Acute human parvovirus B19 infection triggers immune‐mediated transient bone marrow failure syndrome, extreme direct hyperbilirubinaemia and acute hepatitis in patients with hereditary haemolytic anaemias: multicentre prospective pathophysiological study

Author(s):  
Mahmoud I. Elbadry ◽  
Safaa A. A. Khaled ◽  
Nesma M. Ahmed ◽  
Ahmed Abudeif ◽  
Rasha M. Abdelkareem ◽  
...  
2012 ◽  
Vol 96 (6) ◽  
pp. 820-821 ◽  
Author(s):  
Chihiro Kawakami ◽  
Yukako Kono ◽  
Akiko Inoue ◽  
Kimitaka Takitani ◽  
Takayuki Ikemoto ◽  
...  

1993 ◽  
Vol 44 (3) ◽  
pp. 207-209 ◽  
Author(s):  
A. Azzi ◽  
R. Fanci ◽  
S. Ciappi ◽  
K. Zakrzewska ◽  
A. Bosi

2011 ◽  
Vol 3 (2s) ◽  
pp. 7 ◽  
Author(s):  
Antonio M. Risitano ◽  
Fabiana Perna

Acquired aplastic anemia (AA) is the typical bone marrow failure syndrome characterized by an empty bone marrow; an immune-mediated pathophysiology has been demonstrated by experimental works as well as by clinical observations. Immunusuppressive therapy (IST) is a key treatment strategy for aplastic anemia; since 20 years the standard IST for AA patients has been anti-thymocyte globuline (ATG) plus cyclosporine A (CyA), which results in response rates ranging between 50% and 70%, and even higher overall survival. However, primary and secondary failures after IST remain frequent, and to date all attempts aiming to overcome this problem have been unfruitful. Here we review the state of the art of IST for AA in 2010, focusing on possible strategies to improve current treatments. We also discuss very recent data which question the equality of different ATG preparations, leading to a possible reconsideration of the current standards of care for AA patients.


2008 ◽  
Vol 25 (7) ◽  
pp. 699-703 ◽  
Author(s):  
Raghad M. Al-Abdwani ◽  
Faryal A. Khamis ◽  
Abdullah Balkhair ◽  
Mathew Sacharia ◽  
Yasser A. Wali

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5645-5645
Author(s):  
Samar Kulkarni ◽  
John Murray ◽  
David Kaye ◽  
Michael Dennis ◽  
Anna Castleton ◽  
...  

Background: Cytopenia post allograft can be multi-factorial. Known causes include viral infection, septicaemia, graft versus host disease (GVHD), nutritional deficiency, myelotoxic drugs, relapsed malignancy but immune mediated cases are increasingly observed. There remains a group of cases where no obvious cause is identified. The incidence of this complication is small but may be underestimated and treatment options and results are not defined. Aim: This single centre analysis retrospectively evaluated cases of post-transplant cytopenia presumed to be immune mediated or with no obvious cause and response to antiCD20 antibody (Rituximab) therapy. Study period was 2012 to 2019. Data was collected from electronic patient records, case notes and haematology data base. Results: From 2012 to 2019, 988 patients received allograft (n=390) or autograft (n=598) for haematological malignancy or bone marrow failure syndrome. Twenty-four cases received Rituximab for cytopenia post allograft (24/390, 6.2%). Median age was £9yr. (range: 19-68), 19 were males (79.2%) and allograft were done for severe aplastic anaemia (n=4), Ac. Leukaemia (n=6), Hodgkins disease (n=4), non-Hodgkins lymphoma (n=4), MPD/MDS (n=5) and myeloma (n=1). Conditioning was reduced intensity in n22 case, myeloablative in 2 cases and included campath (n=18) or ATG (n=2) in 20 cases (83.3%). Donor was sibling (n=6) or unrelated (n=22) and 23 (96%) patients received PBSC. All allografts were donor/patient CMV matched (NN: 15, PP: 9). Rituximab was used at a median of 171 days post transplant (range: 55-6174). Cytopenia was trilineage in 8, bilineage in 10 and single lineage in 6 cases. Median haematological parameters were as follows: Hb 78gm/L (68-152), WBC: 2x109/L (0-12), Platelets 28x109/L (4-638). DCT was positive in 7 of the 15 cases where results were available. Seventeen of the 22 cases who had bone marrow evaluation showed hypocellular marrow with no malignancy (3 had normocellular marrow) . Seven of the 10 cases where reticulocyte count pre-rituximab was available, showed response above 2% . Cytopenia was not related to infection, viruses, it B12 or folate deficiency. Response to rituximab therapy was defined as CR (normal counts, transfusion independence, no treatment with steroids or G-CSF), Stable (improvement in counts with platelets>50, Hb>100 and ANC>1.0 without support) or no response. Rituximab was delivered weekly in the dose of 375mg/m2 for 4 weeks. Twelve patients achieved complete response (50%), 3 achieved stabilization (12.5%) and 9 did not show any response (37%) for overall response rate of 63%. All patients with positive DCT responded to Rituximab (7/7, 100%) but even in negative DCT group 4 responded (4/8, 50%). Response was 100% in single lineage cytopenia (6/6), 40% in bilineage cytopenia (4/10) and 63% in trilineage cytopenia (5/8) [p=0.052]. Three patients received second course of Rituximab for recurrence of cytopenia and all achieved second complete response (all three had autoimmune haemolysis). Numbers are too small to identify the predictors but there was trend towards better outcome in patients younger than 40 yrs. age (10/12 vs. 5/12, p=0.035) and patients with Hodgkins disease (4/4 vs. 11/20, p=0.09) but there was no effect of gender, intensity of conditioning, use of campath/ATG or CMV status. Treatment was well tolerated and infusion reactions were uncommon. We identify that the main drawback of this analysis is substantial amount of missing data, especially haematological investigations that precludes identification of predictors or trends. Conclusion: Rituximab should be considered as an option for management of post allograft cytopenia with immune aetiology or with no identified cause. Response rate is substantial and the benefit is sustained. It will be useful to have larger cohort of cases to identify the predictors of response. Disclosures Kulkarni: Therakos, Clegene: Honoraria. Murray:Therakos: Honoraria. Castleton:Novartis, Pfizer, Amgen: Consultancy, Honoraria. Cavet:AMGEN, Autolus, Celgene, EUSA, Jansen/J&J, Novartis,: Consultancy, Honoraria, Research Funding, Speakers Bureau. Wiseman:Novartis, Celgene: Consultancy, Honoraria. Somervaille:Novartis: Consultancy. Sommerfeld:Gilead: Other: Educational grant. Bloor:Abvie, Gilead, Novartis, Autolus, Celgene, etc: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Other: Educational grant.


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 ◽  
...  

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.


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