Original Article
A Single Cycle of Rituximab for the Treatment of Severe Pemphigus
N Engl J Med 2007; 357:545-552August 9, 2007
- Abstract
Background
The combination of multiple cycles of rituximab and intravenous immune globulins has been reported to be effective in patients with severe pemphigus. The aim of this study was to assess the efficacy of a single cycle of rituximab in severe types of pemphigus.
Methods
We studied 21 patients with pemphigus whose disease had not responded to an 8-week course of 1.5 mg of prednisone per kilogram of body weight per day (corticosteroid-refractory disease), who had had at least two relapses despite doses of prednisone higher than 20 mg per day (corticosteroid-dependent disease), or who had severe contraindications to corticosteroids. The patients were treated with four weekly infusions of 375 mg of rituximab per square meter of body-surface area. The primary end point was complete remission 3 months after the end of rituximab treatment; complete remission was defined as epithelialization of all skin and mucosal lesions.
Results
Eighteen of 21 patients (86%; 95% confidence interval, 64 to 97%) had a complete remission at 3 months. The disease relapsed in nine patients after a mean of 18.9±7.9 months. After a median follow-up of 34 months, 18 patients (86%) were free of disease, including 8 who were not receiving corticosteroids; the mean prednisone dose decreased from 94.0±10.2 to 12.0±7.5 mg per day (P=0.04) in patients with corticosteroid-refractory disease and from 29.1±12.4 to 10.9±16.5 mg per day (P=0.007) in patients with corticosteroid-dependent disease. Pyelonephritis developed in one patient 12 months after rituximab treatment, and one patient died of septicemia 18 months after rituximab treatment. These patients had a profound decrease in the number of circulating B lymphocytes but normal serum levels of IgG.
Conclusions
A single cycle of rituximab is an effective treatment for pemphigus. Because of its potentially severe side effects, its use should be limited to the most severe types of the disease. (ClinicalTrials.gov number, NCT00213512.)
Media in This Article
Figure 1
Changes in Clinical Lesions, Antidesmoglein Antibodies, and Doses of Prednisone in Patients with Pemphigus Treated with Rituximab.Table 1
Baseline Characteristics of Patients with Pemphigus Treated with Rituximab.Article Activity
- Article
Pemphigus is a life-threatening autoimmune blistering disease affecting the skin and mucosa. It is mediated by pathogenic autoantibodies directed against desmoglein 1 and desmoglein 3, adhesion molecules of the epidermis that are responsible for the cohesion between keratinocytes in skin and mucosa, respectively.1-3 Patients with severe pemphigus require long-term treatment with corticosteroids and other immunosuppressive drugs, which can lead to serious adverse events.4,5
Rituximab, a monoclonal antibody directed against the CD20 antigen of B lymphocytes, has been demonstrated to be effective in various autoimmune diseases6-12 and in occasional cases of life-threatening pemphigus.13-22 Recently, the combination of multiple cycles of rituximab and intravenous immune globulin, another potentially active agent in pemphigus, was reported to be effective in a single-center study of 11 patients with pemphigus.23 We report a multicenter series of 21 patients with severe pemphigus treated by a simple regimen of one cycle of rituximab. Immunologic evaluations explored the mechanism of the short-term and long-term effects of rituximab on these patients.
Methods
Patients
Thirteen centers in France participated in this prospective, open trial. The study was approved by the ethics committee of Seine-Maritime, and written informed consent was obtained from each patient.
Consecutive patients with severe mucosal erosions, superficial blisters, or both suggestive of pemphigus vulgaris or pemphigus foliaceus; a histologic picture of intraepidermal acantholysis; and deposition of IgG, complement component 3 (C3), or both on the keratinocyte membrane detected by direct immunofluorescence24 were included if additional criteria were met. These were the absence of response to an 8-week course of treatment with 1.5 mg of prednisone per kilogram of body weight per day (corticosteroid-refractory cases); the occurrence of at least two cutaneous or mucosal relapses during the period when corticosteroid doses were being decreased, despite prednisone doses higher than 20 mg per day (corticosteroid-dependent cases); and contraindication to corticosteroids because of severe associated medical conditions.
Treatment
The patients were treated with one cycle of four weekly infusions of rituximab at a dose of 375 mg per square meter of body-surface area on days 1, 8, 15, and 22. Corticosteroids were maintained at the initial dose until the disease was controlled, and the corticosteroid dose was then reduced by 10% twice a month. Patients with contraindications to corticosteroids were treated with rituximab alone. Complete remission was defined as the epithelialization of all skin and mucosal lesions, partial remission as the epithelialization of more than 50% of lesions but not of all lesions, and relapse as the occurrence of new cutaneous or mucosal erosions.
End Points
The patients were evaluated clinically and biologically every month during the first year of follow-up and every other month during the second year. The primary end point was the rate of complete remission 3 months after the last infusion of rituximab. The secondary end points were the rate of complete remission during the study period, the time from the start of rituximab treatment to complete remission, the number of relapses and the length of time to each relapse, and adverse effects of treatment.
Immunologic Evaluation
Blood samples were collected at each evaluation. Titers of antibodies against desmoglein 1 and desmoglein 3 were measured by a desmoglein enzyme-linked immunosorbent assay (ELISA) test (MESACUP Desmoglein Test, MBL Medical and Biological Laboratories) with 1:100 diluted serum. For determination of IgG subclass, mouse antihuman IgG1, IgG2, IgG3, and IgG4 antibodies (Sigma) and peroxidase-conjugated goat antimouse IgG (Rockland) were used. IgG reactivity of pemphigus vulgaris serum against the NH2 terminal domains of desmoglein 3 was characterized with the use of ELISA with baculovirus-derived recombinant proteins of desmoglein 3.25
The phenotype of peripheral-blood mononuclear cells was determined by three-color flow cytometry with the use of murine monoclonal antibodies against CD3, CD4, CD5, CD19, CD20, CD21, CD22, CD23, CD24, CD27, CD38, CD56, and CD86 (Coulter). The IgG, IgA, and IgM repertoire of peripheral-blood B lymphocytes was determined with the use of the immunoscope technique, a method that evaluates the diversity of the B-lymphocyte repertoire and monitors its evolution. First, a polymerase chain reaction amplified the heavy-chain variable (HV) region of the IgG, IgA, and IgM molecules. In a second step, the lengths of the complementary determining region 3 (CDR3) were analyzed on an automatic sequencer.26 The serum levels of antibodies against pneumococcal capsule polysaccharide and tetanus toxin were determined on days 0, 90, and 180.27
Statistical Analysis
Two-sided P values less than 0.05 were considered to indicate statistical significance. Continuous variables are expressed as means ±SD. Mean doses of prednisone were compared with the use of the nonparametric Wilcoxon test. Roche, France (the maker of rituximab) had no role in the design of the study, in data accrual or analysis, or in manuscript preparation.
Results
Characteristics of the Patients
Twenty-one patients (14 men and 7 women; 14 with pemphigus vulgaris and 7 with pemphigus foliaceus) were enrolled between January 2003 and December 2004 and followed through March 2007. Their mean (±SD) age was 53.7±15.6 years. The baseline clinical characteristics of the patients are shown in Table 1Table 1
Baseline Characteristics of Patients with Pemphigus Treated with Rituximab.. The mean proportion of the body-surface area involved was 27%. All the patients had severe oral involvement and weight loss of up to 10 kg. In addition, seven patients had severe involvement of one or more other mucosae, including the genital, anal, conjunctival, or pharyngeal mucosae or a combination of these. All patients with corticosteroid-refractory disease and all patients with corticosteroid-dependent disease had been treated previously with various immunosuppressive drugs, intravenous immune globulins, or both without success. The duration of all systemic therapy before study entry ranged from 4 to 168 months (mean, 70.2). Severe associated medical conditions or side effects of corticosteroids were present at baseline in 14 patients (67%). Five patients were treated with rituximab alone because they had contraindications to corticosteroid use. Corticosteroids were contraindicated in two patients because of severe diabetes mellitus, arterial hypertension, or both; in two patients because of a history of severe infection, osteonecrosis of the hip, or both; and in one patient because of old age (84 years) and poor general condition (Table 1).Response to Rituximab Treatment
Eighteen of 21 patients (86%; 95% confidence interval, 64 to 94) had a complete remission at 3 months, including 12 of 14 patients with pemphigus vulgaris and 6 of 7 with pemphigus foliaceus (Table 2Table 2
Complete Remission 3 Months after Rituximab Treatment in Patients with Severe Pemphigus.). Two patients with pemphigus vulgaris had a delayed complete remission on days 180 and 360 (Figure 1Figure 1Changes in Clinical Lesions, Antidesmoglein Antibodies, and Doses of Prednisone in Patients with Pemphigus Treated with Rituximab.). One patient with pemphigus foliaceus with lesions that initially involved the entire body surface was only slightly improved after rituximab, and treatment of this patient was considered to have failed. All the other patients (95%) had a complete remission at some time during the study period. The median delays to partial and complete remission are shown in Table 3Table 3
Median Time to Partial and Complete Remission in Patients with Pemphigus Treated with Rituximab..Of the 20 patients who had a complete remission, 9 (6 with pemphigus vulgaris and 3 with pemphigus foliaceus) had a relapse after a mean period of 18.9±7.9 months. Three patients with corticosteroid-dependent disease had a total of six relapses. Of the nine patients who had a relapse, three were treated with topical corticosteroids only, four with a moderately increased dose of oral corticosteroids, and two with a second course of rituximab. The second course of rituximab was chosen because one of the two patients was 84 years old and was thought to be at high risk for complications from corticosteroids, and the other had a severe relapse. Both patients had a complete remission again. After a median follow-up time of 34 months (range, 26 to 45), 18 patients (86%) were free of disease, including 8 patients (38%) who received no more corticosteroids.
The mean dose of prednisone for patients with corticosteroid-refractory disease decreased from 94.0±10.2 mg per day at baseline to 12.0±7.5 mg per day at the end of the study (P=0.04) (Figure 1). The mean dose of prednisone for patients with corticosteroid-dependent disease decreased from 29.1±12.4 mg per day at baseline to 10.9±16.5 mg per day at the end of the study (P=0.007). Nine patients reported minor and transient side effects during rituximab infusion: headache in three patients, asthenia in three, fever in one, chills in one, and nausea in one. In addition, two severe side effects were observed: one patient had pyelonephritis 12 months after rituximab treatment, and one patient died from septicemia 18 months after rituximab treatment. The patient who died also had rheumatoid arthritis and was concomitantly treated with the anti–tumor necrosis factor agent etanercept.
Immunologic Evaluations
Peripheral-blood B- and T-lymphocyte subpopulations and T-lymphocyte cytokine production were analyzed longitudinally. The B-cell count decreased dramatically from a median of 275 cells per cubic millimeter (range, 29 to 752) to 0 cells per cubic millimeter (range, 0 to 1) at day 21 and remained undetectable until day 180 in all but two patients. Reappearance of B cells began between day 180 and day 270. Ninety percent of them expressed a CD19+CD27− phenotype suggestive of naive B lymphocytes. Twenty-nine percent had a CD19+ CD38highCD24high transitional phenotype suggestive of the migration of B cells from the bone marrow to the periphery. No major changes in T cells or natural killer cells or in T-cell cytokine production were detected after rituximab treatment.
Using the immunoscope method, we followed the evolution of the repertoire of IgG, IgA, and IgM in blood B lymphocytes in two patients. Before treatment, immunoscope profiles showed some peak expansions in the immunoglobulin HV-region genes (IgVH3a, IgVH3b, and IgVH4), the most represented ones, reflecting in vivo antigen-driven responses. Six months later, reappearing blood B cells showed a typical gaussian distribution of the CDR3 lengths for these IgVH families, similar to that found in the naive B cells of cord blood, suggesting the reconstitution of a diverse B-cell repertoire (data not shown).
Antidesmoglein autoantibody response was then analyzed. A dramatic decrease of IgG and IgG4 anti–desmoglein 1 and anti–desmoglein 3 antibodies was observed in 15 of the 18 patients who had a complete remission 3 months after rituximab treatment, whereas persistent high titers were detected in the 2 patients who had a delayed complete remission and in the 1 patient in whom treatment failed. Persistent high titers or rises in anti–desmoglein 1 and anti–desmoglein 3 antibody levels were detected in patients with relapsing disease and, surprisingly, in five patients with pemphigus vulgaris in whom a complete remission was maintained (Figure 1). To disentangle this discrepancy, we retested serum from these patients on recombinant proteins of five extracellular (EC) domains of desmoglein 3 (EC1 to EC5). Antibodies reacting with epitopes of the EC1 to EC2 domains, which are considered the main pathogenic antibodies,28,29 decreased dramatically after rituximab treatment and remained undetectable until day 540, a result that was in accordance with the absence of mucosal lesions in these patients.30,31
Finally, to assess the influence of rituximab on antimicrobial response, we first determined the serum level of IgG and IgM antibodies. No significant change in mean IgG levels was observed after rituximab treatment (P=0.79). On the contrary, mean IgM levels decreased from 1.5±1.1 g per liter at baseline to 1.1±0.9 g per liter on day 180 and 1.0±0.7 g per liter on day 360 (P=0.003). We then determined that the levels of antibodies against pneumococcal capsule polysaccharide and the levels of antibodies against tetanus toxin were not significantly altered between baseline, day 21, and day 90. The two patients who had severe infections, one at 12 months after rituximab treatment and one at 18 months, had normal serum IgG levels (21 g per liter and 13.5 g per liter, respectively), despite low numbers of circulating B lymphocytes (5 per cubic millimeter and 9 per cubic millimeter, respectively) at the times of their infections.
Discussion
Our study demonstrated the efficacy of rituximab for severe pemphigus; 86% of patients were in complete remission 3 months after receiving four weekly infusions of rituximab. After a 34-month follow-up period, 18 patients were free of disease, and 8 of these patients were not receiving any systemic therapy. Overall, treatment with rituximab both resulted in major clinical improvement and permitted a large decrease in the doses of corticosteroids. Our results were similar to those recently reported by Ahmed et al.,23 who obtained a complete remission in 9 of 11 patients (82%). Our patients were treated with one cycle of four weekly infusions of rituximab, and the patients in the study by Ahmed et al. were treated with two induction cycles of rituximab, followed by consolidation therapy and six infusions of intravenous immune globulins, another potentially active agent in pemphigus.23,32,33 Therefore, we believe multiple cycles of rituximab may not be necessary. Accordingly, we suggest restricting the use of additional cycles of rituximab to the few relapses that cannot be adequately controlled with conventional treatments.
Two severe side effects were observed in our study: pyelonephritis developed in one patient 12 months after rituximab treatment, and one patient died from septicemia 18 months after rituximab treatment. It is important to emphasize that rituximab treatment is associated with a risk of death from severe side effects, such as pneumocystis infection, toxic epidermal necrolysis, and progressive multifocal leukoencephalopathy.34,35 The risk of serious infection led Ahmed et al. to propose combining intravenous immune globulins with rituximab during the first 6 months of treatment with rituximab.23 We do not think that 6 months of treatment with immune globulins would have prevented the two serious infections observed in our study, which occurred at 12 and 18 months in patients who had no defect in IgG serum levels or in preformed antibacterial antibodies. It is not known whether the addition of intravenous immune globulins to rituximab reduces the risk of serious infections.36,37
Immunologic investigations demonstrated that one cycle of rituximab induced a prolonged depletion of peripheral-blood B lymphocytes, followed by the reappearance of B cells with a naive phenotype similar to that found in cord blood from neonates. Rituximab induced a modification of the repertoire of B cells, with the disappearance of the initially expanded populations and the reconstitution of a diverse B-cell repertoire that might account for its long-lasting effect.
The clinical response to rituximab in patients with pemphigus foliaceus was closely related to the evolution of anti–desmoglein 1 antibodies, which dramatically decreased in patients who had a complete remission, whereas we were surprised to observe persistently high levels of anti–desmoglein 3 antibodies in a few patients in whom pemphigus vulgaris was in complete remission. The dissociation between anti–desmoglein 1 and anti–desmoglein 3 antibody responses, as well as the absence of major modification of serum levels of antibodies against pneumococcal and tetanus-toxin antigens, suggested some specificity of rituximab for the autoreactive B-cell response.38,39 One hypothesis is that rituximab would differentially affect the turnover of short-life and long-life plasma cells that produce antibodies directed against desmoglein 1 and desmoglein 3.40
Overall, our study suggests that rituximab is a very effective treatment for severe pemphigus. Larger series with a longer follow-up are needed to assess the long-term risks of this treatment.
Presented in part at the December 2006 Congress of the French Society of Dermatology and at the September 2006 Congress of the European Society of Dermatological Research (ESDR), both in Paris.
Supported by the French Society of Dermatology, Paris, and by Roche, France.
No potential conflict of interest relevant to this article was reported.
We thank Marie-France Hellot for her help with the statistical analysis, Vincent Ferranti for monitoring the study, Ken Wood for assistance in editing an earlier version of the manuscript, and Nathalie Jourdain for excellent secretarial assistance.
Source Information
From Rouen University Hospital, Rouen (P.J., P.M.); INSERM Unité 519, Rouen University Hospital, Rouen (P.J., H.M., D.G., S.J., F.T., P.M.); Henri Mondor University Hospital, Créteil (J.-C.R.); Clermont-Ferrand University Hospital, Clermont-Ferrand (M.D.); Pasteur Institute, Paris (M.-L.G.); Limoges University Hospital, Limoges (C.B.); Nantes University Hospital, Nantes (B.D.); Bordeaux University Hospital, Bordeaux (M.-S.D.); Lille University Hospital, Lille (E.D.); Poissy–Saint Germain-en-Laye Intercommunal Hospital, Saint Germain-en-Laye (C. Pauwels); Paris V University, Paris (N.F.); Paris XIII University Hospital, Bobigny (F.C.); Bichat University Hospital, Paris (C. Picard); Paris X University Hospital, Paris (E.T.-B.); and Reims University Hospital, Reims (P.B.) — all in France; and the Faculty of Medicine, Philipp University, Marburg, Germany (R.M., M.H.).
Address reprint requests to Dr. Joly at the Clinique Dermatologique, Hôpital Charles Nicolle, 1 rue de Germont, 76031 Rouen CEDEX, France, or at Pascal.Joly@chu-rouen.fr.
- References
References
1
Stanley JR . Pemphigus and pemphigoid as paradigms of organ-specific, autoantibody-mediated diseases. J Clin Invest 1989;83:1443-1448
CrossRef | Web of Science | Medline2
Stanley JR . Cell adhesion molecules as targets of autoantibodies in pemphigus and pemphigoid, bullous diseases due to defective epidermal cell adhesion. Adv Immunol 1993;53:291-325
CrossRef | Web of Science | Medline3
Amagai M ,Klaus-Kovtun V ,Stanley JR . Autoantibodies against a novel epithelial cadherin in pemphigus vulgaris, a disease of cell adhesion. Cell 1991;67:869-877
CrossRef | Web of Science | Medline4
Bystryn JC ,Steinman NM . The adjuvant therapy of pemphigus: an update. Arch Dermatol 1996;132:203-212
CrossRef | Web of Science | Medline5
McDonald CJ . Cytotoxic agents for use in dermatology. J Am Acad Dermatol 1985;12:753-775
CrossRef | Web of Science | Medline6
Kazkaz H ,Isenberg D . Anti B cell therapy (rituximab) in the treatment of autoimmune diseases. Curr Opin Pharmacol 2004;4:398-402
CrossRef | Web of Science | Medline7
Stasi R ,Stipa E ,Forte V ,Meo P ,Amadori S . Variable patterns of response to rituximab treatment in adults with chronic idiopathic thrombocytopenic purpura. Blood 2002;99:3872-3873
CrossRef | Web of Science | Medline8
Narat S ,Gandla J ,Hoffbrand AV ,Hughes RG ,Mehta AB . Rituximab in the treatment of refractory autoimmune cytopenias in adults. Haematologica 2005;90:1273-1274
Web of Science | Medline9
Zaja F ,De Vita S ,Russo D , et al. Rituximab for the treatment of type II mixed cryoglobulinemia. Arthritis Rheum 2002;46:2252-2254
CrossRef | Web of Science | Medline10
Specks U ,Fervenza FC ,McDonald TJ ,Hogan MC . Response of Wegener's granulomatosis to anti-CD20 chimeric monoclonal antibody therapy. Arthritis Rheum 2001;44:2836-2840
CrossRef | Web of Science | Medline11
Levine TD . Rituximab in the treatment of dermatomyositis: an open-label pilot study. Arthritis Rheum 2005;52:601-607
CrossRef | Web of Science | Medline12
Arzoo K ,Sadeghi S ,Liebman HA . Treatment of refractory antibody mediated autoimmune disorders with an anti-CD20 monoclonal antibody (rituximab). Ann Rheum Dis 2002;61:922-924
CrossRef | Web of Science | Medline13
Dupuy A ,Viguier M ,Bedane C , et al. Treatment of refractory pemphigus vulgaris with rituximab (anti-CD20 monoclonal antibody). Arch Dermatol 2004;140:91-96
CrossRef | Web of Science | Medline14
Espana A ,Fernandez-Galar M ,Lloret P ,Sanchez-Ibarrola A ,Panizo C . Long-term complete remission of severe pemphigus vulgaris with monoclonal anti-CD20 antibody therapy and immunophenotype correlations. J Am Acad Dermatol 2004;50:974-976
CrossRef | Web of Science | Medline15
Morrison LH . Therapy of refractory pemphigus vulgaris with monoclonal anti-CD20 antibody (rituximab). J Am Acad Dermatol 2004;51:817-819
CrossRef | Web of Science | Medline16
Wenzel J ,Bauer R ,Bieber T ,Tuting T . Successful rituximab treatment of severe pemphigus vulgaris resistant to multiple immunosuppressants. Acta Derm Venereol 2005;85:185-186
Medline17
Schmidt E ,Herzog S ,Brocker EB ,Zillikens D ,Goebeler M . Long-standing remission of recalcitrant juvenile pemphigus vulgaris after adjuvant therapy with rituximab. Br J Dermatol 2005;153:449-451
CrossRef | Web of Science | Medline18
Arin MJ ,Engert A ,Krieg T ,Hunzelmann N . Anti-CD20 monoclonal antibody (rituximab) in the treatment of pemphigus. Br J Dermatol 2005;153:620-625
CrossRef | Web of Science | Medline19
Kong HH ,Prose NS ,Ware RE ,Hall RP III . Successful treatment of refractory childhood pemphigus vulgaris with anti-CD20 monoclonal antibody (rituximab). Pediatr Dermatol 2005;22:461-464
CrossRef | Web of Science | Medline20
Herrmann G ,Hunzelmann N ,Engert A . Treatment of pemphigus vulgaris with anti-CD20 monoclonal antibody (rituximab). Br J Dermatol 2003;148:602-603
CrossRef | Web of Science | Medline21
Goebeler M ,Herzog S ,Brocker EB ,Zillikens D . Rapid response of treatment-resistant pemphigus foliaceus to the anti-CD20 antibody rituximab. Br J Dermatol 2003;149:899-901
CrossRef | Web of Science | Medline22
El Tal AK ,Posner MR ,Spigelman Z ,Ahmed AR . Rituximab: a monoclonal antibody to CD20 used in the treatment of pemphigus vulgaris. J Am Acad Dermatol 2006;55:449-459
CrossRef | Web of Science | Medline23
Ahmed AR ,Spigelman Z ,Cavacini LA ,Posner MR . Treatment of pemphigus vulgaris with rituximab and intravenous immune globulin. N Engl J Med 2006;355:1772-1779
Full Text | Web of Science | Medline24
Lever WF . Pemphigus and pemphigoid: a review of the advances made since 1964. J Am Acad Dermatol 1979;1:2-31
CrossRef | Web of Science | Medline25
Muller R ,Svoboda V ,Wenzel E , et al. IgG reactivity against non-conformational NH2-terminal epitopes of the desmoglein 3 ectodomain relates to clinical activity and phenotype of pemphigus vulgaris. Exp Dermatol 2006;15:606-614
CrossRef | Web of Science | Medline26
Lim A, Lemercier B, Werth X, Lesjean Pottier S, Huetz F, Kourilsky P. Most human peripheral blood B cells display a unique heavy chain rearrangement. Int Immunol (in press).
27
Ballet JJ ,Sulcebe G ,Couderc LJ , et al. Impaired anti-pneumococcal antibody response in patients with AIDS-related persistent generalized lymphadenopathy. Clin Exp Immunol 1987;68:479-487
Web of Science | Medline28
Anzai H ,Fujii Y ,Nishifuji K , et al. Conformational epitope mapping of antibodies against desmoglein 3 in experimental murine pemphigus vulgaris. J Dermatol Sci 2004;35:133-142
CrossRef | Web of Science | Medline29
Sekiguchi M ,Futei Y ,Fujii Y ,Iwasaki T ,Nishikawa T ,Amagai M . Dominant autoimmune epitopes recognized by pemphigus antibodies map to the N-terminal adhesive region of desmogleins. J Immunol 2001;167:5439-5448
Web of Science | Medline30
Hacker MK ,Janson M ,Fairley JA ,Lin MS . Isotypes and antigenic profiles of pemphigus foliaceus and pemphigus vulgaris. Clin Immunol 2002;105:64-74
CrossRef | Web of Science | Medline31
Amagai M ,Komai A ,Hashimoto T , et al. Usefulness of enzyme-linked immunosorbent assay using recombinant desmogleins 1 and 3 for serodiagnosis of pemphigus. Br J Dermatol 1999;140:351-357
CrossRef | Web of Science | Medline32
Ahmed AR . Treatment of autoimmune mucocutaneous blistering diseases with intravenous immunoglobulin therapy. Expert Opin Investig Drugs 2004;13:1019-1032
CrossRef | Web of Science | Medline33
Ahmed AR ,Dahl MV . Consensus statement on the use of intravenous immunoglobulin therapy in the treatment of autoimmune mucocutaneous blistering diseases. Arch Dermatol 2003;139:1051-1059
CrossRef | Web of Science | Medline34
Bermudez A ,Marco F ,Conde E ,Mazo E ,Recio M ,Zubizaretta A . Fatal varicella-zoster infection following rituximab and chemotherapy treatment in a patient with follicular lymphoma. Haematologica 2000;85:894-895
Web of Science | Medline35
Quartier P ,Tournilhac O ,Archimbaud C , et al. Enteroviral meningoencephalitis after anti-CD20 (rituximab) treatment. Clin Infect Dis 2003;36:e47-e49
CrossRef | Web of Science | Medline36
Lehrnbecher T . Intravenous immunoglobulins in the prevention of infection in children with hematologic-oncologic diseases. Klin Padiatr 2001;213:Suppl 1:A103-A105
CrossRef | Web of Science | Medline37
Sullivan KM ,Kopecky KJ ,Jocom J , et al. Immunomodulatory and antimicrobial efficacy of intravenous immunoglobulin in bone marrow transplantation. N Engl J Med 1990;323:705-712
Full Text | Web of Science | Medline38
Smith MR . Rituximab (monoclonal anti-CD20 antibody): mechanism of action and resistance. Oncogene 2003;22:7359-7368
CrossRef | Web of Science | Medline39
Maloney DG ,Smith B ,Rose A . Rituximab: mechanism of action and resistance. Semin Oncol 2002;29:Suppl 2:2-9
CrossRef | Web of Science | Medline40
Hoyer BF ,Manz RA ,Radbruch A ,Hiepe F . Long-lived plasma cells and their contribution to autoimmunity. Ann N Y Acad Sci 2005;1050:124-133
CrossRef | Web of Science | Medline
- Citing Articles (87)
Citing Articles
1
Michael Kasperkiewicz, Enno Schmidt, Detlef Zillikens. (2012) Current therapy of the pemphigus group. Clinics in Dermatology 30:1, 84-94
CrossRef2
Giuseppe Cianchini, Francesca Lupi, Cinzia Masini, Rosamaria Corona, Pietro Puddu, Ornella De Pità. (2012) Therapy with rituximab for autoimmune pemphigus: Results from a single-center observational study on 42 cases with long-term follow-up. Journal of the American Academy of Dermatology
CrossRef3
R.J. Feldman, W.G. Christen, A.R. Ahmed. (2012) Comparison of immunological parameters in patients with pemphigus vulgaris following rituximab and IVIG therapy. British Journal of Dermatologyno-no
CrossRef4
M. Kasperkiewicz, I. Shimanovich, M. Meier, N. Schumacher, L. Westermann, J. Kramer, D. Zillikens, E. Schmidt. (2012) Treatment of severe pemphigus with a combination of immunoadsorption, rituximab, pulsed dexamethasone and azathioprine/mycophenolate mofetil: a pilot study of 23 patients. British Journal of Dermatology 166:1, 154-160
CrossRef5
B. Horváth, J. Huizinga, H.H. Pas, A.B. Mulder, M.F. Jonkman. (2012) Low-dose rituximab is effective in pemphigus. British Journal of Dermatologyno-no
CrossRef6
Ziad Reguiai, Thierry Tabary, Michael Maizières, Philippe Bernard. (2012) Rituximab treatment of severe pemphigus: Long-term results including immunologic follow-up. Journal of the American Academy of Dermatology
CrossRef7
A.J. Kanwar, D. Tsuruta, K. Vinay, H. Koga, N. Ishii, T. Dainichi, T. Hashimoto. (2011) Efficacy and safety of rituximab treatment in Indian pemphigus patients. Journal of the European Academy of Dermatology and Venereologyno-no
CrossRef8
Alba Álvarez-Abella, Sara Martín-Sala, Ignasi Figueras Nart, Anna Jucglà. (2011) Tratamiento de los pénfigos. Piel
CrossRef9
Andrea Kneisel, Michael Hertl. (2011) Autoimmune bullous skin diseases. Part 2: diagnosis and therapy. JDDG: Journal der Deutschen Dermatologischen Gesellschaft 9:11, 927-947
CrossRef10
Emma E. Craythorne, Ghulam Mufti, Anthony W. duVivier. (2011) Rituximab used as a first-line single agent in the treatment of pemphigus vulgaris. Journal of the American Academy of Dermatology 65:5, 1064-1065
CrossRef11
Benjamin S. Daniel, Dédée F. Murrell, Pascal Joly. (2011) Rituximab and its Use in Autoimmune Bullous Disorders. Dermatologic Clinics 29:4, 571-575
CrossRef12
Enno Schmidt, Detlef Zillikens. (2011) Diagnosis and Treatment of Patients with Autoimmune Bullous Disorders in Germany. Dermatologic Clinics 29:4, 663-671
CrossRef13
Cheyda Chams-Davatchi. (2011) Prevalence and Treatment of Pemphigus in Iran. Dermatologic Clinics 29:4, 681-683
CrossRef14
Tiffany Clay, Amit G. Pandya. (2011) Minimizing Complications in Autoimmune Blistering Diseases. Dermatologic Clinics 29:4, 577-583
CrossRef15
Nicolas Meyer, Carle Paul, Pascal Joly. (2011) Management of Autoimmune Bullous Diseases in France: A Nationwide Network of 30 Centers. Dermatologic Clinics 29:4, 659-662
CrossRef16
Annette Czernik, Siavash Toosi, Jean-Claude Bystryn, Sergei A. Grando. (2011) Intravenous immunoglobulin in the treatment of autoimmune bullous dermatoses: An update. Autoimmunity110919025640001
CrossRef17
Michael Kasperkiewicz, Iakov Shimanovich, Ralf J. Ludwig, Christian Rose, Detlef Zillikens, Enno Schmidt. (2011) Rituximab for treatment-refractory pemphigus and pemphigoid: A case series of 17 patients. Journal of the American Academy of Dermatology 65:3, 552-558
CrossRef18
J.H. Kim, Y.H. Kim, M.R. Kim, S.-C. Kim. (2011) Clinical efficacy of different doses of rituximab in the treatment of pemphigus: a retrospective study of 27 patients. British Journal of Dermatology 165:3, 646-651
CrossRef19
Emma Craythorne, Anthony du Viver, Ghulam J. Mufti, Saman Warnakulasuriya. (2011) Rituximab for the treatment of corticosteroid - refractory pemphigus vulgaris with oral and skin manifestations. Journal of Oral Pathology & Medicine 40:8, 616-620
CrossRef20
Rachel Brackley, Jean Marie Pagani. (2011) Conjunctival Erosions Associated with Pemphigus Vulgaris. Optometry and Vision Science 88:8, 1010-1013
CrossRef21
Ron J Feldman, A Razzaque Ahmed. (2011) Relevance of rituximab therapy in pemphigus vulgaris: analysis of current data and the immunologic basis for its observed responses. Expert Review of Clinical Immunology 7:4, 529-541
CrossRef22
Olivier Benveniste, Laurent Drouot, Fabienne Jouen, Jean-Luc Charuel, Coralie Bloch-Queyrat, Anthony Behin, Zahir Amoura, Isabelle Marie, Marguerite Guiguet, Bruno Eymard, Danièle Gilbert, François Tron, Serge Herson, Lucile Musset, Olivier Boyer. (2011) Correlation of anti-signal recognition particle autoantibody levels with creatine kinase activity in patients with necrotizing myopathy. Arthritis & Rheumatism 63:7, 1961-1971
CrossRef23
J. Henk Sillevis Smitt, Marcel F. Jonkman. 2011. Pemphigus, Pemphigoid and Epidermolysis Bullosa Acquisita. , 91.1-91.25.
CrossRef24
Polly Livermore, Clarissa Pilkington. 2011. The Use of Emerging Biological Treatments in Children. , 182.1-182.15.
CrossRef25
Jayne L Chamberlain, Kesley Attridge, Chun Jing Wang, Gemma A Ryan, Lucy SK Walker. (2011) B cell depletion in autoimmune diabetes: insights from murine models. Expert Opinion on Therapeutic Targets 15:6, 703-714
CrossRef26
Gerald T. Nepom, E. William St. Clair, Laurence A. Turka. (2011) Challenges in the pursuit of immune tolerance. Immunological Reviews 241:1, 49-62
CrossRef27
Yaohan Li, J.B. Foshee, Richard D. Sontheimer. (2011) Sustained clinical response to rituximab in a case of life-threatening overlap subepidermal autoimmune blistering disease. Journal of the American Academy of Dermatology 64:4, 773-778
CrossRef28
I. Ueki, N. Abiru, M. Kobayashi, M. Nakahara, T. Ichikawa, K. Eguchi, Y. Nagayama. (2011) B cell-targeted therapy with anti-CD20 monoclonal antibody in a mouse model of Graves' hyperthyroidism. Clinical & Experimental Immunology 163:3, 309-317
CrossRef29
P. Joly, C. Sin. (2011) Pemphigus : revue de la littérature. Annales de Dermatologie et de Vénéréologie 138:3, 182-200
CrossRef30
P. Joly. (2011) Maladies bulleuses auto-immunes : un domaine d’excellence de la recherche en dermatologie. Annales de Dermatologie et de Vénéréologie 138:3, 169-171
CrossRef31
Hans-Peter Tony, Gerd Burmester, Hendrik Schulze-Koops, Mathias Grunke, Joerg Henes, Ina Kötter, Judith Haas, Leonore Unger, Svjetlana Lovric, Marion Haubitz, Rebecca Fischer-Betz, Gamal Chehab, Andrea Rubbert-Roth, Christof Specker, Jutta Weinerth, Julia Holle, Ulf Müller-Ladner, Ramona König, Christoph Fiehn, Philip Burgwinkel, Klemens Budde, Helmut Sörensen, Michael Meurer, Martin Aringer, Bernd Kieseier, Cornelia Erfurt-Berge, Michael Sticherling, Roland Veelken, Ulf Ziemann, Frank Strutz, Praxis von Wussow, Florian MP Meier, Nico Hunzelmann, Enno Schmidt, Raoul Bergner, Andreas Schwarting, Rüdiger Eming, Michael Hertl, Rudolf Stadler, Michael Schwarz-Eywill, Siegfried Wassenberg, Martin Fleck, Claudia Metzler, Uwe Zettl, Jens Westphal, Stefan Heitmann, Anna L Herzog, Heinz Wiendl, Waltraud Jakob, Enno Schmidt, Klaus Freivogel, Thomas Dörner, . (2011) Safety and clinical outcomes of rituximab therapy in patients with different autoimmune diseases: experience from a national registry (GRAID). Arthritis Research & Therapy 13:3, R75
CrossRef32
Mi Ri Kim, Hyeon Chang Kim, Soo-Chan Kim. (2011) Long-Term Prognosis of Pemphigus in Korea: Retrospective Analysis of 199 Patients. Dermatology 223:2, 182-188
CrossRef33
Jun Yamagami, Aimee S. Payne, Stephen Kacir, Ken Ishii, Don L. Siegel, John R. Stanley. (2010) Homologous regions of autoantibody heavy chain complementarity-determining region 3 (H-CDR3) in patients with pemphigus cause pathogenicity. Journal of Clinical Investigation 120:11, 4111-4117
CrossRef34
Michael J. Townsend, John G. Monroe, Andrew C. Chan. (2010) B-cell targeted therapies in human autoimmune diseases: an updated perspective. Immunological Reviews 237:1, 264-283
CrossRef35
D Mimouni, H Bar, M Gdalevich, V Katzenelson, M David. (2010) Pemphigus, analysis of 155 patients. Journal of the European Academy of Dermatology and Venereology 24:8, 947-952
CrossRef36
Stefan Beissert, Daniel Mimouni, Amrinder J Kanwar, Neil Solomons, Veena Kalia, Grant J Anhalt. (2010) Treating Pemphigus Vulgaris with Prednisone and Mycophenolate Mofetil: A Multicenter, Randomized, Placebo-Controlled Trial. Journal of Investigative Dermatology 130:8, 2041-2048
CrossRef37
O. Thaunat, E. Morelon, T. Defrance. (2010) Am"B"valent: anti-CD20 antibodies unravel the dual role of B cells in immunopathogenesis. Blood 116:4, 515-521
CrossRef38
Spiro Getsios, Jens Waschke, Luca Borradori, Michael Hertl, Eliane J Müller. (2010) From Cell Signaling to Novel Therapeutic Concepts: International Pemphigus Meeting on Advances in Pemphigus Research and Therapy. Journal of Investigative Dermatology 130:7, 1764-1768
CrossRef39
David R. Carr, Michael P. Heffernan. (2010) Innovative Uses of Rituximab in Dermatology. Dermatologic Clinics 28:3, 547-557
CrossRef40
C. Stephen Foster, Peter Y. Chang, A. Razzaque Ahmed. (2010) Combination of Rituximab and Intravenous Immunoglobulin for Recalcitrant Ocular Cicatricial Pemphigoid. Ophthalmology 117:5, 861-869
CrossRef41
S. M. Breathnach, C. H. Smith, R. J. G. Chalmers, R. J. Hay. 2010. Systemic Therapy. , 1-53.
CrossRef42
F. Perosa, M. Prete, V. Racanelli, F. Dammacco. (2010) CD20-depleting therapy in autoimmune diseases: from basic research to the clinic. Journal of Internal Medicine 267:3, 260-277
CrossRef43
Ralf Müller, Nicolas Hunzelmann, Vera Baur, Guido Siebenhaar, Elke Wenzel, Rüdiger Eming, Andrea Niedermeier, Philippe Musette, Pascal Joly, Michael Hertl. (2010) Targeted Immunotherapy with Rituximab Leads to a Transient Alteration of the IgG Autoantibody Profile in Pemphigus Vulgaris. Dermatology Research and Practice 2010, 1-9
CrossRef44
S. M. Breathnach. 2010. , 1.
CrossRef45
Maria Beatrice Di Bisceglie, Alberta Lucchese, Vito Crincoli. (2009) Pemphigus: The promises of peptide immunotherapy. Immunopharmacology and Immunotoxicology 31:4, 509-515
CrossRef46
E William St Clair. (2009) Novel targeted therapies for autoimmunity. Current Opinion in Immunology 21:6, 648-657
CrossRef47
Thomas Dörner, David Isenberg, David Jayne, Heinz Wiendl, Detlef Zillikens, Gerd Burmester. (2009) Current status on B-cell depletion therapy in autoimmune diseases other than rheumatoid arthritis. Autoimmunity Reviews 9:2, 82-89
CrossRef48
Jennifer H. Anolik, R. John Looney, Frances E. Lund, Troy D. Randall, Iñaki Sanz. (2009) Insights into the heterogeneity of human B cells: diverse functions, roles in autoimmunity, and use as therapeutic targets. Immunologic Research 45:2-3, 144-158
CrossRef49
A. Cavailhes, B. Balme, D. Gilbert, F. Skowron. (2009) Succès de l’association rituximab–corticoïdes généraux dans le traitement d’une épidermolyse bulleuse acquise récalcitrante. Annales de Dermatologie et de Vénéréologie 136:11, 795-799
CrossRef50
Deshan Sebaratnam, Dédée F Murrell. (2009) Treatment of pemphigus vulgaris and pemphigus foliaceus. Expert Review of Dermatology 4:5, 469-481
CrossRef51
Oliver A. Perez, Timothy Patton. (2009) Novel Therapies for Pemphigus Vulgaris. Drugs & Aging 26:10, 833-846
CrossRef52
Angela Nagel, Eva Podstawa, Markus Eickmann, Hans-Helge Müller, Michael Hertl, Rüdiger Eming. (2009) Rituximab Mediates a Strong Elevation of B-Cell-Activating Factor Associated with Increased Pathogen-Specific IgG but Not Autoantibodies in Pemphigus Vulgaris. Journal of Investigative Dermatology 129:9, 2202-2210
CrossRef53
Enno Schmidt, Kirsten Hennig, Christian Mengede, Detlef Zillikens, Arno Kromminga. (2009) Immunogenicity of rituximab in patients with severe pemphigus. Clinical Immunology 132:3, 334-341
CrossRef54
Enno Schmidt, Matthias Goebeler, Detlef Zillikens. (2009) Rituximab in Severe Pemphigus. Annals of the New York Academy of Sciences 1173:1, 683-691
CrossRef55
M. Alter, M. Wittmann, B. Völker, A. Kapp, T. Werfel, R. Gutzmer. (2009) Erfolgreiche Therapie des Pemphigus foliaceus mit Rituximab. Der Hautarzt 60:9, 743-748
CrossRef56
Vickie McDonald, Maria Leandro. (2009) Rituximab in non-haematological disorders of adults and its mode of action. British Journal of Haematology 146:3, 233-246
CrossRef57
M. C. Levesque. (2009) Translational Mini-Review Series on B Cell-Directed Therapies: Recent advances in B cell-directed biological therapies for autoimmune disorders. Clinical & Experimental Immunology 157:2, 198-208
CrossRef58
E. Schmidt. (2009) Therapieoptimierung bei schweren bullösen Autoimmundermatosen. Der Hautarzt 60:8, 633-640
CrossRef59
W.W. Li, X.X. Chen, J. Yu, Y. Wang, D.F. Bu, P. Tu. (2009) Haemolytic anaemia following rituximab treatment in a patient with pemphigus vulgaris. British Journal of Dermatology 161:1, 205-206
CrossRef60
Michael Hertl. (2009) Research in practice: Treatment of autoimmune bullous disorders. Journal der Deutschen Dermatologischen Gesellschaft 7:6, 500-505
CrossRef61
Z. Reguiaï, T. Tchen, G. Perceau, P. Bernard. (2009) Efficacité du rituximab dans une pemphigoïde bulleuse en échec thérapeutique. Annales de Dermatologie et de Vénéréologie 136:5, 431-434
CrossRef62
Masayuki Amagai, Shigaku Ikeda, Hiroshi Shimizu, Hajime Iizuka, Katsumi Hanada, Setsuya Aiba, Fumio Kaneko, Seiichi Izaki, Kunihiko Tamaki, Zenro Ikezawa, Masahiro Takigawa, Mariko Seishima, Toshihiro Tanaka, Yoshiki Miyachi, Ichiro Katayama, Yuji Horiguchi, Sachiko Miyagawa, Fukumi Furukawa, Keiji Iwatsuki, Michihiro Hide, Yoshiki Tokura, Masutaka Furue, Takashi Hashimoto, Hironobu Ihn, Sakuhei Fujiwara, Takeji Nishikawa, Hideoki Ogawa, Yasuo Kitajima, Koji Hashimoto. (2009) A randomized double-blind trial of intravenous immunoglobulin for pemphigus. Journal of the American Academy of Dermatology 60:4, 595-603
CrossRef63
A.B. Alexandroff, K.E. Harman. (2009) Blistering skin disorders: an evidence-based update. Conference report. British Journal of Dermatology 160:3, 502-504
CrossRef64
A. España, C. Panizo, S. Fernández, M. Marquina, M. Pretel, L. Aguado, A. Sánchez-Ibarrola. (2009) Remisión clínica completa prolongada en pacientes con pénfigo vulgar grave después del tratamiento con ciclos intravenosos de ciclofosfamida. Actas Dermo-Sifiliográficas 100:2, 113-120
CrossRef65
Angela Nagel, Michael Hertl, Rüdiger Eming. (2009) B-Cell-Directed Therapy for Inflammatory Skin Diseases. Journal of Investigative Dermatology 129:2, 289-301
CrossRef66
Linda K Martin, Anna Liza Agero, Victoria Werth, Elmer Villanueva, Janet Segall, Dedee F Murrell, Dedee F Murrell. 2009. Interventions for pemphigus vulgaris and pemphigus foliaceus. .
CrossRef67
Hakan M. Gürcan, Derin B. Keskin, Joel N.H. Stern, Matthew A. Nitzberg, Haris Shekhani, A. Razzaque Ahmed. (2009) A review of the current use of rituximab in autoimmune diseases. International Immunopharmacology 9:1, 10-25
CrossRef68
Rüdiger Eming, Angela Nagel, Sonja Wolff-Franke, Eva Podstawa, Dirk Debus, Michael Hertl. (2008) Rituximab Exerts a Dual Effect in Pemphigus Vulgaris. Journal of Investigative Dermatology 128:12, 2850-2858
CrossRef69
D. Janisson-Dargaud, Z. Reguiaï, G. Perceau, C. Eschard, P. Bernard. (2008) Pemphigus vulgaire de l’enfant. Annales de Dermatologie et de Vénéréologie 135:12, 843-847
CrossRef70
Giovanna Zambruno, Luca Borradori. (2008) Rituximab Immunotherapy in Pemphigus: Therapeutic Effects Beyond B-Cell Depletion. Journal of Investigative Dermatology 128:12, 2745-2747
CrossRef71
Hugo Mouquet, Philippe Musette, Marie-Lyse Gougeon, Serge Jacquot, Brigitte Lemercier, Annick Lim, Danièle Gilbert, Ingrid Dutot, Jean C Roujeau, Michel D'Incan, Christophe Bedane, François Tron, Pascal Joly. (2008) B-Cell Depletion Immunotherapy in Pemphigus: Effects on Cellular and Humoral Immune Responses. Journal of Investigative Dermatology 128:12, 2859-2869
CrossRef72
Julia Tzu, Nancy Kim, Robert S Kirsner. (2008) Why Rituximab Works. Journal of Investigative Dermatology 128:12, 2744-2744
CrossRef73
Donna A. Culton, Ye Qian, Ning Li, David Rubenstein, Valeria Aoki, Gunter Hans Filhio, Evandro A. Rivitti, Luis A. Diaz. (2008) Advances in pemphigus and its endemic pemphigus foliaceus (Fogo Selvagem) phenotype: A paradigm of human autoimmunity. Journal of Autoimmunity 31:4, 311-324
CrossRef74
Wendell A. Edgin, Taylor C. Pratt, Ronald E. Grimwood. (2008) Pemphigus Vulgaris and Paraneoplastic Pemphigus. Oral and Maxillofacial Surgery Clinics of North America 20:4, 577-584
CrossRef75
A. Nagel, M. Hertl, R. Eming. (2008) Einsatz B-Zell-depletierender Antikörper bei Hauterkrankungen. Der Hautarzt 59:10, 793-805
CrossRef76
Johannes Schulze, Peter Bader, Ulrike Henke, Markus A. Rose, Stefan Zielen. (2008) Severe Bullous Pemphigoid in an Infant- Successful Treatment with Rituximab. Pediatric Dermatology 25:4, 462-465
CrossRef77
Clifton O. Bingham. (2008) Immunomodulatory approaches to the management of chronic urticaria: An immune-mediated inflammatory disease. Current Allergy and Asthma Reports 8:4, 277-287
CrossRef78
Christian Veldman, Claudio Feliciani. (2008) Pemphigus: A Complex T Cell-dependent Autoimmune Disorder Leading to Acantholysis. Clinical Reviews in Allergy & Immunology 34:3, 313-320
CrossRef79
Enno Schmidt, Matthias Goebeler. (2008) CD20-directed therapy in autoimmune diseases involving the skin: role of rituximab. Expert Review of Dermatology 3:3, 259-278
CrossRef80
Michael Hertl, Detlef Zillikens, Luca Borradori, Leena Bruckner-Tuderman, Harald Burckhard, Rüdiger Eming, Andreas Engert, Matthias Goebeler, Silke Hofmann, Nicolas Hunzelmann, Franz Karlhofer, Ocko Kautz, Undine Lippert, Andrea Niedermeier, Martin Nitschke, Martin Pfütze, Marcel Reiser, Christian Rose, Enno Schmidt, Iakov Shimanovich, Michael Sticherling, Sonja Wolff-Franke. (2008) Recommendations for the use of rituximab (anti-CD20 antibody) in the treatment of autoimmune bullous skin diseases. JDDG 6:5, 366-373
CrossRef81
Pamela Vezzoli, Emilio Berti, Angelo V Marzano. (2008) Rationale and efficacy for the use of rituximab in paraneoplastic pemphigus. Expert Review of Clinical Immunology 4:3, 351-363
CrossRef82
Luigi Bartalena, Adriana Lai, Maria Laura Tanda. (2008) Perspectives in pharmacological management of Graves’ hyperthyroidism and orbitopathy. Expert Review of Clinical Immunology 4:3, 321-329
CrossRef83
Sue Jessop, Nonhlanhla P Khumalo. (2008) Pemphigus. American Journal of Clinical Dermatology 9:3, 147-154
CrossRef84
Marc C. Levesque, E. William St. Clair. (2008) B cell–directed therapies for autoimmune disease and correlates of disease response and relapse. Journal of Allergy and Clinical Immunology 121:1, 13-21
CrossRef85
C. Paul. (2007) Quoi de neuf en thérapeutique ?. Annales de Dermatologie et de Vénéréologie 134, 8S64-8S75
CrossRef86
C. Mühlhoff, M. Megahed. (2007) Behandlung eines therapieresistenten Pemphigus vulgaris mit Rituximab und Immunglobulinen. Der Hautarzt 58:11, 924-926
CrossRef87
Diaz, Luis A., . (2007) Rituximab and Pemphigus — A Therapeutic Advance. New England Journal of Medicine 357:6, 605-607
Full Text
