Pathology Deterioration in a Pure β-zero Thalassemia Heterozygote After mRNA COVID-19 Vaccination: A Case Report and Literature Review

Background: β-thalassemia heterozygotes produce sensitive levels of fetal hemoglobin and hemoglobin A2 to remain asymptomatic for life compared to β-thalassemia intermedia and β-thalassemia major patients. The asymptomatic β0 thalassemia minor individuals rarely deteriorate to the point of requiring a blood transfusion. Case report: An asymptomatic individual with a pure β0-thalassemia trait, after his first and only Pfizer modified mRNA COVID-19 injection, immediately developed cardiological, neurological, and other clinically important symptoms. The patient’s severe physical impairments resembled a presyncope (about to feint) syndrome. Multiple hematological tests prior to and after the Pfizer injection revealed that the patient sustained a medically important rise in fetal hemoglobin and concurrently a remarkable drop of his hemoglobin A2 levels, compared to prior to mRNA injection. Moreover, the alterations in his life sustaining fetal hemoglobin and hemoglobin A2 levels was accompanied by a clinically significant lowering of blood hemoglobin concentration that required blood transfusion. The patient’s antibody response to the spike protein remains very high (> 10,000 AU/ml) even almost three years after the Pfizer injection. Furthermore, the elevated levels of C-reactive protein — through May 2024 — after the mRNA injection, apart from pointing to multi-organ systemic inflammation, are consistent with his elevated levels of anti-p53 autoantibodies. Conclusions: The simultaneous decrease of patient blood hemoglobin levels was consistent with the hematological readings of mean corpuscular volume, hematocrit, ferritin, folate, and zinc level deteriorations soon after the mRNA injection, which, apart from his double digit rise in C-reactive protein, resemble overall the pathological manifestations of a β-thalassemia worsening condition. By performing an investigative literature review we conclude that an autoimmune hematological disorder contributed to the patient’s severe hematological stress.