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Orthoplastic Surgery & Orthopedic Care International Journal

Image of Interest Secondary Hyperparathyroidism

SM Rabiul Islam*

Department of Orthopaedic Surgery, Ripas Hospital, Brunei

*Corresponding author: SM Rabiul Islam, Department MS Ortho, FICS Ortho, Orthopaedic Surgeon, Ripas Hospital, Ministry of Health Brunei, Brunei

Submission: January 20, 2018;Published: March 26, 2018

DOI: 10.31031/OOIJ.2018.01.000520

ISSN: 2578-0069
Volume1 Issue4

Case Report

35 year old lady with CKD on haemodialysis for 10 years was admitted with left hip pain after a trivial trauma.Plain radiograph of pelvis including both hips was advised. Based on the pelvic radiographic findingfurther radiographs of hand, shoulder, skull, and spine were obtained (Figure 1).

Figure 1: Examples of biological function of ncRNAs in the heart.

What is the diagnosis?

a. Secondary hyperparathyroidism: Fracture in this case was the result of relatively trivial trauma, raising suspicion of cortical thinning, difficult to manage by ORIF due to poor bone quality. We applied skin traction with close monitoring to avoid bed redden complication and manage fracture. Work up for secondary hyperparathyroidism confirm by serum parathyroid hormone (PTH> 389.9pmol/L), calcium (1.91mmol/L), and phosphorus level (1.55mmol/L).Secondary hyperparathyroidism is characterized by pronounced parathyroid gland hyperplasia resulting from end-organ resistance to parathyroid hormone (PTH). The consequent hyper secretion of PTH depresses calcium levels [1]. The most important cause of secondary hyperparathyroidism is chronic renal insufficiency. The clinical manifestation of secondary hyperparathyroidism includes bone and joint pain, as well as limb deformities.

b. Pathology: Increased levels of parathyroid hormone (PTH) lead to increased osteoclastic activity. The resultant bone resorption produces cortical thinning (subperiosteal resorption) and osteopaenia [2].

c. Preferred examination: Radiographs are the main stays diagnosis of secondary hyperparathyroidism, because the predominant changes are skeletal, with abnormal calcifications at various sites; these calcifications are well depicted on conventional radiographs [2].

What is the typical radiological finding?

a. List of typical radiological findings: Lacativ et al. [3] was obtained from 73 chronic hemodialysis patients with severe HPT2. The regions of radiographic studied were the skull, hands, wrists, clavicles, thoracic and lumbar column, long bones and pelvis. The most common abnormality was subperiosteal bone resorption, mostly at the phalanges and distal clavicles 94%, ‘Rugger jersey spine’ sign was found in 27%. Pathological fractures and deformities were seen in 27% and 33%, respectively. Calcifications were presented in 80%. Brown tumors were present in 37%.

b. Subperiosteal resorption: Classically at the distal phalangeal tufts (acroosteolysis) and along the radial margins of the second and third middle phalanges.

c. Trabecular resorption: Resorption within medullary bone gives bone a granular appearance, with loss of distinct trabecular detail. In the skull, the diploic space is replaced by connective tissue, leading to a speckled appearance (“salt and pepper” skull).

d. Brown tumors: Accumulations of osteoclasts and fibrous tissue. Tend to heal after treatment of the underlying disorder. Eccentric/intracortical, lytic and often expansile. Incidence is greater in primary hyperparathyroidism, but more commonly seen with secondary hyperparathyroidism due to the higher prevalence [3,4].

e. Soft tissue calcifications: More commonly seen in secondary Hyperparathyroidism.

f. Bone sclerosis: More commonly seen in secondary hyperpararthyroidism. Can be seen in the metaphyses of long bones, the skull, or the vertebral body endplates (rugger jersey spine). Progressive hypertrophy of the facial and cranial hones can produce “leontiasis ossea” (lion face), and can mimic Paget disease and fibrous dysplasia [4].


  1. Terai K, Nara H, Takakura K, Mizukami K, Sanagi M, et al. (2009) Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels. Br J Pharmacol 156 (8): 1267-78.
  2. Khan A, Bilezikian J (2000) Primary hyperparathyroidism: pathophysiology and impact on bone. CMAJ 163(2): 184-187.
  3. Lacativa PG, Franco FM, Pimentel JR, Patrício Filho PJ, Gonçalves MD, et al. (2009) Prevalence of radiological findings among cases of severe secondary hyperparathyroidism. Sao Paulo Med J 27(2): 71-77.
  4. Resnick D (2002) Parathyroid disorders and renal osteodystrophy. In: Diagnosis of Bone and Joint Disorders, (4th edn), Saunders, USA.

© 2018 SM Rabiul Islam. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and build upon your work non-commercially.