Musculoskeletal ImagingHyperparathyroidism
a condition in which increased levels of
parathyroid hormone are found in the blood. Three types are recognized: primary, secondary and tertiary. In the primary form increased
parathyroid hormone secretion occurs as a result of abnormality in one or more of the
parathyroid glands, usually owing to the presence of
adenoma or
carcinoma. In this form the fundamental biochemical finding is persistent
hypercalcaemia. The secondary form is associated with abnormalities of
parathyroid gland function induced by a sustained hypocalcaemic stimulus, often resulting from chronic
renal failure or malabsorption states. In this variety,
renal abnormality is associated with additional soft tissue and skeletal changes, and the entire complex is termed
renal
osteodystrophy. Tertiary hyperparathyroidism is found in patients with chronic
renal failure or malabsorption and secondary hyperparathyroidism of long duration who develop relatively autonomous
parathyroid function and hypercalcaemia. The clinical features of primary and secondary hyperparathyroidism differ in some respects (Table 1).
Hyperparathyroidism, Table 1. Primary versus secondary hyperparathyroidism.
| Findings | Primary hyperparathyroidism | Secondary hyperparathyroidism * |
|---|
| Brown tumours | Common | Less common |
| Osteosclerosis | Rare | Common |
| Chondrocalcinosis | Not infrequent | Rare |
| Periostitis | Rare | Not infrequent |
* Additional findings of renal osteodystrophy are observed in association with secondary hyperparathyroidism, including rickets, osteomalacia, and soft tissue and vascular calcification.
Hyperparathyroidism leads to considerable bone erosion involving subperiosteal, intracortical, endosteal, trabecular, subchondral and subligamentous foci. In renal osteodystrophy, additional features are noted, including osteomalacia, osteoporosis, and soft tissue and vascular calcification. Haemodialysis and renal transplantation may cause these findings to become exaggerated or arrested.
Bone tissue in hyperparathyroidism demonstrates osteitis fibrosa cystica, with replacement of marrow elements by highly vascular fibrous tissue, as well as osteoporosis and osteomalacia. Localized cysts or brown tumours may also be seen.
Bone resorption in the hands can be identified in the early stages of the disease by high quality radiography of this region. Subperiosteal resorption of cortical bone is virtually diagnostic of hyperparathyroid bone disease. Brown tumours, representing localized accumulations of fibrous tissue and giant cells, can replace bone and even may produce osseous expansion (Fig.1).
Brown tumours appear as single or multiple well-defined lesions of the axial or appendicular skeleton. Common sites of involvement are the facial bones, pelvis, ribs and femora.
Bone sclerosis, marked by diffuse increase in bone density, may be apparent in the metaphyseal regions of the long bones, the skull or the vertebral endplates. In addition, deposition of bone in the subchondral areas of the vertebral bodies leads to the appearance of radiodense bands across the superior and inferior margins (rugger jersey spine).
Primary hyperparathyroidism is frequently associated with chondrocalcinosis. Other rheumatologic manifestations include capsular and ligamentous laxity, as well as rupture, contributing to joint instability, traumatic synovitis, and cartilaginous and osseous destruction. Monosodium urate crystal deposition and clinical gout have also been described in patients with hyperparathyroidism.
Familial multiple en endocrine neoplasia, type I, an autosomal dominant disease associated with primary hyperparathyroidism, is characterized by nonsecretory neoplastic masses, including lipomas, pituitary chromophobe adenomas, carcinoid tumours and adrenal and thyroid adenomas.
DR/RB
DR/RB