Sigbjørn Berentsen, MD, PhD / Ilene C. Weitz, MD - Demystifying Cold Agglutinin Disease: A Visual Exploration of Mechanism, Diagnosis, and the Role of Complement Inhibition in Addressing Unmet Needs

PeerView Clinical Pharmacology CME/CNE/CPE Audio Podcast - A podcast by PVI, PeerView Institute for Medical Education - Thursdays

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Go online to PeerView.com/WQY860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Autoimmune hemolytic anemia (AIHA) has traditionally been considered the simplest and most scholastic example of antibody-mediated autoimmune disease. However, AIHA has recently been identified as a greatly heterogeneous disease because of several immunological mechanisms involved beyond antibodies, complement, and antibody-dependent cell-mediated cytotoxicity. In addition, AIHA may be associated with conditions where the immunologic mechanisms are unpredictably involved. Given the many conditions, an accurate diagnostic approach to AIHA is fundamental for a comprehensive risk assessment and proper therapy. In this activity, based on a recent live symposium, a panel of expert faculty discusses a sufficient diagnostic workup in any patient with AIHA to help determine the possibility of CAD and the rationale for inhibition of complement C1s as an effective long-term therapy for CAD. In addition, they address how to implement classical complement pathway-targeted therapies into treatment plans for CAD based on efficacy and safety data, patient-specific characteristics, and other potential prescribing considerations. Upon completion of this activity, participants should be better able to: Describe the main clinical characteristics and pathogenic mechanisms of autoimmune hemolytic anemia (AIHA); Perform a sufficient diagnostic workup in any patient with AIHA to establish the subtype, including the possibility of cold agglutinin disease (CAD); Discuss the rationale for inhibition of complement C1s as an effective long-term therapy for CAD, particularly symptoms influenced predominantly by activation of the classical complement pathway (eg, chronic hemolysis, anemia, and fatigue); and Integrate classical complement pathway-targeted therapies into treatment plans for CAD based on efficacy and safety data, patient-specific characteristics, and other potential prescribing considerations