Here, we present a case of an HIV patient with persistent parvovirus infection resulting in chronic anemia requiring long-term maintenance immunoglobulin therapy with an excellent therapeutic response
Here, we present a case of an HIV patient with persistent parvovirus infection resulting in chronic anemia requiring long-term maintenance immunoglobulin therapy with an excellent therapeutic response. strong class=”kwd-title” Keywords: hematology, hiv, intravenous immunoglobulins, parvovirus b19, anemia Introduction Parvovirus is a single-stranded DNA virus that gets its name from the Latin word “parvum,” which means small [1]. persistent infection by infecting the erythroid precursors Hederasaponin B in the bone marrow [2]. Patients with immunocompromised states, e.g., HIV-infected, undergoing chemotherapy or organ transplantation, are particularly at the risk of persistent and severe anemia secondary to parvovirus infections [3]. In addition, these patients are susceptible to infection relapses, highlighting the significance of ongoing monitoring and maintenance therapy. Intravenous immunoglobulin (IVIg) is an effective treatment for parvovirus-induced pure red cell aplasia; however, there are no specific treatment guidelines for chronic parvovirus infection [4]. We discuss the management and therapeutic response of a 38-year-old HIV-positive male with persistent parvovirus infection treated with monthly immunoglobulin therapy. Case presentation A 38-year Hispanic male with a medical history of HIV and surgical history of splenectomy for pancytopenia?around 10 years ago presented to the emergency room (ER) with severe Hederasaponin B fatigue and palpitations for one week. His initial laboratory findings (Table ?(Table1)1) showed a hemoglobin (Hb) level Hederasaponin B of 3.3 g/dl with normocytic normochromic red blood cells (RBCs). The patient’s absolute reticulocyte count was 0.011 x 106/L, and the reticulocyte index was 0.08%. His baseline hemoglobin one year ago was 11 g/dl. He admitted to not taking his HIV medications for the last year. In the ER, he received blood transfusions. Table 1 Summary of laboratory results on initial presentationLDH:?Lactate dehydrogenase; PCR:?Polymerase chain reaction; Ab: Antibody; Ig:?Immunoglobulin; PV B19:?Parvovirus?B19. Laboratory test (Feb 2020) Results Unit Reference range Hemoglobin 3.3 g/dl 13.2-17.5 Hematocrit 9.8 % 40-53 Mean corpuscular volume 83.1 fL 80-100 White blood cells 9,000 /L 4,500-11,000 Platelets 587,000 /L 140,000-400,000 LDH 119 U/L 91,000-200,000 Haptoglobin 173 mg/dL 30-225 Reticulocyte count 0.91 % 0.40-2.50 Absolute reticulocyte count 0.011 x 10? /L 0.010-0.110 HIV RNA PCR 1226 Copy/ml None Parvovirus DNA Hederasaponin B Detected ? None Ab IgM PV B19 3.20 ? = 0.89 Ab IgG PV B19 1.59 ? = 0.89 Open in a separate window The patient’s workup was negative for opportunistic infections, including toxoplasma IgM, cryptococcal antigen (Ag), syphilis enzyme immunoassay (EIA), and acid-fast blood culture, and he had normal hemoglobin electrophoresis?along with an unremarkable iron panel, vitamin B12, and folate levels. However, parvovirus B19 quantitative polymerase chain reaction (PCR) was 100,000,000 with peripheral blood smear showing atypical lymphocytosis,?abnormal RBC morphology, target cells (1+),?red cell distribution width of 15.3%, and CD4 count of 45 cells/mm3. Due to the patient’s unwillingness, a bone marrow biopsy was not performed in our case, and there was no medication explaining the anemia. Provisionally, the patient was diagnosed with chronic parvovirus infection with pure red cell aplasia causing severe anemia on initial admission and received IVIg of 2 g/kg total dose. He was also restarted on anti-retroviral medication, including an emtricitabine-rilpivirine-tenofovir combination of one tablet daily. By the time of discharge, his blood counts p35 responded, and his Hb was stable at 7.2 g/dL; however, he was found to have persistent viral titers of parvovirus B19. After discharge, the patient did not follow up in the clinic. Unfortunately, the patient had a relapse about six months later and presented to the ER with a Hb of 4.8 g/dl and Hederasaponin B normocytic normochromic anemia with an absolute reticulocyte count of 0.060 x 106/L and reticulocyte index of 0.46%. He underwent endoscopy with findings of plaques in the esophagus but no active bleeding ulcers, lesions, or evidence of carcinoma. Relevant laboratory findings are shown in Table ?Table22. Table 2 Summary of laboratory results on repeat presentationLDH:?Lactate dehydrogenase; CD4.