathyroidism. Elevated parathyroid hormone levels cause increased osteoclastic activity, bone resorption and reactive fibroblastic proliferation leading to the formation of Brown tumor. Although Brown tumors are more commonly seen in the maxilla and mandible, it can occur in the long, flat bones or any bone. It is less commonly seen in the spine. In this report, we discuss the presentation, management, difficulties with histopathological diagnosis, and follow-up of a Brown tumor in a 55-year-old gentleman undergoing renal dialysis who presented with thoracic compressive myelopathy. Our patient underwent a T4 laminectomy, tumor debulking, and T2–T6 instrumented posterior fusion. Based on histopathological examination of the tissue specimen and raised serum parathyroid hormone levels, we arrived at a diagnosis of Brown tumor. Our review of the literature revealed 62 cases of vertebral Brown tumor resulting in neurologic symptoms. The lesion was more common in females (58%), those aged between 40 and 49 years (26%), and in the thoracic spine (51.6%). Early surgical intervention and management of the underlying cause of hyperparathyroidism lead to sustained symptomatic improvement. Brown tumor should be considered in the differential diagnosis of expansile vertebral lesions in the presence of hyperparathyroidism or chronic kidney disease. Treatment of the underlying hyperparathyroidism and decompression of the neural structures with or without stabilization is recommended.

Keywords: Brown tumor, chronic kidney disease, hyperparathyroidism


How to cite this article:
Ramachandraiah MK, Kishen TJ. Brown tumor causing thoracic compressive myelopathy: A case report and review of literature. Indian Spine J 2021;4:203-13

How to cite this URL:
Ramachandraiah MK, Kishen TJ. Brown tumor causing thoracic compressive myelopathy: A case report and review of literature. Indian Spine J [serial online] 2021 [cited 2021 Dec 4];4:203-13. Available from: https://www.isjonline.com/text.asp?2021/4/2/203/316665




  Introduction Top


Brown tumor, also termed osteitis fibrosa cystica or Recklinghausen’s disease of bone, is a benign bone lesion resulting from either primary, secondary or tertiary hyperparathyroidism.[1] The primary function of parathyroid hormone (PTH) is to regulate the blood calcium levels by tubular reabsorption of calcium in the kidney, release of skeletal calcium stores, increased 1,25-dihydroxy-cholecalciferol production and increased calcium reabsorption from the gastrointestinal tract. Elevated parathyroid hormone levels lead to increased osteoclastic activity and bone resorption which can cause reactive fibroblastic proliferation leading to the formation of a Brown tumor.[2] Brown tumor is uncommon even in the presence of hyperparathyroidism with an incidence less than 5% in primary hyperparathyroidism and 13% in secondary hyperparathyroidism.[3]

Vertebral Brown tumors are rare[4] and were first reported by Shaw and Davies in 1968.[5] The symptoms of vertebral Brown tumor include pain, radiculopathy, and myelopathy depending on its location in the spine.[6] In this report, we discuss the presentation, management, difficulties with histopathological diagnosis and follow-up of a Brown tumor in a 55-year-old gentleman undergoing renal dialysis who presented with thoracic compressive myelopathy.


  Case Report Top


A 55-year-old gentleman presented with buckling of both knees, difficulty in getting up from supine and sitting position in the last 6 months, inability to walk unsupported and tingling sensation in the lower abdomen and both lower limbs for 10 days. There was no history of back pain, radiating leg pain, trauma, fever, or constitutional symptoms. He was a diabetic and hypertensive on regular hemodialysis for chronic kidney disease for the last twelve years. Examination of the spine revealed tenderness over the mid-thoracic region with painfully restricted thoracolumbar movements. Motor power was normal in both lower limbs with hypoesthesia in T11-S1 dermatomes bilaterally, exaggerated deep tendon reflexes in both lower limbs and an extensor plantar reflex. The upper limb neurology was normal.

Magnetic resonance imaging (MRI) scan of the thoracic spine revealed an expansile mixed intensity lesion in the right posterolateral aspect of T4 vertebral body with involvement of pedicle, transverse process, and spinous process compressing the spinal cord causing myelomalacic changes [Figure 1]A and [B]. With an MRI appearance suggestive of metastasis, a basic metastatic workup including a CT scan of chest and abdomen, prostate-specific antigen level, and serum protein electrophoresis was performed and found to be normal. In view of progressive neurological deterioration, surgery in form of T4 laminectomy and posterior decompression with tumor debulking and T2-T6 instrumented posterior fusion was performed [Figure 2]. The neurological status improved following surgery and he was able to ambulate with a walker. Serum parathyroid hormone level (normal range 10–65 pg/mL) was found to be high (384.3 pg/mL).
Figure 1: Sagittal (A) and axial (B) T2W MRI images showing expansile mixed intensity lesion in the right posterolateral aspect of T4 vertebral body with involvement of pedicle, transverse process and spinous process and compressing the spinal cord causing myelomalacia changes

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Figure 2: Anteroposterior (A) and lateral (B) post-operative radiographs after posterior decompression with tumor debulking and T2–T6 instrumented posterior fusion

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GeneXpert for tuberculosis and aerobic culture of the tissue obtained during surgery was negative. Histopathological examination of the tissue showed numerous osteoclastic giant cells separated by stromal cells which were mononuclear with vesicular nuclei and moderate cytoplasm. There was no mitosis, nuclear pleomorphism, or necrosis [Figure 3]. Although it was initially reported as a giant cell tumor, further correlation with the raised parathyroid hormone levels led to a histopathological diagnosis of Brown tumor. A subsequent 99 mTc-Sestamibi (CARDIOLITE) parathyroid scan did not reveal a parathyroid adenoma/lesion [Figure 4] and a final diagnosis of secondary hyperparathyroidism due to chronic kidney disease was made. In view of the increased parathyroid hormone levels, oral Cinacalcet (30 mg per day) (a calcimimetic drug) was initiated which consequently reduced the serum parathyroid hormone level to 42 pg/mL at the end of one month. Thereafter, the dose of Cinacalcet was reduced to 15 mg per day for the next 3 months and subsequently stopped. However, the PTH level rose to 599 pg/mL within one month after stopping Cinacalcet and hence it was restarted at a dose of 15 mg/day with the aim to maintain a PTH level between 2 and 9 times the upper limit of the assay according to the KDIGO (Kidney Disease: Improving Global Outcomes) guidelines of 2017. The PTH level was 558 pg/mL at the one year mark and Cinacalcet (15 mg/day) is being continued. The levels of calcium, phosphorus, vitamin D and PTH are mentioned in [Table 1].
Figure 3: H and E stained specimen (×100 magnification) showing numerous osteoclastic giant cells separated by stromal cells

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Figure 4: 99 mTc-Sestamibi (CARDIOLITE) parathyroid scan showing no definite evidence of hyperfunctioning parathyroid adenoma

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Table 1: Serum calcium, phosphorus, vitamin D and PTH levels immediately after surgery and during follow-up

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At 18 months of follow-up, he was ambulating independently without any neurological deficits and a repeat MRI scan [Figure 5] performed after 18 months revealed that the Brown tumor had healed with no ongoing spinal cord compression.
Figure 5: Sagittal (A) and axial (B) T2W MRI images at 18 months of follow-up showing no evidence of the lesion or cord compression

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  Discussion Top


Brown tumor is a classical manifestation of hyperparathyroidism (primary, secondary or tertiary) and is characterized by bone pain and radiographic features of bone resorption.[7] Hyperparathyroidism is referred to as primary when the pathology lies in the overactive parathyroid glands (adenoma or hyperplasia of the glands) that secrete excess of PTH and secondary when the parathyroid glands are stimulated to excrete excess PTH in response to low serum calcium, high serum phosphorus or low vitamin D levels all of which can result from chronic kidney disease.[4],[8] Long-standing secondary hyperparathyroidism can lead to autonomous and unregulated parathyroid function (unregulated by serum calcium levels), a condition referred to as tertiary hyperparathyroidism.[8] Hence, ascertaining the actual cause of the hyperparathyroidism plays an important part in the management of Brown tumor. Although primary hyperparathyroidism was responsible for most Brown tumors in the past, the incidence of Brown tumor in secondary hyperparathyroidism is on the rise due to increased life expectancy with chronic kidney disease.[4] The first case of secondary hyperparathyroidism involving the spine was reported by Ericsson et al.[9] Hyperparathyroidism leads to increased mobilization of calcium from bones through osteoclastic bone resorption and when boss loss is rapid, the osteoclastic cavities are filed with granulation tissue and proliferating fibrous tissue interspersed with hemorrhagic areas and hemosiderin deposits.[10],[11] The accumulation of hemosiderin gives the surrounding stroma a Brown color[4] from which the term “Brown” tumor is derived.

Brown tumors usually develop in the third or fourth decades of life and can involve facial bones (mandible and maxilla), long bones, ribs, and pelvis.[12],[13] They usually present as a slow-growing mass and symptoms depend on the particular anatomical region involved.[14],[15] Vertebral Brown tumors, though rarely asymptomatic,[16],[17] usually present with slowly progressive back pain and weakness of the limbs[15] and occasionally may follow an acute course with paraplegia due to spinal cord compression.[4],[18] On imaging studies, vertebral Brown tumors either present as a solitary lesion resembling an aneurysmal bone cyst or giant cell tumor or as disseminated lesions resembling osteolytic metastasis or multiple myeloma.[19] On computed tomographic (CT) imaging, Brown tumors appear as lytic lesions with soft tissue density and may resemble metastasis or multiple myeloma. The MRI appearance of Brown tumors is described as hypointense on T1-weighted images and hyper- or hypointense on T2-weighted images.[4] Interestingly, Brown tumors with radiographic blood-fluid levels have also been described.[20] The presence of hemosiderin in lytic bone lesions on CT/MRI imaging in the setting of hyperparathyroidism, excludes most other diagnoses, including giant cell tumors, giant cell reparative granulomas, and pigmented villonodular synovitis.[21] Histologically they resemble other giant cell lesions such as giant cell tumor or aneurysmal bone cyst and are characterized by the presence of hemosiderin pigment deposits and osteoclastic giant cells arranged in groups, separated by richly vascularized fibrous tissue.[10]

Our review of the literature yielded 62 cases of vertebral Brown tumors [Table 2] being more common in females (58%) with a predilection for the thoracic spine (51%) and secondary hyperparathyroidism following chronic kidney disease being the commonest predisposing condition (56%). Lesions arose from the vertebral bodies or posterior elements without an obvious anatomical predilection.
Table 2: Reported cases of vertebral brown tumor in chronological order

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Management of vertebral Brown tumors involves a two-pronged strategy to treat the hyperparathyroidism and the vertebral lesion. Total or subtotal parathyroidectomy is the treatment of choice for primary hyperparathyroidism[4],[26],[69] leading to rapid decrease in the parathyroid hormone level and complete regression of the bony lesions with remineralization.[4],[24] A cinacalcet-based regimen, including active vitamin D analogs and phosphate binders, based on individual patient requirement is the recommended treatment of secondary hyperparathyroidism in chronic kidney disease.[70] Maintaining an optimum level of PTH is crucial to prevent the recurrence of Brown tumors (high bone turnover state) due to excessive PTH and adynamic bone disease (low bone turnover state resulting from a reduced number of osteoclasts and osteoblasts without osteoid accumulation) due to low PTH levels.[31] The KDIGO (The Kidney Disease: Improving Global Outcomes) guidelines of 2017 recommend a target PTH level between 2 and 9 times the upper limit of the assay.[59] Early spinal decompression with or without stabilization has to be considered when neural compression leads to motor and sensory deficits.[4],[69],[71],[72]

The 55-year-old gentleman with chronic kidney disease on regular dialysis, discussed in this report, presented with inability to walk. MRI scan revealed an expansile lesion in the T4 vertebrae involving the posterior vertebral body, pedicle and posterior elements with spinal cord compression and cord signal changes suggestive of myelomalacia. In view of his neurological deterioration spinal decompression, tumor debulking and stabilization was carried out. Although the initial histopathological diagnosis was giant cell tumor, further correlation with high serum parathyroid hormone level led to a diagnosis of Brown tumor. Cinacalcet therapy is being continued to maintain an optimum serum parathyroid hormone level. At 18 months follow-up, the patient was ambulating independently without any neurological deficits and a repeat MRI scan revealed that the Brown tumor had healed with no ongoing spinal cord compression.


  Conclusion Top


Brown tumor should be considered in the differential diagnosis of expansile vertebral lesions in the presence of hyperparathyroidism or chronic kidney disease. Treatment of the underlying hyperparathyroidism and decompression of the neural structures with or without stabilization is recommended. Maintaining an optimal level of PTH will prevent the recurrence of Brown tumors (due to excessive levels of PTH) and adynamic bone disease (due to very low levels of PTH).

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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