Work overview

Section 01 of 09

Introduction

Complement‐Dominant Relapse of Mixed Autoimmune Hemolytic Anemia After Rituximab Response

Naru Tomigaki, Seiji Kakiuchi, Akimasa Sakamoto, Shutaro Fujioka, Isamu Harima, Hiroaki Akiyama, Ryotaro Niwa, Ikumi Takagi, Yoko Kozuki, Yoshiharu Miyata, Sou Tanaka, Hiroyuki Tsuji, and Nobuko Iwata · 2026

Contents

Section 01 of 09

  1. 01Introduction
  2. 02Case Presentation
  3. 03Discussion
  4. 04Conclusion
  5. 05Section 5
  6. 06Funding
  7. 07Ethics Statement
  8. 08Consent
  9. 09Conflicts of Interest
Text size
Work overview

Section 1 of 9

Introduction

Naru Tomigaki, Seiji Kakiuchi, Akimasa Sakamoto, Shutaro Fujioka, Isamu Harima, Hiroaki Akiyama, Ryotaro Niwa, Ikumi Takagi, Yoko Kozuki, Yoshiharu Miyata, Sou Tanaka, Hiroyuki Tsuji, and Nobuko Iwata · about 1 minutes

Mixed autoimmune hemolytic anemia (AIHA) comprises warm‐ and cold‐reactive autoantibody components whose relative contributions to hemolysis may vary over time. Because serologic findings capture the dominant phenotype at a single time point, longitudinal reassessment may be required when relapse is not concordant with the initial classification. Rituximab targets CD20‐positive B cells, whereas sutimlimab blocks the classical complement pathway through C1s inhibition [1, 2, 3, 4]. Evidence for complement‐directed treatment in mixed AIHA remains limited.

We previously reported the initial course of this same patient, in whom warm AIHA was diagnosed at presentation and cold‐triggered relapse led to reassessment as mixed AIHA, followed by hematologic improvement after rituximab [5]. The present report describes the subsequent longitudinal follow‐up. During the following winter, complement‐dominant hemolysis recurred after the previously identified κ‐restricted CD20‐positive population was no longer detectable by marrow flow cytometry. Hemoglobin increased without transfusion after sutimlimab initiation. We interpreted this episode as a cold‐ and complement‐dominant relapse within mixed AIHA rather than newly developed isolated cold agglutinin disease.