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Year : 2020  |  Volume : 35  |  Issue : 3  |  Page : 253-254  

Skeletal changes in hypoparathyroidism: X-ray to bone scintigraphy


Department of Nuclear Medicine, Jawaharlal Institute of Post Graduate Medical Education and Research, Puducherry, India

Date of Submission29-Feb-2020
Date of Acceptance16-Mar-2020
Date of Web Publication01-Jul-2020

Correspondence Address:
Dr. Vishnukumar Rajaraman
Department of Nuclear Medicine, Jawaharlal Institute of Post Graduate Medical Education and Research, Puducherry
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnm.IJNM_40_20

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   Abstract 


Parathyroid hormone (PTH) is a key in maintaining calcium homeostasis. Decreased PTH will result in decreased bone remodeling and increased bone density. The major cause is iatrogenic injury to parathyroid gland. X-ray and dual-energy X-ray absorptiometry are used to identify the skeletal changes. Typical skeletal changes are metaphyseal sclerosis in long bones and sclerosis of vertebrae and pelvic bones. 99mTc methylene diphosphonate scintigraphy is used to identify metabolic bone diseases. There are no typical scan findings in case of hypoparathyroidism. We like to report an interesting image of skeletal scintigraphy in case of hypoparathyroidism.

Keywords: Bone scan, hypoparathyroidism, 99mTc methylene diphosphonate


How to cite this article:
Seetharam S J, Rajaraman V, Pandit N. Skeletal changes in hypoparathyroidism: X-ray to bone scintigraphy. Indian J Nucl Med 2020;35:253-4

How to cite this URL:
Seetharam S J, Rajaraman V, Pandit N. Skeletal changes in hypoparathyroidism: X-ray to bone scintigraphy. Indian J Nucl Med [serial online] 2020 [cited 2020 Aug 9];35:253-4. Available from: http://www.ijnm.in/text.asp?2020/35/3/253/288462



Parathyroid hormone (PTH) is a key in maintaining calcium homeostasis. Decreased PTH will result in decreased bone remodeling and increased bone density. Causes include iatrogenic, autoimmune diseases, genetic or infiltrative disorders, and ionizing radiation exposure, with the major cause being accidental removal or injury of parathyroid glands during neck surgeries.[1]

Skeletal changes are diagnosed using X-ray and dual-energy X-ray absorptiometry. Bone scan is not routinely done to rule out the involvement, but can show findings related to bone metabolism. Radiographic features include generalized or localized osteosclerosis and ossification or calcification of anterior longitudinal ligaments of spine. Occasionally, dense metaphyseal bands and enthesopathy can be seen on radiographs.[2],[3]

We had done dual-phase 99m Tc methylene diphosphonate (MDP) skeletal scintigraphy for a 21-year-old male patient, who was incidentally diagnosed to have hypoparathyroidism (serum PTH – 6 pg/ml; intact PTH – 7.4 pg/ml; serum calcium – 6 mg/dl; and serum inorganic phosphorous – 5.5 mg/dl). The patient had no neck surgeries in the past. He was also a known case of nephrotic syndrome. He was being evaluated for idiopathic hypoparathyroidism or autoimmune hypoparathyroidism. The patient had no history of trauma to bones. X-ray of the pelvis[Figure 1] showed sclerotic bands in the bilateral acetabulum (right > left) and head and neck of the bilateral femur. X-ray of bilateral knee joints [Figure 2] showed metaphyseal sclerotic band in the distal 3rd of bilateral femur and proximal 3rd of bilateral tibia.
Figure 1: X-ray of the pelvis showing sclerotic bands in the bilateral acetabulum (right > left) and head and neck of bilateral femur

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Figure 2: X-ray of bilateral knee joints showing metaphyseal sclerotic bands in the distal 3rd of bilateral femur and proximal 3rd of bilateral tibia

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Tissue-phase images [Figure 3] showed abnormally increased tracer distribution in the regions of bilateral costochondral junction, bilateral iliac bone, bilateral sacroiliac joints, bilateral hip joints, and bilateral tibia. Delayed images [Figure 3] showed abnormally increased tracer uptake in the proximal 3rd of bilateral humerus; bilateral sternoclavicular joint; bilateral costochondral junction; costovertebral junctions; bilateral sacroiliac joints; bilateral iliac crest; bilateral acetabulum (right >left); head, neck, and distal 3rd of bilateral femur; and proximal 3rd of bilateral tibia. Relatively less uptake is noted in bilateral ribs. Increased tracer uptake is noted along the sclerotic areas. Additional bilateral costochondral and costovertebral junction involvement was noted in bone scan. It can be due to enthesitis, which can rarely happen in chronic hypoparathyroidism or can be due to renal osteodystrophy due to the underlying nephrotic syndrome. Focal increased tracer uptake noted in the right maxillary region was due to sinusitis.
Figure 3: Dual-phase bone scan images showing increased tracer uptake in multiple bones in both phases

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Limited literature is available regarding the bone scan changes in hypoparathyroidism. PTH is responsible for the modulation of osteoprogenitor cells. It reduces the conversion of osteoclasts to osteoblasts. In chronic hypoparathyroidism, there can be net increase in osteoblastic activity, leading to the increased bone mineral density and sclerosis noted in multiple long bones.[4],[5] In some cases, enthesitis of spinal ligaments can happen similar to psoriatic arthritis.[6]99m Tc MDP uptake is expected in the sites of increased osteoblastic activity. This explains the uptake pattern noted in our case. Bone scan can be useful to identify the skeletal involvement in cases of hypoparathyroidism.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Silva BC, Rubin MR, Cusano NE, Bilezikian JP. Bone imaging in hypoparathyroidism. Osteoporos Int 2017;28:463-71.  Back to cited text no. 1
    
2.
Guglielmi G, Scalzo G, Cascavilla A, Salaffi F, Grassi W. Imaging of the seronegative anterior chest wall (ACW) syndromes. Clin Rheumatol 2008;27:815-21.  Back to cited text no. 2
    
3.
Lenchik L, Sartoris DJ. Orthopedic aspects of metabolic bone disease. Orthop Clin North Am 1998;29:103-34.  Back to cited text no. 3
    
4.
Hod N, Bistritzer T, Mordish Y, Horne T. Multiple vertebral compression fractures induced by hypocalcemic tetany in a patient with DiGeorge's syndrome detected on bone scintigraphy. Isr Med Assoc J 2005;7:348.  Back to cited text no. 4
    
5.
Krishnamurthy GT, Brickman AS, Blahd WH. Technetium-99m-Sn-pyrophosphate pharmaco-kinetics and bone image changes in parathyroid disease. J Nucl Med 1977;18:236-42.  Back to cited text no. 5
    
6.
Chang CY, Rosenthal DI, Mitchell DM, Handa A, Kattapuram SV, Huang AJ. Imaging Findings of metabolic bone disease. Radiographics 2016;36:1871-87.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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