Effectiveness of rituximab for chemotherapy‐resistant multiple tumoral B‐LPD in a haemopoietic stem cell recipient

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

“…23,26 Rituximab has also been used as therapy for EBV reactivation and posttransplantation lymphoproliferative disease. [27][28][29][30][31][32][33][34] In our study, responses were noted in patients with cutaneous and musculoskeletal disease, a finding that has previously been reported. 14,16,17 Although it is possible that other involved organs (such as the eyes and oral mucosa) did not respond because of the destruction of target tissues (such as the lacrimal and salivary glands), or because our clinical measurement tools were inadequate to detect improvement, it is notable that rituximab is now being used successfully in autoimmune conditions resembling cutaneous and musculoskeletal chronic GVHD.…”

Prolonged hypogammaglobulinemia following rituximab treatment for post transplant Epstein–Barr virus-associated lymphoproliferative disease

“…5,7 Our case might be exceptional, because he needed two courses (a total of 16 infusions) because of very refractory multiple LPD masses in the adrenal glands, lungs, kidneys, liver and para-aortic lymph nodes as well as no availability of donor-derived EBV-specific CTLs at the time. 4 It is possible that this intensive treatment might be responsible for such prolonged B-cell deficiency in our patient, but in the case of Castagnola et al, 3 only a single dose was administered. A correlation between the duration of B lymphopenia and numbers (doses) of rituximab administered needs to be analyzed in future studies.…”

“…The patient recovered remarkably after the treatment, with steadily regressed LPD masses, as described in detail in our previous publication. 4 Since then, the patient has had hypogammaglobulinemia for more than 2.5 years despite continuous replacement therapy with intravenous Ig (IVIG) as high-titer anti-CMV-gammaglobulin, partly because of his history of cytomegalovirus retinitis ( Figure 1). Before allogeneic BMT performed on October 27, 1998, the patient had normal serum Ig levels: IgG 1131 (normal 870-1700) mg/dl, IgA 165 (normal 110-410) mg/dl and IgM 129 (normal 33-190) mg/dl.…”