ABSTRACT
During an acute SARS-CoV-2 infection, a diagnosis of Aplastic Anaemia associated with Paroxysmal Nocturnal Haemoglobinuria (AA/PNH) was made in a 78-year-old woman who had presented to the emergency department with severe pancytopenia. It is possible that she had subclinical AA/PNH that was unmasked during the acute COVID-19 infection, but we can also suspect a direct role of the virus in the pathogenesis of the disease, or we can hypothesize that COVID-19 infection changed the phosphatidylinositol glycan class A (PIGA) gene pathway.
Subject(s)
Anemia, Aplastic , COVID-19 , Hemoglobinuria, Paroxysmal , Pancytopenia , Aged , Anemia, Aplastic/complications , Anemia, Aplastic/diagnosis , Anemia, Aplastic/genetics , COVID-19/complications , Female , Glycosylphosphatidylinositols , Hemoglobinuria, Paroxysmal/complications , Hemoglobinuria, Paroxysmal/diagnosis , Humans , Pancytopenia/complications , SARS-CoV-2ABSTRACT
The detailed clinical course of coronavirus disease 2019 (COVID-19) in patients with hairy cell leukemia (HCL) is rarely reported. We report the first case of HCL diagnosed with prolonged pancytopenia after COVID-19 infection in Japan. We describe the case of a 56-year-old man who was diagnosed with COVID-19. Computed tomography revealed ground-glass opacities in the bilateral lung lobes as well as splenomegaly. Remdesivir and dexamethasone were administered for the treatment of COVID-19. Since the pancytopenia persisted, bone marrow examination was performed, and he was diagnosed with HCL. Although pancytopenia can occur with COVID-19 alone, clinicians should be alerted regarding the presence of hematologic malignancies in patients in whom pancytopenia persists after COVID-19 treatment or in those with splenomegaly. Further, the condition of all previously reported patients with COVID-19 associated with HCL was severe enough to require mechanical ventilation. This is the first case in which the disease was not severe. The interleukin-6 (IL-6) level was lower in this case than in previous cases, suggesting that racial differences in IL-6 production may have contributed to COVID-19 severity.