Rituximab for steroid-refractory chronic graft-versus-host disease

Cutler, Corey; Miklos, David B.; Kim, Haesook T.; Treister, Nathaniel S.; Woo, Sook‐Bin; Bienfang, Don C.; Klickstein, Lloyd B.; Levin, Jesse; Miller, Kathleen L.; Reynolds, Carol; Macdonell, Rebecca; Pasek, Mildred; Lee, Stephanie J.; Ho, Vincent T.; Soiffer, Robert J.; Antin, Joseph H.; Ritz, Jérôme; Alyea, Edwin P.

doi:10.1182/blood-2006-01-0233

Cited by 399 publications

(307 citation statements)

References 37 publications

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“…4,6,22,29 Nevertheless, resolution of graft-versus-host disease and post hematopoietic cell transplant membranous glomerulonephritis with this anti-B-cell agent supports the hypothesis that B-cell alloreactivity may play a role in both of these entities. 16,35,37 Interestingly, our study also identified two patients with biopsy proven membranous glomerulonephritis after autologous hematopoietic cell transplantation. As these patients have not received foreign cells, classic graft-versus-host disease is, by definition, not possible.…”

Section: Discussionmentioning

confidence: 59%

“…35 Others demonstrated the development of anti-nephrin autoantibodies and mesangioproliferative glomerulonephritis in a mouse model of chronic graftversus-host disease after non-myeloablative transplantation. 36 Small studies have separately characterized efficacy of the anti-CD20 agent rituximab in treatment of chronic graft-versus-host disease, 37 and idiopathic membranous glomerulonephritis. [38][39][40][41] Thus, it is not unexpected that rituximab-treated hematopoietic cell transplantation recipients with biopsy proven membranous glomerulonephritis responded well (three allogeneic and one autologous transplant).…”

Section: Discussionmentioning

confidence: 99%

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Renal pathology in hematopoietic cell transplantation recipients

et al. 2008

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Renal pathology in hematopoietic cell transplantation recipients

et al. 2008

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“…13 Rituximab, which depletes B cells in vivo, was reported to have a preventive and curative potential for GVHD. [14][15][16] However, the optimal strategy for B-cell depletion has yet to be investigated. To optimize B-cell depletion, an effective immunologic guide to identifying patients most at risk for developing cGVHD is needed.…”

Section: Introductionmentioning

confidence: 99%

Allogeneic HY antibodies detected 3 months after female-to-male HCT predict chronic GVHD and nonrelapse mortality in humans

Nakasone¹,

Tian

Sahaf³

et al. 2015

Blood

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Key Points• Detection of multiple HY-Abs at 3 months post-F→M HCT predicts cGVHD incidence, severity, and nonrelapse mortality.• Patients with a high HY score may be good candidates for cGVHD prevention trials, especially those targeting allogeneic B cells.Allogeneic antibodies against minor histocompatibility antigens encoded on the Y chromosome (HY-Abs) develop after hematopoietic cell transplant (HCT) of male recipients with female donors (F→M). However, the temporal association between HY-Ab development and chronic graft-versus-host disease (cGVHD) has yet to be elucidated. We studied 136 adult F→M HCT patients, with plasma prospectively collected through 3 years posttransplant, and measured immunoglobulin G against 6 H-Y antigens. Multiple HY-Abs were frequently detected beginning at 3 months posttransplant: 78 (57%) of F→M patients were seropositive for at least 1 of the 6 HY-Abs, and 3-month seropositivity for each HYAb was associated with a persistent seropositive response throughout the posttransplant follow-up period (P < .001 in each). There were no associations between pretransplant features and 3-month overall HY-Ab development. Detection of multiple HY-Abs at 3 months (represented by HY score) was significantly associated with an increased risk of cGVHD (P < .0001) and nonrelapse mortality (P < .01). Compared to clinical factors alone, the addition of HY score to clinical factors improved the predictive potential of cGVHD (P < .01). Monitoring HY-Ab development thus stratifies cGVHD risk in F→M HCT patients and may support preemptive prophylaxis therapy for cGVHD beginning at 3 months posttransplant. (Blood. 2015;125(20):3193-3201)

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“…Rituximab, which is a monoclonal chimeric antibody to B cell surface antigen CD20, has shown activity in GVHD. Cutler et al [122] reported a response rate of 70 % with rituximab in treatment of steroid-refractory cGVHD. In another meta-analysis involving 111 patients a cumulative response rate of 66 % was observed with rituximab [123].…”

Section: Rituximabmentioning

confidence: 99%

State-of-the-art acute and chronic GVHD treatment

Jamil

Mineishi

2015

Int J Hematol

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owing to the advancement in reduced intensity conditioning (RIC) and in patients without HLA-matched donors due to the use of cord blood and haploidentical HSCT [4][5][6]. Although marked improvement has been made in supportive care, immunosuppressive therapy and DNA-based Human Leukocyte Antigen (HLA) typing, graft vs host disease (GVHD) remains a major cause of morbidity and non-relapse mortality among allogeneic HSCT recipients. It was first described by Billingham in 1966 as a syndrome where immunocompetent T cells from the donor recognize and damage the host tissue in an immunocompromised recipient. It presents with heterogeneous symptoms involving multiple organ systems including gastrointestinal tract, skin, mucosa, liver and lungs [7]. In the past clinical features occurring within 100 days after HSCT was called acute GVHD (aGVHD) and those happening after 100 days were labeled chronic GVHD (cGVHD) [8,9]. This definition was rather unsatisfactory thus National Institute of Health (NIH) consensus criteria were developed and have been revised. The criteria have added new categories such as late-onset aGVHD (acute GVHD occurring after 100 days) and overlap syndrome which includes features of both acute and chronic GVHD to the classification, and also have introduced new definitions for organ system involvement [10][11][12]. The categorization of acute vs chronic GVHD is based on the combination of clinical symptoms rather than the time of onset. Depending upon a number of variables associated with patients, donors, and types of transplant, the incidence of aGVHD varies with incidence of grade II-IV GVHD at 40 % in matched related donor (MRD) transplant to 50 % in MUD transplant. The main risk factors for aGVHD include degree of HLA mismatch, age of the patient, previous all immunization of the donor and the kind of GVHD prophylaxis used. About 30-70 % of allogeneic HSCT recipients alive after 100 days will Abstract Graft-versus-host disease (GVHD) remains as the major obstacle for successful hematopoietic stem cell transplant (HSCT). Roughly half of the patients undergoing HSCT develop GVHD which requires treatment, and above 10 % of the patient may die because of it. However, GVHD presents with anti-tumor activity, called graft-versus-tumor (GVT) effect, and it carries significant anti-tumor activity, thus suppressing GVHD completely may increase the relapse of original disease. Thus, it is important to control GVHD to the appropriate level.

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Rituximab for steroid-refractory chronic graft-versus-host disease

Cited by 399 publications

References 37 publications

Renal pathology in hematopoietic cell transplantation recipients

Renal pathology in hematopoietic cell transplantation recipients

Allogeneic HY antibodies detected 3 months after female-to-male HCT predict chronic GVHD and nonrelapse mortality in humans

State-of-the-art acute and chronic GVHD treatment

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