How does hctz cause hyperglycemia
Alterations in the extracellular potassium concentration to which these cells are exposed could potentially lead to decreased insulin secretion. If this mechanism is correct, it would imply that thiazide-induced hyperglycemia occurs by a different mechanism decreased insulin secretion than the standard type 2 diabetes peripheral insulin resistance , and furthermore that thiazide-induced hyperglycemia is reversible with normalization of potassium levels. Thus, it is probably not necessary to remove thiazides from the list of useful first-line agents for treatment of hypertension.
That being said, as a budding nephrologist I am always looking for a good reason to prescribe an ACE-inhibitor or ARB, and therefore I personally tend to add one of the RAAS blockers first given the population of clinic patients that I see. Save my name, email, and website in this browser for the next time I comment.
Follow ASNKidney. Read Later Share. In recent years, there has been the suggestion that thiazide diuretics—long considered a front-line therapy for hypertension based on the ALLHAT study and others—may increase the risk of diabetes. What do we think about this data and should it change our clinical practice of prescribing thiazide monotherapy to an individual recently diagnosed with hypertension?
Also, why should thiazides result in hyperglycemia? Previous Post Refeeding Syndrome. Heart J. Pisanti F. Download references. Armanni, 5, , Napoli, Italy. You can also search for this author in PubMed Google Scholar. Reprints and Permissions. Papaccio, G. Hyperglycemic effects of hydrochlorothiazide and propranolol. A biochemical and ultrastructural study.
Acta diabet. Download citation. Received : 02 June Issue Date : October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article.
Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search SpringerLink Search. Summary The authors studied the glycemic disturbances provoked by two antihypertensive drugs, propranolol and hydrochlorothiazide, administered alone or in combination to normal and diabetic rats, using biochemical and ultrastructural parameters.
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