Rituxan sold under the brand name Rituximab is a chimeric monoclonal antibody against the protein CD20, which is primarily found on the surface of immune system B cells. CD20 is widely expressed on B cells, from early pre-B cells to later in differentiation, but it is absent on terminally differentiated plasma cells. When it binds to this protein it triggers cell death.
The following effects have been found:
- The Fc portion of rituximab mediates antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).
- Rituximab has a general regulatory effect on the cell cycle.
- It increases MHC II and adhesion molecules LFA-1 and LFA-3 (lymphocyte function-associated antigen).
- It elicits shedding of CD23.
- It downregulates the B cell receptor.
- It induces apoptosis of CD20+ cells.
It is used to treat adults with non-Hodgkin lymphoma and chronic lymphocytic leukemia. It is also indicated for the treatment of certain autoimmune diseases such as rheumatoid arthritis and pemphigus vulgaris, and both pediatric and adult patients with granulomatosis with polyangiitis (Wegener’s granulomatosis) and microscopic polyangiitis.
Rituxan destroys both normal and malignant B cells that have CD20 on their surfaces and is therefore used to treat diseases which are characterized by having too many B cells, overactive B cells, or dysfunctional B cells. It is used to treat cancers of the white blood system such as leukemias and lymphomas, including non-Hodgkin’s lymphoma, chronic lymphocytic leukemia, and lymphocyte predominant subtype, of Hodgkin’s Lymphoma.This also includes Waldenström’s macroglobulinemia a type of NHL.
Rituxan is used in combination with fludarabine and cyclophosphamide to treat previously untreated and previously treated CD20-positive chronic lymphocytic leukemia. Riutuxan is used in combination with methotrexate to treat moderately-to severely-active rheumatoid arthritis with inadequate response to one or more TNF antagonist therapies. Rituxan is used in combination with glucocorticoids to treat both granulomatosis with polyangiitis and microscopic polyangiitis.
Rituxan is being used off-label in the management of kidney transplant recipients. This drug may have some utility in transplants involving incompatible blood groups. It is also used as induction therapy in highly sensitized patients going for kidney transplantation.
Patients require close monitoring during rituximab infusion due to the potential for serious infusion-related reactions. Severe reactions typically occurred during the first infusion with time to onset of 30 to 120 minutes. Institute medical management (e.g., glucocorticoids, epinephrine, bronchodilators, or oxygen) for infusion reactions as needed.
General adverse events have been reported with rituximab, although it should be noted that fever, chills, rigors, flushing, pain, and cytokine release syndrome have been associated with reactions related to the infusion that can be severe and/or fatal.
There have been a limited number of reports of bronchiolitis obliterans presenting up to 6 months post-rituximab infusion and a limited number of reports of pneumonitis.
Cardiovascular adverse events have been reported with rituximab, although it should be noted that hypotension, hypertension, myocardial infarction, ventricular fibrillation, and cardiogenic shock have been associated with reactions related to the infusion that can be severe and/or fatal.
Hematologic reactions includes lymphopenia as the most common and others include neutropenia, leukopenia, granulocytopenia and anemia.
Rituximab may cause hepatitis B virus (HBV) reactivation, resulting in hepatitis B exacerbation, during or after receipt. Other viral infections may also be reactivated.
Mucocutaneous reactions, some with fatal outcomes, have been reported and these includes bullous rash/vesicular rash, lichenoid dermatitis (lichen planus-like eruption), paraneoplastic pemphigus (an uncommon disorder associated with the underlying malignancy), Stevens-Johnson syndrome, and toxic epidermal necrolysis.
Tumor lysis syndrome (TLS) due to rapid reduction of tumor cells may result in renal insufficiency, acute renal failure requiring dialysis, hyperkalemia, hypocalcemia, hyperuricemia, or hyperphosphatemia.