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Table of Contents    
CASE REPORT
Year : 2019  |  Volume : 67  |  Issue : 5  |  Page : 1334-1340

Tumor-induced Osteomalacia due to a Phosphaturic Mesenchymal Tumor in the Cervical Spine: A Case Report and Literature Review


1 Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India
2 Department of Pathology, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication19-Nov-2019

Correspondence Address:
Dr. Nitish Agarwal
R-10/B-3 and B-4, New Rajnagar, Ghaziabad - 201 002, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.271274

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 » Abstract 


Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome of certain mesenchymal tumors which secrete fibroblast growth factor-23 (FGF-23) responsible for causing features of hypophosphatemia and osteomalacia in these patients. Most of them involve the appendicular skeleton and occasionally the craniofacial regions. Involvement of spine is exceedingly rare. Through this paper, the authors present a rare case of a 71-year-old male with TIO due to a lesion in the cervical spine (right C2 lamina) which was proven to be a phosphaturic mesenchymal tumor-mixed connective tissue type on histopathology. This is the fifth reported case of TIO localized to the cervical spine. The patient underwent a hemilaminectomy and gross total resection of the tumor following which he made a gradual but steady recovery and does not have any recurrence 24 months after surgery. The authors not only provide a comprehensive literature review of all 18 spinal cases reported till date but also discuss the management of these patients in light of the published literature.


Keywords: Cervical spine, fibroblast growth factor-23, paraneoplastic syndrome, phosphaturic mesenchymal tumor-mixed connective tissue, tumor-induced osteomalacia
Key Messages: Tumor-induced osteomalacia (TIO) due to a phosphaturic mesenchymal tumor-mixed connective tissue in the spine is exceedingly rare. A complete surgical resection of the lesion with wide margins is the therapy of choice as it ensures biochemical remission and prevents recurrences in most cases.


How to cite this article:
Agarwal N, Kale SS, Kumari K. Tumor-induced Osteomalacia due to a Phosphaturic Mesenchymal Tumor in the Cervical Spine: A Case Report and Literature Review. Neurol India 2019;67:1334-40

How to cite this URL:
Agarwal N, Kale SS, Kumari K. Tumor-induced Osteomalacia due to a Phosphaturic Mesenchymal Tumor in the Cervical Spine: A Case Report and Literature Review. Neurol India [serial online] 2019 [cited 2019 Dec 10];67:1334-40. Available from: http://www.neurologyindia.com/text.asp?2019/67/5/1334/271274


TIO is a rare paraneoplastic syndrome in which tumors, usually of mesenchymal origin and generally histologically benign, secrete molecules that induce renal phosphate wasting.[1] One such molecule, fibroblast growth factor-23 (FGF-23) is a protein notorious for inhibiting renal tubular reabsorption of phosphate, thereby causing hypophosphatemia. Other accompanying abnormalities include inappropriately low blood levels of calcitriol, low-normal serum levels of calcium, and evidence of impaired bone mineralization. In most cases, the clinical symptoms and biochemical derangements resolve soon after complete resection of the lesion.[2]

In this manuscript, we present the case of a 62-year-old man with TIO due to benign lesion involving C2 lamina. Histopathology revealed a PMT-MCT type. His symptoms significantly improved following a complete resection of the lesion and C2 hemilaminectomy and he continues to be disease free at 24 months follow-up. TIO is a rare disorder with over 200 cases reported. Most of them involve the appendicular skeleton and occasionally the craniofacial regions.[3] To the best of our knowledge, only 18 cases of TIO localized to the spine have been so far reported with the present case being only the fifth involving the cervical spine [Table 1].[30],[31],[32],[33],[34],[35],[36],[37],[38]
Table 1: A comprehensive literature review of spinal tumors causing TIO

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We discuss the management of TIO involving the axial skeleton and also present a review of literature.


 » Case History Top


This 62-year-old man presented with a 4-year history of backache, mild to moderate in intensity, aggravating on walking, and partially relieved with rest and analgesics. He also complained of proximal muscle weakness of 3 years with no specific pattern of progression. He also complained of truncal muscle weakness. At the time of presentation, he was unable to do his activities of daily living without the support of family members and was bed bound. However, he denied any sensory loss and bladder or bowel complaints. Only comorbid illness included systemic hypertension of 15 years controlled on medication. There was no history of similar illness in the family. He had received a course of teriparatide 1 year back in view of osteoporosis and multiple vertebral fractures.

On physical examination, the patient was alert and oriented. Cranial nerves II–XII were grossly intact. Motor strength was poor in proximal muscles in all extremities with good distal muscle power and intact sensations throughout. He had no focal or lateralizing neurological deficits.

On evaluation, we found low phosphate (1.3 mg/dl; normal range 2.5–4.5 mg/dl), normal calcium (8.5 mg/dl; normal range 8.1–10.4 mg/dl), normal PTH (79.3 pg/ml; normal range 16–87 pg/ml) and low-normal Vitamin D (35.9 ng/ml; normal range 25–50 ng/ml), low TmP/GFR (0.51; normal range 2.0–3.4 mg/dl), and elevated alkaline phosphatase (ALP) (702 IU/l; normal range 80–240 IU/l).

A skeletal survey revealed diffuse osteopenia (lumbar spine T score – 3.4; Z score – 2.7), multiple vertebral compression fractures, and pseudofracture of right femur. A 68-Ga DOTANOC PET-CT study revealed two nodules in the posterior cervical region at the level of C2 with increased radiotracer uptake [Figure 1]. It was isointense on T1W MRI of cervical spine and heterogeneously hyperintense on T2W sequence. On contrast enhanced MRI, it appeared as a well-defined lesion of heterogenous contrast enhancement abutting the left C2 lamina on its posterolateral aspect and infiltrating the substance of the overlying inferior oblique muscle without any restriction on DWI, suggesting a mesenchymal tumor [Figure 2]. A CT-guided biopsy confirmed the suspicion of a PMT – showing a spindle cell lesion with areas of fibrosis. The cells had small oval nucleus with indistinct cell margins. Immunohistochemically, the cells were positive for Bcl-2 (focal and weak) and MIC2 (focal and weak) but negative for SMA and CD34 [Figure 3].
Figure 1: Preoperative 68-Ga DOTANOC PET Maximum Intensity Projection (MIP) image (left) and fused PET/CT image (right) showing increased radiotracer uptake in the region of left C2 lamina

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Figure 2: Preoperative axial T2W MR image (left) and axial gadolinium enhanced T1W MR image (right) showing tumor involving the left C2 lamina

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Figure 3: Photomicrograph depicting a cellular spindle cell tumor arranged in pattern-less pattern, alternate hypocellular area, interspersed hyalinized vessels, and areas of hemorrhage (a, H and E, ×200). Tumor cell composed of bland spindle cells with indistinct cell border, vesicular nuclei, and inconspicuous nucleoli. Mitotic figure and necrosis are absent (b, ×400). Hemangiopericytoma-like vasculature and microcyst formation (c, ×400). Tumor cells are immunopositive for vimentin (d, ×400). Immunonegative for cytokeratin, EMA, Mic-2, Bcl 2, CD 34, desmin, SMA, and Stat 6 (e-l ×400)

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Decision to excise the offending lesion was taken and a written informed consent obtained. Intraoperatively, on exposure of C1–C3 posterior elements, there was evidence of a grayish-white, moderately vascular, firm lesion attached to left C2 lamina, also involving the overlying obliquus capitis inferior muscle. All of the macroscopically visible tumor was excised with margins along with a left C2 hemilaminectomy. Care was taken to avoid injury to C1 nerve root and the horizontal part of vertebral artery within the suboccipital triangle. Rectus capitis muscles appeared normal and were left untouched.

Patient had an uneventful postoperative course and was discharged on the second postoperative day.

On follow-up, patient had a good clinical recovery. Serum phosphate was within normal range on the sixth postoperative day and was 3.5, 3.9, and 4.1 mg/dl at 3, 12, and 24-month follow–up, respectively. He started walking with support of a frame at 3 months and without support at 6 months post-op. Back pain gradually improved over a period of 12 months. On 24 months follow-up visit, patient had no e/o residual/recurrent disease [Figure 4] and could perform all his activities of daily living without difficulty and presently taking oral calcitriol supplementation alone.
Figure 4: Postoperative non contrast computed tomographycervical spine axial image (right) at C2 level with evidence of left hemilaminectomy. Twenty-four months postoperative axial T2W MR image (left) and axial gadolinium enhanced T1W MR image (center) showing postoperative changes at C2 level and no e/o residual/recurrent tumor

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 » Discussion Top


Osteomalacia is the impaired mineralization of bone matrix proteins. Apart from calcium and vitamin D deficiency, osteomalacia may also occur with chronic hypophosphatemia.[1] Tumor-induced osteomalcia is a syndrome of hypophosphatemia characterized by excessive secretion of FGF-23 by certain mesenchymal tumors.[4]

TIO was first described by McCance in 1947 in a young girl who presented with vitamin D-resistant osteomalacia acquired at the age of 15 years.[5] Prader and colleagues, in 1959, first described a “rachitogenic” substance secreted from a “giant cell tumor” in a rib as the basis of this disease in a 11.5-year old girl with rickets.[6] FGF-23 is one such substances which inhibits reabsorption of phosphate in the proximal renal tubule. In addition, it inhibits the hydroxylation of 25 hydroxy vitamin D (25OHD) leading to decreased plasma levels of calcitriol.[7]

Clinically, patients of TIO present with bone pains, insufficiency fractures, and proximal muscle weakness.[2] In pediatric patients, the disease manifests as rickets and growth retardation.[8] More commonly, it involves the appendicular skeleton or craniofacial regions. Involvement of axial skeleton is rare. To the best of our knowledge, only 18 cases, including the present case, have been reported thus far with the present case being only fifth reported case in cervical spine. In a literature review of all spinal cases of TIO, thoracic spine was found to be the most common site of involvement. Bone pain was the most consistent symptom (all cases) with no gender predilection of the disease (nine male and nine female patients). Diagnosis is often delayed due to small size and peculiar locations. In the present case, diagnosis with precise localization of tumor could be done after 4 years. This was similar to the findings of the literature review – mean duration of disease at diagnosis was 3 years 10 months.

Hypophosphatemia due to hyperphosphaturia is the most consistent lab finding, although nonphosphaturic variant has also been reported.[9] Raised serum FGF-23 supports the diagnosis; however, it is not diagnostic as constitutive overexpression is seen in X-linked and autosomal-dominant hypophosphatemia rickets.[10] Serum FGF levels were not done in the present case due to logistic issues. Other notable biochemical abnormalities include low serum vitamin D3 levels due to inhibition of one alpha hydroxylase by FGF-23, leading to fall in levels of serum phosphorus and a profound hypophosphatemia. This dual defect of renal phosphate wasting and impaired calcitriol synthesis is the cause of poor bone mineralization and fractures.[2] Increased bone turnover results in raised serum ALP levels.

In addition to clinical and laboratory parameters, diagnosis and localization of a PMT relies on optimal imaging investigations. Chong and colleagues,[8] in their review article, lucidly describe a stepwise approach in the utilization of imaging – first performing functional imaging – FDG-PET/CT,111 Indium octreotide scintigraphy, ideally combined with single photon emission CT and CT (SPECT/CT), and the more recently advocated 68Ga-DOTANOC PET/CT. There is evidence in favor of octreotide scintigraphy with SPECT/CT as the best initial study as it provides the combination of best specificity and sensitivity.[11],[12] Following identification of suspicious areas or when no lesions are identified on functional imaging, anatomic imaging X-rays, CT, and MRI may be carried out.

In this literature review of spinal cases of TIO, PET/CT was useful in localizing the tumor in almost all cases where the lesion could not be clinically localized. For others, MRI or CT specific to the clinical level could detect lesion in most cases. Chua et al. demonstrated the diagnostic value of FDG-PET in localizing oncogenic osteomalacia causing nonmesenchymal tumors in the setting of background postoperative changes, including bone grafting and metallic artifacts where MRI could not be used.[13] Maehara et al. concluded that a 68-Ga DOTATOC PET/CT for somatostatin receptor imaging for localization of PMT is better than MRI or CT.[14] Short tau inversion recovery whole body MRI has been found to be highly useful (although very costly) in detection of tumors causing oncogenic osteomalacia in various case reports.[1],[3],[6],[10] In the present case, lesion at C2 level was detected using an 68-Ga DOTANOC PET/CT. Subsequent MRI and CT scan of the cervical spine revealed the anatomical extent of the lesion.

On histopathology, majority of the tumors (13 out of 18) were phosphaturic mesenchymal tumors. Osteoblastoma, osteosarcoma, hemangiopericytoma, and plasmacytoma were the other causes of oncogenic osteomalacia in this review. In 2004, Folpe et al. did a comprehensive review of mesenchymal tumor-associated oncogenic osteomalacia and concluded that most of these cases belong to a single histopathologic entity of PMT-MCT variant.[3] These tumors are mostly benign with low cellularity, myxoid change, bland spindled cells, distinctive “grungy”-calcified matrix, fat, HPC-like vessels, microcysts, hemorrhage, osteoclasts, and an incomplete rim of membranous ossification, although malignant hypercellular variants with cytological atypia are also known to occur.[3] Weidner and Cruz[15] studied four PMT-MCT tumors immunohistochemically and three of these tumors revealed only vimentin immunoreactivity within the primitive-appearing tumor cells. All other reagents (desmin, S-100 protein, leu-M 1, chromogranin, cytokeratin, neuron-specific enolase, leukocyte common antigen, and factor VIII-related antigen) were nonreactive in tumor cells. The tumor cells in the present case had similar findings on immunohistochemistry [Figure 3].

A complete surgical resection of the lesion with wide margins to ensure biochemical remission and prevent recurrences is the therapy of choice.[16],[17],[18] There is evidence in literature which suggests that for phosphaturic mesenchymal tumors arising from bone, intralesional procedures may not be sufficient and wide resection should be performed wherever possible.[17] Care should be taken to make all cuts in the bone outside the tumor margin to ensure minimal spillage.[19],[20] Sciubba et al.[21] and Meng et al.[19] have suggested en bloc spondylectomy for these tumors. In regions where resection with wide margins is technically difficult, intralesional excision should be considered. Nakamura and colleagues performed an intralesional excision and demonstrated successful bony union with noninstrumented fusion using iliac struts in a patient with tumor of C5 vertebra. They found no evidence of local recurrence or metastasis after a 5-year follow-up.[22]

In addition, a key point is that osteomalacia may predispose to nonunion or delayed union; hence, rigid internal fixation with multiple fixation points and augmented pedicular screws should be considered and effective postoperative bracing can be helpful.[23],[24]

In the previously reported cases in spine, persistent serum abnormalities were reported in all 3 cases where a subtotal tumor excision was performed and in only 1 of the 15 cases where a gross total excision was done [Table 1]. In eight cases of fusion following tumor excision in the spine (out of a total of 18 cases), only one in the cervical spine has been a noninstrumented fusion [Table 1].

Fusion was not necessary in the present case as a complete excision with margins could be achieved with hemilaminectomy. Following surgery, serum phosphate levels usually return to normal within a week and symptomatic improvement is seen over a period of 3–6 months.[18],[25]

Radiotherapy is the therapeutic option for unresectable tumors or for incompletely resected tumors.[16],[26],[27]

For patients with no clear documented evidence of tumor with symptomatic hypophosphatemic osteomalacia/rickets, medical management is advised.[8],[16],[18] It includes phosphorus and calcitriol supplementation. However, it is not effective in long term and patients should be monitored for potential complications of hyperparathyroidism, hypercalcemia, and nephrolithiasis.[18]

Other proposed treatment options include radiofrequency ablation for small bony tumors in critical locations[28] and a new treatment approach using cinacalcet, a calcium sensing receptor agonist.[29]

Serum phosphate and FGF-23 levels correlate with recurrence of disease and can be used for postoperative screening. FGF-23, although a more direct marker of tumor activity, is expensive and logistically demanding. The test was not performed in the present case due to its unavailability at our center. The patient did not show any symptomatic, radiological, or biochemical evidence of tumor recurrence at 18-month follow-up.


 » Conclusion Top


TIO due to a PMT-MCT in the spine is exceedingly rare. This manuscript presents a case of this tumor in the cervical spine which is only the fifth reported case in this region. The patient had a drastic improvement in terms of clinical and biochemical parameters following complete resection and continued to be disease free at 24 months follow-up. The manuscript also includes an exhaustive literature review of all the published cases of TIO due to a tumor in the spine to the best of our knowledge.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Khosla S. Hypercalcemia and hypocalcemia [Internet]. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill Education; 2015.  Back to cited text no. 1
    
2.
janlebeursm.pdf [Internet]. Available from: http://www.hopkinsmedicine.org/johns_hopkins_bayview/_docs/education_training/grand_rounds_presentations/janlebeursm.pdf. [Last accessed on 2017 Oct 04].  Back to cited text no. 2
    
3.
Folpe AL, Fanburg-Smith JC, Billings SD, Bisceglia M, Bertoni F, Cho JY, et al. Most osteomalacia-associated mesenchymal tumours are a single histopathologic entity: An analysis of 32 cases and a comprehensive review of the literature. Am J Surg Pathol 2004;28:1-30.  Back to cited text no. 3
    
4.
Fukumoto S. Diagnostic modalities for FGF23-producing tumours in patients with tumour-induced osteomalacia. Endocrinol Metab 2014;29:136-43.  Back to cited text no. 4
    
5.
McCance RA. Osteomalacia with Looser's nodes (Milkman's syndrome) due to a raised resistance to vitamin D acquired about the age of 15 years. Q J Med 1947;16:33-46.  Back to cited text no. 5
    
6.
Prader A, Illig R, Uehlinger E, Stalder G. Rickets following bone tumour. Helv Paediatr Acta 1959;14:554-65.  Back to cited text no. 6
    
7.
Quarles LD. Role of FGF23 in vitamin D and phosphate metabolism: Implications in chronic kidney disease. Exp Cell Res 2012;318:1040–8.  Back to cited text no. 7
    
8.
Chong WH, Molinolo AA, Chen CC, Collins MT. Tumour-induced osteomalacia. Endocr Relat Cancer 2011;18:R53-77.  Back to cited text no. 8
    
9.
Mavrogenis AF, Sakellariou VI, Soultanis K, Mahera H, Korres DS, Papagelopoulos PJ. A Nonphosphaturic mesenchymal tumour mixed connective tissue variant of the sacrum. Orthopedics 2010;33:851.  Back to cited text no. 9
    
10.
Jonsson KB, Zahradnik R, Larsson T, White KE, Sugimoto T, Imanishi Y, et al. Fibroblast growth factor 23 in oncogenic osteomalacia and x-linked hypophosphatemia. N Engl J Med 2003;348:1656-63.  Back to cited text no. 10
    
11.
Chong WH, Andreopoulou P, Chen CC, Reynolds J, Guthrie L, Kelly M, et al. Tumour localization and biochemical response to cure in tumour-induced osteomalacia. J Bone Miner Res 2013;28:1386-98.  Back to cited text no. 11
    
12.
Jadhav S, Kasaliwal R, Lele V, Rangarajan V, Chandra P, Shah H, et al. Functional imaging in primary tumour-induced osteomalacia: Relative performance of FDG PET/CT vs somatostatin receptor-based functional scans: A series of nine patients. Clin Endocrinol (Oxf) 2014;81:31-7.  Back to cited text no. 12
    
13.
Chua SC, O'Connor SR, Wong WL, Ganatra RH. Case report: Solitary plasmacytoma of bone with oncogenic osteomalacia: Recurrence of tumour confirmed by PET/CT. A case report with a review of the radiological literature. Br J Radiol 2008;81:e110-4.  Back to cited text no. 13
    
14.
Maehara J, Yamashita K, Hiwatashi A, Togao O, Kikuchi K, Matsumoto Y, et al. Primary phosphaturic mesenchymal tumour of the lumbar spine: Utility of 68Ga-DOTATOC PET/CT findings. BJR Case Rep 2016;2. doi: 10.1259/bjrcr.20150497.  Back to cited text no. 14
    
15.
Weidner N, Cruz DS. Phosphaturic mesenchymal tumours. A polymorphous group causing osteomalacia or rickets. Cancer 1987;59:1442-54.  Back to cited text no. 15
    
16.
Hautmann AH, Hautmann MG, Kölbl O, Herr W, Fleck M. Tumour-induced osteomalacia: An up-to-date review. Curr Rheumatol Rep 2015;17:512.  Back to cited text no. 16
    
17.
Ledford CK, Zelenski NA, Cardona DM, Brigman BE, Eward WC. The phosphaturic mesenchymal tumour: Why is definitive diagnosis and curative surgery often delayed? Clin Orthop 2013;471:3618-25.  Back to cited text no. 17
    
18.
Zuo Q, Wang H, Li W, Niu X, Huang Y, Chen J, et al. Treatment and outcomes of tumour-induced osteomalacia associated with phosphaturic mesenchymal tumours: Retrospective review of 12 patients. BMC Musculoskelet Disord 2017;18:403.  Back to cited text no. 18
    
19.
Meng T, Zhou W, Li B, Yin H, Li Z, Zhou L, et al. En bloc resection for treatment of tumour-induced osteomalacia: A case presentation and a systematic review. World J Surg Oncol 2015;13:176.  Back to cited text no. 19
    
20.
Puthenveetil PJ, Hattab EM, Peacock M, Horn EM. Thoracic phosphaturic mesenchymal tumours causing oncogenic osteomalacia. J Clin Neurosci 2013;20:1057-61.  Back to cited text no. 20
    
21.
Sciubba DM, Petteys RJ, Shakur SF, Gokaslan ZL, McCarthy EF, Collins MT, et al. En bloc spondylectomy for treatment of tumour-induced osteomalacia. J Neurosurg Spine 2009;11:600-4.  Back to cited text no. 21
    
22.
Nakamura T, Aizawa T, Hoshikawa T, Ozawa H, Ito N, Fukumoto S, et al. Tumour-induced osteomalacia caused by phosphaturic mesenchymal tumour of the cervical spine. J Orthop Sci 2015;20:765-71.  Back to cited text no. 22
    
23.
DeWald CJ, Stanley T. Instrumentation-related complications of multilevel fusions for adult spinal deformity patients over age 65: Surgical considerations and treatment options in patients with poor bone quality. Spine 2006;31:S144-51.  Back to cited text no. 23
    
24.
Dipaola CP, Bible JE, Biswas D, Dipaola M, Grauer JN, Rechtine GR. Survey of spine surgeons on attitudes regarding osteoporosis and osteomalacia screening and treatment for fractures, fusion surgery, and pseudoarthrosis. Spine J 2009;9:537-44.  Back to cited text no. 24
    
25.
Yu WJ, He JW, Fu WZ, Wang C, Zhang ZL. Reports of 17 Chinese patients with tumour-induced osteomalacia. J Bone Miner Metab 2017;35:298-307.  Back to cited text no. 25
    
26.
Hautmann AH, Schroeder J, Wild P, Hautmann MG, Huber E, Hoffstetter P, et al. Tumour-induced osteomalacia: Increased level of FGF-23 in a patient with a phosphaturic mesenchymal tumour at the tibia expressing periostin. Case Rep Endocrinol [Internet] 2014;2014. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4158256/. [Last accessed on 2017 Oct 10].  Back to cited text no. 26
    
27.
Tarasova VD, Trepp-Carrasco AG, Thompson R, Recker RR, Chong WH, Collins MT, et al. Successful treatment of tumour-induced osteomalacia due to an intracranial tumour by fractionated stereotactic radiotherapy. J Clin Endocrinol Metab 2013;98:4267-72.  Back to cited text no. 27
    
28.
Hesse E, Rosenthal H, Bastian L. Radiofrequency ablation of a tumour causing oncogenic osteomalacia. N Engl J Med 2007;357:422-4.  Back to cited text no. 28
    
29.
Geller JL, Khosravi A, Kelly MH, Riminucci M, Adams JS, Collins MT. Cinacalcet in the management of tumour-induced osteomalacia. J Bone Miner Res 2007;22:931-7.  Back to cited text no. 29
    
30.
Boriani S, Campanacci M. Osteoblastoma associated with osteomalacia (presentation of a case and review of the literature). Ital J Orthop Traumatol 1978;4:379-82.  Back to cited text no. 30
    
31.
Stone MD, Quincey C, Hosking DJ. A neuroendocrine cause of oncogenic osteomalacia. J Pathol 1992;167:181-5.  Back to cited text no. 31
    
32.
Yu GH, Katz RL, Raymond AK, Gagel RF, Allison A, McCutcheon I. Oncogenous osteomalacia: Fine needle aspiration of a neoplasm with a unique endocrinologic presentation. Acta Cytol 1995;39:831-2.  Back to cited text no. 32
    
33.
Terek RM, Nielsen GP. Case 29-2001 — A 14-year-old boy with abnormal bones and a sacral mass. NEJM 2001;345:903-8.  Back to cited text no. 33
    
34.
Dissanayake AM, Wilson JL, Holdaway IM, Reid IR. Oncogenic osteomalacia: Culprit tumour detection whole body magnetic resonance imaging. Intern Med J 2003;33:615-6.  Back to cited text no. 34
    
35.
Pirola E, Vergani F, Casiraghi P, Leone EB, Guerra P, Sganzerla EP. Oncogenic osteomalacia caused by a phosphaturic mesenchymal tumour of the thoracic spine. J Neurosurg Spine 2009;10:329-33.  Back to cited text no. 35
    
36.
Marshall AE, Martin SE, Agaram NP, Chen JH, Horn EM, Douglas-Akinwande AC, et al. A 61-year-old woman with osteomalacia and a thoracic spine lesion. Brain Pathol Zurich Switz 2010;20:499-502.  Back to cited text no. 36
    
37.
Akhter M, Sugrue PA, Bains R, Khavkin YA. Oncogenic osteomalacia of the cervical spine: A rare case of curative resection and reconstruction. J Neurosurg Spine 2011;14:453-6.  Back to cited text no. 37
    
38.
Gandhi GY, Shah AA, Wu KJ, Gupta V, Shoraka AR. Tumour-induced osteomalacia caused by primary fibroblast growth factor 23 secreting neoplasm in axial skeleton: A case report. Case Rep Endocrinol 2012;2012:185454.  Back to cited text no. 38
    


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