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Noticias A Review of Rituximab in Cutaneous Medicine
Noticias A Review of Rituximab in Cutaneous Medicine | A Review of Rituximab in Cutaneous Medicine |
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Noah Scheinfeld Dermatol Online J. 2006;12(1) (c)2006 Arthur C. Huntley, MD Posted 03/02/2006 Abstract and Introduction Abstract
The rituximab antibody is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigenfound on the surface of normal and malignant B lymphocytes. Rituximabis indicated for the treatment of patients with relapsed or refractory, low-grade or follicular, CD20-positive, B-cell non-Hodgkinlymphoma. Rituximab is also commonly used to treat chronic lymphocyticleukemia, Waldenstrom's macroglobulinemia, and immune or idiopathic thrombocytopenic purpura (ITP). Rituximab is an effective treatmentfor primary cutaneous B-cell lymphoma and other cutaneous lymphomas. Rituximab is an effective treatment for mixed cryoglobulinemia. Rituximab is a promising treatment for systemic lupus erythematosus,dermatomyositis, pemphigus, vasculitis, and a variety of hematologicdiseases. Black-box warnings on rituximab include fatal infusionreactions, tumor lysis syndrome, and severe mucocutaneous reactions. Avariety of cardiac, pulmonary, renal, and hematologic side effects can occur. It commonly causes mild cutaneous side effect and rarely hascaused paraneoplastic pemphigus, Stevens-Johnson syndrome, lichenoiddermatitis, vesiculobullous dermatitis, and toxic epidermal necrolysis.
Introduction
Rituximab is indicated for the treatment of patients with relapsed or refractory, low-grade or follicular, CD20-positive, B-cell non-Hodgkinlymphoma.[1] Rituximab is also commonly used to treat chroniclymphocytic leukemia, Waldenstrom macroglobulinemia, and immune or idiopathic thrombocytopenic purpura (ITP). It is a promising agent forthe treatment on any disease called by B-Cells and the pathogenicantibodies that they produce.[1]
The rituximab antibody is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigenfound on the surface of normal and malignant B lymphocytes. Theantibody is an IgG1-κ immunoglobulin containing murine light-chain and heavy-chain variable region sequences and human constant regionsequences. Rituximab is composed of two heavy chains of 451 aminoacids and two light chains of 213 amino acids (based on cDNA analysis) and has an approximate molecular weight of 145 kD. Rituximab has abinding affinity for the CD20 antigen of approximately 8.0 nM.[1]
ituximab binds specifically to the antigen CD20 (human B lymphocyterestricted differentiation antigen, Bp35), a hydrophobic transmembrane protein with a molecular weight of approximately 35 kD located on pre-and mature-B lymphocytes. The antigen is also expressed on > 90percent of B-cell non Hodgkin lymphomas (NHL), but is not found on hematopoietic stem cells, pro-B cells, normal plasma cells, or othernormal tissues. CD20 regulates early steps in the activation processfor cell-cycle initiation and differentiation, and possibly functions as a calcium ion channel. CD20 is not shed from the cell surface anddoes not internalize upon antibody binding. Free CD20 antigen is notfound in the circulation.[1]
The Fab domain of Rituximab binds to the CD20 antigen on B lymphocytes, and the Fc domain recruits immune effector functions tomediate B-cell lysis in vitro. Possible mechanisms of cell lysisinclude complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC). The antibody has been shown toinduce apoptosis in the DHL-4 human B-cell lymphoma line. Rituximabbinding has been observed on lymphoid cells in the thymus, the white pulp of the spleen, and a majority of B lymphocytes in peripheral blood and lymph nodes. Little or no binding was observed in thenonlymphoid tissues examined.[1]
Treatment of Cutaneous B Cell Lymphoma
,11,12] This is even true in cases of primary cutaneous B-cell lymphoma that have relapsed or failed othertherapies.[13]
Rituximab is an effective therapy of atypical B-cell-lymphoma variants. Primary cutaneous large B-cell lymphoma mimicking pyodermagangrenosum of the leg has been effectively treated withrituximab.[14,15,16,17] Cutaneous large B-cell lymphoma of the leg masquerading as a chronic venous ulcer can be treated withrituximab.[18] Systemic therapy of primary cutaneous B-cell lymphoma,marginal-zone type, with rituximab, has been successful.[19]
Regression of cutaneous intravascular lymphoma with rituximab has been noted.[20]
Intralesional therapy with anti-CD20 monoclonal antibody rituximab hasbeen found to be an effective treatment of primary cutaneous B-cell lymphoma.[21,22,23] In comparison to intravenous administration,intralesional application of the drug allows the use of lower dosages.
Treatment Failures. With rituximab therapy lymphomas can lose CD20expression and, with that, susceptibility to rituximab. Cutaneous B-cell lymphoma with loss of CD20 immunoreactivity after rituximabtherapy has occurred.[24,25] Relapse of diffuse large B cell lymphomato CD20-negative multiple cutaneous tumors immediately after anti-CD20 monoclonal antibody (rituximab) therapy has been reported.[26]
Treatment of Other Lymphomas and Lymphoma With Unique Presentations Some types of lymphoma of the skin can be effectively treated withrituximab. Successful treatment of isolated cutaneous relapse offollicular lymphoma with rituximab has been noted.[27] Cutaneous immunocytoma (which most commonly manifests as extremity basedclustered erythematous brown papules) can be treated withrituximab.[28] Intravascular lymphoma commonly presents with skin findings of tender indurated plaques and nodules, but has a rarevariant manifesting as telangectatic plaques that can be treated byrituximab.[29] Retreatment with rituximab alone can induce sustained remission in patients with follicular lymphoma with multipleextranodal sites of involvement, relapsing soon after primarytreatment with fludarabine-rituximab.[30]
Isolated EBV lymphoproliferative disease in a child with Wiskott-Aldrich syndrome manifesting as cutaneous lymphomatoidgranulomatosis responded to treatment with rituximab. [31] EBV-associated cutaneous plasmocytoma in a renal transplant patienthas been treated effectively with rituximab.[32,33]
Cryoglobulinemia
Rituximab has been found to be effective therapy of mixed cryoglobulinemia, with decreases in cryoglobulin values andimprovement in complement values.[34,35,36] In a study of 15 people,Rituximab proved an effective treatment of cryoglobulinemia with skinvasculitis manifestations (ulcers, purpura, and urticaria), subjectivesymptoms of peripheral neuropathy, low-grade B-cell lymphoma,arthralgias, and fever. Nephritis of recent onset went into remission in one case. Laboratory features, that is, significantly decreased serum rheumatoid factor and cryoglobulins and increased C4, wereconsistent with the clinical efficacy. Treatment with rituximab iswell tolerated, with few infectious complications. Thrombosis of retinal artery or self-limiting panniculitis occurred in one patienteach. Rituximab may represent a safe and effective alternative tostandard immunosuppression in cryoglobulinemia.[37] Initial increase in the cryoglobulin level after rituximab therapy for type-IIcryoglobulinemia secondary to Waldenstrom macroglobulinemia does notindicate failure of response.[38]Collagen Vascular DiseaseRituximab is a promising treatment for systemic lupus erythematosus(SLE).[39,40] and dermatomyositis.[41] It can be used for long term therapy of SLE[42] It also might have utility in the treatment of thecutaneous manifestations of lupus[43] This is even true in treatment resistant cases.[44,45] Treatment complications exist and includeextremely high titers of anti-human chimeric antibody followingre-treatment with rituximab in a patient with active systemic lupus erythematosus.[46] Rituximab has been used in childhood systemic lupuserythematosus refractory to conventional immunosuppression.[47]Complex cases of SLE have abated with rituximab treatment.
Catastrophic systemic lupus erythematosus with Rosai-Dorfman sinus histiocytosis has been treated successfully with rituximab.[48] Saigalreported a case of hypocomplementemic urticarial vasculitis andrecurrent angioedema in a patient with systemic lupus erythematosus unresponsive to mycophenolate mofetil, high-dose methylprednisolone,and intravenous immunoglobulin; that patient responded rapidly torituximab.[49] In summary, systemic autoimmune diseases can respond to rituximab.[50]
Hematological Diseases
Many hematological diseases are related to pathologic B-cells and the antibodies that they produce. Unsurprisingly, rituximab, which blocksthe function of such B-cells, ameliorates a variety of hematologicdiseases. Long-term remission from life-threatening hypercoagulable state associated with lupus anticoagulant (LA) following rituximabtherapy has been reported.[51] Rituximab is a useful treatment foradult refractory idiopathic thrombocytopenic purpura.[52] Lian noted a 43-year-old patient who developed factor-V inhibitor 6 months afterliver transplantation for primary biliary cirrhosis in associationwith Sjogren syndrome/systemic lupus erythematosus who suffered from ecchymoses in the lower extremities; rituximab dissipated the factor-Vinhibitor after 10 weekly doses of 375-500 mg.[53] B-cell depletionmay lead to normalization of anti-platelet, anti-erythrocyte, and antiphospholipid antibodies in systemic lupus erythematosus.[54]Sustained response to rituximab of autoimmune hemolytic anemiaassociated with antiphospholipid syndrome has been noted.[55]Rituximab was an effective treatment for refractory autoimmunethrombocytopenia in a girl with systemic lupus erythematosus.[56]
Waldenstrom's Macroglobulinemia
Waldenstrom's macroglobulinemia (WM) is a cancer of mature plasma cells, B lymphocytes, that causes overproduction of monoclonalmacroglobulin (IgM antibody). It is sometimes referred to as alymphoplasmacytic disorder. WM often results in the overproduction of IgM, which causes the blood to become too thick. This hyperviscosityinterferes with blood flow through small vessels and leads to many ofthe symptoms of the disease. Some 35-50 percent of WM patients respond to single rituximab therapy, with limited toxicity.[57] Extended rituximab therapy may lead to more major responses than standard doserituximab in WM.[58]
Pemphigus
Rituximab is a useful treatment for pemphigus vulgaris.[59,60,61] This in not surprising because pemphigus is an antibody driven disease andrituximab blocks the function of B-cells and the production ofantibodies. Rituximab is even effective treatment for recalcitrant, life-threatening pemphigus vulgaris.[62,63,64,65,66,67] This is alsotrue in juvenile pemphigus vulgaris.[68] Treatment-resistant pemphigusfoliaceus rapidly responds to rituximab.[69]
The use of rituximab can result in the remission of paraneoplastic pemphigus because of its effects on the underlyingneoplasm.[70,71,72,73] It is effective treatment for refractoryerosive stomatitis secondary to CD20(+) follicular lymphoma-associated paraneoplastic pemphigus.[74,75]
Vasculitis
Autoimmune varieties of vasculitis can be effectively treated with rituximab. Rituximab has been found to be a useful adjunct in thetreatment of giant-cell arteritis.[76] Eriksson noted nine patientswith anti-neutrophil cytoplasmic antibody-positive vasculitis successfully treated with rituximab.[77] It has been found to be auseful treatment for refractory Wegener granulomatosis.[78,79,80,81]Keogh noted induction of remission by B-lymphocyte depletion in eleven patients with refractory antineutrophil cytoplasmicantibody-associated vasculitis.[82] As vasculitis is a type-IIIhypersensitivity reaction, which involves antibody immune complex, the
decrease of antibody production that rituximab engenders is a useful therapy.Side Effects
Cutaneous Side Effects
The cutaneous side effects of rituximab are frequent but usually not serious. In a study of 356 patients treated in nonrandomized,single-arm studies of rituximab administered as a single agent 44percent of patient suffered some side effect involving the skin and appendages. Specifically, 15 percent of patients suffered nightsweats, 15 percent of patients suffered "skin rash," 14 percent ofpatients suffered pruritus, and 8 percent suffered urticaria.[83] Observed side-effects in a systemic eight-cycle rituximab therapy inprimary cutaneous B-cell lymphomas were two bacterial infections, twopatients with shivering during infusion, one patient with sweating for
months and one patient with persistent pruritus.[84]
In the trial of 356 patients, 2 percent suffered serious cutaneous side effects. The package insert notes a spectrum of serious sideeffects that include paraneoplastic pemphigus (an uncommon disorderthat is a manifestation of the patient's underlying malignancy), Stevens-Johnson syndrome, lichenoid dermatitis, vesiculobullousdermatitis, and toxic epidermal necrolysis.[85] The onset of thereaction in the reported cases has varied from 1 to 13 weeks following rituximab exposure.
Since rituximab's approval, a variety of serious side effectsinvolving the skin have been reported. Several reports note that rituximab can cause serum sickness.[86] Rituximab-induced vasculitishas been reported.[87] Lowndes reported a case of Stevens-Johnsonsyndrome after treatment with rituximab; it occurred in a 36-year-old man with relapsed follicular lymphoma. The patient developed mucositisand fevers after the first two injections, followed by a floridmaculopapular rash with severe orogenital ulceration after the thirdinfusion. Over several weeks his symptoms progressed with severe cutaneous, orogenital and conjunctival ulceration, leading to visualproblems and malnutrition. No improvement occurred with steroids and immunosuppressant therapy.[88]
Buda-Okreglak described a novel, delayed, proinflammatory syndrome that occurred at or near completion of a 4-week dose-intense coursewith rituximab in a 58-year-old man with Waldenstrommacroglobulinemia; this syndrome mimicked acute rheumatoid arthritisaffecting the hands and the knees.[89]
To treat B-cell lymphomas, rituximab (at a dose of 250 mg QW) is sometimes administered with ibritumomab tiuxetan, an immunoconjugatein which the monoclonal antibody ibritumomab is covalently bound totiuxetan, a high-affinity, linker-chelator for the radioisotopes yttrium-90 (Y-90) or indium-111 (In-111).[90] The antibody moiety ofibritumomab tiuxetan is ibritumomab, a murine IgG1-κ monoclonalantibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. The tiuxetan chelator provides a stable linkage between the antibody and the radioisotope,permitting radiation to be directed against antigen-positive cells.The β emission from Y-90 induces cell damage by the formation of free
radicals in the target and neighboring cells. Severe mucocutaneous reactions, some with fatal outcome, have been reported in associationwith the ibritumomab tiuxetan therapeutic regimen, which includesrituximab, In-111 ibritumomab tiuxetan, and Y-90.
It is possible that, as an immunosuppressant, rituximab may increase the likelihood for development of cancer. There is one report ofMerkel cell carcinoma (MCC) occurring in CLL patients soon aftertreatment with 2-CdA and/or rituximab, suggesting that thiscomplication rarely observed in CLL patients may have a link with strongly immunosuppressive therapy with 2-CdA and rituximab.[91]Non
Cutaneous Side Effects
Although an extensive discussion of noncutaneous side effects in beyond the scope of this paper, a brief survey is useful forphysicians contemplating the use of rituximab. Black box warnings include the following[1]:
Fatal Infusion Reactions. Deaths within 24 hours of rituximab infusion have been reported. These fatal reactions followed an infusionreaction complex which included hypoxia, pulmonary infiltrates, acuterespiratory distress syndrome, myocardial infarction, ventricular fibrillation or cardiogenic shock. Approximately 80 percent of fatalinfusion reactions occurred in association with the first infusion.
Tumor Lysis Syndrome (TLS). Acute renal failure requiring dialysis with instances of fatal outcome has been reported in the setting ofTLS following treatment with rituximab.
Severe Mucocutaneous Reactions (discussed above). Severe mucocutaneous reactions, some with fatal outcome, have been reported in associationwith rituximab treatment. Other side effects listed in the package insert include the following[1]: Hepatitis B reactivation with related fulminant hepatitis:
Hypersensitivity reactions:
Serious or life-threatening cardiac arrhythmias (hypotension can occur as well) Severe renal toxicity, including acute renal failure requiringdialysis and, in some cases, a fatal outcome.Certain precautions should be taken when using rituximab.[1] Because rituximab targets all CD20-positive B lymphocytes, malignant andnonmalignant, complete blood counts (CBC) and platelet counts shouldbe obtained at regular intervals during rituximab therapy and more frequently in patients who develop cytopenias. The duration ofcytopenias caused by rituximab can extend well beyond the treatmentperiod. Renal toxicity was seen with this drug in combination with cisplatin in clinical trials. Human antichimeric antibody (HACA) wasdetected in 4 of 356 patients and 3 had an objective clinicalresponse.
Rituximab can increase the risk of infection.[1] In trials, infectious events occurred in 31 percent of patients: 19 percent of patients hadbacterial infections, 10 percent had viral infections, 1 percent hadfungal infections, and 6 percent were unknown infections. Serious infectious events including sepsis, occurred in 2 percent of patients.Immune/autoimmune events have been reported, including uveitis, opticneuritis in a patient with systemic vasculitis, pleuritis in a patient with a lupus-like syndrome,Rixuximab has a variety of hematologic side effects.[1]
In clinical trials, series cytopenias were reported in 48 percent of patients treated with rituximab; these include: lymphopenia (40 %), neutropenia(6 %), leukopenia (4 %), anemia (3 percent ), and thrombocytopenia (2%). The median duration of lymphopenia was 14 days (range 1-588 days)and of neutropenia was 13 days (range, 2 to 116 days). A single occurrence of transient aplastic anemia (pure red cell aplasia) andtwo occurrences of hemolytic anemia following rituximab therapy were reported.
The most common respiratory system adverse events experienced were increased cough, rhinitis, bronchospasm, dyspnea, and sinusitis.[1] Inboth clinical studies and post-marketing surveillance, there have been a limited number of reports of bronchiolitis obliterans presenting upto 6 months post-rituximab infusion and a limited number of reports of pneumonitis (including interstitial pneumonitis) presenting up to 3months post-rituximab infusion, some of which resulted in fatal
outcomes.
Conclusion
Rituximab is a promising agent for the treatment of B-Cell related diseases. It has many side effects, some common and some not common.It has transformed the treatment of non-Hodgkin's lymphoma, chroniclymphocytic leukemia, Waldenstrom macroglobulinemia, and immune or
idiopathic thrombocytopenic purpura. As future research defines the role of the B-cell in disease, the uses of rituximab will likelyincrease.
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