Diagnostic Radiology/Musculoskeletal Imaging/Metabolic Basic/Primary 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
editThe 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 a parathyroid gland abnormality
- 80% parathyroid adenoma
- 12% parathyroid hyperplasia (rarely from Multiple endocrine neoplasia)
- 1-3% parathyroid carcinoma
Radiology
editOsteopenia and bone demineralization
editOsteopenia and bone demineralization are present in all forms of hyperparathyroidism
===Subperiosteal .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
editAcroosteolysis 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
editBrown Tumors
editBrown 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 from 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. xxxxxxxxPrimer of Diagnostic Imaging. Second Edition. Mosby, 1997.