Foscarnet Resolves Refractory Anemia in Lupus Patient With Parvovirus B19

A single case reported in Clinical Case Reports describes a woman in her 30s with systemic lupus erythematosus and autoimmune hemolytic anemia whose severe, transfusion-resistant anemia was ultimately traced to pure red cell aplasia driven by parvovirus B19 infection. After more than 50 days of immunosuppressive therapy and intravenous immunoglobulin failed to raise her hemoglobin, the addition of the antiviral drug foscarnet on 3 May 2025 produced a marked response: hemoglobin began rising within three days, normalized and stabilized within ten days, and parvovirus B19 DNA subsequently became undetectable.

The patient’s illness began two years before the recurrent episode, when she presented to a hospital with fatigue. Routine laboratory testing at that time showed a white blood cell count of 10.26 × 10⁹/L, a hemoglobin level of just 32.00 g/L, a platelet count of 275 × 10⁹/L, indirect bilirubin of 100.4 μmol/L, and lactate dehydrogenase of 662 U/L. Bone marrow examination was consistent with proliferative anemia. Serologic testing revealed strongly positive anti-SSA antibody and a positive antinuclear antibody, and both direct and indirect antiglobulin tests were positive. On the basis of these findings she was diagnosed with systemic lupus erythematosus complicated by autoimmune hemolytic anemia, an immune-mediated destruction of red blood cells that is a recognized hematologic complication of lupus.

Initial treatment combined corticosteroids, rituximab, methotrexate, and hydroxychloroquine, and her condition gradually improved. The corticosteroid dose was tapered and then maintained. This stability did not last. In January 2025 her anemia recurred: the reticulocyte count and hemoglobin level both fell, and she responded poorly to blood transfusion. Poor transfusion response is itself a clue in this setting, because the autoantibodies produced in autoimmune hemolytic anemia can shorten the survival of transfused cells, so a falling hemoglobin in a lupus patient with known hemolysis is easily attributed to recurrent immune destruction rather than to a new process.

That interpretive trap is central to the case. When the hemoglobin declined, her clinicians initially assumed that hemolysis related to lupus had recurred or worsened, and the dose of immunosuppressive therapy was increased. Pure red cell aplasia was not initially considered. Because the clinical response remained unsatisfactory, the team proceeded to repeated bone marrow aspiration. Before that step, other causes of anemia had been systematically excluded, including iron, folic acid, and vitamin B12 deficiencies, gastrointestinal bleeding, menorrhagia, hemorrhoids, inflammation, and hypothyroidism. Bone marrow pathology then showed active proliferation of hematopoietic tissue with an increased proportion of granulocytes, decreased erythroid proliferation, and giant proerythroblasts, with megakaryocytes still visible. A marrow aspirate smear showed decreased erythroid precursors and a giant pronormoblast on Wright-Giemsa stain at 1000× magnification. These findings supported a diagnosis of pure red cell aplasia.

Pure red cell aplasia is a rare bone marrow failure disorder characterized primarily by normocytic normochromic anemia and a decreased reticulocyte count. Although erythroid precursor cells in the bone marrow are often absent or markedly reduced, granulocytes and megakaryocytes are usually preserved, which distinguishes it from aplastic anemia, a condition that typically presents with multilineage hypoplasia. The authors also note that PRCA must be differentiated from myelofibrosis and from myelosuppression after radiotherapy or chemotherapy, distinctions that can be made through bone marrow biopsy and clinical history. The disorder can be congenital or acquired, and major causes of acquired disease include drugs, viral infections, thymoma, and hematopoietic stem cell transplantation, with thymoma-related disease the most common form of secondary PRCA. Once PRCA was confirmed at the referral center by repeated marrow aspiration, the clinicians investigated primary and secondary causes, including thymoma, drug-related disease, B-cell dyscrasia, transplantation-related disease, and infections. Parvovirus B19 DNA testing came back positive.

Parvovirus B19 is a common viral cause of PRCA; other viral causes include Epstein-Barr virus and hepatitis C virus. The virus may remain latent in the general population and is more likely to cause active infection in immunocompromised patients, including organ transplant recipients. Beyond the marrow, it can cause myocarditis, central nervous system involvement, and gastrointestinal disorders, and some infected individuals develop pure red cell aplasia. In this patient, the combination of long-term immunosuppression for lupus and the viral infection set the stage for a form of anemia that does not respond to the drugs usually used for either lupus or PRCA.

Treatment proceeded in stages, and the sequence matters for interpreting the outcome. Standard PRCA therapy relies on immunosuppressive agents such as cyclosporine and sirolimus, but the authors note that the efficacy of immunosuppression is limited in virus-associated PRCA. Corticosteroid doses were reduced, from prednisone acetate 15 mg once daily down to 5 mg every other day, and cyclosporine was tapered from 150 mg twice daily to 50 mg twice daily and then discontinued on 14 April 2025. Intravenous immunoglobulin was given at 10 g/day for three days, then changed to 10 g once every five days; after 20 days, hemoglobin had not increased significantly. The dose was raised to 20 g/day for five days without benefit, and intermittent dosing of 12.5 g on 16 April, 15 g on 23 April, and 20 g on 29 April 2025 also left hemoglobin low. Because no specific antiviral drug is established for parvovirus B19, high-dose immunoglobulin combined with conventional low-dose immunosuppression is the commonly described approach, and it failed here despite more than 50 days of treatment.

Foscarnet was started on 3 May 2025. Hemoglobin gradually increased after three days and normalized and stabilized after ten days, and parvovirus B19 DNA subsequently became negative. Foscarnet is used primarily as antiviral treatment for cytomegalovirus in immunocompromised patients, including patients with AIDS. It selectively inhibits the pyrophosphate-binding site of virus-specific DNA polymerase, which accounts for its antiviral activity, and its use has also been reported for parvovirus B19 infection. At follow-up to the time of the report, parvovirus B19 testing has remained negative, hemoglobin has stayed within the normal range, and the patient has returned to daily activities and work. The authors state that the potential synergistic mechanism between foscarnet and the other measures warrants further investigation, and they frame the temporal improvement after foscarnet as an observation from a single case rather than a demonstrated treatment effect.

Context from the published literature underscores how unusual this presentation and response are. The authors reviewed English-language PubMed case reports of parvovirus B19-associated secondary PRCA published since 1990 and summarized 18 previously reported cases alongside their own. Most reported patients had undergone organ transplantation, including pancreas, heart, kidney, and liver transplantation, and others had underlying conditions ranging from T-cell immunodeficiency and HIV to chronic lymphocytic leukemia, ulcerative colitis, iron deficiency anemia, allogeneic hematopoietic stem cell transplantation, neurofibromatosis type 1, and lupus. Improvement was generally observed after intravenous immunoglobulin treatment, with some patients receiving prednisolone and some receiving no specific treatment, and most reported outcomes were stable. One patient, an 82-year-old woman with lupus reported in 2007, died. Against that pattern, the present patient’s poor response to immunoglobulin and her recovery only after foscarnet stand out as the distinctive feature of the case.

The clinical lesson the authors draw is procedural rather than therapeutic. First, in patients with lupus and autoimmune hemolytic anemia who respond poorly to immunotherapy and blood transfusion, pure red cell aplasia should be considered, because refractory anemia in this population is easily misread as recurrent hemolysis and the resulting delay carries a relatively high risk of missed diagnosis. Second, once PRCA is identified, the underlying cause should be sought, since immunosuppressive therapy may be ineffective when a virus is driving the marrow failure. Third, when intravenous immunoglobulin alone fails, antiviral therapy may be considered in combination with immunoglobulin; the authors list the nucleotide analog cidofovir, its lipid conjugate brincidofovir, and foscarnet as reported options. As a single-case report, the findings establish what happened to one patient under a specific treatment sequence and identify a diagnostic pathway for similar presentations; they do not establish foscarnet as a validated therapy for parvovirus B19-associated pure red cell aplasia, a question the authors themselves say requires further study.

Subject of Research: A case report of parvovirus B19-associated pure red cell aplasia in a patient with systemic lupus erythematosus and autoimmune hemolytic anemia, treated with foscarnet after immunosuppression and IVIG failed.

Article Title: SLE Complicated With AIHA and Parvovirus B19 Infection Secondary to PRCA: A Case Report

Article References: Xing, M., Zhang, S., Zhang, Y., Sun, X., & Ge, H. (2026). SLE Complicated With AIHA and Parvovirus B19 Infection Secondary to PRCA : A Case Report. Clinical Case Reports, 14(11), Article e73784. https://doi.org/10.1002/ccr3.73784

Image Credits: AI Generated

DOI: 10.1002/ccr3.73784

Keywords: pure red cell aplasia, parvovirus B19, systemic lupus erythematosus, autoimmune hemolytic anemia, foscarnet, intravenous immunoglobulin, bone marrow failure, case report, refractory anemia, antiviral therapy, immunosuppression, hematology