A Case of COVID-19 in a Patient with Asymptomatic Hemoglobin D Thalassemia and Glucose-6-Phosphate Dehydrogenase Deficiency

Abstract

Patient: Gender, 26-year-old Final Diagnosis: COVID-19 Symptoms: Cough • fever Medication:— Clinical Procedure: — Specialty: Hematology Objective: Rare co-existance of disease or pathology Background: Beta-hemoglobinopathies and glucose-6-phosphate dehydrogenase (G6PD) deficiency are genetic disorders that cause hemolytic anemia when exposed to oxidative stress. Their co-existence is, however, not proven to enhance the severity of anemia. Case Report: We report the case of a young man with no known co-morbidities, who came with fever and cough and was diagnosed with COVID-19 pneumonia. He was found to have hemoglobin D thalassemia and G6PD deficiency during further evaluation. Hydroxychloroquine therapy started initially, was discontinued after 3 doses once the G6PD deficiency was diagnosed. His hospital course showed a mild drop in hemoglobin with evidence of hemolysis on peripheral smear. However, the hemoglobin improved without any need for transfusion. Conclusions: Hydroxychloroquine therapy can induce hemolytic crises in patients with underlying G6PD deficiency or hemoglobinopathies and should be avoided or closely monitored. Immediate intervention to stop hydroxychloroquine after 3 doses saved our patient from a major hemolytic crisis. The significance of this case report is that it is the first report that outlines the clinic course of COVID-19 pneumonia in a patient with underlying hemoglobin D disease and G6PD deficiency.

The Affinity of Hemoglobin for Oxygen Is Not Altered During COVID-19

“…Later, it was stated that AIHA could concern 12% of the subgroup of anemic COVID-19 patients (Algassim et al, 2021). Fourteen additional patients were described: five with paroxysmal nocturnal hemoglobinuria (Kulasekararaj et al, 2020;Pike et al, 2020) and 9 with previously undiagnosed glucose-6-phosphate dehydrogenase (G6PD) deficiency uncovered in context of acute hemolysis (Aguilar and Averbukh, 2020;Beauverd et al, 2020;De Franceschi et al, 2020;Kuipers et al, 2020;Maillart et al, 2020;Palmer et al, 2020;Sasi et al, 2020;Sgherza et al, 2020;Lopes et al, 2021). Indeed, infections are the most common trigger for hemolysis in G6PD-deficient individuals, and it is unclear if the use of chloroquine or hydroxychloroquine in these patients can worsen the phenomenon (Afra et al, 2020a,b).…”

A Southeast Asian Perspective on the COVID-19 Pandemic: Hemoglobin E (HbE)-Trait Confers Resistance Against COVID-19

“…The high number of cases in Singapore seems to stem from clusters in male migrant workers living in close proximity in crowded living quarters, promoting higher infectious spread [ 33 ]. These migrant workers are from various ethnic groups (e.g., Bengali and Tamil) with higher HbE/thalassemia trait prevalence but also higher glucose-6-phosphate dehydrogenase (G6PD) deficiency rates, compared to resident Singaporeans [ 32 , 34 , 35 ]. G6PD-deficient patients have been shown to be highly susceptible to enteroviruses, human dengue virus, and human coronavirus 229E infection.…”

Can Hydroxychloroquine Cause G6PD-Related Hemolysis? A Case Study

“…Despite the warning by the manufacturing company regarding the association between HCQ and hemolysis in G6PD-deficient patients, this drug was reported in the literature as a safe drug; in 1 retrospective study which was carried out at the Duke University Medical Center on rheumatology patients published in 2017, they found 11 patients who were tested deficient for the enzyme G6PD and were treated with HCQ; there were no reports of hemolysis in more than 700 months of HCQ exposure among these 11 G6PD-deficient patients [ 8 ]. However, hemolysis due to HCQ was reported in 1 case which was published in April 2020 of a 68-year-old male who was started on HCQ for the treatment of COVID-19 that led to severe hemolysis, and the HB level dropped from 12 to 6.5 g/dL few days after starting the treatment [ 9 , 10 ].…”