Rapidly Progressive Mixed Autoimmune Hemolytic Anemia With Multiorgan Dysfunction Syndrome

Sunday, March 22, 2026

11:00 AM - 12:00 PM Central Time

Location: Connections Central - RST 16

AC

Arkaketan Chatterjee, MD

Disclosure(s): No relevant financial relationship(s) to disclose.
RB

Rohan Bhan, MD

Dr.
OBH-Brookdale University Hospital Medical Center

Disclosure information not submitted.
CR

Cristian Rodriguez, MD

Resident Physician
Brookdale University Hospital Medical Center

Disclosure information not submitted.
MH

Mohammad Hassoon, MD

MD
Brookdale University Hospital Medical Center

Disclosure information not submitted.
MA

Mina Al-Saeedi, MD

MD
Brookdale University Hospital Medical Center

Disclosure information not submitted.
SO

Stephanie Ogbonda, MD.

Dr.
OBH-Brookdale University Hospital & Medical Center

Disclosure information not submitted.
Emmanuel Ukenenye, MD.

New York

Disclosure(s): No relevant financial relationship(s) to disclose.
AS

Anup Shreshtha, MD

Dr
Brookdale University Hospital Medical Center

Disclosure information not submitted.
MT

Muhammad S. Tahir, MD

Dr
Brookdale University Hospital Medical Center

Disclosure information not submitted.
OO

Omar Oudit, MD

MD
Brookdale University Hospital Medical Center

Disclosure information not submitted.

Introduction: Autoimmune hemolytic anemia (AIHA) is a condition characterized by destruction of red blood cells (RBCs) due to autoantibodies against RBC surface antigens. AIHA is classified as either warm AIHA, mediated by IgG antibodies, or cold AIHA, mediated by IgM antibodies with complement activation. Mixed-type AIHA is characterized by the presence of both warm and cold autoantibodies. We present a case of rapidly progressing mixed AIHA with multiorgan dysfunction syndrome (MODS), possibly associated with recent cabotegravir-rilpivirine (CR) injection.

Description: A 58 year old woman with HIV (CD4 700, viral load undetectable) on monthly CR injections started 2 months prior, who presented with syncope preceded by a week of progressive weakness and red colored urine. Initial labs showed Hb 7.9 g/dl, indirect bilirubin 4.8 mg/dl, LDH 983, and haptoglobin < 10, confirming hemolytic anemia. Antibodies (Ab) were noted on initial type and screen. Direct antiglobulin test returned positive with pan-IgG Ab, indicating AIHA. Analysis of antibodies returned positive for cold and warm auto-Ab, of both anti-IgG and anti-C3 types. No allo-Ab and no specificity to RBC antigens were detected. The patient deteriorated clinically, with further drop in Hb to 3.8, worsening hypoxia requiring intubation, hemodynamic instability requiring norepinephrine, severe coagulopathy, and renal failure with metabolic acidosis. She was started on methylprednisone, bicarbonate drip, and received 5 total units of PRBCs, 2 units of platelets, and 1 unit each of fresh frozen plasma and cryoprecipitate. Her clinical status worsened, developing type 2 myocardial infarction, and ischemic hepatitis requiring N-acetylcysteine infusion. She received intravenous immunoglobulin (IVIG), and rituximab was ordered. Unfortunately, before rituximab could be initiated, the patient experienced a cardiac arrest due to MODS and she expired.

Discussion: Mixed AIHA requires timely recognition and prompt initiation of treatment as it can potentially be life threatening. While warm AIHA often responds well to corticosteroids, the cold component can be refractory. Additional agents such as rituximab, IVIG/plasmapheresis, or bendamustine may be necessary. To our knowledge, this is the first case of mixed AIHA presenting with MODS.