[Erythrocytosis induced by SGLT2 inhibitors].

Sodium-glucose cotransporter (SGLT) 2 inhibitors have been demonstrated to induce hypoglycemic effects by inhibiting glucose reabsorption in the kidneys and promoting its excretion into urine. SGLT2 inhibitors also contribute to a reduction in heart failure and prevention of kidney disease progression, thus making these drugs increasingly attractive for use in patients with heart failure and chronic kidney disease in addition to patients with diabetes. A novel observation has emerged in recent years that SGLT2 inhibitors induce erythrocyte proliferation, a phenomenon that warrants consideration in the differential diagnosis of erythrocytosis. The prevailing hypothesis explaining the mechanism of erythrocytosis has been the decrease in fluid volume and increase in concentration of the blood which is attributable to the diuretic effect of SGLT2 inhibitors. However, a novel mechanism involving increased production of erythropoietin has also been postulated. A study of patients with erythrocytosis caused by SGLT2 inhibitors reported that careful consideration should be given to discontinuing SGLT2 inhibitors for erythrocytosis in addition to phlebotomy.

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Publication Details

Journal
PubMed
Published
2025-01-01
DOI
https://doi.org/10.11406/rinketsu.66.220
Primary Topic
Diabetes Treatment and Management
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article
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article

[Erythrocytosis induced by SGLT2 inhibitors].

Yoko Edahiro
PubMed
Diabetes Treatment and Management
article

[Erythrocytosis induced by SGLT2 inhibitors].

Yoko Edahiro
article en

Abstract

Sodium-glucose cotransporter (SGLT) 2 inhibitors have been demonstrated to induce hypoglycemic effects by inhibiting glucose reabsorption in the kidneys and promoting its excretion into urine. SGLT2 inhibitors also contribute to a reduction in heart failure and prevention of kidney disease progression, thus making these drugs increasingly attractive for use in patients with heart failure and chronic kidney disease in addition to patients with diabetes. A novel observation has emerged in recent years that SGLT2 inhibitors induce erythrocyte proliferation, a phenomenon that warrants consideration in the differential diagnosis of erythrocytosis. The prevailing hypothesis explaining the mechanism of erythrocytosis has been the decrease in fluid volume and increase in concentration of the blood which is attributable to the diuretic effect of SGLT2 inhibitors. However, a novel mechanism involving increased production of erythropoietin has also been postulated. A study of patients with erythrocytosis caused by SGLT2 inhibitors reported that careful consideration should be given to discontinuing SGLT2 inhibitors for erythrocytosis in addition to phlebotomy.

PubMedVol. 66(4)
Juntendo University (JP)
Diabetes Treatment and Management
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