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. Author manuscript; available in PMC: 2008 Nov 23.
Published in final edited form as: J Pediatr. 2007 Apr;150(4):338–344.e1. doi: 10.1016/j.jpeds.2006.12.038

Treatment with Rituximab in Benign and Malignant Hematologic Disorders in Children

Lisa B Giulino 1, James B Bussel 1, Ellis J Neufeld 2; and the Pediatric and Platelet Immunology Committees of the TMH clinical trial network
PMCID: PMC2586083  NIHMSID: NIHMS21145  PMID: 17382107

Monoclonal antibodies (mAbs) have had a major impact on the diagnosis and treatment of many disorders. First discovered in the 1980s, the original monoclonal antibodies were composed entirely of mouse protein which resulted in the development of human anti-mouse antibodies (HAMA) preventing repeated use. Advances in antibody engineering resulted in chimeric antibodies, with both human and mouse components, and more recently humanized antibodies comprised of almost all human protein (>90%)1. The reduction in the mouse components of monoclonal antibodies has allowed for these treatments to be repeated by lessening or eliminating development of human anti-mouse antibodies. Tens of thousands of monoclonal antibodies have been produced but less than 20 have been licensed for use in patients in the United States.

Rituximab is a chimeric monoclonal antibody specific for CD20, an antigen expressed on B cells. In 1997, it was the third monoclonal antibody approved by the FDA following OKT3 and abciximab. The efficacy of rituximab for the treatment of non-Hodgkin’s B cell lymphoma and its relative lack of toxicity lead to its incorporation in most standard treatment protocols for B cell lymphomas and its use in a wide spectrum of B cell disorders, including autoimmune diseases and other malignancies2. Over 540,000 patients have been treated with rituximab worldwide, primarily for B cell lymphomas3. There are only two monoclonal antibodies that have been more widely used, both of which are also chimeric: abciximab, an anti-integrin used in more than one million cardiac patients, and infliximab, an anti-TNF-alpha used in approximately 770,000 patients with Crohn disease and rheumatoid arthritis4.

Although rituximab has been widely used in adults for 10 years, studies in the pediatric population are limited and include primarily case reports, small retrospective and small prospective cohort studies. Specifically, there have been no randomized controlled studies of the safety or efficacy of rituximab in children. The package insert states that rituximab has not been studied in children, however, rituximab has been explored in children for a number of hematologic conditions including autoimmune hemolytic anemia (AIHA), chronic immune thrombocytopenic purpura (ITP), antibodies to factors VIII and IX, post transplant lymphoproliferative disease (PTLD), pre B cell acute lymphoblastic leukemia (ALL), and B cell non Hodgkins lymphoma (NHL). This paper will review the current literature on these uses of rituximab in children including articles and abstracts through July 2006.

Mechanism of Effect

Rituximab is a chimeric monoclonal antibody composed of murine variable regions fused with human IgG1 heavy chains and kappa light chains. Rituximab is specific for the CD20 antigen, a 35kd transmembrane protein expressed on all normal and malignant mature B-lymphocytes. CD20 is not expressed on stem cells, pro-B-cells, most pre-B-cells, most plasma cells, or any other normal human tissue. CD20 does not circulate in plasma5, is not shed from or internalized by the B-cell, and is not downregulated upon antibody binding6. The physiologic role of CD20 is poorly understood. There is no known natural ligand and CD20 knockout mice show no significant defects in B cell function7. Based on structural homologies, CD20 is hypothesized to be a calcium channel subunit8 involved in B-cell activation, differentiation, and/or cell cycle progression9.

Rituximab binds to CD20 causing rapid depletion of circulating CD20+ B-cells10. Although circulating B-cells are profoundly depleted, the number of B-cells found in lymph nodes are reduced11. Rituximab is postulated to induce B-cell destruction through a variety of mechanisms, including antibody-dependent cellular cytotoxicity (ADCC), complement-mediated lysis, apoptosis, inhibition of cell growth, and sensitization to chemotherapy12-14. The importance of the Fc gamma receptor IIIa (FcγRIIIa), a receptor found on natural killer cells and macrophages which binds to IgG1, has been well documented. A polymorphism in this receptor (specifically V/F158) has been correlated with differences in rituximab-induced ADCC and clinical response to rituximab for the treatment of NHL15, Waldenstrom’s macroglobulinemia16, and systemic lupus erythematous (SLE)17. Rituximab-induced sensitization to chemotherapy is thought to be mediated by downregulation of Bcl-2, an inhibitor of apoptosis18. As its mechanism of action is distinct from that of conventional chemotherapy, combining rituximab with standard treatment may have additive, if not synergistic, effects.

Safety Profile

The standard dose of rituximab is 375 mg/m2/dose administered intravenously on a weekly schedule for 4 weeks. This dose, however, was not chosen based on any studies of pharmacokinetics or the response to the drug, and other dosing schedules have been successfully used. Rituximab has been generally well tolerated in adult and pediatric patients. The majority of reported side effects are mild or moderate and infusion-related.

The first infusion often causes a syndrome of chills, fever, headache, and occasional dyspnea, nausea, pruritis, angioedema, or hypotension19. These symptoms are mediated by the release of inflammatory cytokines such as TNF-alpha, IL-8, and IFN-gamma both directly secondary to B cell destruction, as well as indirectly by macrophage activation20. Among lymphoma patients, reactions are more common and more severe in patients with a high tumor burden. The symptoms usually resolve completely with slowing or temporary interruption of the infusion. Premedications such as antihistamines, antipyretics, and corticosteroids are commonly used and can be re-administered to mitigate the reactions.21 Subsequent infusions are much less likely to cause such reactions.

Among the approximately 540,000 patients who have been treated worldwide, tumor lysis syndrome and severe infusion reactions have been reported rarely, a small number of which were fatal. The most severe cases were in patients with high tumor burden, multiple rounds of previously administered chemotherapy, advanced age, and comorbid conditions, such as pulmonary or cardiovascular disease. Anaphylactoid reactions have been reported which may be exaggerated “first infusion” cytokine reactions. Severe mucocutaneous syndromes have also been reported rarely, including Stevens-Johnson syndrome22, paraneoplastic pemphigus, and toxic epidermal necrolysis19. In October 2004, the manufacturer issued a warning stating that carriers of hepatitis B are at risk for its reactivation with development of fulminant hepatitis19.

Serum sickness has been a relatively infrequent occurrence despite the fact that rituximab is chimeric rather than humanized. Two recent reports, however, suggest that serum sickness may develop in 5-10% of children receiving rituximab to treat ITP 23,24.

An important concern with the use of rituximab has been the risk of developing new infections which generally do not occur despite the immunologic changes. Treatment with rituximab results in immediate, marked B-cell depletion with levels remaining low for 2-6 months and returning to pretreatment levels in 6-12 months25. Physicians should not administer immunizations at any age until the B-cell population has returned. Despite substantial prolonged B-cell depletion, an increased incidence of infection has not been demonstrated. Furthermore studies, primarily in adults, have looked at immunoglobulin levels and generally found very little to no change21. This is likely due to the persistence both of plasma cells and also of B-cells in lymph nodes11. Despite the general lack of change of immunoglobulin levels, prophylactic treatment with IVIG has been employed following rituximab in younger children, as they are thought to be at higher risk of transient hypogammaglobulinemia. Studies of rituximab in combination with chemotherapy for lymphoma report a higher rate of neutropenia than with chemotherapy alone, but again without significant increases in infections26. There has been a small number of case reports describing serious viral infections in patients receiving rituximab in conjunction with pre- and post- transplant chemotherapy.

Methods

A literature search of articles and abstracts published on the use of rituximab in pediatric hematologic and oncologic disorders was performed. Cohorts, case reports, and abstracts published by July 2006 were included. Reports on the use of rituximab for the following diseases were reviewed: AIHA, chronic ITP, antibodies to factor VIII/IX, PTLD, pre-B-cell ALL, and B-cell NHL. No articles were identified describing the use of rituximab in pediatric patients with thrombotic thrombocytopenic purpura. Although there have been a number of reports on the use of rituximab in other autoimmune disorders, such as SLE27, they are outside the scope of this review.

Case reports were presented separately from cohort studies given their bias in favor of positive results. Case reports were arbitrarily defined as three or fewer patients. Publications were analyzed for the following variables: age, sex, diagnosis, treatment prior to rituximab, rituximab dose, response to treatment and duration of response, and adverse events. Results are summarized by treatment indication in the Table.

Table.

Diagnosis – study type N % Male/Female Age range (median) Other Diagnoses Previous Treatment Doses of Rituximab range (median) Response Rate Follow-up range (median) Toxicity/Side Effects
AIHAcohort studies 25 38/62 4mo-15yr (35mo) SLE, rheumatoid arthritis,ITP steroids, IVIG, cyclosporine, cyclophospamide, splenectomy, azathioprine, tacrolimus 1-6(4) 92% 7 - 28mo (16 mo) E. Coli pyelonephritis, bronchitis, varicella pneumonia, varicella zoster (2), Pneumocytis carinii pneumonia
AIHA case reports 14 54/46 2mo-18yr (7yr) Beta-thalassemia, severe combinedimmunodeficiency, SLE,ITP, diabetes mellitus, Evans syndrome steroids, IVIG, cyclosporine,cyclophospamide,azathioprine, 2-8 (4) 93% 1- 30 mo (14 mo) Fatal RSV pneumonia,fungal infection
ITP cohort studies 82 48/52 2yr-19yr(11 yr) Evans syndrome (n = 6) splenectomy, IVIg, anti-D, danazol,cyclophospamide,azothioprine, vincristine 1-4(4) 43% 3-30mo(9 mo) Neutropenia (3),serum sickness(3), hypotensionwith 3rddose,primary varicella
ITPcase reports 10 33/67 3mo-16yr (8yr) SLE Anti-D, steroids, IVIg,splenectomy 3-4 (4) 70% 80d-22mo (12 mo) none
Antibody toFactor VIII/IX case reports 8 100/0 7y–17y(14y) none Immune tolerance 4-every 10wks (4) 63% 11- 15 mo ( 13 mo) none
PTLD cohort studies 71 not reported 11mo-16yr (8yr) Transplant:bone marrow (12)umbilical cord blood (5),liver (11), small bowel(3), heart (15), kidney (11), lung (9), other (5) reduction ofimmunosuppression,ganciclovir, CMV Ig 1-9 (4) 70% 12d-41mo (28 mo) Fatal staphlococcalsepsis,anaphylaxis
PTLDcase reports 14 69/31 9mo-19yr(5yr) Transplant:bone marrow (6),umbilical cord blood (1),heart (2), liver (3), kidney(1), small bowel (1) reduction ofimmunosuppression,maternal lymphocytes,acyclovir 1-4(4) 93% 6mo-3yr(10mo) none
Lymphomacase reports 6 67/33 4-14yr (9yr) none conventionalchemotherapy 4-8 (4) 83% 4-5 yr none
Leukemia case reports 6 67/33 2-12yr(6yr) none conventionalchemotherapy 1-5(4) 100% 6mo-4yr(12mo) none
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Results

Autoimmune Hemolytic Anemia (AIHA)

AIHA, an autoimmune disorder characterized by anti-red cell antibodies, is usually a self limited disorder treated with short courses of steroids. Resistant disease, however, has been difficult to manage. Immunosuppressants and splenectomy are not consistently effective and may carry a risk of infection. Often children require prolonged use of high dose steroids which is associated with serious adverse effects.

Cohort studies have described the use of rituximab for AIHA in a total of 25 children, all of whom had failed conventional treatments28-30. The standard dose of rituximab was given weekly for 1-6 weeks (median = 4 doses). Remarkably, 23 of the 25 children (92%) had a complete response ongoing from 7-28 months (median = 16 months) at the time of the last follow up. Only 3 of these 23 responders had relapsed, including one patient who had had two relapses. All relapses were successfully retreated with rituximab.

There have been 14 single case reports published on the use of rituximab for AIHA in children31-44. Ninety three percent of children demonstrated a complete response. The mean response duration was 14 months, and all patients had ongoing responses at the time of publication.

These results differ in comparison with adult studies. Adults with AIHA often have cold agglutinun disease with IgM anti-red cell autoantibodies unlike children who most commonly have warm antibody AIHA. Although some adult studies report a high response rate2, the largest study of 27 adults receiving 37 courses of rituximab treatment for cold agglutinin disease reported a response in 54%, 20 out of 37 courses, with a complete response in only one patient45.

Given the high degree of efficacy of rituximab in pediatric patients and the difficulty of treating AIHA, it seems appropriate to consider early use of rituximab in these patients, especially in steroid intolerant children. In the treatment of small children, despite the absence of data on serial immunoglobulin levels, prophylactic monthly IVIG has been used.

Chronic Immune Thrombocytopenic Purpura

Chronic ITP, characterized by autoantibodies to platelets, is treated with observation, corticosteroids, immunosuppressants, anti-D, and/or intravenous immunoglobulin (IVIG). Splenectomy and immunosuppressants are reserved for those with persistent disease.

Wang 23 (n=24), Taube46 (n=22) and Bennett24 (n=36) reported series of children with chronic ITP refractory to multiple prior treatments treated with rituximab. Children in the Wang and Bennett studies were given the standard dose of rituximab weekly for 4 weeks, whereas children in the Taube study received only a single dose. A response defined as platelet count >50,000/uL was seen in 71% in the study by Wang, most of which were a complete response (CR), and 31% in the study by Bennett. Taube reported a CR (platelets >100,000/uL) in 32% and partial response (platelets > 30,000/uL) in 27%. The lower response rate in the Bennett study was probably a result of a more severely affected patient population. All but 1 CR in the study by Wang occurred within 4 weeks of the first rituximab infusion. Case reports published on a total of 10 children with ITP receiving four doses of rituximab showed a response rate of 70%47-53. Neither Wang nor Bennett could identify clear predictors of response to rituximab. Of note, Bennett (2) and Wang (3) reported 5 children who experienced serum sickness, a rate which appears to be higher than in any other rituximab-treated patient group.

Bennett noted in their children (ages 2.6 to 18.3, median > 10 years of age) that IgG levels were unchanged. IgM levels fell significantly but not to levels out of the normal range. Pharmacokinetics on 14 children demonstrated that clearance of rituximab following the first infusion was more rapid than clearance following the fourth infusion.

Data in adults with ITP treated with rituximab is similar to that reported in children except that children with ITP who respond to rituximab appear to do so more quickly than adults. Conversely, 15 of 17 adults in one study who attained a CR maintained that response for > 1 year 21 whereas in the Wang study children appeared to relapse sooner.

In conclusion, infusions of rituximab have the potential to avoid splenectomy in children with chronic ITP but apparently in not more than 50% of cases. Specific indications for rituximab and when treatment with it should be initiated remain uncertain. The development of serum sickness can be readily managed with prednisone but requires discontinuation of treatment.

Antibodies to Factor VIII/IX (Inhibitors)

Approximately 20-30% of patients with severe hemophilia A and 5% of patients with severe hemophilia B develop inhibitory antibodies. Hemophiliacs with inhibitors commonly receive bypassing agents for acute bleeds and immune tolerance in an attempt to eliminate the inhibitor.

No cohort studies have been published on the use of rituximab for inhibitors. Four case reports describe 8 children with congenital hemophilia treated with rituximab for antibodies against factors VIII and IX54-57. Five of 8 (63%) had an initial response. Two had relapses at 11mo and 8mo, only one of which responded to a second course of rituximab.

Two studies reported 14 adults, 13 with acquired hemophilia, treated with rituximab58,59. A response was seen in 11 of the 13 patients with acquired hemophilia and in the patient with congenital hemophilia. The two patients who did not initially achieve remission both had inhibitor levels greater than 100 Bethesda Units; both achieved a complete response with a combination of rituximab and cyclophosphamide.

A projected single arm study of the efficacy of rituximab in 43 children and adults with inhibitors in congenital hemophilia is beginning in September 2006.

Post Transplant Lymphoproliferative Disease

Post transplant lymphoproliferative disease is a B-cell proliferative disorder induced by infection with Epstein-Barr virus in the setting of chronic immunosuppression. This is particularly prevalent in the post transplant setting. Standard treatment is withdrawal of immunosuppression, acyclovir and alpha interferon.

Seventy one children with PTLD have been treated with rituximab60-64 including preliminary results of a phase II trial65. Twelve patients had undergone bone marrow transplantation, 5 umbilical cord blood transplantation, and 54 solid organ transplantation. The patients who had received solid organ grafts had refractory PTLD defined as no response to reduced immunosuppression, progressive or relapsed disease, and/or concomitant allograft rejection. The 12 children who had undergone bone marrow transplantation received rituximab as first line treatment.

The 71 children received the standard dose of rituximab weekly for 1-9 weeks. Fifty (70%) had a complete response followed for a mean of 28 months with few adverse events. Case reports on 14 children treated with rituximab describe similar results66-77. The authors of one study suggested that rituximab should be first-line treatment for refractory PTLD after solid organ transplant 65.

Two large studies in adults reported lower response rates of 46 and 65%.78,79 A recent study piloted the use of rituximab in combination with cyclophosphamide and prednisone; complete responses were seen in 5 of 6 adults80.

Overall it may be appropriate to use rituximab as first line therapy in PTLD in children in view of the high response rate.

Lymphoma

Rituximab was licensed in the United States based on of its efficacy in adults with B cell non-Hodgkin lymphoma. Treatment of children with Burkitt lymphoma has been far more restricted. This is in large part due to the much smaller number of cases of B-cell NHL in children compared to adults.

No cohort studies have been published on the used of rituximab for pediatric lymphoma. Five case reports describe the use of rituximab for six children with B-cell NHL81-85. All had had relapsed disease. Rituximab was infused at the standard dose weekly for 4-8 weeks and, in one case, repeated every 6 months. Five children had a response to rituximab, which was sustained in four. Two deaths were reported, one from relapse of disease and the other from graft versus host disease related to stem cell transplant five years after rituximab treatment.

Current Children’s Oncology Group protocols incorporate rituximab in first line treatment protocols for B-cell NHL (Burkitt’s Lymphoma).

Leukemia

As most pre B-cells do not express CD20, the great majority of pre B-cell ALL in children is CD20 negative. Four case reports describe 6 children with relapsed, CD20+ pre B cell ALL treated with rituximab82,86-88. All had been treated previously with conventional chemotherapy and subsequently relapsed. Rituximab added to a chemotherapy resulted in remission for all six patients. One patient died of a CD20 negative relapse 6 months after treatment. Five children were in remission at the time of publication.

Conclusions

Rituximab has emerged as an important new drug for the treatment of autoimmune B cell mediated disease and B-cell malignancies in both the adult and pediatric populations. Although there are relatively few published reports in children describing rituximab treatment of hematologic diseases and their sample size is typically small, they appear to demonstrate that rituximab is a safe and effective treatment especially for AIHA, chronic ITP, and PTLD. Although rituximab was generally used when conventional treatments have failed, the findings suggest a role for rituximab as first-line therapy in PTLD and, in AIHA, in cases failing or intolerant of steroids. In these diseases, and perhaps chronic ITP, rituximab appears to be more effective in children than in adults. The toxicities in children appear to be similar to those seen in adults with the exception of serum sickness in children with ITP.

Future studies should include randomized, controlled trials to examine long-term outcomes as well as pharmacokinetic and pharmaco dynamic studies to help determine optimal dosing. Other questions that remain to be answered include:

  1. Are there reliable predictors of response?

  2. Is there a benefit to monthly IVIG infusion following rituximab, beyond infection prophylaxis, by virtue of suppression of rebound autoantibody production?

  3. In cases where rituximab is effective, is there a role for maintenance infusions?

  4. When is it appropriate to initiate rituximab treatment?

Given the more limited follow up available in studies of non-malignant disease, caution regarding long term potential side effects of rituximab is warranted. The effect of rituximab to transiently deplete B-cells generally is not accompanied by infectious complications, but little to no data exists on the long-term effects on immune responses. Questions regarding reactivation of existing infections and acquisition of new infections need to be addressed. Nonetheless, early results of treatment of hematologic B cell mediated diseases with rituximab remain impressive and worthy of further investigation.

Abbreviations

ADCC

antibody-dependent cellular cytotoxicity

AIHA

autoimmune hemolytic anemia

ALL

acute lymphoblastic leukemia

CR

complete response

ITP

immune thrombocytopenic purpura

IVIG

intravenous immune globulin

NHL

non Hodgkins lymphoma

PTLD

post-transplant lymphoproliferative disease

SLE

systemic lupus erythematosus

Footnotes

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