Immune-Mediated Pancytopenia Associated with Graves’ Disease Mimicking Evans Syndrome and Carbimazole-Induced Agranulocytosis
https://doi.org/10.15605/jafes.041.S1
- Author:
Ahmad Syahmi Yusof Zaki
1
;
Ezelea Elwina Walter Sandosam
2
;
Nur Izat Muhamad
2
;
Wan Mohd Izani Wan Mohamed
2
Author Information
1. Faculty of Medicine, University Sultan Zainal Abidin;Department of Internal Medicine, School of Medical Sciences, University Science Malaysia
2. Department of Internal Medicine, School of Medical Sciences, University Science Malaysia
- Publication Type:Journal Article
- MeSH:
Evans Syndrome;
Carbimazole;
Pancytopenia;
Agranulocytosis;
Graves Disease
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):103-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Autoimmune thyroid disease is frequently associated with
other immune-mediated disorders; however, clinically
significant pancytopenia is rare. In patients with Graves’
disease receiving antithyroid therapy, leukopenia raises
concern for drug-induced agranulocytosis, a rare but
potentially life-threatening complication characterized
by severe neutropenia requiring immediate drug withdrawal. The coexistence of hemolytic anemia and thrombocytopenia may instead suggest Evans syndrome, defined
by autoimmune hemolytic anemia with immune thrombocytopenia, with or without neutropenia. Importantly,
uncontrolled thyrotoxicosis itself may cause immunemediated cytopenias, creating a diagnostic challenge.
Case:We report a 55-year-old female with thyroid receptor
antibody-positive Graves’ disease who presented with
jaundice and pancytopenia while receiving carbimazole therapy. Laboratory evaluation demonstrated anemia
with reticulocytosis and a positive direct antiglobulin
test, thrombocytopenia and leukopenia. Complement
testing revealed reduced C3 with normal C4, consistent
with immune-mediated hemolysis. Peripheral blood
film showed no blast cells or marrow infiltration, and
autoimmune screening, including antinuclear antibodies
and anti–double stranded DNA, was negative.
The coexistence of Coombs-positive hemolysis and
thrombocytopenia initially raised suspicion for Evans
syndrome, while leukopenia during carbimazole therapy
prompted concern for drug-induced agranulocytosis.
However, neutropenia was not severe, and the absence
of marrow infiltration or systemic autoimmune disease
made alternative causes of pancytopenia less likely.
Importantly, blood counts progressively improved
following the optimization of thyroid control despite
continuation of carbimazole at a reduced dose, without the
use of immunosuppressive therapy. This clinical course
supported the interpretation of thyrotoxicosis-associated
immune cytopenia rather than primary Evans syndrome
or carbimazole-induced agranulocytosis.
Conclusion:This case highlights thyrotoxicosis-associated immune
cytopenia as an important mimic of Evans syndrome and
carbimazole-related hematological toxicity. Recognizing
this entity is essential to avoid unnecessary discontinuation of antithyroid therapy or inappropriate immunosuppressive treatment.
- Full text:2026080416544645199EP_A150.pdf
