Low incidence of adenovirus hemorrhagic cystitis following autologous hematopoietic stem cell transplantation in the rituximab era

Abstract

Viral hemorrhagic cystitis (HC) is a frequent complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT) but is rare after autologous peripheral blood stem cell transplantation (auto-PBSCT) because immunosuppression is not required in the absence of an allogeneic immune reaction. Recently, auto-PBSCT has been combined with novel anticancer agents targeting specific molecules, such as rituximab; however, these may cause severe immune deficiency and increase the susceptibility of transplant recipients to opportunistic infections. To address this issue, we performed a retrospective analysis of the incidence of viral HC in auto-PBSCT recipients. Of 158 recipients, only 4 cases (2.5%) were diagnosed with viral HC due to adenovirus (ADV), which was significantly less frequent compared with the incidence in allo-HSCT recipients (15.8%). The incidence of HC did not increase with rituximab treatment. This was a single-center retrospective analysis with a small sample size; however, incorporation of rituximab into the treatment of auto-PBSCT recipients did not appear to be a risk factor for developing viral HC.Viral HC is a noteworthy complication after HSCT because of its negative effects on the quality of life and its potential to cause therapy-related mortality [1]. We recently reported different risk factors associated with two viral HCs in allo-HSCT recipients [2]: ADV-HC and BKV-HC. ADV-HC is associated with severe immunodeficiency caused by immunosuppression therapies such as T-cell purging, whereas BKV-HC is associated with allogeneic immune hyperactivity such as graft-versus-host disease (GVHD) or the pre-engraftment immune reaction (PIR) [3]. Auto-PBSCT is characterized by rapid hematologic and immune reconstitution and does not trigger an allogeneic immune reaction that would require immunosuppressive therapy either for prophylaxis or for treatment. Consequently, there is lower incidence and severity of opportunistic infection including viral HC in auto-PBSCT recipients [4,5].The survival of auto-PBSCT recipients has significantly improved over the recent years because of the incorporation of novel anticancer agents targeting specific molecules into the treatment regimen [6]. One such anticancer agent widely used in this context is rituximab, a chimeric monoclonal anti-CD20 antibody that causes B-lymphocyte depletion. When used alone in patients with lymphoma, rituximab has few effects on the incidence of infectious complications [7,8]. However, the combination of rituximab and high-dose chemotherapy (HDC) may increase the risk of viral infections [9][10][11], including that caused by the hepatitis-B virus (HBV) [12]. This retrospective study was conducted to clarify the prevalence, clinical features, and risk factors of viral HC after auto-PBSCT and to compare these variables with those of allo-HSCT. A total of 158 patients with hematological disorders or solid tumors hospitalized at our institute from 2000 to 2010 were enrolled. The clinical characteristics of these patients are summarized...

Adenovirus: Epidemiology, Global Spread of Novel Serotypes, and Advances in Treatment and Prevention

“…The incidence of AdV infections among HSCT recipients is highly variable (range, 3-47%). 2,4,[25][26][27][28]42,[153][154][155][156][180][181][182][183][184] The incidence is much higher among allogeneic (range, 5-47%) 4 compared with autologous (range, 2.5-14%) [185][186][187] HSCT recipients. Higher rates of AdV infections reflect prospective studies with regular (often weekly) sampling of plasma for AdV DNA (by PCR).…”

Hemorrhagic cystitis after allogeneic hematopoietic cell transplantation: risk factors, graft source and survival

“…1–4 Early urinary bleeding after transplant is usually attributed to toxic effects of the preparative regimens, while HC attributable to factors other than chemotherapy is usually noted more than 2 weeks after alloHCT 1 . Many factors from toxic effects of the preparative regimens to viruses have been implicated in the etiology of HC 1, 5–12 .…”