Diagnostic Radiology/Musculoskeletal Imaging/Metabolic Basic/Secondary hyperparathyroidism

Parathyroid hormone is the main hormone that maintains a balance of calcium and phosphate in our bodies. When released, parathyroid hormone increases the release of calcium from the bone, reabsorption from the kidney, and secondarily stimulates absorption of calcium from the intestines. It also stimulates secretion of phosphate in the kidney. Hyperparathyroidism is the abnormal secretion of parathyroid hormone.

Clinical Findings edit

The classic medical school clinical findings are "Stones, Bones, abdominal moans, and psychiatric overtones," referring to renal calculi, bone pain, peptic ulcers, pancreatitis, and CNS symptoms (confusion lethargy, weakness). Depending on the etiology, the serum calcium may be elevated and phosphate may be decreased.

Etiology edit

Excessive parathyroid hormone due to an abnormality elsewhere in the body. Most often this is from chronic renal failure where elevated phosphate and +/- decreased calcium lead to chronic stimulation of the parathyroid gland.

Radiology edit

Osteopenia and bone demineralization edit

Osteopenia and bone demineralization are present in all forms of hyperparathyroidism

Subperiosteal resorption edit

Subperiosteal resorption is virtually pathognomonic for hyperparathyroidism and is typically seen at the radial aspect of the middle phalanx of the index and middle fingers.

Phalangeal tuff resorption/acroosteolysis edit

Acroosteolysis differential diagnosis Mnemonic from The Primer:

  • PINCH FO
    • Psoriasis
    • Injury (thermal/frostbite)
    • Neuropathy (congenital insensitivity to pain, diabetes, leprosy, myelomeningocele)
    • Collagen vascular disease (Scleroderma, Raynaud's)
    • Hyperparathyroidism
    • Familial (Hadju-Cheney)
    • Other (Polyvinyl chloride exposure, snake/scorpion venom)

Subchondral resorption edit

  • Subchondral resorption
    • Sacroiliac joints
    • Distal clavicle
    • Pubic symphysis

Salt and Pepper Skull edit

Brown Tumors edit

Brown tumor are more common in patients with primary hyperparathyroidism, however, due to the increased prevalence of secondary hyperparathyroidism, there are more brown tumors from secondary hyperparathyroidism than form primary hyperparathyroidism. It is difficult to differentiate a Brown Tumor from a giant cell tumor or fibrous dysplasia; however, other signs of hyperparathyroidism should be present.

Soft Tissue Calcification edit

  • Primary > Secondary

Chondrocalcinosis edit

  • Secondary > Primary
  • Knee
  • Triangular fibrocartilage
  • Symphysis Pubis

Osteosclerosis edit

  • Secondary > Primary

Periostitis edit

  • Secondary > Primary

Tendon and ligament laxity edit

  • May lead to rupture

Renal osteodystrophy edit

  • General term for the radiology changes associated with renal failure
  • Secondary hyperparathyroidism (as describe above)
  • Also includes:
    • Osteomalacia (Normal osteoid, abnormal mineralization)
    • Demineralized coarsened bones
    • Looser's zones
      • Axillary margin of the scapula
      • Inner femoral neck
      • Ribs
      • Pubic and ischial rami

Looser's zones in the inferior femoral neck

Fig. 9 Looser's zones in the inferior femoral neck

  • Osteosclerosis
  • Rugger Jersey spine

Rugger Jersey spine

Fig. 10 Rugger Jersey spine

  • Soft tissue calcification
  • Vascular calcification

References edit

  • Hyperparathyroidism by Adam Myhre, M.D., University of Washington Department of Radiology
  • Cooper KL. Radiology of metabolic bone disease. Endocrinology Metabolism Clinics of North America. 1989; 18(4): 955-76.
  • Manaster BJ, et al. Musculoskeletal Imaging: the Requisites. Second Edition. Mosby, 2002.
  • Weissleder R, et al. Primer of Diagnostic Imaging. Second Edition. Mosby, 1997.