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TEXTBOOK PRESENTATION
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Thiazide diuretics cause mild hypercalcemia. This hypercalcemia is associated with a normal or elevated PTH 98% of the time.
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Thiazide diuretics cause hypocalciuria.
Sodium depletion causes increased sodium and calcium retention in the proximal tubule.
Thiazides probably also augment the renal effect of PTH.
Thiazide-induced hypercalcemia has traditionally thought to be mild and short-lived because in response to the hypocalciuria-induced hypercalcemia, PTH secretion is suppressed, normalizing calcium levels.
A recent study, however, suggests that hypercalcemia is discovered, on average, about 5 years after initiation of therapy.
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EVIDENCE-BASED DIAGNOSIS
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The diagnosis of thiazide-induced hypercalcemia depends on documenting hypercalcemia in a patient taking a thiazide diuretic.
Upon discontinuation of thiazide, approximately one-third of patients will have resolution of hypercalcemia.
Of the remaining two-thirds, about 80% will be found to have primary hyperparathyroidism.
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A patient with transient hypercalcemia after beginning a thiazide does not need treatment. Those with persistent hypercalcemia after discontinuing therapy should be evaluated for primary hyperparathyroidism.