Chronic pure red cell aplasia caused by parvovirus B19 in AIDS: Use of intravenous immunoglobulin—A report of eight patients

Koduri, Prasad Rao; Kumapley, Rudolf; Valladares, Jose; Teter, Caroline

doi:10.1002/(sici)1096-8652(199905)61:1<16::aid-ajh4>3.3.co;2-p

Cited by 14 publications

(19 citation statements)

References 9 publications

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“…This treatment is usually ameliorative and very often curative (105,107,169,171), leading to a marked increase in reticulocyte count and corresponding rise in hemoglobin. On a more experimental note, generation of neutralizing human monoclonal antibodies directed against B19 proteins have been proposed as an immunotherapy of chronically infected individuals and acutely infected pregnant women (111).…”

Section: Treatmentmentioning

confidence: 99%

Human Parvovirus B19

2002

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Parvovirus B19 (B19) was discovered in 1974 and is the only member of the family Parvoviridae known to be pathogenic in humans. Despite the inability to propagate the virus in cell cultures, much has been learned about the pathophysiology of this virus, including the identification of the cellular receptor (P antigen), and the control of the virus by the immune system. B19 is widespread, and manifestations of infection vary with the immunologic and hematologic status of the host. In healthy immunocompetent individuals B19 is the cause of erythema infectiosum and, particularly in adults, acute symmetric polyarthropathy. Due to the tropism of B19 to erythroid progenitor cells, infection in individuals with an underlying hemolytic disorder causes transient aplastic crisis. In the immunocompromised host persistent B19 infection is manifested as pure red cell aplasia and chronic anemia. Likewise, the immature immune response of the fetus may render it susceptible to infection, leading to fetal death in utero, hydrops fetalis, or development of congenital anemia. B19 has also been suggested as the causative agent in a variety of clinical syndromes, but given the common nature, causality is often difficult to infer. Diagnosis is primarily based on detection of specific antibodies by enzyme-linked immunosorbent assay or detection of viral DNA by dot blot hybridization or PCR. Treatment of persistent infection with immunoglobulin reduces the viral load and results in a marked resolution of anemia. Vaccine phase I trials show promising results

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Section: Treatmentmentioning

confidence: 99%

Human Parvovirus B19

2002

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“…This has been well documented with HIV infection [15], use of immunosuppressive drugs [16], congenital immunodeficiency states [17], and, rarely, in immunocompetent individuals [18,19]. Treatment options include observation alone, supportive care with PRBC transfusions, or IVIG depending on the clinical setting [20].…”

Section: Discussionmentioning

confidence: 99%

Chronic parvovirus infection and G6PD deficiency masquerading as Diamond-Blackfan anemia

Parekh

Perez²,

Yang

et al. 2005

Am. J. Hematol.

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Bone marrow aplasia due to parvovirus B19 infections is usually mild and self-limited. In patients with hereditary or acquired hemolytic anemias, B19 infection can cause a severe and life-threatening anemia due to the shortened half-life of red cells, but here, too, the transient nature of the infection soon remits the symptoms. Chronic infections with parvovirus are more characteristically associated with immunodeficiency states. We report here a case of B19-induced anemia in a patient with G6PD deficiency and hypogammaglobulinemia which was mislabeled as Diamond-Blackfan anemia until the use of modern laboratory techniques allowed a correct diagnosis to be made. Am. J. A 24-year-old African-American male was admitted for generalized weakness, palpitations, and shortness of breath due to severe anemia. Since 11 months of age, he carried a diagnosis of Diamond-Blackfan anemia. He had received his first blood transfusion at the age of 2 years, and remained transfusion-dependent ever since. In early adolescence, he was noted to have low immunoglobulin titers and treated with intravenous immunoglobulin with a temporary reduction in transfusion requirements. At a prior admission for pneumonia, he was told that he was possibly G6PD deficient and to refrain from taking aspirin or sulfa drugs. His family history was significant for a younger brother who had died of an unspecified ''anemia'' at the age of 11 months.On examination, his blood pressure was 110/57 mmHg supine and 96/42 mmHg upright; his heart rate was 95/min supine and 105/min upright. A grade III/VI systolic ejection murmur was heard at the left sternal border. Lungs were clear to auscultation, and there was no palpable lymphadenopathy, organomegaly, or edema. He had normal stature and no congenital anomalies.Laboratory testing showed a hemoglobin of 2.7 g/dL, hematocrit of 7.5%, red cell count 0.80 Â 10 12 /L, MCV 93 fL, MCH 33.5 pg, MCHC 35.8 g/dL, and RDW 18.2. Platelet count was 401 Â 10 9 /L. White cell count was 1.8 Â 10 9 /L with 30% granulocytes, 25% monocytes, and 45% lymphocytes. His chemistries were normal except for an ALT of 61 IU/L (normal<40 IU/L). LDH was 198 U/L, and total bilirubin was 0.2 mg/dL. Examination of the peripheral blood smear showed mild to moderate anisocytosis, poikilocytosis, and dysplastic white cells. A bone marrow biopsy was hypercellular (90%) with left-shifted myelopoiesis, megaloblastic changes, and absolute erythroid hyperplasia with an M/E ratio of 1:1. Giant pronormoblasts were not seen. However, pale pink intranuclear inclusions (Fig. 1) characteristic of parvovirus were seen, which, on immunohistochemical staining for VP2 structural protein using a high-sensitivity streptavidin-biotinperoxidase system (DakoCytomation Inc., Carpinteria, CA), stained positive in 5-10% of cells (Fig. 2). The negative control was a similarly diluted solid-phase

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“…A deficiency in generating specific antibodies either qualitatively (e.g., patients with congenital or acquired immunodeficiencies) or quantitatively (e.g., patients with leukemia) is considered responsible for persistent B19 infections (32,49). Consequently, supplementation of specific immunoglobulins is the accepted therapy of choice (29,30,32,33,49). Commercial preparations of immunoglobulins contain specific parvovirus B19 antibodies, which are deemed responsible for clinical effectiveness.…”

Section: Discussionmentioning

confidence: 99%

New LightCycler PCR for Rapid and Sensitive Quantification of Parvovirus B19 DNA Guides Therapeutic Decision-Making in Relapsing Infections

Harder¹,

Hufnagel

Zahn³

et al. 2001

J Clin Microbiol

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The human erythrovirus B19, a member of the family Parvoviridae, causes a broad and seemingly expanding spectrum of disorders (7,12,23,44). The clinical picture depends on the immune status and age of the patient (14,36,43). Parvovirus B19 shows a remarkable tropism for erythroid progenitor cells in the bone marrow, which is partly based on binding to its receptor, the blood group P antigen (6). Viral replication, and possibly also the induced immune response, interferes with physiological functions and loss of the erythroid progenitor cells, resulting in a usually subclinical reticulocytopenia (8). In patients with an underlying hematologic disorder and high blood cell turnover (e.g., hemolytic anemia), transient aplastic anemia may ensue. Immunocompromised patients, who have an increased risk of developing a persistent B19 infection, are threatened by a chronic reticulocytopenic anemia, also known as pure red cell anemia (2,8).Diagnosis of uncomplicated cases of acute B19 infection (fifth disease or arthropathy) is usually clinically based and can be accomplished by detection of specific immunoglobulin M (IgM) antibodies except in immunocompromised patients, who are prone to persistent infection and who may generate IgMspecific B19 antibodies less reliably (7,19). Likewise, specific IgG is not a reliable marker for discriminating a reconvalescent status from chronic persistent infection (35), although recent data indicate that IgG antibodies specific for nonstructural protein 1 (NS-1) of B19 are more frequently associated with persistent infection (24). Detection of DNA by hybridization or PCR has been reported to be superior in the diagnosis of prenatal B19 infections and in children with oncologic or hematologic disorders (5,11,34). Several qualitative and quantitative PCR methods targeting different regions of the parvovirus genome have been published (1,4,9,10,13,15,17,22,25,40). These PCR approaches are based on conventional block thermocycling and combined single-round PCRs with subsequent oligohybridization or use a nested format.The recently developed LightCycler (LC) DNA amplification technology (Roche Diagnostics, Mannheim, Germany) combines rapid glass capillary thermal cycling with real-time microvolume fluorescence monitoring (47). Detection of amplicons is achieved during the run in real time. Melting point analysis of the amplicons at the end of the run is used as a specificity control when the fluorochrome SYBR green is used for detection of double-stranded DNA. Alternatively, specificity can be tested during the run by using two target-specific hybridization probes which utilize fluorescence resonance energy transfer (FRET) to generate a measurable signal. In the latter case, two oligonucleotide probes (HybProbe) bind to immediately adjacent regions of the respective amplicon. The upstream probe (referred to as the probe) is labeled at its 3Ј end with fluorescein, while the 5Ј end of the downstream probe (referred to as the anchor) is labeled with either of the fluorochromes LC-Red 640 and LC-...

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Chronic pure red cell aplasia caused by parvovirus B19 in AIDS: Use of intravenous immunoglobulin—A report of eight patients

Cited by 14 publications

References 9 publications

Human Parvovirus B19

Human Parvovirus B19

Chronic parvovirus infection and G6PD deficiency masquerading as Diamond-Blackfan anemia

New LightCycler PCR for Rapid and Sensitive Quantification of Parvovirus B19 DNA Guides Therapeutic Decision-Making in Relapsing Infections

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