What are the Clinical Features of Hyperpara­thyroidism?

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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.


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