Acute fulminant hepatitis with bone marrow failure in an adult due to parvovirus B19 infection

Hepatology ◽  
2011 ◽  
Vol 55 (1) ◽  
pp. 329-330 ◽  
Author(s):  
Li Sun ◽  
Jiu-Cong Zhang
Keyword(s):  
Bone Marrow ◽  
Fulminant Hepatitis ◽  
Parvovirus B19 ◽  
Bone Marrow Failure ◽  
Parvovirus B19 Infection

Severe bone marrow failure associated with human parvovirus B19 infection in a case with no underlying disorder

2012 ◽  
Vol 96 (6) ◽  
pp. 820-821 ◽  
Author(s):  
Chihiro Kawakami ◽  
Yukako Kono ◽  
Akiko Inoue ◽  
Kimitaka Takitani ◽  
Takayuki Ikemoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Parvovirus B19 ◽  
Bone Marrow Failure ◽  
Human Parvovirus B19 ◽  
Parvovirus B19 Infection ◽  
Underlying Disorder

scholarly journals Clinical presentation of parvovirus B19 infection in HIV-infected patients with and without AIDS

2003 ◽  
Vol 36 (2) ◽  
pp. 299-302 ◽  
Author(s):  
Sérgio Setúbal ◽  
Maria Cristina Jorge-Pereira ◽  
Anadayr Leite Martins de Sant'Anna ◽  
Solange Artimos de Oliveira ◽  
Anna Ricordi Bazin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Parvovirus B19 ◽  
Bone Marrow Failure ◽  
Pure Red Cell Aplasia ◽  
Hiv Positive ◽  
Aids Patients ◽  
Knowing That ◽  
Parvovirus B19 Infection ◽  
Hematological Manifestations ◽  
Morbilliform Rash

Human parvovirus B19 replicates in erythrocyte precursors. Usually, there are no apparent hematological manifestations. However, in individuals with high erythrocyte turnover, as in patients with sickle-cell disease and in the fetus, the infection may lead to severe transient aplasia and hydrops fetalis, respectively. In AIDS patients, persistent infection may result in chronic anemia. By contrast, in HIV-positive patients without AIDS the infection evolves as a mild exanthematous disease. Two clinical descriptions exemplify these forms of presentation. In the first, an AIDS patient presented with bone marrow failure that responded to immunoglobulin. In the second, an HIV-positive patient without AIDS had a morbilliform rash, and needed no treatment. Knowing that an AIDS patient has chronic B19 anemia lessens concern about drug anemia; protects the patient from invasive diagnostic maneuvers; and prevents the patient from disseminating the infection. In AIDS patients with pure red cell aplasia, a search for parvovirus B19 DNA in the serum or in the bone marrow is warranted.

Human parvovirus B19 infection in bone marrow transplantation patients

1993 ◽  
Vol 44 (3) ◽  
pp. 207-209 ◽  
Author(s):  
A. Azzi ◽  
R. Fanci ◽  
S. Ciappi ◽  
K. Zakrzewska ◽  
A. Bosi
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Marrow Transplantation ◽  
Parvovirus B19 ◽  
Human Parvovirus B19 ◽  
Parvovirus B19 Infection

Parvovirus B19 and Aplastic Anemia: Case Control Study: Preliminary Report from the ITESM Hematology Study Group.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3765-3765
Author(s):  
Jose R. Borbolla Escoboza ◽  
Marcos E. Garza-Madrid ◽  
Luis Villela ◽  
Manuel A. Lopez-Hernandez ◽  
Jorge Vela-Ojeda
Keyword(s):  
Bone Marrow ◽  
Aplastic Anemia ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Parvovirus B19 ◽  
Bone Marrow Failure ◽  
Control Group ◽  
Number Of Patients ◽  
Two Samples ◽  
Sense Primer

Abstract Aplastic anemia (AA) is a classic bone marrow failure syndrome simply defined as peripheral blood pancytopenia and a hypocelular bone marrow, yet the diagnosis must be made by excluding other causes of bone marrow failure. The incidence rate of AA reported by the International Aplastic Anemia and Agranulocytosis Study (IAAAS) in the 1980s was 2 cases per 1 million people. This disease is known to be caused by exposure to radiation, chemotherapy and some viral agents, yet most of the cases are idiopathic. Epstein Barr virus and non-A, non-B or non-C Hepatitis virus have classically been related to the development of some AA cases. Recently there have been some reports of AA following Parvovirus B19 (PvB19) infection. This virus, the only parvoviridae virus capable of infecting humans, attacks erythrocyte precursors attaching to the P antigen in their surface and requiring Beta1 integrin for viral entry. Although PvB19 seems to infect only erytroid precursors, it is widely recognized that the infection with this virus can cause not only anemia, but neutropenia and thrombocytopenia as well, producing aplastic crisis of varying intensity. A correlation has recently been found between PvB19 DNA in peripheral blood and AA in children. We pretend to corroborate this observation and include adult patients in order to improve our understanding of the relationship between PvB19 and AA. So far we have taken peripheral blood samples from 9 AA patients and 9 controls paired by age, sex and community; we plan to include 100 AA patients and their controls from several hospitals around Mexico. DNA was extracted using the PUREGENE DNA extraction kit (Gentra, Minneapolis MN). Nested PCR was performed using the sense primer (P1) 5-AATACACTGTGGTTTTATGGGCCG-3, antisense (P2) 5-CCATTGCTGGTTATAACCACAGGT-3 for the first round and the sense primer (P3) 5-AATGAAAACTTTCCATTTAATGATGTAG-3 and antisense primer (P4) 5-CTAAAATGGCTTTTGCAGCTTCTAC-3for the second round. A DNA sample from a patient with active infectious mononucleosis with positive IgG and IgM against PvB19 in serum was used as positive control. Two samples from the AA group (22%) and 1 from the control group (11%) have turned positive for PvB19 DNA. The reported incidence for the presence of this virusDNA in the peripheral blood of the population is 3%. We expect that, as the number of patients grows, the percentage of positive samples in the control group will decrease, while the percentage of positive samples in the AA group will rise or be sustained. Our partial results point towards a possible relationship between AA and the presence of PvB19 DNA in the peripheral blood cells. It is possible that this virus is one of many factors capable of precipitating the development of AA by limiting the bone marrows capacity to produce blood cells. We are in the process of gathering more samples to prove if a relationship really exists and, if so, future studies will likely shed light upon the mechanism by which PvB19 contributes to the development of AA and other marrow failure syndromes.

Changes in erythron peripheral component during chemotherapy in patients with malignant lymphomas and parvovirus B19 infection.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e20086-e20086
Author(s):  
Nailya K. Guskova ◽  
Tatiana A. Zykova ◽  
Irina B. Lysenko ◽  
Ekaterina A. Guskova ◽  
Anastasia S. Nozdricheva ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Viral Load ◽  
Parvovirus B19 ◽  
Microcytic Anemia ◽  
Malignant Lymphomas ◽  
Hypochromic Microcytic Anemia ◽  
Before And After ◽  
Parvovirus B19 Infection ◽  
Expected Increase ◽  
Timely Treatment

e20086 Background: The purpose of the study was to analyze changes in the erythron peripheral component during chemotherapy for malignant lymphomas in patients infected with parvovirus B19 (B19V). Methods: The study included 34 patients with lymphomas (48.7±4.3 years). B19V infection was determined by the presence of IgM/IgG antibodies to B19V in blood serum and DNA in blood plasma and bone marrow before chemotherapy (CT). Parameters of the erythron peripheral component - RBC, HGB, MCW, MCH, MCHC, RDW, PLT, RET (#), IRF, LFR, MFR, HFR (%), and myelogram were evaluated before and after CT (Sysmex XE 2100, Japan). Results: 82.5% of patients had IgG to B19V, including IgM in 11.8%. B19V DNA was detected in 23.4% of patients: in the bone marrow and blood in 11.7%, only in the bone marrow in 11.7%. The range of viral load in the bone marrow was 1435-79573 IU/ml, in the blood 2-349 IU/ml. RBC in all patients before CT was within the reference range, with a tendency to decrease in the group with B19V: 4.01±0.06×1012/L with B19V and 4.57±0.08×1012/L without B19V. Levels of HGB before CT were respectively 112±1.26 g/L and 116±1.26 g/L, decreasing after CT by 1.5 and 1.3 times (p < 0.05) depending on the viral load. MCV, MCH and MCHC varied: 78.6 – 84.8 fl, 24.9 – 28.0 pg and 314–330 g/L in the group with B19V, and 89.7–91.3 fl, 29.5–29.8 pg and 324–337 g/L, respectively, in the group without B19V, which indicates the development of hypochromic microcytic anemia. RET levels before CT in the group with B19V were 38.3±3.44×109/L, after CT – 10.6±2.7×109/L, being lower than in the group without B19V by 1.8 and 3.8 times (p < 0.001), respectively. IRF, MFR and HFR in patients with B19V before CT were 10.6±2.23%, 9.5±1.54% and 1.1±0.022%, being lower than in non-infected patients by 1.6, 1.3 and 3.6 times, respectively. After CT, the downward trend in the proportion of young fractions continued. The noted changes in the erythron peripheral unit indicated inhibition of erythropoiesis, more pronounced in patients with B19V, and were consistent with the myelogram data. Conclusions: The development of anemia without the expected increase in RET, and in particular immature forms - IRF, MFR, HFR - in patients with lymphomas and B19V infection indicates inhibition of erythropoiesis. Early manifestation of these changes allows for timely treatment correction.

Acute parvovirus B19 infection associated with fulminant hepatitis of favourable prognosis in young children

The Lancet ◽  
1998 ◽  
Vol 352 (9142) ◽  
pp. 1739-1741 ◽  
Author(s):  
Etienne Marc Sokal ◽  
Marie Melchior ◽  
Chantal Cornu ◽  
Anne-Thérèse Vandenbroucke ◽  
Jean Paul Buts ◽  
...  
Keyword(s):  
Young Children ◽  
Fulminant Hepatitis ◽  
Parvovirus B19 ◽  
Favourable Prognosis ◽  
Parvovirus B19 Infection
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