A comparison of toxicities in acute myeloid leukemia patients with and without renal impairment treated with decitabine

Abstract

Purpose There are limited data regarding the clinical use of decitabine for the treatment of acute myeloid leukemia in patients with a serum creatinine of 2 mg/dL or greater. Methods We retrospectively evaluated 111 patients with acute myeloid leukemia who had been treated with decitabine and compared the development of toxicities during cycle 1 in those with normal renal function (creatinine clearance greater than or equal to 60 mL/min) to those with renal dysfunction (creatinine clearance less than 60 mL/min). Results Notable differences in the incidence of grade ≥3 cardiotoxicity (33% of renal dysfunction patients vs. 16% of normal renal function patients, p = 0.042) and respiratory toxicity (40% of renal dysfunction patients vs. 14% of normal renal function patients, p = 0.0037) were observed. The majority of heart failure, myocardial infarction, and atrial fibrillation cases occurred in the renal dysfunction group. The odds of developing grade ≥3 cardiotoxicity did not differ significantly between patients with and without baseline cardiac comorbidities (OR 1.43, p = 0.43). Conclusions This study noted a higher incidence of grade ≥3 cardiac and respiratory toxicities in decitabine-treated acute myeloid leukemia patients with renal dysfunction compared to normal renal function. This may prompt closer monitoring, regardless of baseline cardiac comorbidities. Further evaluation of decitabine in patients with renal dysfunction is needed.

miR‐155 increases stemness and decitabine resistance in triple‐negative breast cancer cells by inhibiting TSPAN5

“…As a specific DNA methyltransferase (DNMT) inhibitor, DCA can induce the differentiation of tumor cells into normal cells and tumor cell apoptosis by reversing the DNA methylation process 5 . The mechanism involved in DCA resistance in TNBC is complex.…”

“…As a specific DNA methyltransferase (DNMT) inhibitor, DCA can induce the differentiation of tumor cells into normal cells and tumor cell apoptosis by reversing the DNA methylation process. 5 The mechanism involved in DCA resistance in TNBC is complex. Our previous studies showed that miR-155 is upregulated in TNBC, but whether miR-155 is involved in stemness and DCA resistance in BC has not been studied.…”

Cardiac failure in patients treated with azacitidine, a pyrimidine analogue: Case reports and disproportionality analyses in Vigibase

“…In the literature, some data on cardiac disorders associated with AZA such as atrial fibrillation and pleuro‐pericardial effusion were retrieved (see Table ), but with a frequency below 5%. Furthermore, data about the occurrence of CF in patients treated with AZA are scarce.…”

“…reported a case of rapid heart failure in a patient treated with capecitabine, a pyrimidine analogue of AZA . Cardiac toxicity was also observed in patients treated with decitabine, another hypomethylating agent . An immune reaction or dose‐dependent toxicity have also been suggested as a possible mechanism.…”

Decitabine Induced Delayed Cardiomyopathy in Hematologic Malignancy

“…A recent retrospective study of 111 patients with AML treated with decitabine showed a higher incidence of cardiotoxic side effects in patients with renal dysfunction. New onset heart failure was noted only in patients with renal dysfunction [ 15 ]. Our patient developed cardiac dysfunction despite normal kidney function.…”