{"doi":"10.1111/bjh.17415","title":"COVID‐19 infection in patients with severe aplastic anaemia","abstract":"The coronavirus disease 2019 (COVID-19) pandemic has caused concern among physicians caring for immunosuppressed patients. Aplastic anaemia (AA) is a rare life-threatening bone marrow failure disorder that presents with severe pancytopenia and a hypocellular marrow.1 Patients with severe disease are at increased risk of infection due to neutropenia and immunosuppressive therapy (IST), particularly if the absolute neutrophil count (ANC) is <200/μl. Additionally, standard IST regimens for AA include anti-thymocyte globulin (ATG), high-dose corticosteroids, and cyclosporine (CsA), which suppress T-cell function and can lead to viral reactivation, particularly of herpesviruses. Preceding viral infection as an initial trigger of AA or of disease relapse is possible as viruses can lead to immune destabilisation. Many viruses are known to cause transient cytopenias, but sustained marrow aplasia has mainly been associated with parvovirus.2, 3 Questions regarding AA in the COVID-19 era include: (i) Do patients with AA have a higher susceptibility to COVID-19? (ii) If infected, do patients with AA suffer more severe disease? And (iii) Can newly diagnosed patients with severe AA (SAA) safely receive IST? Because AA is rare, the literature is currently limited to case reports that show varying severities of infection with different treatments and outcomes.4, 5 In another chronic haematological condition, sickle cell disease (SCD), patients have been found to experience a mild infectious course but are at risk of having acute SCD-related complications.6, 7 In the present case series, we report the clinical outcomes of five patients with SAA who developed COVID-19 infection. The median (range) age of the patients with SAA at the time of COVID-19 diagnosis was 32 (21–61) years. Four patients had a previous diagnosis of SAA while unique patient number (UPN)-4 was diagnosed with SAA and COVID-19 simultaneously. Patients received standard IST and eltrombopag (EPAG) on clinical protocols NCT01623167 or NCT04304820. By 6 months, three had achieved haematological response and one (UPN-2) was a non-responder. Of the responders, one patient (UPN-1) had relapsed, was treated with a second round of IST (alemtuzumab and, later, EPAG), and regained response. UPN-2, who had not responded to first-line IST, required two additional therapies and had stable blood counts (Table I). UPN-1 had mild symptoms at COVID-19 diagnosis and recovered after 3 days of symptomatic outpatient management. He presented 1 month later with new onset right shoulder and back pain and was diagnosed with herpes zoster reactivation. UPN-2, a 61-year-old overweight former smoker, had fever, upper respiratory tract symptoms, and pneumonia on imaging. Mild hypoxia not requiring oxygen occurred, which improved with outpatient dexamethasone treatment. UPN-3, a young male with extensive cardiovascular history, was tested for COVID-19 due to precipitous drop in ANC on routine blood monitoring for SAA and was found to be positive. He was admitted briefly for monitoring and treated with granulocyte-colony stimulating factor (G-CSF) with improvement in ANC. UPN-4 presented with severe pancytopenia and was diagnosed with asymptomatic COVID-19 infection and SAA simultaneously. Administration of horse-ATG (h-ATG) was delayed for 3 months until a negative COVID-19 polymerase chain reaction (PCR) test was obtained, but he was started on CsA and EPAG soon after SAA diagnosis. However, he experienced recurrent ileitis and small bowel obstruction necessitating surgical resection. Non-specific pathology showed only inflammation, and a diagnosis of post-COVID-19 immune colitis was made. UPN-5 had mild symptoms of COVID-19 and had recovered fully with symptomatic treatment at home. At last follow-up, all patients had recovered completely from the infection (Table I). Four patients (UPN-1, -2, -3, and -4) received antibody tests and were found to have severe acute respiratory syndrome coronavirus-2 (SA","journal":"British Journal of Haematology","year":2021,"id":190864,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":13,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9692,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2021-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":726790,"name":"Liza Mathews","orcid":"0000-0002-9977-7631","position":1,"is_corresponding":false},{"id":218230,"name":"Emma M. Groarke","orcid":"0000-0002-4648-5926","position":2,"is_corresponding":false},{"id":417532,"name":"Olga Rios","orcid":"0000-0001-6790-9313","position":3,"is_corresponding":false},{"id":265130,"name":"Jennifer Lotter","orcid":null,"position":4,"is_corresponding":false},{"id":218228,"name":"Bhavisha A. Patel","orcid":"0000-0002-2974-7701","position":5,"is_corresponding":false},{"id":218269,"name":"Neal S. Young","orcid":"0009-0007-0999-2519","position":6,"is_corresponding":false},{"id":755686,"name":"Casey Paton","orcid":"0000-0002-9365-1421","position":0,"is_corresponding":true}],"reference_count":15,"raw_metadata":null,"created_at":"2026-07-18T23:49:31.121780Z","pmid":"33928632","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}