Parathyroid Hormone (PTH)

PTH is the master regulator of blood calcium. It's secreted by four small parathyroid glands behind the thyroid in response to low calcium and raises calcium by three mechanisms: pulling calcium out of bone, activating vitamin D in the kidney (which boosts intestinal absorption), and reducing renal calcium loss. The clinically critical rule: PTH must always be interpreted alongside simultaneous serum calcium — the pair, not either alone, makes the diagnosis. Primary hyperparathyroidism (autonomous parathyroid adenoma) gives high PTH + high calcium. Secondary hyperparathyroidism (response to vitamin-D deficiency or CKD) gives high PTH + normal or low calcium. Hypoparathyroidism gives low PTH + low calcium.

• Primary hyperparathyroidism — solitary parathyroid adenoma (~85%) or hyperplasia; high calcium, low/normal phosphate, mildly elevated PTH.
• Secondary hyperparathyroidism (vitamin-D deficient) — body raises PTH to maintain calcium when D is low; low/normal calcium, low vitamin D.
• Secondary hyperparathyroidism (CKD) — kidney can't activate vitamin D or excrete phosphate; high phosphate, low calcium, PTH can be very high.
• Tertiary hyperparathyroidism — autonomous gland overgrowth after long-standing CKD on dialysis.
• Lithium therapy — alters calcium-sensing receptor; chronic users.

• Hypoparathyroidism — surgical (post-thyroidectomy is the commonest), autoimmune, congenital (DiGeorge syndrome).
• Hypercalcaemia of malignancy — PTHrP from tumour suppresses the real PTH; calcium high, PTH suppressed.
• Severe hypomagnesaemia — magnesium is needed for PTH secretion; correct magnesium first.