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Year : 2002  |  Volume : 12  |  Issue : 2  |  Page : 267-270
Extensive skeletal manifestations in a case of primary hyperparathyroidism

Radiology & Imaging Department, International Hospital, GS Road, Giwahati-5 Assam, India

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Keywords: Hyperparathyroidism, Parathyroid Adenoma, Brown Tumors

How to cite this article:
Goswami P, Sarma P K, Sethi S, Hazarika S. Extensive skeletal manifestations in a case of primary hyperparathyroidism. Indian J Radiol Imaging 2002;12:267-70

How to cite this URL:
Goswami P, Sarma P K, Sethi S, Hazarika S. Extensive skeletal manifestations in a case of primary hyperparathyroidism. Indian J Radiol Imaging [serial online] 2002 [cited 2020 Dec 4];12:267-70. Available from:
Classical findings of advanced hyperparathyroid skeletal disease are rarely being encountered today, probably reflecting the earlier detection rate, the greater preponderance of benign chemical hyperparathyroidism and possible preventive effect on bone resorption due to a changing diet with abundant calcium, phosphate and vitamin D. Less than half of the patients with hyperparathyroidism manifest skeletal lesions. We are presenting here classical findings of primary hyperparathyroidism caused by a parathyroid adenoma in a patient along with infrequent and additional atypical findings.

   Case report Top

A thirty eight years old man was admitted in our hospital with a history of severe pain in the right thigh following trivial injury. Even before the injury, he had history of pain in the thigh along with painful movements of the hip joint for more than a year. Radiograph of the thigh revealed a pathological fracture of the right femur. An US examination of the abdomen revealed low echoic collections in the iliac fossa regions bilaterally. Relevant abnormal biochemical parameters were -raised serum calcium (13.8 mg/dl), raised alkaline phosphatase (592 U/L) and low inorganic phosphorus (1.4 mg/dl). Protein electrophoresis for M band was negative. In view of the pathological fracture of the femur, a skeletal survey performed. Findings of the skeletal survey favoured the diagnosis of hyperparathyroidism. The radiographic findings were as follows -

Skull [Figure - 1]: Granular decalcification of the skull, with multiple radiolucent areas due to brown tumors. Multiple radiolucent areas were also seen in the mandible along with loss of lamina dura at places.

Hands [Figure - 2]: Subperiosteal resorption of bone in the radial aspect of the proximal phalanx of the left second finger, erosive changes of the tuft of the right middle finger, brown tumors in the left fifth and right fourth metacarpals and in the right distal radius.

Pelvis [Figure - 3]: Brown tumors and distorted trabecular pattern throughout the pelvis. Brown tumors in both femora with pathological fracture of the right femur.

Knee joints [Figure - 4]: Brown tumors in both femora and right tibia

Chest [Figure - 5]: Brown tumors in the right fourth and fifth ribs

Vertebrae: Multiple wedge vertebrae.

CT thorax was performed which demonstrated the brown tumors in the ribs on the right side more precisely. Rib erosion was also noted on the left side [Figure - 6].

CT of the lower neck was performed which revealed a parathyroid adenoma posterior to the inferior pole of the thyroid gland on the right side [Figure - 7].

In view of the USG Abdomen findings, CT abdomen was performed, which showed low attenuation collections in the iliac fossa regions bilaterally along the lateral margins of the iliopsoas muscles and medial to the iliac bones. The ilium showed brown tumors [Figure - 8]. Guided aspiration of the collection revealed haemorrhagic fluid.

The patient underwent surgery, a right lower parathyroidectomy with partial thyroidectomy was performed. Histopathological examination of the specimen confirmed the diagnosis of a parathyroid adenoma.

   Discussion Top

There are 3 types of hyperparathyroidism primary, secondary and tertiary. Primary hyperparathyroidism is due to a solitary adenoma in 80% of the patients and to glandular hyperplasia in 20%. Rarely is the condition caused by a carcinoma of parathyroid gland. Primary hyperparathyroidism may be associated with multiple endocrine neoplasia (MEN 1 and II) syndromes. Primary hyperparathyroidism primarily involves patients between the age of 40 and 80, with a female predominance of 3: 1. Secondary hyperparathyroidism is a compensatory mechanism that may be due to rickets, osteomalacia, pregnancy, renal insufficiency, calcium deprivation or maternal hypoparathyroidism. Today it most commonly occurs with chronic renal disease [1]. Tertiary hyperparathyroidism is due to the development of autonomous parathyroid hyperplasia after long-standing secondary hyperparathyroidism, most often in renal failure.

The spectrum of manifestations in primary hyperparathyroidism has evolved considerably since 1891, when von Recklinghausen first described the bone disease of osteitis fibrosa cystica. The association of this skeletal disorder with parathyroid gland hyperfunction was not established until 1926, when Mandl performed the first parathyroidectomy on a patient with cystic bone disease [2].

The skeletal changes of primary and secondary hyperparathyroidism are identical. The classical radiographic features of hyperparathyroidism are subperiosteal cortical bone erosions, generalized deossification, bone softening, local destructive bone lesions (brown tumors) and calcification of the soft tissue. Pathological fractures may occur but, are infrequent [1]. Osteosclerosis in primary hyperparathyroidism is rare. It is more commonly associated with secondary hyperparathyroidism [1],[3]. Soft tissue calcification is also commoner in secondary hyperparathyroidism. However, joint cartilage calcification is a common finding in primary hyperparathyroidism [4].

All the skeletal lesions have been described in the literature. However, this patient had an additional atypical finding of low density collections (haemorrhagic on aspiration) in the iliac fossae along the lateral margins of the iliopsoas muscles and medial to the iliac bones. Available literature was reviewed for this atypical finding, but nothing relevant was found. Another finding observed in this patient was a pathological fracture, which is uncommon in hyperparathyroidism.

   References Top

1.Edeiken J, Dalinka M, Karasick D. Metabolic and dystrophic bone disease. In: Edeiken's Roentgen Diagnosis of Diseases of Bone 4th ed. Vol. 2. Baltimore: Williams and Wilkins, 1990: 1150 - 1178.  Back to cited text no. 1    
2.Genant HK, Heck LL, Lanzl LH, Rossmann K, Horst JV, Paloyan E, Primary Hyperparathyroidism: A Comprehensive Study of Clinical, Biochemical and Radiographic Manifestations. Radiology 1973; 109: 513-524.  Back to cited text no. 2    
3.Genant HK, Baron JM, Straus FH II, Paloyan E, Jowsey J. Osteosclerosis in primary hyperparathyroidism. Am J Med 1975; 59: 104 - 113.  Back to cited text no. 3    
4.Dodds WJ, Steinbach HL, Primary hyperparathyroidism and articular cartilage calcification. AJR 1968; 104: 884 - 892.  Back to cited text no. 4    

Correspondence Address:
P Goswami
Radiology & Imaging Department, International Hospital, GS Road, Giwahati-5 Assam
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Source of Support: None, Conflict of Interest: None

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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8]

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