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
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.