Hyperparathyroid and Hypoparathyroid Laboratory Patterns

Parathyroid hormone raises serum free calcium through three source-described actions:

• increasing osteoclast activity;
• increasing intestinal calcium and phosphate absorption indirectly through vitamin D activation; and
• increasing distal renal calcium reabsorption while decreasing proximal phosphate reabsorption.

Chief cells regulate serum ionized calcium through PTH secretion. As ionized calcium rises, negative feedback suppresses PTH. This relationship makes an elevated calcium level with normal or elevated PTH inappropriate and supports primary hyperparathyroidism.

Primary hyperparathyroidism originates in the parathyroid gland itself. Its laboratory pattern includes:

• increased PTH and serum calcium;
• decreased serum phosphate; and
• increased urinary cyclic AMP and serum alkaline phosphatase.

Primary causes are:

• a single-gland parathyroid adenoma in more than 80 percent of source-described cases;
• less commonly, sporadic four-gland hyperplasia; or
• less commonly, parathyroid carcinoma.

Chronic renal failure reduces phosphate excretion. Rising phosphate binds free calcium, stimulating all four parathyroid glands. The resulting pattern is:

• increased PTH;
• decreased serum calcium; and
• increased serum phosphate and alkaline phosphatase.

Vitamin D deficiency lowers calcium and elicits increased PTH secretion. The pattern is:

• increased PTH;
• decreased plasma calcium; and
• decreased plasma phosphate because elevated PTH inhibits renal phosphate reabsorption.

In primary hypoparathyroidism:

• PTH secretion is inadequate;
• plasma calcium falls; and
• plasma phosphate rises.

Without PTH, the kidney reabsorbs more of its filtered phosphate load instead of excreting it.

Hypocalcemia increases motor-neuron excitability, producing muscular spasm and tetany. Tapping the facial nerve can elicit Chvostek sign, while inflation of an upper-arm pressure cuff can elicit carpal spasm as Trousseau sign.

Pseudohypoparathyroidism is target-tissue resistance to PTH. It produces the signs and symptoms of primary hypoparathyroidism, but its biochemical pattern is:

• high PTH;
• low calcium; and
• high phosphate.

Excess vitamin D raises calcium and suppresses PTH. The secondary hypoparathyroid pattern is:

• decreased PTH;
• increased plasma calcium; and
• increased plasma phosphate with normal or decreased phosphate excretion.

When calcium and phosphate move in opposite directions, the source says a primary disorder is usually responsible. When they move in the same direction, the origin is usually secondary. Chronic renal failure is an explicit exception to a simple primary-versus-secondary shortcut.