Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: Hydroxychloroquine (HCQ) is frequently used to treat autoimmune diseases. The HCQ package insert and online drug information resources report an increased risk of hemolytic anemia in patients with G6PD deficiency. However, no published studies quantify this potential risk, and the genetic forms of severe G6PD enzyme deficiency are very rare in the United States. A single abstract reported a 170 chart review, finding one G6PD deficient patient on HCQ with no adverse event. Through a retrospective chart review, we aimed to quantify the percentage of G6PD deficient patients with clinically significant hemolysis attributed to HCQ.
Methods: The Duke Medicine IRB granted approval for this study. We used a clinical search engine (Duke Enterprise Data Unified Content Explorer [DEDUCE]) to identify all patients who had a clinical visit with Duke Rheumatology, HCQ usage, and a G6PD level checked at Duke Health since 1996. A retrospective chart review was performed on all identified patients, recording demographics, G6PD levels, laboratory values consistent with hemolysis, etiology of hemolysis, and outcome of HCQ use. Data were analyzed using simple statistics.
Results: Two hundred seventy five patients met inclusion criteria by having a prior G6PD level and a prescription for HCQ. Our study population included 232 (84%) females and 43 (16%) males; 126 (46%) African Americans, 131 (48%) Caucasians, and 18 (6%) others. The leading diagnoses included 88 (32%) patients with lupus, 80 (29%) patients with rheumatoid arthritis, and 37 (14%) patients with other forms of inflammatory arthritis. Of the 275 charts reviewed, 11 (4%) of patients were G6PD deficient. The G6PD deficient patients had a total of 711 months of exposure to HCQ. One of the 11 G6PD deficient patients (9%) was found to have sulfamethoxazole/trimethoprim (TMP/SMX) induced hemolysis prior to the initiation of HCQ. This patient was later started on HCQ with no clinical adverse events noted. In 3 of 11 G6PD deficient patients, HCQ was discontinued: one after discovering G6PD deficiency (< 3 months HCQ exposure), one self-discontinued (24 months HCQ exposure), and one discontinued by hematology due to neutropenia (108 months exposure). Of the 264 patients with normal G6PD levels, 14 (5%) had hemolytic anemia at some point, caused by TTP (n=4), autoimmune hemolytic anemia (n=9), and pure red cell aplasia (n=1).
Conclusion: This is the largest study to date evaluating G6PD deficiency with concurrent use of HCQ. Among 11 patients with G6PD deficiency, only 1 had evidence of hemolytic anemia, induced by TMP/SMX prior to successfully tolerating HCQ for SLE without further hemolysis episodes. In this cohort, no G6PD deficient patients developed hemolytic anemia attributable to HCQ during 711 months exposure to the drug. These data do not support routine G6PD level measurement prior to initiating HCQ therapy.
To cite this abstract in AMA style:Mohammad S, Clowse MEB, Eudy A, Criscione-Schreiber L. Hydroxychloroquine Is Not Associated with Hemolytic Anemia in Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Patients [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/hydroxychloroquine-is-not-associated-with-hemolytic-anemia-in-glucose-6-phosphate-dehydrogenase-g6pd-deficient-patients/. Accessed December 5, 2020.
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