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| LETTER TO EDITOR |
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| Year : 2015 | Volume
: 63
| Issue : 1 | Page : 110-112 |
Cervical burst fracture caused by brown tumor
Fatih Aydemir1, Ozgur Kardes1, Melih Cekinmez1, Kadir Tufan1, Nazim Emrah Kocer2
1 Department of Neurosurgery, Baskent University Faculty of Medicine, Adana Practice and Research Center, Adana, Turkey
2 Department of Pathology, Baskent University Faculty of Medicine, Adana Practice and Research Center, Adana, Turkey
| Date of Web Publication | 4-Mar-2015 |
Correspondence Address:
Fatih Aydemir
Department of Neurosurgery, Baskent University Faculty of Medicine, Adana Practice and Research Center, Adana
Turkey
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.152680
How to cite this article:
Aydemir F, Kardes O, Cekinmez M, Tufan K, Kocer NE. Cervical burst fracture caused by brown tumor. Neurol India 2015;63:110-2 |
Sir,
Brown tumors (BT) are benign focal bony lesions caused by increased osteoclastic activity and fibroblastic proliferation. They are encountered in primary or secondary hyperparathyroidism. [1] Patients with chronic renal failure (CRF) on long-term hemodialysis are at risk of developing secondary hyperparathyroidism due to phosphate retention and lowered calcitriol levels. [2] BTs can arise as a solitary or multiple lesions of any bone and are more common in the extremities, clavicles, ribs, and pelvis. [3] Spinal involvement is very rare. The diagnosis and treatment options of a C7 vertebral burst fracture caused by secondary hyperparathyroidism (SHP) are discussed in this presentation.
A 29-year-old male patient was admitted with neck pain, and left hand numbness and weakness. In his medical history, he had been undergoing hemodialysis for the past 10 years as he was suffering from chronic renal failure. About 7 years ago, he had been diagnosed to be having SHP and had undergone a total parathyroidectomy. His neurological examination revealed hypoactive left triceps reflex and loss of flexion of the distal phalanx of the left hand (4/5 power). Cervical computed tomography (CT) of the patient revealed a burst fracture (and a lytic lesion) of the C7 vertebral body as well as lytic lesions in the C6 spinous process and the T2 vertebral body. Cervical magnetic resonance imaging (MRI) revealed an expansile-lytic lesion in the C7 vertebral body that was hypointense on T1 and T2 imaging and contrast enhancing following gadolinium injection [Figure 1]. The laboratory findings were as follows; parathyroid hormone: 3377 pg/ml (normal range; 10-70 pg/ml), calcium: 8,77mg / dL (normal range: 8.4-10.2mg/dl), phosphate: 6.46 mg/dL (normal range: 2.7-4.5mg/dL), alkaline phosphatase: 1429 IU/L (normal range: 25-100 IU/L), respectively. Parathyroid scintigraphy and neck MRI revealed an 18 x 18 x 11 mm lesion behind the manubrium sterni consistent with parathyroid tissue. A C7 anterior corpectomy was performed. Fusion with polyether ether ketone (PEEK) cage and synthetic bone putty and C6-T1 anterior plate-screw fixation were performed. A repeat parathyroidectomy of the residual tissue was performed by the general surgeons in the same session. No postoperative neurological deficits were detected and laboratory values of parathyroid hormone and calcium on the first postoperative day were 18.68 pg/ml and 6.06 mg/dl, respectively. Histopathological examination of the resected tissue revealed a BT [Figure 2]. In the early postoperative period, the CT scan showed relief of cord compression and restoration of C7 body height. A cervical MRI and CT scan done after a year showed a proper PEEK cage placement [Figure 3]. | Figure 1: Lytic lesion in C7 vertebral body causing burst fracture and spinal cord compression on T2-weighted sagittal (a) and axial MR images (b), sagittal CT images (c) and axial CT images (d)
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 | Figure 2: Microphotograph reveals the lesion adjacent to cortical bone (a). Lesion is composed of numerous osteoclastic giant cells embedded in spindle cell stroma (b) (a: HE x40, b:HE x100)
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 | Figure 3: Postoperative three-dimensional CT (a) shows the placement of PEEK cage, plates and screws. At one year follow up, T2-weighted sagittal MR images (b) and sagittal CT images (c), it is seen that the cord compression has ceased and the height of C7 vertebral body has been restored
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A total of 47 cases BT (including the present case) have been reported in literature. Twenty eight of them were due to SHP and 19 were due to primary hyperparathyroidism [4],[5] SHP may occur in any condition that causes chronic low calcium levels in serum. A plasmocytoma, lymphoma, giant cell tumor, and metastasis are included in the differential diagnosis of BTs. [4],[5],[6],[7]
BTs are brown in color on gross examination due to a rich vascularity, hemorrhage, and hemosiderin deposition. The microscopic examination shows typically osteoclast-like multinucleated giant cells and hemosiderin scattered in a fibrovascular stroma. BTs are histologically similar to other giant cell lesions such as a giant cell tumor, aneurysmal bone cyst, and a reparative giant cell granuloma. [5] There are no obvious radiological features. Only the clinical manifestations and endocrinological status help in differentiating BTs from other giant cell lesions.
The mainstay in the treatment or prevention of occurrence of a BT is the elimination of the underlying metabolic disorder. Keeping calcium and phosphate levels within a normal range in patients with CRF is essential for the prevention of SHP. Total or subtotal parathyroidectomy may be indicated as it promotes bony remineralization, rapid bone healing, and resolution of the tumor tissue. [6] Patients without neurological deficit often show tumor regression following a parathyroidectomy and medical treatment for hyperparathyroidism. [7],[8],[9],[10] Even when surgery is required for a lesion compressing the thecal sac, to ensure complete tumor resolution and to prevent recurrence, a parathyroidectomy and bisphosphonate therapy before and after surgery may be necessary. [3] Serum phosphate levels should be controlled, dietary phosphorus intake restricted, and a high phosphate clearance dialyzer selected. Use of phosphate binders, vitamin D, oral calcium supplements, and calcimimetics are recommended as treatment. [4] The present case represents the second published report of a patient with a BT induced by residual parathyroid tissue. [6]
The aim of surgery in the present case was to eliminate pressure on the thecal sac and to promote spinal stability. Osteoporosis and impaired bone healing may often interfere with bony fusion. [11]
Thus, BTs should be considered in the differential diagnosis of spinal lesions of patients with CRF. Patients who have had a parathyroidectomy should be followed at regular interval for recurrence.
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[Figure 1], [Figure 2], [Figure 3]
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