Abstract
Hypertension is common (prevalence up to 75 %) in patients with sporadic primary hyperparathyroidism and can be cured by parathyroidectomy. However, there is still uncertainty about the pathophysiology of parathyroid hypertension. The limited and partly controversial data available may be explained by the low prevalence of sporadic primary hyperparathyroidism, the chance of coexisting primary hypertension, and the low number of studies comparing pathogenic mechanisms before and after successful parathyroidectomy. Parathyroid hypertension is associated with reversible pathogenic mechanisms : a) higher plasma norepinephrine (NE) levels, suggesting sympathetic activation; b) a tendency to develop hyperaldosteronism regardless of largely normal plasma renin activity; c) functional and structural changes of blood vessels; 4) increased cytosolic free calcium and reduced intracellular magnesium levels in blood cells, and 5) increased secretion of a hypertensive parathyroid factor resulting in a generalized rise in intracellular cytosolic calcium. Total peripheral vascular resistance is increased in parathyroid hypertension and may be related, at least in part, to an imbalance between cardiovascular NE responsiveness and circulating NE levels. The majority of hypertensive patients with sporadic primary hyperparathyroidism have hypertension stage 1, but occasionally hypertensive crisis occurs in parathyroid hypertension. The death risk of hypertensive patients with primary hyperparathyroidism is 50 % higher than that of normotensive patients with primary hyperparathyroidism. Parathyroid hypertension can be normalized by antihypertensive therapy. Uncomplicated hypertension per se is not a generally accepted indication for parathyroidectomy.
Keywords: Parathyroid hypertension, primary hyperparathyroidism, sympathetic nerve system activity, intracellular free calcium, cardiovascular NE hyperresponsiveness, parathyroidectomy, parathyroid glands, normocalcemic patients, hypercalcemia
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