Prevalence of myelodysplastic syndrome and acute myeloid leukemia among hospitalizations with sickle cell disease: A National Inpatient Sample analysis.

Abstract

e18545 Background: Sickle cell disease (SCD) is characterized by chronic bone marrow stress, inflammation, and high cellular turnover, which may predispose patients to clonal hematopoiesis and myeloid malignancies. However, population-level data comparing the burden of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) among SCD hospitalizations are limited. We evaluated the prevalence of MDS and AML among SCD hospitalizations. Methods: We conducted a retrospective cross-sectional study using the National Inpatient Sample (NIS) from 2016–2020. Adult hospitalizations (age ≥18 years) with SCD were identified using the ICD-10 diagnosis code D57 and excluding sickle cell trait (D57.3). Outcomes included MDS (D46) and AML (C92.0–C92.5). Survey-weighted analyses estimated hospitalization-level prevalence of MDS and AML among SCD versus non-SCD admissions. Multivariable survey-weighted logistic regression adjusted for age, sex, race, payer, ZIP-income quartile, hospital characteristics, and year. Adjusted prevalence estimates and absolute differences were derived using marginal effects. Results: Among an estimated 148.8 million adult hospitalizations, AML prevalence was lower among SCD hospitalizations than non-SCD hospitalizations (unadjusted: 0.11% vs 0.28%). After adjustment, SCD was associated with lower odds of AML (aOR 0.63, 95% CI 0.49–0.80; p<0.001), corresponding to an adjusted prevalence of 0.17% versus 0.28% and an absolute difference of −0.10%. In contrast, SCD was associated with higher odds of MDS (aOR 1.80, 95% CI 1.40–2.31; p<0.001), with adjusted prevalence of 0.48% versus 0.27% and an absolute increase of 0.21%. Conclusions: Among U.S. adult hospitalizations, SCD is associated with a higher adjusted prevalence of MDS but a lower adjusted prevalence of AML compared with non-SCD hospitalizations. These findings suggest differential myeloid disease patterns in SCD and underscore the need for further investigation into clonal hematopoiesis and bone marrow dysregulation in this population.