In primary hyperparathyroidism, there is excess secretion of PTH by a tumor of the parathyroid gland or by ectopic parathyroid tissue. Excess PTH leads to:
(i) increased plasma Ca2+ and decreased plasma inorganic phosphate concentrations;
(ii) increased urinary excretion of phosphate (phosphaturia), cyclic AMP, and hydroxyproline; and
(iii) muscle weakness and fatigability.
In secondary hyperparathyroidism, the increased secretion of PTH occurs in response to hypocalcemia caused by:
(i) vitamin D-deficient diet;
(ii) poor absorption of fat, leading to the concomitant decreased absorption of fat-soluble vitamins (A, D, E, and K);
(iii) impaired synthesis of calcitriol due to renal disease;
(iv) increased demand for Ca2+ as during pregnancy and lactation.