What is it?
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.
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.
Excessive parathyroid hormone due to a parathyroid gland abnormality
80% parathyroid adenoma
12% parathyroid hyperplasia (rarely from Multiple endocrine neoplasia)
1-3% parathyroid carcinoma
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.
Excessive parathyroid hormone due to autonomous secretion of parathyroid hormone.
Often this is from prolonged secondary hyperparathyroidism from renal failure. Then,
when the patient receives a renal transplant, cause of the secondary
hyperparathyroidism is taken away, but the parathyroid glands continue
to over secrete parathyroid hormone.
Radiology of Hyperparathyroidism
Osteopenia and bone demineralization are present in all forms of hyperparathyroidism
is virtually pathognomonic for hyperparathyroidism and is typically
seen at the radial aspect of the middle phalanx of the index and middle
Figure 1: Subperiosteal resorption as well as acroosteolysis, the next sign of hyperparathyroidism
Figure 2: Subperiosteal resorption in a child
3: Compare the finger on a patient with
hyperparathyroidism, to his normal appearing finger after treatment
Phalangeal tuff resorption/acroosteolysis
Figure 4: Acroosteolysis (also subperiosteal resorption)
Acroosteolysis differential diagnosis Mnemonic from The Primer:
(Presented because I can never remember it)
Neuropathy (congenital insensitivity to pain, diabetes, leprosy, myelomeningocele)
Collagen vascular disease (Scleroderma, Raynaud's)
Other (Polyvinyl chloride exposure, snake/scorpion venom)
Salt and pepper skull
Figure 5: Salt and pepper skull
Figure 6: Normal skull in the same patient following treatment of hyperparathyroidism
Brown tumors 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
Figure 7: Brown tumor in the phalanx (also subperiosteal resorption, tuft resorption, and osteopenia)
Figure 8: Brown tumor in the inferior obturator ramus
Soft tissue calcification
Primary > Secondary
Secondary > Primary