Rheumatic Manifestations of Endocrine Diseases

Joseph A. Markenson


Curr Opin Rheumatol. 2010;22(1):64-71. 

In This Article


Parathyroid hormone (PTH) along with vitamin D and calcitonin controls calcium homeostasis. These hormones are responsible for bone metabolism and remodeling in addition to maintaining serum calcium in a very narrow range. In primary hyperparathyroidism this balance is altered due to changes in the parathyroid gland, whereas changes in other organs of the body which result in calcium loss and vitamin D deficiency with increased secretion of PTH are called secondary hyperparathyroidism.[32] In 1959 Bywaters[33] first reported articular symptoms related to these skeletal changes and descriptions of other rheumatic syndromes soon followed.

Approximately 1–2% of the population has hypercalcemia with 10–20% of these having hyperparathyroidism (HPT).[34] Most patients with HPT have a single adenoma, carcinoma is rare and in secondary hyperparathyroidism diffuse hyperplasia is seen related to hypocalcaemia or resistance to PTH. Secondary HPT is most commonly the result of osteomalacia, vitamin D deficiency and renal failure. Skeletal symptoms include arthralgias, as well as radiographic findings such as osteitis fibrosa cystic and subperiosteal resorption along the radial side of the phalanges. In addition the distal tufts of the phalanges may also reveal superiosteal resorption. Arthritis involves the small joints of the hand (possibly becoming erosive) and sparing the proximal interphalangeal (PIP) joints. In this respect it can mimic RA but the presence of subsperiosteal resorption is very distinctive. In contrast to RA these patients generally have low erythrocyte sedimentation rates, negative rheumatoid factors, and labs consistent with HPT.[35] HPT has more involvement of the radiocarpral, inferior radio ulnar and metacarpophalangeal (MCP) joints than RA. Lytic lesions secondary to HPT in the skeleton (Brown tumors) are localized areas of fibrous tissue resulting from increased osteoclastic activity, giant cells, and decomposing blood.[36] CPPD (pseudogout or chondrocalcinosis) described by McCarty et al.[37] in 1992 is associated with HPT. Attacks of gout can also be seen in HPT and the concomitant occurrence of uric acid and CPPD crystals can be found in synovial fluid aspirated from acutely inflamed joints.

In addition to the acute attacks of CPPD in chronic CPPD disease erosive disease may also be seen.[38]

Muscle involvement can occur in HPT presenting with proximal muscle weakness. Enzymes are not elevated and EMG studies as well as muscle biopsy demonstrate a picture of denervation.


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