BK virus (BKV) plasma dynamics in patients with BKV-associated hemorrhagic cystitis following allogeneic stem cell transplantation

2013 ◽  
Vol 15 (3) ◽  
pp. 276-282 ◽  
Author(s):  
R.J. Drew ◽  
A. Walsh ◽  
B. Ní Laoi ◽  
E. Conneally ◽  
B. Crowley
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Allogeneic Stem Cell Transplantation ◽  
Hemorrhagic Cystitis ◽  
Bk Virus ◽  
Plasma Dynamics

scholarly journals BK virus-associated hemorrhagıc cystitis in patients wıth allogeneıc hematopoıetıc cell transplantation: report of three cases

2017 ◽  
Vol 9 (2) ◽  
Author(s):  
Duygu Mert ◽  
Hikmetullah Batgi ◽  
Alparslan Merdin ◽  
Sabahat Çeken ◽  
Mehmet Sinan Dal ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Allogeneic Stem Cell Transplantation ◽  
Hemorrhagic Cystitis ◽  
Immunosuppressive Treatment ◽  
Active Agent ◽  
Bk Virus ◽  
Cell Transplant ◽  
Hematopoietic Stem

BK virus is a human polyoma virus. It is acquired in early childhood and remains life-long latent in the genitourinary system. BK virus replication is more common in receiving immunosuppressive therapy receiving patients and transplant patients. BK virus could cause hemorrhagic cystitis in patients with allogeneic stem cell transplantation. Hemorrhagic cystitis is a serious complication of hematopoietic stem cell transplantation. Hemorrhagic cystitis could cause morbidity and long stay in the hospital. Diagnosis is more frequently determined by the presence of BK virus DNA detected with quantitative or real-time PCR testing in serum or plasma and less often in urine. The reduction of immunosuppression is effective in the treatment of BK virus infection. There are also several agents with anti-BK virus activity. Cidofovir is an active agent against a variety of DNA viruses including poliomyoma viruses and it is a cytosine nucleotide analogue. Intravenous immunoglobulin IgG (IVIG) also includes antibodies against BK and JC (John Cunningham) viruses. Hereby, we report three cases of hemorrhagic cystitis. Hemorrhagic cystitis developed in all these three cases of allogeneic stem cell transplantation due to acute myeloid leukemia (AML). BK virus were detected as the cause of hemorrhagic cystitis in these patients. Irrigation of the bladder was performed. Then levofloxacin 1×750 mg intravenous and IVIG 0.5 gr/kg were started. But the hematuria did not decreased. In the first case, treatment with leflunomide was started, but patient died due to refractory AML and severe graft-versus-host disease after 4th day of leflunamide and levofloxacin treatments. Cidofovir treatment and the reduction of immunosuppressive treatment decreased the BK virus load and resulted symptomatic improvement in the second case. Initiation of cidofovir was planned in the third case. Administration of cidofovir together with the reduction of immunosuppression in the treatment of hemorrhagic cystitis associated with BK virus in allogeneic stem cell transplant recipients could be a good option.

High Incidence of BK-Virus-Related Hemorrhagic Cystitis after Busulfan/Fludarabine Myeloablative Conditioning in Allogeneic Stem Cell Transplantation Recipients.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 5254-5254
Author(s):  
Gorgun Akpek ◽  
Ashraf Badros ◽  
Aaron P. Rapoport ◽  
Kathleen Ruehle ◽  
Kristen Barton ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Allogeneic Stem Cell Transplantation ◽  
Hemorrhagic Cystitis ◽  
Conditioning Regimen ◽  
Bk Virus ◽  
Unrelated Donor ◽  
Myeloablative Conditioning ◽  
High Incidence

Abstract Busulfan (BU) and Fludarabine (F) has been reported by de Lima et al. to be a well-tolerated myeloablative conditioning regimen with 3% incidence of hemorrhagic cystitis (Blood2004;104:857). Between 5/2005 and 5/2006, we performed allogeneic stem cell transplantation (SCT) in 29 patients following BU+F (n=17) and other (n=12) myeloablative regimens. Nineteen (66%) patients were in remission and 10 (34%) had active disease at BMT. Twenty patients had AML, 4 ALL and 5 had other malignancies. Busulfan was given at 130mg/M2 over 3 hours on 4 successive days, along with Fludarabine 40mg/M2 on 4 successive days. Eighteen (72%) had matched-related 7 (24%) had matched-unrelated donor (MUD) transplant. GVHD prophylaxis consisted of Tacrolimus and low-dose Methotrexate. Thymoglobulin (n=4) and CAMPATH (n=3) were given along with conditioning in MUD/one-antigen mismatch transplant recipients (5 BU+F and 2 other). As of August 1st, 2006, 19 (65%) patients are alive. Of 26 evaluable patients, the incidence of bacterial (59% vs. 89%), fungal (29% vs. 11%) infections were similar between Bu+F and other group, respectively. CMV reactivation was observed in 78% in other group as compared to 35% in BU+F recipients (p=0.09). Hemorrhagic cystitis (HC) occurred in 6 patients (35%) in BU+F group and in 1 (11%) patient in other group (p=0.35). BK virus was detected by quantitative PCR in all patients with HC. Two BK(+) cases were in BU+F+CAMPATH group. Considering 18 AML patients who received transplant in remission and had at least 2 months of follow-up, 5 patients (38%) in BU+F group relapsed within 6 months of transplant. Two out of 5 patients relapsed in the other group. Our findings suggest that BU+F myeloablative conditioning appears to be associated with high incidence of BK-related hemorrhagic cystitis and may have long-term consequences. Further studies are warranted.

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