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Thiazide therapy for high blood pressure may cause volume depletion and secondary hyperaldosteronism, potentially blunting its antihypertensive efficacy.
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This letter highlights the potential for secondary hyperaldosteronism to blunt the antihypertensive efficacy of thiazide diuretics.
To the Editor.— We have recently read Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, (237:255, 1977). The report as a whole is a commendable document, but it contains a number of scientific errors and omissions. The following suggestions are provided to reduce possible hazard to certain patients and to allow greater therapeutic efficacy on many occasions. In Step 1 of the Stepped-Care Approach section, the important therapeutic consideration that secondary hyperaldosteronism may lessen efficacy has not been mentioned. A concluding comment could be added to this section in a future edition of the report, to read as follows: The volume depletion produced by thiazide therapy may cause increased secretion of aldosterone, resulting in fluid and sodium retention and a lesser reduction in blood pressure. When secondary hyperaldosteronism is suspected of blunting antihypertensive efficacy in Step 1, the physician should consider adding an
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Sanford Cobb (1977) conducted a letter in High blood pressure. Thiazide therapy was evaluated. Thiazide therapy for high blood pressure may cause volume depletion and secondary hyperaldosteronism, potentially blunting its antihypertensive efficacy.
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