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In this single-institution retrospective study of 30 patients with sodium-glucose cotransporter-2 (SGLT-2) inhibitor–induced erythrocytosis, the median patient age was 64 years, 67% were males, patients were on SGLT2 inhibitors for a median of 1.7 years, and the median for baseline and peak hemoglobin was 15.8 g/dL and 17.9 g/dL, respectively. Antiplatelet therapy was prescribed for almost half of the patients (n=14), and another 5 patients were already taking systemic anticoagulation for another indication. After a median follow up of 2.2 years, there were 2 cases of major arterial thrombosis. SGLT2 inhibitor therapy was discontinued in a minority of cases (n=7, 23%).
SGLT2 therapy should be recognized as a cause of erythrocytosis, which seems to correlate with the cardioprotection associated with this drug class. Further studies are warranted to further understand patient outcomes and to establish appropriate management recommendations.
Erythrocytosis referrals to hematology are frequently triggered by hemoglobin/hematocrit (Hgb/Hct) levels that exceed conventional criteria thresholds for polycythemia vera (PV), (Hgb/Hct above 16.5 g/dL/49% in males and 16 g/dL/48% in females)1. Foremost, PV should always be excluded by absence of a JAK2 mutation (V617F exon 14 and exon 12) and/or subnormal serum erythropoietin (EPO) level2, following which a systematic workup for secondary erythrocytosis is recommended3. The latter includes review of medications associated with erythrocytosis; testosterone, androgen, erythropoiesis stimulating agents, diuretics, and contemporary antidiabetic agents (sodium-glucose cotransporter-2 (SGLT-2) inhibitors, e.g., canagliflozin, empagliflozin, dapagliflozin and ertugliflozin). In addition to management of diabetes mellitus, the FDA- approval of SGLT-2 inhibitors has recently expanded to include patients with heart failure and chronic renal disease4-6. Importantly, studies have implied shared molecular mechanisms for SGLT-2 inhibitor associated erythrocytosis and cardioprotection, whereby a drug induced hypoxic and nutrient-deprived state activates sirtuin 1 (SIRT1) and hypoxia-inducible factor (HIF2α/1α)7,8. Current literature on the subject is limited to five cases of marked erythrocytosis (Hct >53%) induced by SGLT-2 inhibitor therapy, two of which occurred in the context of co- administration of testosterone9, one case resulted in unmasking of PV10, while the remainder two were without another predisposing factor11. Therefore, we sought to investigate the presenting features, degree and duration of erythrocytosis, management strategies and outcomes of 30 consecutive cases of SGLT-2 inhibitor induced erythrocytosis that underwent hematological evaluation at our institution between 2015 and 2021.