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Year : 2005  |  Volume : 15  |  Issue : 4  |  Page : 485-487
Classical case of primary hyperparathyroidism


S.S.G. Hospital, Medical College Baroda, Vadodara, Gujarat - 390001, India

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Keywords: Hyperparathyroidism, Skeletal, Neoplasia

How to cite this article:
Sharma P, Parikh K, Chhabra A P, Kapadia B, Vorha P A, Verma S. Classical case of primary hyperparathyroidism. Indian J Radiol Imaging 2005;15:485-7

How to cite this URL:
Sharma P, Parikh K, Chhabra A P, Kapadia B, Vorha P A, Verma S. Classical case of primary hyperparathyroidism. Indian J Radiol Imaging [serial online] 2005 [cited 2020 Jul 7];15:485-7. Available from: http://www.ijri.org/text.asp?2005/15/4/485/28780

   Introduction Top


Primary hyperparathyroidism is a condition caused by an overproduction of PTH, in excess of the amount required by the body. The classical findings of advanced hyperparathyroid skeletal disease are rarely encountered today in western countries but are still seen in developing countries. 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.


   Case report Top


A forty years old female was admitted in our hospital with a history of severe pain in the left forearm and left ankle following trivial injury. She had difficulty in walking and a swelling in left lower leg. She had pain in the ankle along with painful movements of the ankle joint for about two years.

Radiograph of the forearm revealed a pathological fracture of both radius and ulna and the radiograph of the left lag with ankle revealed an expansile lytic multiseptated lesion [Figure - 1]. In view of the pathological fracture of the forearm and swelling in left ankle radiographs of the hands and skull were taken. An ultrasound examination of the abdomen revealed no abnormality. The skull radiograph [Figure - 2] granular appearance of the skull with multiple areas of normal bone interspaced between giving typical "Pepper pot skull" appearance with loss of distinction of inner & outer table and loss of lamina dura. The radiographs of the hands [Figure - 3] showed osteopinea with acroosteolysis with lytic expansile lesions in the metacarpals.

Ultrasound neck [Figure - 4]of the patient reveled There was a 1.5 x 1.5 cm hypoechoic lesion noted on the left side near the postero-inferior surface of the thyroid gland with few specks of calcification seen within it. Possibility of parathyroid adenoma was kept and fine needle aspiration cytology advised.

Relevant abnormal biochemical parameters were -raised serum calcium (11.9 mg/dl [Normal - 9-10.5mg/dL]), raised alkaline phosphatase (717 U/L[Normal - 30-120U/L]), low inorganic phosphorus (1.3 mg/dl[Normal - 3-4.5mg/dL]) and raised serum parathyroid hormone (1265 pg/l[Normal - 10-60pg/mL]). Protein electrophoresis for M band was negative.

Fine needle aspiration cytology confirmed the diagnosis of a parathyroid adenoma. Fine needle aspiration cytology from the left ankle swelling revealed some hemorrhagic fluid. The patient underwent surgery and a left lower parathyroidectomy was performed. After surgery the serum PTH(56pg/mL) and serum calcium (10.1 mg/dL) returned to normal.


   Discussion Top


The diagnosis of hyperparathyroidism can be made on the basis of laboratory tests. The value of plain radiography lies not in initial diagnosis but in assessing the severity of the condition and in establishing a means of objective follow up of the patient i.e. in primary hyperparathyroidism skeletal changes are an accepted indication for surgery. In secondary hyperparathyroidism and renal osteodystrophy the production of bone changes or increased soft tissue calcification may reflect the need for changes in therapy. There are three types of hyperparathyroidism primary, secondary and tertiary. In 75-80% of cases of primary hyperparathyroidism, one or more adenomas account for the overproduction, whereas approximately 20% of cases are secondary to diffuse hyperplasia of all glands. Carcinoma accounts for less than 2% of all cases [1],[2],[3]. Adenoma of the parathyroid gland usually involves a single gland, with incidence of multiple adenomas being six percent [1]. Primary hyperparathyroidism primarily involves patients between the age of 40 and 80, with a female predominance of 3 : 1. Secondary hyperparathyroidism involves an increase in PTH levels to meet some bodily requirement. It is a compensatory mechanism that may be due to rickets, osteomalacia, pregnancy, renal insufficiency, calcium deprivation or maternal hypoparathyroidism [1]. Tertiary hyperparathyroidism is due to the development of autonomous parathyroid hyperplasia after long-standing secondary hyperparathyroidism, most often in renal failure.

The effects of hyperparathyroidism on bone are same for primary and secondary hyperparathyroidism. There is increase in bone breakdown (osteoclastic resorption) with subsequent fibrous replacement and reactive osteoblastic activity. There may be microfractures, with subsequent hemorrhage and growth of fibrous tissue and an influx of macrophages. The resulting mass is called a brown tumor because of the brown color of the vascular elements and blood in the mass. This results in the characteristic radiologic features of generalized bone demineralization, resorption, cysts, brown tumors, erosion of the dental lamina dura, and pathologic fractures. Joint cartilage calcification is a common finding in primary hyperparathyroidism [6]. Osteosclerosis and soft tissue calcification in primary hyperparathyroidism is rare. These are more commonly associated with secondary hyperparathyroidism [3]. Other effects of hypercalcemia include nephrolithiasis or nephrocalcinosis, neurologic changes, peptic ulcer disease and pancreatitis [1],[2],[3].

On ultrasound a parathyroid adenoma is seen as a hypoechoic solid mass with Echogenicity less than thyroid gland. About 2% have cystic changes due to degeneration. Rarely may contain specks of calcification. On CT-scan adenoma are seen as hypoattenuating masses with contrast enhancement in 20% cases. On Magnetic Resonance Imaging adenoma has variable appearances mostly intermediate signal intensity on T1 weighted images and increased signal intensity or isointense with fat on T2 weighted images. Technetium 99m pertechnetate-thallium 201 scintigraphy and Magnetic Resonance Imaging are useful in localization of ectopic parathyroid gland. MR imaging and 99mTc 2-methoxyisobutyl-isonitrile (MIBI) scintigraphy have similarly good sensitivity and positive predictive value for the detection of hyperfunctioning parathyroid tissue in patients after surgery. The combination of the two tests provided a substantial increase in sensitivity and positive predictive value [5].

Hereditary hyperparathyroidism is seen in Multiple Endocrine Neoplasia Type - 1 (MEN-1) syndrome with tumors of the anterior pituitary gland and pancreas. In Multiple Endocrine Neoplasia Type - 2a (MEN-2a) parathyroid disease occurs in conjunction with medullary cancer of the thyroid & pheochromocytoma. Another rare syndrome called Jaw Tumor Syndrome is associated with hyperparathyroidism in which there are fibrous jaw tumors with parathyroid adenomas, thyroid cancer, renal cysts and Wilms tumors [8].

Treatment is parathyroidectomy and at higher centers minimally invasive parathyroidectomy using intraoperative nuclear mapping {also called minimally invasive radioguided parathyroidectomy (MIRP)} has become the preferred method of removing parathyroid tumors [7].

 
   References Top

1.Matheson N. The parathyroid and adrenal glands. In: Mann CP, Russel RC (eds). Bailey and Love's Short practice of Surgery 21 ed, London: Chapman & Hall, 1991: 769-775.  Back to cited text no. 1    
2.Yousem DM, Scheff AM. Thyroid and Parathyroid. In: Son PM, Curtin HD. Head and neck imaging 3 ed. Vol 2. St. Louis: Mosby, 1996: 952-975.  Back to cited text no. 2    
3.Resnick D, Niwayama G Parathyroid disorders and renal osteodystrophies In: Resnick D. Diagnosis of bone and joint disorders. 3 ed, Philadelphia: WB Saunders, 1995: 2012-2075  Back to cited text no. 3    
4.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 & Wilkins, 1990 : 1150 - 1178.  Back to cited text no. 4    
5.Gotway MB, Reddy GP, Webb WR, et al: Comparison between MR imaging and 99mTc MIBI scintigraphy in the evaluation of recurrent of persistent hyperparathyroidism. Radiology 2001 Mar; 218(3): 783-90.  Back to cited text no. 5    
6.Dodds WJ, Steinbach HL, Primary hyperparathyroidism and articular cartilage calcification. AJR 1968 ; 104 : 884 - 892.  Back to cited text no. 6    
7.Scott F. Gallagher MD, Daphne W. Denham MD, Michel M. Murr MD and James G. Norman MD. The impact of minimally invasive parathyroidectomy on the way endocrinologists treat primary hyperparathyroidism. "Surgery" 2003:134;910-917.  Back to cited text no. 7    
8.Szabo, J.; Heath, B.; Hill, V.M, et al: Hereditary hyperparathyroidism-jaw tumor syndrome: the endocrine tumor gene HRPT2 maps to chromosome 1q21-q31. Am J Hum Genet ; 56 ; 4 ;Apr 1995: 944-950.  Back to cited text no. 8    

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Correspondence Address:
P Sharma
B-103, Sapan Flats, Near Mother School, Harinagar Road,Gotri, Vadodara
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-3026.28780

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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]

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