Potassium Magnesium Citrate Is Superior to Potassium Chloride in Reversing Metabolic Side Effects of Chlorthalidone.


Journal

Hypertension (Dallas, Tex. : 1979)
ISSN: 1524-4563
Titre abrégé: Hypertension
Pays: United States
ID NLM: 7906255

Informations de publication

Date de publication:
Dec 2023
Historique:
medline: 17 11 2023
pubmed: 17 10 2023
entrez: 17 10 2023
Statut: ppublish

Résumé

Thiazide diuretics (TD) are the first-line treatment of hypertension because of its consistent benefit in lowering blood pressure and cardiovascular risk. TD is also known to cause an excess risk of diabetes, which may limit long-term use. Although potassium (K) depletion was thought to be the main mechanism of TD-induced hyperglycemia, TD also triggers magnesium (Mg) depletion. However, the role of Mg supplementation in modulating metabolic side effects of TD has not been investigated. Therefore, we aim to determine the effect of potassium magnesium citrate (KMgCit) on fasting plasma glucose and liver fat by magnetic resonance imaging during TD therapy. Accordingly, we conducted a double-blinded RCT in 60 nondiabetic hypertension patients to compare the effects of KCl versus KMgCit during chlorthalidone treatment. Each patient received chlorthalidone alone for 3 weeks before randomization. Primary end point was the change in fasting plasma glucose after 16 weeks of KCl or KMgCit supplementation from chlorthalidone alone. The mean age of subjects was 59±11 years (30% Black participants). Chlorthalidone alone induced a significant rise in fasting plasma glucose, and a significant fall in serum K, serum Mg, and 24-hour urinary citrate excretion (all KMgCit is superior to KCl, the common form of K supplement used in clinical practice, in preventing TD-induced hyperglycemia. This action may improve tolerability and cardiovascular safety in patients with hypertension treated with this drug class.

Sections du résumé

BACKGROUND UNASSIGNED
Thiazide diuretics (TD) are the first-line treatment of hypertension because of its consistent benefit in lowering blood pressure and cardiovascular risk. TD is also known to cause an excess risk of diabetes, which may limit long-term use. Although potassium (K) depletion was thought to be the main mechanism of TD-induced hyperglycemia, TD also triggers magnesium (Mg) depletion. However, the role of Mg supplementation in modulating metabolic side effects of TD has not been investigated. Therefore, we aim to determine the effect of potassium magnesium citrate (KMgCit) on fasting plasma glucose and liver fat by magnetic resonance imaging during TD therapy.
METHODS UNASSIGNED
Accordingly, we conducted a double-blinded RCT in 60 nondiabetic hypertension patients to compare the effects of KCl versus KMgCit during chlorthalidone treatment. Each patient received chlorthalidone alone for 3 weeks before randomization. Primary end point was the change in fasting plasma glucose after 16 weeks of KCl or KMgCit supplementation from chlorthalidone alone.
RESULTS UNASSIGNED
The mean age of subjects was 59±11 years (30% Black participants). Chlorthalidone alone induced a significant rise in fasting plasma glucose, and a significant fall in serum K, serum Mg, and 24-hour urinary citrate excretion (all
CONCLUSIONS UNASSIGNED
KMgCit is superior to KCl, the common form of K supplement used in clinical practice, in preventing TD-induced hyperglycemia. This action may improve tolerability and cardiovascular safety in patients with hypertension treated with this drug class.

Identifiants

pubmed: 37846572
doi: 10.1161/HYPERTENSIONAHA.123.21932
doi:

Substances chimiques

Antihypertensive Agents 0
Blood Glucose 0
Chlorthalidone Q0MQD1073Q
Citrates 0
magnesium citrate RHO26O1T9V
Potassium RWP5GA015D
Potassium Chloride 660YQ98I10
Sodium Chloride Symporter Inhibitors 0

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

2611-2620

Auteurs

Wanpen Vongpatanasin (W)

Department of Internal Medicine, Hypertension Section (W.V., J.M.G., D.P., A.M., G.K.), University of Texas Southwestern Medical Center, Dallas.
Charles and Jane Pak Center for Mineral Metabolism and Clinical Research (W.V., O.W.M., C.C.Y.P.), University of Texas Southwestern Medical Center, Dallas.

John M Giacona (JM)

Department of Internal Medicine, Hypertension Section (W.V., J.M.G., D.P., A.M., G.K.), University of Texas Southwestern Medical Center, Dallas.
Department of Applied Clinical Research (J.M.G., J.W.), University of Texas Southwestern Medical Center, Dallas.

Danielle Pittman (D)

Department of Internal Medicine, Hypertension Section (W.V., J.M.G., D.P., A.M., G.K.), University of Texas Southwestern Medical Center, Dallas.

Ashley Murillo (A)

Department of Internal Medicine, Hypertension Section (W.V., J.M.G., D.P., A.M., G.K.), University of Texas Southwestern Medical Center, Dallas.

Ghazi Khan (G)

Department of Internal Medicine, Hypertension Section (W.V., J.M.G., D.P., A.M., G.K.), University of Texas Southwestern Medical Center, Dallas.

Jijia Wang (J)

Department of Applied Clinical Research (J.M.G., J.W.), University of Texas Southwestern Medical Center, Dallas.

Talon Johnson (T)

Advanced Imaging Research Center (T.J., J.R.), University of Texas Southwestern Medical Center, Dallas.

Jimin Ren (J)

Advanced Imaging Research Center (T.J., J.R.), University of Texas Southwestern Medical Center, Dallas.

Orson W Moe (OW)

Charles and Jane Pak Center for Mineral Metabolism and Clinical Research (W.V., O.W.M., C.C.Y.P.), University of Texas Southwestern Medical Center, Dallas.
Department of Internal Medicine, Division of Nephrology (O.W.M.), University of Texas Southwestern Medical Center, Dallas.
Department of Physiology (O.W.M.), University of Texas Southwestern Medical Center, Dallas.

Charles C Y Pak (CCY)

Charles and Jane Pak Center for Mineral Metabolism and Clinical Research (W.V., O.W.M., C.C.Y.P.), University of Texas Southwestern Medical Center, Dallas.

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Classifications MeSH