Bullous Systemic Lupus Erythematosus (BSLE) 

Updated: Mar 13, 2018
Author: Sarah Sweeney Pinney, MD, FAAD; Chief Editor: Dirk M Elston, MD 

Overview

Background

Bullous systemic lupus erythematosus is an autoantibody-mediated subepidermal blistering disease that occurs in patients with systemic lupus erythematosus (see the image below).[1, 2, 3, 4]

Tense vesiculobullous lesions on the neck of a pat Tense vesiculobullous lesions on the neck of a patient with bullous systemic lupus erythematosus.

The diagnosis of bullous systemic lupus erythematosus requires the following elements (see Presentation and Workup):

  • Fulfillment of the American College of Rheumatology criteria for systemic lupus erythematosus (see also Systemic Lupus Erythematosus)

  • An acquired vesiculobullous eruption (see the image above)

  • Histologic evidence of a subepidermal blister and a predominantly neutrophilic dermal infiltrate

  • Direct immunofluorescence (DIF) microscopy demonstrating immunoglobulin G (IgG, with or without immunoglobulin A [IgA] and immunoglobulin M [IgM]) deposits at the basement membrane zone (BMZ)

  • Evidence of antibodies to type VII collagen via DIF or indirect immunofluorescence (IIF) on salt-split skin, immunoblotting, immunoprecipitation, enzyme-linked immunosorbent assay (ELISA), or immunoelectron microscopy[5]

All 5 criteria listed above are needed for a diagnosis of type 1 bullous systemic lupus erythematosus, whereas only the first 4 criteria are needed to diagnose type 2 (undetermined location of antigen or dermal antigen other than type VII collagen) and type 3 (epidermal antigen) bullous systemic lupus erythematosus. Type VII collagen, a component of anchoring fibrils, is also targeted in epidermolysis bullosa acquisita (EBA). However, unlike epidermolysis bullosa acquisita, bullous systemic lupus erythematosus tends to respond dramatically to treatment with dapsone. (See Differentials and Treatment.)

Not all blistering eruptions that occur in patients with lupus erythematosus represent bullous systemic lupus erythematosus as defined above. Vesiculobullous skin lesions can also develop as a result of extensive damage to the epidermal basal layer (and even suprabasal keratinocytes), due to an intense interface dermatitis in the setting of lupus erythematosus–specific skin disease. Such patients may present with a severe form of acute or subacute cutaneous lupus erythematosus (SCLE) that resembles erythema multiforme (Rowell syndrome)[6] or toxic epidermal necrolysis (TEN). (See Differentials.)[7, 8, 9]

Because epidermolysis bullosa acquisita and bullous systemic lupus erythematosus share the same target antigen, distinguishing between the 2 may be difficult. (See Etiology below.)

 For patient education information, see Lupus (Systemic Lupus Erythematosus).

Etiology

The production of autoantibodies represents a central feature of systemic lupus erythematosus. For example, antinuclear antibodies (ANAs) are detected in almost all affected individuals. In addition to this general tendency, injury to the dermoepidermal junction by the interface dermatitis of cutaneous lupus erythematosus may expose new epitopes and precipitate the development of antibodies that specifically target the BMZ.

The autoantibody repertoire of systemic lupus erythematosus can include nonpathogenic and pathogenic anti-BMZ antibodies. Patients with nonbullous systemic lupus erythematosus often have circulating antibodies to various components of the BMZ (including bullous pemphigoid antigens 1 and 2), which may have a role in formation of the lesional lupus band (ie, granular antibody deposition at the BMZ in normal-appearing skin).[10]

Although the lupus band appears to colocalize with type VII collagen, the noncollagenous-1 (NC1) domain of this protein does not represent the target antigen for circulating antibodies in systemic lupus erythematosus patients without clinical blistering.

In patients with bullous systemic lupus erythematosus, antibodies directed at the BMZ likely mediate the blistering phenotype by directly interfering with adhesive connections at the dermoepidermal junction and through induction of complement-dependent inflammation that leads to tissue injury and dermoepidermal separation. Proteolytic damage caused by recruited neutrophils contributes to the latter process.

In patients with systemic lupus erythematosus without vesiculobullous eruptions, an increase of circulating antitype VII collagen antibodies may precede the onset of type 1 bullous systemic lupus erythematosus. The autoantibodies then increase after disease onset and decrease with remission of eruptions.[11] In type 1 bullous systemic lupus erythematosus (which accounts for most cases), antibodies against type VII collagen may weaken or block anchoring fibril-mediated connections between the lamina densa of the basement membrane and the papillary dermis.

In epidermolysis bullosa acquisita and bullous systemic lupus erythematosus, antigenic epitopes reside within the NC1 and NC2 domains of type VII collagen, which are localized to the lamina densa and the underlying dermis, respectively.[12] The cartilage matrix protein (CMP) subdomain of the NC1 domain has been shown to bind to antibodies from patients with epidermolysis bullosa acquisita and systemic lupus erythematosus, suggesting this subdomain serves as an immunodominant antigenic epitope.[13]

Subepidermal blisters can be induced in mice by the passive transfer of such autoantibodies from patients with epidermolysis bullosa acquisita, but not the Fab fragments alone.[14, 15] This demonstrates that human epidermolysis bullosa acquisita autoantibodies are pathogenic and that complement-mediated inflammation (which requires the Fc fragment) has an important role in the blistering process.

Antibodies recognizing bullous pemphigoid antigen 1, laminin-5, and laminin-6 have also been described in patients with bullous systemic lupus erythematosus.[16] While autoreactive helper T cells and dysregulation of regulatory T cells may play a role in other autoimmune blistering disorders, such as pemphigus and bullous pemphigoid, autoimmunity to type VII collagen has not been shown to involve aberrant regulatory T cell function.[17, 18, 19]

The term acute syndrome of apoptotic pan-epidermolysis (ASAP) has been proposed for the toxic epidermal necrolysis–like cutaneous injury pattern that can occur in settings of lupus erythematosus, acute graft versus host disease, pseudoporphyria, and the classic drug-hypersensitivity syndrome.[20] Fas-Fas ligand interactions have been implicated in the massive keratinocyte apoptosis that characterizes ASAP.

Toxic epidermal necrolysis–like cutaneous lupus erythematosus (which can be triggered by intensive ultraviolet exposure) must be differentiated from drug-induced toxic epidermal necrolysis occurring in a patient with lupus erythematosus.[21]

Genetic predisposition

Certain individuals may have a genetic predisposition to develop autoimmunity to BMZ antigens and to systemic lupus erythematosus. For example, epidermolysis bullosa acquisita, bullous systemic lupus erythematosus, and systemic lupus erythematosus are all associated with an increased prevalence of the HLA class II DR2 haplotype.

The antigen-presenting protein encoded by the DR2-associated DRB1*1501 allele (found in epidermolysis bullosa acquisita and bullous systemic lupus erythematosus patients) has been postulated to be involved in presenting type VII collagen epitopes to T lymphocytes.

Epidemiology

Bullous systemic lupus erythematosus accounts for 2-3% of cases of autoimmune subepidermal blistering disease, with an estimated incidence of fewer than 0.5 cases per million population per year.

Persons of any race can develop bullous systemic lupus erythematosus, but it occurs most frequently in African Americans. Bullous systemic lupus erythematosus affects women more often than men, reflecting the female preponderance in systemic lupus erythematosus.

Bullous systemic lupus erythematosus most often manifests in the second through fourth decades of life, but it has been reported in children and older adults.[22, 23]

Prognosis

The course of bullous systemic lupus erythematosus is often remitting. Fortunately, unlike epidermolysis bullosa acquisita, treatment with dapsone is successful in most cases of bullous systemic lupus erythematosus. The disorder frequently resolves spontaneously in less than 1 year. In some cases, postinflammatory hypopigmentation may remain.[24]

The development of bullous systemic lupus erythematosus in patients with systemic lupus erythematosus does not typically lead to increased mortality. Morbidity depends on the extent of the eruption and the response to therapy.

Toxic epidermal necrolysis–like lupus erythematosus can result in considerable morbidity and even mortality if extensive areas of skin are denuded, especially in the context of severe systemic manifestations of lupus erythematosus.

 

Presentation

History

Bullous systemic lupus erythematosus is characterized by the rapid development of a widespread vesiculobullous eruption. The blistering activity does not necessarily correlate with that of the patient's lupus erythematosus–specific skin or systemic disease, but parallel exacerbations (often involving lupus nephritis) have been described. Bullous systemic lupus erythematosus occasionally represents the initial clinical manifestation of systemic lupus erythematosus in both children and adults.[25]  

Bullous systemic lupus erythematosus may be accompanied by pruritus of variable intensity. Mucosal lesions are often painful. Patients can exhibit any of the symptoms associated with systemic lupus erythematosus. These can include the following:

  • Fever

  • Weight loss

  • Fatigue

  • Photosensitivity

  • Arthralgias

  • Arthritis

  •  Esophagitis[26]

  • Manifestations of renal, pulmonary, cardiac, and/or central nervous system disease[24]

Patients with toxic epidermal necrolysis–like acute cutaneous lupus erythematosus often have significant systemic disease activity (eg, lupus nephritis or cerebritis).

See also Systemic Lupus Erythematosus and Neurologic Manifestations of Systemic Lupus Erythematosus.

Physical Examination

Extracutaneous findings of systemic lupus erythematosus may include joint tenderness and swelling, pallor or petechiae (reflecting hematologic abnormalities), and auscultation evidence of a pulmonary or pericardial effusion.

Morphology of bullous systemic lupus erythematosus skin lesions

Blisters range from large, tense bullae (resembling bullous pemphigoid) to small, grouped vesicles (resembling dermatitis herpetiformis). They often arise on erythematous skin and may be preceded by urticarial papules and plaques. An annular or figurate configuration is occasionally observed. Bullae contain clear or hemorrhagic fluid. Rupture results in erosions and crusts, which typically heal with postinflammatory hyperpigmentation or hypopigmentation. (See the image below.)

Tense vesiculobullous lesions on the neck of a pat Tense vesiculobullous lesions on the neck of a patient with bullous systemic lupus erythematosus.

Although bullous systemic lupus erythematosus was initially defined as a nonscarring bullous disease, a mechanobullous presentation resembling classic epidermolysis bullosa acquisita has been reported. In such patients, vesicles and bullae arise within noninflamed skin of trauma-prone sites (reflecting skin fragility) and heal with milia and scarring.

Distribution of bullous systemic lupus erythematosus

Bullous systemic lupus erythematosus frequently manifests in a widespread, symmetrical distribution of skin lesions. The eruption favors the upper part of the trunk, proximal upper extremities (flexural and extensor aspects), neck, and face, but blisters can occur anywhere on the cutaneous surface. Usually, no clear association exists between sun exposure and the development of lesions, which involve sun-protected and sun-exposed sites. Blisters and erosions can also affect the oral, pharyngeal, nasal, and vulvar mucous membranes.

Lesions of classic epidermolysis bullosa acquisita–like bullous systemic lupus erythematosus are localized to trauma-prone areas, such as the dorsal hands, feet, elbows, and knees.

Lupus erythematosus–specific vesiculobullous skin disease

These vesiculobullous lesions are distinct from those of bullous systemic lupus erythematosus, representing severe variants of acute, subacute, or (rarely) discoid cutaneous lupus erythematosus. The eruptions can develop rapidly or evolve over several weeks.

In toxic epidermal necrolysis–like acute cutaneous lupus erythematosus, photodistributed diffuse or patchy erythema evolves (usually rapidly) into flaccid bullae (positive Nikolsky sign, unlike bullous systemic lupus erythematosus) and widespread, sheetlike, full-thickness epidermal detachment.

Toxic epidermal necrolysis–like subacute cutaneous lupus erythematosus manifests as widespread blistering and full-thickness epidermal detachment in the context of preexisting photodistributed annular or papulosquamous skin lesions and anti-Ro/SS-1 and/or anti-La/SS-2 antibody production. Involvement of the oral, conjunctival, and genital mucosae occurs in some cases of toxic epidermal necrolysis–like lupus erythematosus.

Erythema multiforme–like lesions occurring in the context of acute, subacute, or (as initially described by Rowell and colleagues in 1963) discoid cutaneous lupus erythematosus have been referred to as Rowell syndrome. The development of these targetoid erythematous plaques with central (or, in the setting of subacute cutaneous lupus erythematosus, peripheral) blistering and erosions is thought to represent a limited form of toxic epidermal necrolysis–like lupus erythematosus. Mucosal involvement is often observed.[27, 28, 29]

Some authors[30] identify Rowell syndrome as a rare but distinct clinical entity with specific diagnostic criteria. The diagnosis of Rowell syndrome requires the presence of all redefined major criteria and at least 1 of the minor criteria. Major criteria include the coexistence of lupus erythematous, erythema multiforme–like lesions, and a speckled pattern of antinuclear antibodies. Minor criteria include chilblains, positive anti-Ro (SS-A) or anti-La (SS-B) antibodies, and a reactive rheumatoid factor.

Vesicles or erosions at the advancing edge of active annular subacute lupus erythematosus lesions represent a relatively common observation.

Other mucocutaneous findings

Specific cutaneous lesions of acute, subacute, and chronic (discoid) cutaneous lupus are observed in a minority of patients with bullous systemic lupus erythematosus. (See also Acute Lupus Erythematosus, Subacute Cutaneous Lupus Erythematosus, and Discoid Lupus Erythematosus.)

Nonspecific cutaneous findings of lupus erythematosus, such as periungual telangiectasias, livedo reticularis, and nonscarring alopecia, also may be present. Chilblain lupus can occur in association with Rowell syndrome.

 

DDx

Diagnostic Considerations

The clinical, histologic, and immunohistochemical features of bullous systemic lupus erythematosus can resemble epidermolysis bullosa acquisita (the inflammatory form more often than the classic mechanobullous form), dermatitis herpetiformis, and bullous pemphigoid.

Toxic epidermal necrolysis–like lupus erythematosus demonstrates clinical and histologic overlap with drug-induced toxic epidermal necrolysis and toxic epidermal necrolysis–like variants of acute graft versus host disease and pseudoporphyria. Usually these cases have a previous history of SLE, as well as serologic markers for SLE, and lack a history of drug ingestion.[31] A similar clinical presentation is occasionally observed in patients with fulminant linear IgA bullous dermatosis (especially the drug-induced variety).

Differential Diagnoses

 

Workup

Approach Considerations

Bullous systemic lupus erythematosus occurs in the setting of systemic lupus erythematosus; thus, ANA test results generally are positive. Anti-dsDNA, anti-Sm, anti-Ro/SS-A, anti-La/SS-B, and anticardiolipin antibodies may also be detected.

Other laboratory abnormalities related to systemic lupus erythematosus can include low levels of complement (ie, C3, C4, CH50), anemia, leukopenia, thrombocytopenia, proteinuria or cellular casts upon urinalysis, and an elevated erythrocyte sedimentation rate. (See also Systemic Lupus Erythematosus and Lupus Nephritis.)

Laboratory findings in persons with toxic epidermal necrolysis–like lupus erythematosus vary depending on the underlying type of lupus erythematosus present.

Although the lupus erythematosus patients with erythema multiforme–like skin lesions who were originally described by Rowell and colleagues had immunologic features that included a speckled pattern of ANAs, anti-Ro/SS-A and/or La/SS-B antibodies, and a positive rheumatoid factor, these findings are not consistently observed in lupus erythematosus patients with this clinical presentation. Anticardiolipin antibodies and lupus anticoagulant have also been reported in individuals with Rowell syndrome.

Procedures

Diagnosis of bullous systemic lupus erythematosus requires skin biopsy specimens for routine light microscopy (preferably from the edge of a fresh blister, including adjacent, clinically unblistered skin) and DIF microscopy (from perilesional skin).

Histologic Findings

Light microscopy

Histologically, bullous systemic lupus erythematosus is characterized by dermoepidermal separation beneath an intact epidermis. A predominantly neutrophilic infiltrate is observed in an edematous upper dermis, either concentrated in the dermal papillae (similar to dermatitis herpetiformis) or distributed in a continuous band beneath the BMZ (similar to linear IgA bullous dermatosis).

Nuclear dust is often apparent, and a variable number of eosinophils and mononuclear cells are present within the dermal infiltrate. Basal keratinocyte vacuolization and other histologic features of cutaneous lupus erythematosus are typically absent.

Immunofluorescence microscopy

DIF microscopy of perilesional skin reveals deposition of IgG (with and without IgM and IgA) and complement in a linear or granular bandlike pattern at the BMZ.[4]

In type 1 bullous systemic lupus erythematosus, DIF of salt-split perilesional skin and/or IIF microscopy following incubation of the patient's serum with salt-split normal human skin reveals immunoglobulin deposits localized to the dermal floor of the split.[32] Immunoblot and immunoprecipitation studies using the patient's serum can confirm that these antibodies recognize the 290- and 145-kd proteins of type VII collagen. An enzyme-linked immunosorbent assay (ELISA) test for rapid detection of anti–type VII collagen NC1 domain antibodies has also been developed.

In addition, direct immunoelectron microscopy can be used to demonstrate that the immunoglobulin deposits are codistributed with anchoring fibrils/type VII collagen within and just below the lamina densa.

Cases with negative IIF and an undetermined sublocalization of anti-BMZ antibodies (or antibodies recognizing a dermal antigen other than collagen VII) are referred to as type 2 bullous systemic lupus erythematosus. Of note, circulating antibodies to type VII collagen are less likely to be present in patients with a granular pattern of fluorescence on DIF. Bullous systemic lupus erythematosus characterized by immunoglobulin binding the epidermal roof (type 3 bullous systemic lupus erythematosus) or the roof and the dermal floor of salt-split skin has also been observed. Antigens in such patients have included bullous pemphigoid antigen 1, laminin-5, and laminin-6.

Histologic findings in toxic epidermal necrolysis–like and erythema multiforme–like lupus erythematosus lesions

The histologic features of toxic epidermal necrolysis–like lupus erythematosus consist of full-thickness epidermal necrosis and a sparse lymphocytic infiltrate in the upper dermis, as are seen in drug-induced toxic epidermal necrolysis.

Rowell syndrome is characterized by a vacuolar interface dermatitis with lymphocyte exocytosis; prominent necrotic keratinocytes in all layers of the epidermis; a mild, superficial, perivascular lymphocytic infiltrate; and dermal edema, features suggestive of erythema multiforme but also compatible with early, hyperacute cutaneous lupus erythematosus. DIF findings are usually negative.

 

Treatment

Approach Considerations

Bullous systemic lupus erythematosus generally responds well to medical therapy, and treatment with dapsone is particularly effective. Although type 1 bullous systemic lupus erythematosus and epidermolysis bullosa acquisita are characterized by antibodies targeting type VII collagen, epidermolysis bullosa acquisita differs considerably in its marked resistance to therapy.

A dermatologist may be consulted for the evaluation and management of bullous systemic lupus erythematosus, toxic epidermal necrolysis, erythema multiforme–like lupus erythematosus, or another cutaneous manifestation of lupus erythematosus.

An internist/rheumatologist may be consulted for the evaluation and management of extracutaneous (eg, renal, cardiac, pulmonary) manifestations of systemic lupus erythematosus.

Pharmacologic Therapy

Dapsone is the initial treatment of choice for bullous systemic lupus erythematosus.[3, 33] The response is usually dramatic, with cessation of new blister formation within 1-2 days and rapid healing of existing lesions. Low doses (25-50 mg/d) are often effective, although a higher dosage is sometimes required. Rapid recurrences may occur upon withdrawal of dapsone, with prompt remission after reinstitution of therapy. However, discontinuance of dapsone therapy is usually possible within a year. Dapsone has the potential adverse effects of hemolytic anemia and agranulocytosis, especially in patients with a history of anemia and leukopenia.

Prednisone may be effective in patients who cannot tolerate dapsone (eg, those with glucose-6-phosphate dehydrogenase [G-6-PD] deficiency), have a poor response to dapsone, or require treatment of concurrent systemic manifestations of systemic lupus erythematosus. Combination therapy with prednisone and dapsone can also be beneficial.  For patients with parallel exacerbations such as lupus nephritis, additional therapeutics such as corticosteroids and other immunosuppressive agents should be considered.[25]

Methotrexate (MTX), azathioprine, mycophenolate mofetil, and rituximab represent additional therapeutic options.[34, 35, 36]

Rituximab is an anti-CD20 monoclonal antibody hypothesized to reduce the number of antitype VII collagen antibodies by depletion of mature B cells. It may useful for select patients who do not respond to dapsone or other immunosuppressive agents.[35, 37]

Extensive eruptions of toxic epidermal necrolysis–like lupus erythematosus require prompt institution of therapy with intravenous immunoglobulin (IVIG) and/or systemic corticosteroids.[38] IVIG is a viable treatment option when dapsone is contraindicated.[39] However, further studies are needed to determine the true efficacy and safety of IVIG in the treatment of bullous systemic lupus erythematosus. As in drug-induced toxic epidermal necrolysis, intravenous immunoglobulin represents an important therapeutic option for the Fas-mediated massive epidermal necrosis of fulminant toxic epidermal necrolysis–like lupus erythematosus.

Less fulminant manifestations of erythema multiforme–like lupus erythematosus can be treated with antimalarials (including hydroxychloroquine), corticosteroids (topical or systemic, depending on the severity and presence of systemic disease), and other agents in the therapeutic armamentarium for lupus erythematosus. (See also Subacute Cutaneous Lupus Erythematosus.)

Lenalidomide, a thalidomide analogue, has been shown to be effective for a spectrum of cutaneous manifestations of systemic lupus erythematosus in adults. A small study from 2016 showed resolution of cutaneous manifestations, including bullous lesions, of pediatric systemic lupus erythematosus.[40] However, more study is needed to clarify the role of lenalidomide in treating the cutaneous manifestations of systemic lupus erythematosus in both children and adults.

 

Medication

Medication Summary

Bullous systemic lupus erythematosus generally responds well to medical therapy. Dapsone represents the mainstay of treatment, typically leading to rapid clearance of lesions. Dapsone has the potential adverse effects of hemolytic anemia and agranulocytosis, especially in patients with a history of anemia and leukopenia.

As in drug-induced toxic epidermal necrolysis, intravenous immunoglobulin represents an important therapeutic option for the Fas-mediated massive epidermal necrosis of fulminant toxic epidermal necrolysis–like lupus erythematosus.

Antimycobacterial Agents

Class Summary

Therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Dapsone

The general mechanism of action of dapsone is similar to that of sulfonamides, in which competitive antagonism of para-aminobenzoic acid (PABA) prevents the formation of folic acid, inhibiting bacterial growth.

The anti-inflammatory mechanism of dapsone is believed to result from suppression of neutrophils by the inhibition of neutrophil myeloperoxidase and inflammation-inducing oxygen intermediates. Dapsone has been shown to inhibit some forms of neutrophil chemotaxis, suppress leukocyte integrin function, and decrease the attachment of neutrophils to endothelial cell junctions.

Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone

Prednisone decreases inflammation; in particular, it suppresses neutrophil presence and activity at sites of inflammation by inhibition of endothelial cell adhesion molecule expression and chemoattractant production. Prednisone also inhibits antigen presentation, T lymphocyte activity, and (at higher doses) antibody production.

Immunosuppressive Agents

Class Summary

These drugs have anti-inflammatory effects.

Methotrexate (Trexall, Rheumatrex)

Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) synthesis in lymphocytes and other immune cells. Anti-inflammatory effects also result from the inhibition of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) transformylase (increasing tissue concentrations of the anti-inflammatory mediator adenosine) and methionine synthetase (reducing production of the proinflammatory mediator S-adenyl methionine).

Azathioprine (Imuran, Azasan)

Azathioprine antagonizes purine metabolism and inhibits the synthesis of DNA, ribonucleic acid (RNA), and proteins. It may decrease the proliferation of immune cells, in that way lowering autoimmune activity.

Mycophenolate mofetil (CellCept) or mycophenolic acid (Myfortic)

Mycophenolate mofetil has been shown to useful in the treatment of autoimmune diseases.

Blood Products

Class Summary

These are used to improve the clinical and immunologic aspects of the disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.

Immune globulin intravenous (Gamunex, Octagam, Gammaplex , Gammagard)

This provides an antibody-mediated blockade of Fas-Fas ligand interactions involved in the epidermal necrosis of toxic epidermal necrolysis–like cutaneous lupus erythematosus.

Antineoplastics, Anti-CD20 Monoclonal Antibodies

Rituximab (Rituxan)

Rituximab is an anti­CD20 monoclonal antibody that depletes the number of mature B ­cells.