scholarly journals Intravesical alprostadil as a promising agent in BK virus-associated hemorrhagic cystitis: A report of a refractory case

2021 ◽  
Vol 2021 (3) ◽  
Author(s):  
Shahin Shamsian ◽  
Ali Saffaei ◽  
Fatemeh Malek ◽  
Zahra Khafafpour ◽  
Abtin Latifi ◽  
...  
Keyword(s):  
At Risk ◽  
Stem Cell ◽  
Hemorrhagic Cystitis ◽  
Antiviral Agents ◽  
Bk Virus ◽  
Special Role ◽  
Cell Transplant ◽  
Saline Irrigation ◽  
Forced Diuresis ◽  
Clinical Benefits

Allogeneic stem cell transplant recipients are at risk of BK virus-associated hemorrhagic cystitis. This condition causes a significant morbidity and worsens clinical outcomes. The standard cares for BK virus-associated hemorrhagic cystitis are saline irrigation and forced diuresis. Notably, several beneficial roles are proposed for antiviral and anti-inflammatory agents against BK virus-associated hemorrhagic cystitis. However, cases who are at risk of cystectomy remain refractory. Herein, we present a 13-year-old boy with severe hematuria by passing two months from his allogeneic stem cell transplantation. The laboratory work up showed high BK viremia >1.1 ×  10 copies/ml in this case's urine sample. The patient was treated with antiviral agents in combination with supportive care. Moreover, intravesical alum was administered, but no clinical benefits were achieved. Finally, intravesical alprostadil was prepared under the supervision of a pediatric clinical pharmacist. In this regard, an alprostadil solution was prepared by constitution of 250 μg alprostadil in 50 mL saline. After administrating the first dose of intravesical alprostadil, an acceptable clinical response was observed, and hematuria stopped. Of note, alprostadil induces platelet aggregation and vasoconstriction. Thus, bleeding can be controlled after the administration of intravesical alprostadil. This strategy may be associated with several side effects including bladder spasm. This study is the first report describing the special role of intravesical alprostadil in refractory cases of BK virus-associated hemorrhagic cystitis. In such refractory cases, clinicians can use intravesical alprostadil rather than invasive therapies in the treatment of BK virus-hemorrhagic cystitis.

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.

Steroid Refractory Acute and Chronic Graft Versus Host Disease (GVHD) - Response to Photophoresis+/− Rituximab.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5358-5358 ◽  
Author(s):  
Ramakrishnan Parameswaran ◽  
Maggie Sekeramayi ◽  
Kelly McCaul ◽  
Bill Bradfeldt
Keyword(s):  
Stem Cell ◽  
Acute Gvhd ◽  
Hemorrhagic Cystitis ◽  
Chronic Gvhd ◽  
Bk Virus ◽  
High Dose ◽  
Unrelated Donor ◽  
Cell Transplant ◽  
Gi Tract ◽  
Steroid Refractory

Abstract Acute GVHD is an important complication following hematopoeitic stem cell transplantation (HSCT), with significant attendant morbidity and mortality. High dose steroids remain the cornerstone of therapy. Steroid refractory GVHD carries a very poor prognosis. Various therapies are available for steroid refractory acute GVHD, but response is not uniform. Among the less intensive regimens, extracorporeal photopheresis (ECP) and rituximab, a chimeric humanized anti CD 20 monoclonal antibody have been shown to be useful in treating refractory acute and chronic GVHD. We describe 8 patients who developed GVHD following transplantation of HLA-identical stem cells, from siblings in 7 and from an unrelated donor in one. 2 patients had steroid refractory chronic GVHD of the liver, 3 patients had a refractory chronic GVHD of the skin and one had a steroid responsive restrictive pulmonary syndrome. Of the patients with skin GVHD, 2 had chronic scelrodermatous GVHD, which was of 20 years duration in one patient and 8 in the other. 2 patients had acute GVHD of the GI tract. The age range was 21– 53 years. All patients were in complete remission from their primary disease at the time of therapy for GVHD. 3 patients had a diagnosis of acute lymphoblasitc leukemia and 5 acute myeloid leukemia All had failed treatment with high dose steroids and/or tacrolimus and/or cellcept, and, one had also failed ATG therapy. Then therapy for refractory GVHD was initiated with rituximab in 3 patients and with photopheresis in 5. 7 patients received ECP. One patient with refractory chronic GVHD of the liver received rituximab alone in addition of steroids and tacrolimus. The patients with acute GVHD were treated with daily ECP for 10 days and then were weaned down to two procedures every 2 weeks. Patients with chronic GVHD received ECP 2 to 3 times a week for 6 weeks and were subsequently similarly weaned down. In the patients with acute GVHD of the GI tract complete responses occurred at 10 days in one patient and 45 days in the second as determined by complete cessation of diarrhea, cramps and nausea. Both patients with chronic GVHD of the liver achieved normalization of the serum bilirubin by 26 and 38 days after initiation of therapy. All patients tolerated successful taper of steroid therapy. The two patients with sclerodermatous GVHD have shown marked improvement in skin texture and range of motion at the involved joints. The patient with the pulmonary symptoms has shown complete normalization of pulmonary function. 5 patients were at risk of CMV reactivation, but failed to do so. One patient developed BK virus associated hemorrhagic cystitis that required therapy with cidofovir. There were 3 admissions for neutropenic fever, three for pneumonia and one each for gastroenteritis, HSV gingivostomatitis and line related sepsis. Two patients had line related thrombosis. None of the patients had relapse of their disease. 2 of the responders had an ECOG performance status 2, two of 3, one of 4 and four of </= 1 while being treated. All patients demonstrated improvement in functional status. ECP and rituximab is a well tolerated and effective modality for therapy of steroid refractory chronic and acute GVHD in both related and unrelated marrow stem cell transplant recipients.

scholarly journals BK Virus Encephalitis in HIV-Infected Patients: Case Report and Review

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Luciana Antoniolli ◽  
Rafael Borges ◽  
Luciano Z. Goldani
Keyword(s):  
Stem Cell ◽  
Case Report ◽  
Clinical Features ◽  
Hematopoietic Stem Cell Transplant ◽  
Stem Cell Transplant ◽  
Hemorrhagic Cystitis ◽  
Bk Virus ◽  
Cell Transplant ◽  
Transplant Recipients ◽  
Hematopoietic Stem

Encephalitis and meningitis due to BKPyV are unusual and emerging condition. Only a few cases of BKPyV encephalitis have been reported in hematopoietic stem cell transplant recipients, with the majority of cases presenting with concurrent hemorrhagic cystitis and HIV-infected patients. The authors report two HIV-infected patients with the diagnosis of BKPyV encephalitis and discuss the main clinical, diagnostic, and therapeutic aspects of this infection in patients with AIDS. Physicians should be aware to recognize the main clinical features and diagnose BKPyV central nervous infection in the setting of AIDS.

scholarly journals Hemorrhagic cystitis: A successful outcome for a challenging complication in stem cell transplant

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Sergio Pinzón Mariño ◽  
Samira Bakali Badesa ◽  
María Jesús Viso Soriano ◽  
Isabel Izquierdo Garcia
Keyword(s):  
Stem Cell ◽  
Hemorrhagic Cystitis ◽  
Successful Outcome ◽  
Cell Transplant ◽  
Dna Viruses ◽  
Allogenic Stem Cell Transplantation ◽  
Nucleotide Analog ◽  
Forced Diuresis ◽  
Successful Case ◽  
Bk Polyomavirus

Hemorrhagic cystitis (HC) secondary to BK polyomavirus (BKPyV) is a frequent complication related to allogenic stem cell transplantation. With an important morbidity and mortality, this disease doesn’t have a stablished standard treatment or prophylaxis strategies. At this moment, the supportive therapies approved to treat included hyperhydration, forced diuresis and transfusion support. Cidofovir is a nucleotide analog of deoxycytidine monophosphate against DNA viruses and it has been described for the treatment of BKPyV-HC, but at this moment, is not a front-line therapy. We report a successful case after the use of Cidofovir without Probenecid. No adverse effect was developed under the treatment, and after 4 weeks of treatment, the patient achieved an excellent response.

Defining Treatment Paradigms for BK Virus-Induced Hemorrhagic Cystitis in the Post-Allogeneic Hematopoietic Stem Cell Transplant Setting

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4468-4468
Author(s):  
Devi D Morrison ◽  
Samith Thomas Kochuparambil ◽  
David Deremer ◽  
Ethan Speir ◽  
Kristen Sterling ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Hematopoietic Stem Cell Transplant ◽  
Stem Cell Transplant ◽  
Hemorrhagic Cystitis ◽  
Bk Virus ◽  
Cell Transplant ◽  
Hematopoietic Stem ◽  
Cell Dose ◽  
The Mean

Abstract Abstract 4468 Introduction: BK viuria is an important and frequent infection in the post-allogeneic hematopoietic stem cell transplant (allo-HSCT) setting that results in significant morbidity and mortality. Over the years our understanding of the disease process has improved significantly but treatment algorithms remain poorly defined and developed. A variety of anti-viral therapies have been utilized in conjunction with reduced immunosuppression with modest benefits. We therefore present our institutional data and recommend a clinical practice guideline that could potentially improve the outcomes of patients with BK-virus infections. Method: Our retrospective analysis included 75 consecutive patients who underwent allo-HSCT from 2001–2011. Data was collected on patients with PCR proven BK-viuria under existing IRB approved protocols. SPSS version 13.0 was used for statistical analysis. Kaplan-Meier method was used to calculate survival outcomes. Result: 12% (9/75) of all patients developed PCR proven hemorrhagic cystitis (HC). The median age of patients at transplant was 37-years (range 28–61). 77% were male. 66% had acute myeloid or lymphoblastic leukemia and the median number of prior therapies was three. 33% had a matched unrelated donor transplant while 66% received reduced intensity conditioning regimen and 33% received anti-thymocyte globulin (ATG). The mean CD34+ cell dose infused was 4.8×106/kg and the mean CD3+ cell dose was 8.6×1011/kg. Median days to neutrophil engraftment were 11 and for platelet engraftment were 14. The median ECOG performance status was 1 (range 0–2). The median time of onset of HC from day 0 of transplant was 44-days (range 4–158) and lasted for an average of 53-days (range 7–157). 33% patients were neutropenic at the onset of HC and the mean absolute neutrophil count was 4300/ul. Most common symptoms were dysuria in 66%, bladder spasms in 44% and urinary retention in 22%. All patients had received GVHD prophylaxis with methotrexate and tacrolimus and 77% were on concurrent steroids and mycophenolate. 88% of patients had concurrent acute graft-vs.-host disease (GVHD) at the time of HC. 88% also had concurrent CMV viremia and 11% had EBV viremia at the time of HC. 44% developed BK-viremia while 55% had BK-virus induced nephropathy defined as an increase of serum creatinine >1.5. Management approach was tiered into prophylaxis, symptomatic relief and anti-viral therapy. All patients received ciprofloxacin and 88% received intravenous immunoglobulin (IVIg). No single therapy component including reduced immunosuppression, cidofovir and leflunomide was independently identified as a more efficacious option (p>0.05) but of the patients who received cidofovir, 75% had resolution of symptoms and were able to clear the BK-viuria with the median duration of treatment of 4.5 weeks. Conclusion: Our analysis supports existing data that BK-virus induced HC is the result of multifaceted host and donor interactions and the concurrent use of immune altering therapies. To address the need of reduced morbidity and improved outcomes of this commonly encountered scenario in the post allo-HSCT setting, we have developed a multi-tiered approach that includes prophylactic intervention with ciprofloxacin for patients undergoing T-cell depleting regimens; symptomatic management with continuous bladder irrigation, pyridium and oxybutynin; and antiviral therapy with cidofovir and leflunomide in select subsets of patients. This approach will provide us a tool to uniformly manage our patients with BK-viuria and HC, and continually analyze and improve outcomes in a prospective manner. Disclosures: No relevant conflicts of interest to declare.

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