Original Article
A Novel Targeted T-Cell Modulator, Efalizumab, for Plaque Psoriasis
N Engl J Med 2003; 349:2004-2013November 20, 2003
- Abstract
Background
Interactions between leukocyte-function–associated antigen type 1 (LFA-1) and intercellular adhesion molecules are important in the pathogenesis of psoriasis. Efalizumab, a humanized monoclonal antibody, binds to the α subunit (CD11a) of LFA-1 and inhibits the activation of T cells.
Methods
In a phase 3, multicenter, randomized, placebo-controlled, double-blind study, we assign 597 subjects with psoriasis to receive subcutaneous efalizumab (1 or 2 mg per kilogram of body weight per week) or placebo for 12 weeks. Depending on the response after 12 weeks, subjects received an additional 12 weeks of treatment with efalizumab or placebo. Study treatments were discontinued at week 24, and subjects were followed for an additional 12 weeks.
Results
At week 12, there was an improvement of 75 percent or more in the psoriasis area-and-severity index in 22 percent of the subjects who had received 1 mg of efalizumab per kilogram per week and 28 percent of those who had received 2 mg of efalizumab per kilogram per week, as compared with 5 percent of the subjects in the placebo group (P<0.001 for both comparisons). Efalizumab-treated subjects had greater improvement than those in the placebo group as early as week 4 (P<0.001). Among the efalizumab-treated subjects who had an improvement of 75 percent or more at week 12, improvement was maintained through week 24 in 77 percent of those who continued to receive efalizumab, as compared with 20 percent of those who were switched to placebo (P<0.001 for both comparisons). After the discontinuation of efalizumab at week 24, an improvement of 50 percent or more in the psoriasis area-and-severity index was maintained in approximately 30 percent of subjects during the 12 weeks of follow-up. Efalizumab was well tolerated, and adverse events were generally mild to moderate.
Conclusions
Efalizumab therapy resulted in significant improvements in plaque psoriasis in subjects with moderate-to-severe disease. Extending treatment from 12 to 24 weeks resulted in both maintenance and improvement of responses.
Media in This Article
Figure 1
Study Design.Figure 2
Disposition of the Subjects.Article Activity
- Article
Chronic plaque psoriasis affects approximately 2 percent of the world's population and results in disability similar to or exceeding that associated with other major illnesses, such as diabetes mellitus, arthritis, depression, and cancer.1,2 Systemic therapies are limited by toxic effects (e.g., end-organ damage, bone marrow suppression, cancer, and teratogenesis), interactions with other drugs, and the need for extensive laboratory monitoring.3-7 The unmet need for safe and effective therapies, coupled with an improved understanding of the pathogenesis of psoriasis, has prompted the development of targeted biologic therapies.
Psoriasis is an incurable autoimmune disease that is mediated by T lymphocytes.8 A T-lymphocyte adhesion molecule, leukocyte-function–associated antigen type 1 (LFA-1), binds with intercellular adhesion molecule 1 (ICAM-1), facilitating processes relevant to the pathogenesis of psoriasis, including the migration of T lymphocytes from the circulation into dermal and epidermal tissues, with subsequent reactivation.9 Monoclonal antibodies against LFA-1 inhibit the activation of T lymphocytes and their adhesion to the vascular endothelium, providing the basis for the targeting of LFA-1 for psoriasis.10-13 Efalizumab, a humanized monoclonal IgG1 antibody, binds to the α subunit of LFA-1 (CD11a), inhibiting the binding of T lymphocytes to endothelial cells, their movement from the circulation into dermal and epidermal tissues, and their activation and reactivation. This activity differentiates efalizumab from the biologic agent that has been approved for psoriasis, alefacept, in that efalizumab inhibits T-lymphocyte activation without depleting memory effector T lymphocytes.14
Efalizumab's biologic effects and clinical activity were demonstrated in phase 1 and 2 studies.15-18 Efalizumab saturated CD11a on peripheral T lymphocytes and decreased epidermal thickness, the numbers of epidermal and dermal T lymphocytes, and the expression of keratin 16 and ICAM-1. These changes were accompanied by significant clinical improvement. We conducted a phase 3 trial to evaluate the efficacy and safety of efalizumab in subjects with moderate-to-severe plaque psoriasis.
Methods
Conduct of the Study
Employees of Genentech and academic investigators, including the authors of this article, collaborated in the design of the study. All the investigators were responsible for gathering the data, and Genentech employees held and analyzed the data. All authors had full access to the data and participated in their interpretation. Dr. Lebwohl made the decisions about publication.
Study Subjects
The criteria for eligibility were an age of 18 to 70 years, plaque psoriasis that had been clinically stable for at least three months and that had been moderate to severe for at least six months, a psoriasis area-and-severity index of at least 12.0 at screening, the presence of plaque psoriasis covering at least 10 percent of the body-surface area, and candidacy for systemic therapy. The criteria for exclusion included a history of or ongoing uncontrolled infection, the presence of cancer or a history of cancer within the previous five years (excluding resolved basal-cell or squamous-cell skin cancers), hepatic or renal dysfunction, a white-cell count of less than 4000 per cubic millimeter or more than 14,000 per cubic millimeter, a history of severe allergic or anaphylactic reaction to humanized monoclonal antibodies, and previous treatment with efalizumab. After enrollment, the following factors resulted in withdrawal from the study: pregnancy, treatment with a live-virus or live-bacteria vaccine, the use of systemic or topical therapies for psoriasis (including phototherapy) that were not permitted in the study, the use of immunosuppressive agents, the use of experimental treatments, and any medical condition that could jeopardize the subject's safety. All subjects provided written informed consent. The institutional review board at each site approved the study protocol.
Study Design
This phase 3, randomized, double-blind, placebo-controlled, parallel-group, multicenter trial (conducted from May 4, 2000, through June 6, 2001) involved three consecutive phases: the first-treatment phase (weeks 0 through 12), the extended-treatment phase (weeks 13 through 24), and the follow-up phase (weeks 25 through 36) (Figure 1Figure 1
Study Design.). In the first phase, subjects were randomly assigned in a ratio of 2:2:1 to 1 mg of subcutaneous efalizumab (anti-CD11a, Raptiva, Genentech) per kilogram of body weight per week, 2 mg of efalizumab per kilogram per week, or an equivalent volume of matching placebo. To maintain blinding, two different volumes of placebo were used to match the two doses of active drug. Randomization was performed according to a dynamic approach (urn adaptive biased-coin)19 and was balanced within subgroups defined according to the base-line psoriasis area-and-severity index (≤16 vs. >16), receipt or nonreceipt of previous systemic treatment for psoriasis, and study site.In the second phase, subjects who had been receiving active treatment were stratified into three subgroups on the basis of their level of improvement on the psoriasis area-and-severity index from base line to week 12 (≥75 percent, 50 to 74 percent, or <50 percent). Subjects in the first two strata were randomly assigned to continue receiving 2 mg of efalizumab per kilogram either weekly or every other week or to receive placebo. Rerandomization for efalizumab-treated subjects was balanced within subgroups defined according to the dose received during the first-treatment phase, with the use of static randomization tables with a block size of six. Subjects in the third stratum (<50 percent improvement) were randomly assigned to either an increased dose of efalizumab (4 mg per kilogram per week) or placebo. In the follow-up phase, the treatments were discontinued, and subjects were followed for an additional 12 weeks.
The use of Eucerin cream (Beiersdorf), tar or salicylic acid preparations for psoriasis on the scalp, limited application of low-potency (group VII) corticosteroids, and oral antipruritic agents was permitted. Subjects could self-administer approximately half the injections during weeks 13 through 24 at home. All other injections were administered in the clinic.
Assessment of Responses
Responses were assessed with the use of the psoriasis area-and-severity index, a measure used by the Food and Drug Administration (FDA) in clinical trials to assess the efficacy of therapies for psoriasis. The score, based on the extent of the skin-surface area involved and the severity of erythema, desquamation, and plaque induration, ranges from 0 to 72, with higher scores indicating more severe disease and a reduction in the score indicating improvement.20
Statistical Analysis
The investigators, the sponsor, and the contract research organization remained unaware of the treatment-group assignments until all data analyses were completed. The population included in the primary analysis was the intention-to-treat population consisting of all the subjects who underwent randomization. Subjects were considered to have had a treatment failure if the value for the psoriasis area-and-severity index at week 12 was missing.
Fisher's exact test was used for the comparison of each efalizumab group with the placebo group in terms of the proportion of subjects who had an improvement of at least 75 percent in the psoriasis area-and-severity index, the primary end point. For all analyses of weeks 1 through 12, data for the two placebo groups were combined. To maintain a two-sided type I error of 0.05, the Hochberg–Bonferroni procedure for multiple comparisons was used. If both comparisons resulted in a difference in favor of efalizumab with a P value of less than 0.05, the data from both efalizumab groups were considered to be significantly different from those in the placebo group. If the P value for one comparison exceeded 0.05, the data from the other efalizumab group were considered to be significantly different from those in the placebo group if the difference in favor of efalizumab was associated with a P value of less than 0.025.
The planned accrual was 500 subjects (400 randomly assigned to efalizumab and 100 to placebo). The probability that there would be at least one type of adverse event with an actual rate of 1 percent in a group of 200 subjects was 0.866, and the probability that there would be at least one type with an actual rate of 2 percent was 0.982. The estimation of the statistical power was based on the assumption of a response rate of 25 percent in the efalizumab groups and 2 percent in the placebo group. The study had more than 95 percent power to detect the difference in the rate of the primary end point at the 0.025 level with the use of Fisher's exact test. For secondary analyses, two-sample t-tests using the pooled error term from an analysis of variance including all treatment groups were used for continuous variables, and Fisher's exact test was used for dichotomous variables.
Results
Characteristics of the Subjects
A total of 597 subjects underwent randomization (Figure 2Figure 2
Disposition of the Subjects.), and there were no significant differences among the treatment groups with respect to demographic characteristics, other base-line characteristics, or the severity of disease. Overall, 65 percent of the subjects were male, the mean age was 46 years, the mean duration of psoriasis was 19 years, the mean base-line psoriasis area-and-severity index was 20.0, and 67 percent of the subjects had received previous systemic therapy for psoriasis. Seventy-seven percent of the subjects received all 12 doses of study drug during the first-treatment phase, with a relatively even distribution among the groups.A total of 434 subjects underwent rerandomization for the extended-treatment phase (Figure 2). The groups for this phase were similar in terms of base-line characteristics. Seventy percent of the subjects who were assigned to receive efalizumab weekly during the extended-treatment phase and 87 percent of the subjects assigned to receive efalizumab every other week received all scheduled doses, either at home or in the clinic.
Treatment Efficacy
First-Treatment Phase
The subjects in both efalizumab groups had a significantly better response than those in the placebo group, as determined by the assessment of the primary end point and all other prespecified measures (P<0.001 for the comparisons with the placebo group in the proportion of subjects with an improvement of at least 50 percent and the proportion with an improvement of at least 75 percent) (Table 1Table 1
Improvements in the Psoriasis Area-and-Severity Index at Week 12 among All Subjects and at Week 24 among Subjects Treated with Efalizumab during Weeks 0 through 12.). Responses in various subgroups defined according to site, sex, age group, base-line psoriasis area-and-severity index, or receipt or nonreceipt of previous systemic therapy were generally consistent with those in the overall study population. Efalizumab therapy resulted in a significantly lower mean psoriasis area-and-severity index at week 12 than that found in the placebo group (9 vs. 17, P<0.001 according to a post hoc analysis); there was a mean improvement of 51 percent in the 1-mg–efalizumab group and 52 percent in the 2-mg–efalizumab group, as compared with 17 percent in the placebo group (P<0.001 for both comparisons). Improvement in the efalizumab groups significantly diverged from that in the placebo group at week 4 (P<0.001 for both comparisons) (Figure 3Figure 3
Mean Improvements in the Psoriasis Area-and-Severity Index during the First-Treatment Period.). Photographs illustrating improvement are shown in Figure 4Figure 4
Representative Responses to Efalizumab..Extended-Treatment Phase
Of the 121 efalizumab-treated subjects who had an improvement of at least 75 percent in the psoriasis area-and-severity index at week 12, 119 underwent rerandomization to the continuation of efalizumab treatment with 2 mg per kilogram either weekly or every other week or to the cessation of active treatment (the administration of placebo). An improvement of 75 percent or more in the psoriasis area-and-severity index was maintained in a significantly greater proportion of the subjects who were treated with efalizumab during this phase than of those given placebo (P<0.001 for the comparisons between each of the efalizumab groups and the placebo group). Therefore, continued therapy with efalizumab either weekly or every other week was beneficial (Table 1).
Of the subjects in the efalizumab groups who had an improvement of 50 to 74 percent in the psoriasis area-and-severity index at week 12, 138 underwent rerandomization to the continuation of efalizumab treatment with 2 mg per kilogram either weekly or every other week or to placebo. An improvement of 75 percent or more in the psoriasis area-and-severity index was achieved in a significantly greater proportion of the efalizumab-treated subjects than of those given placebo. Therefore, continued therapy with efalizumab either weekly or every other week was also beneficial in these subjects (Table 1).
Of the 182 subjects who received efalizumab and had an improvement of less than 50 percent in the psoriasis area-and-severity index at week 12, 177 underwent rerandomization to the continuation of efalizumab treatment with 4 mg per kilogram per week or to placebo. An improvement of 75 percent or more in the psoriasis area-and-severity index was achieved at week 24 in a significantly greater proportion of efalizumab-treated subjects than of those given placebo (P=0.02) (Table 1). Therefore, there is evidence to suggest that the escalation of the dose was beneficial in the subjects who had had a limited response to the initial dose.
Follow-up Phase
At week 36, 12 weeks after the discontinuation of the study treatment, 50 percent or more of the improvement that had been achieved during treatment was maintained in approximately one third of the subjects who had received continuous efalizumab therapy for 24 weeks. Among the remaining subjects, the mean psoriasis area-and-severity index gradually regressed toward the base-line value. The time to relapse (loss of at least 50 percent of the improvement in the psoriasis area-and-severity index that had been achieved between base line and week 24) among subjects who had had an improvement of at least 50 percent at week 24 was approximately 84 days.
Safety
In general, efalizumab therapy was well tolerated. The rates of adverse events that were reported in at least 5 percent of the subjects in any treatment group and that occurred at a rate at least 1 percentage point higher in an efalizumab group than in the placebo group are shown in Table 2Table 2
Adverse Events during the First-Treatment Phase.. During weeks 0 through 12, 10 types of adverse events occurred at a rate at least 5 percentage points higher in an efalizumab group than in the placebo group. Of these events, headache, chills, fever, nausea, and myalgia were predefined as acute adverse events when they occurred on the day of or within two days after the administration of a dose of the study drug. Acute adverse events were most frequent after the first dose, were generally mild to moderate, and decreased in frequency over time. By the third dose and for subsequent doses, the percentage of subjects in each group who had acute adverse events was similar. Serious adverse events and adverse events leading to withdrawal from the study were infrequent, and their rates were similar in the efalizumab groups and the placebo group (Table 2).During weeks 13 through 24, the rates of adverse events were similar to those observed during weeks 0 through 12, with the exception of a lower rate of occurrence of acute adverse events. Adverse events resulting in early withdrawal from the study were more common among subjects receiving placebo than among those receiving efalizumab. The rate of infection among subjects who continued to receive efalizumab was similar to that observed during the first 12 weeks, after adjustment for the season during which the treatment was received.
During the follow-up phase, the types of adverse events that occurred in at least 5 percent of all subjects were nonspecific infection (in 13 percent), worsening psoriasis (9 percent), pruritus (6 percent), and arthritis (5 percent). Thirteen subjects (3 percent) had a serious adverse event (five of which were nonfatal infections and three of which were psoriasis-related events); none of these events resulted in withdrawal from the study.
Anti-efalizumab antibodies developed in 5 percent of the subjects who were treated with efalizumab. There was no difference between the safety profile among these subjects and that among the subjects who did not have anti-efalizumab antibodies. The absolute lymphocyte, eosinophil, and total white-cell counts were transiently elevated during efalizumab treatment; they returned to their base-line levels on the discontinuation of treatment. Alkaline phosphatase and serum glutamate pyruvate transaminase levels were slightly elevated transiently during efalizumab treatment, although these elevations were deemed not to be clinically relevant. There were no other notable changes in laboratory results or vital signs.
Discussion
Efalizumab therapy resulted in significant improvement and was well tolerated in subjects with moderate-to-severe plaque psoriasis. At week 12, significantly more subjects in the efalizumab groups than in the placebo group had an improvement of 75 percent or more in the psoriasis area-and-severity index. Improvement in the efalizumab group diverged significantly from that in the placebo group by week 4. A response to phototherapy, including psoralen–ultraviolet A therapy, generally occurs after eight weeks. With systemic therapy, a response to cyclosporine typically occurs at four weeks, a response to methotrexate at four to six weeks, and a response to retinoids and alefacept even later (at more than eight weeks). Thus, efalizumab has a rapid onset of action that compares favorably with those of current therapies.21,22
Continued efalizumab therapy provided continued benefit. In most subjects in the efalizumab group who had an improvement of 75 percent or more in the psoriasis area-and-severity index at week 12, the response was maintained with continued treatment through week 24. In approximately 90 percent of these subjects, an improvement of at least 50 percent in the psoriasis area-and-severity index was maintained at week 24, illustrating the benefit of continued therapy. The high percentage of subjects in the placebo group who had an improvement of at least 50 percent during weeks 13 through 24 may reflect the fact that these subjects received efalizumab during weeks 0 through 12 and had residual clinical benefit. In addition, extending the efalizumab treatment from 12 to 24 weeks resulted in improved responses in many subjects who did not initially have improvement of 75 percent or more.
The gradual loss of clinical benefit observed after the discontinuation of efalizumab therapy may have been due in part to the fact that the study design dictated an abrupt discontinuation of efalizumab treatment, without tapering or a transition to other therapies for psoriasis, which is not consistent with general practice. The natural course of psoriasis is marked by fluctuations in severity over time,23 and given that psoriasis is incurable, the disease eventually returns after the discontinuation of all psoriasis therapies. We speculate that psoriasis might be best controlled by the continuous administration of efalizumab.
The psoriasis area-and-severity index is widely used to evaluate efficacy during clinical trials. However, the responses to traditional psoriasis therapies vary among different groups of patients and according to the severity of the psoriasis being examined and the type of monitoring that is performed (which, in turn, depends on whether the study is initiated by a drug manufacturer or independent investigators). Such variations make it difficult to compare emerging biologic therapies with FDA-approved agents in terms of the levels of improvement in the psoriasis area-and-severity index. This lack of comparability is highlighted by the recent trial comparing methotrexate with cyclosporine for the treatment of plaque psoriasis.24 For example, the base-line characteristics of the patients in that study were different from those in our study; on average, the patients were younger (41.6 years and 38.3 years vs. 46 years) and had a lower psoriasis area-and-severity index at base line (13.4 and 14.0 vs. 20.0). The time point at which the primary efficacy end point was assessed differed, and the protocols differed in terms of whether or not active therapies for psoriasis were permitted during the follow-up period. Thus, despite a standardized efficacy end point, the comparison of efficacy between trials is complicated.
The adverse events that were attributed to efalizumab in our study were primarily mild to moderate. Except for acute adverse events — most commonly, headache, nausea, chills, and fever — the safety profile of efalizumab was similar during the 12-week treatment period and during the 24-week treatment period. Acute adverse events, observed primarily after the first or second dose, were managed easily and did not preclude further treatment. Acute adverse events are not uncommon after the administration of monoclonal antibodies or fusion proteins.25,26 The rate of infection was not increased with efalizumab, and there was no evidence of end-organ toxicity, which limits the use of some systemic therapies. Finally, the low incidence of the development of anti-efalizumab antibodies (5 percent) may make the long-term administration of efalizumab feasible.
Efalizumab compares favorably with approved antipsoriasis agents, demonstrating both rapid and sustained improvement. Although the long-term safety and efficacy of efalizumab in the treatment of psoriasis have not been established, the results of this trial show that the extension of efalizumab treatment resulted in the maintenance of and improvement in the responses in most subjects, thus demonstrating the benefit of continued treatment.
Supported by Genentech.
Dr. Lebwohl reports having received consulting and lecture fees from Biogen, Centocor, Genentech, and Wyeth–Amgen. Dr. Hamilton reports having received consulting and lecture fees from Amgen, Biogen, and Genentech. Dr. Toth reports having received consulting and lecture fees from Genentech. Dr. Tawfik reports having received consulting and lecture fees from Genentech. Dr. Walicke reports having equity ownership or stock options in Genentech, Pfizer, and Johnson & Johnson. Dr. Dummer reports having equity ownership or stock options in Genentech. Dr. Wang reports having equity ownership or stock options in Genentech and Applied Materials. Dr. Garovoy reports having equity ownership or stock options in Xoma. Dr. Pariser reports having received consulting and lecture fees from Amgen, Biogen, and Genentech and having received grant support from these companies as well as from Centocor.
We are indebted to Kirsten Duncan, Pharm.D., for assistance in the preparation of the manuscript.
Source Information
From the Mt. Sinai School of Medicine, New York (M.L.); the University of Texas Medical Branch, Galveston (S.K.T.); the Atlanta Dermatology, Vein, and Research Center, Alpharetta, Ga. (T.K.H.); Probity Medical Research, Windsor, Ont., Canada (D.T.); Buffalo Grove, Ill. (S.G.); the Welborn Clinic, Evansville, Ind. (N.H.T.); Genentech, South San Francisco, Calif. (P.W., W.D., X.W.); Xoma, Berkeley, Calif. (M.R.G.); and the Eastern Virginia Medical School and Virginia Clinical Research, Norfolk, Va. (D.P.).
Address reprint requests to Dr. Lebwohl at the Mt. Sinai School of Medicine, 5 E. 98th St., 12th Fl., Box 1048, New York, NY 10029-6574.
- References
References
1
Christophers E . Psoriasis -- epidemiology and clinical spectrum. Clin Exp Dermatol 2001;26:314-320
CrossRef | Web of Science | Medline2
Rapp SR ,Feldman SR ,Exum ML ,Fleischer AB Jr ,Reboussin DM . Psoriasis causes as much disability as other major medical diseases. J Am Acad Dermatol 1999;41:401-407
CrossRef | Web of Science | Medline3
Tristani-Firouzi P ,Krueger GG . Efficacy and safety of treatment modalities for psoriasis. Cutis 1998;61:Suppl:11-21
Medline4
Lebwohl M . Strategies to optimize efficacy, duration of remission, and safety in the treatment of plaque psoriasis by using tazarotene in combination with a corticosteroid. J Am Acad Dermatol 2000;43:S43-S46
CrossRef | Web of Science | Medline5
Wollina U ,Stander K ,Barta U . Toxicity of methotrexate treatment in psoriasis and psoriatic arthritis -- short- and long-term toxicity in 104 patients. Clin Rheumatol 2001;20:406-410
CrossRef | Web of Science | Medline6
Grossman RM ,Chevret S ,Abi-Rached J ,Blanchet F ,Dubertret L . Long-term safety of cyclosporine in the treatment of psoriasis. Arch Dermatol 1996;132:623-629
CrossRef | Web of Science | Medline7
Stern RS . The risk of melanoma in association with long-term exposure to PUVA. J Am Acad Dermatol 2001;44:755-761
CrossRef | Web of Science | Medline8
Bos JD ,Hulsebosch HJ ,Krieg SR ,Bakker PM ,Cormane RH . Immunocompetent cells in psoriasis: in situ immunophenotyping by monoclonal antibodies. Arch Dermatol Res 1983;275:181-189
CrossRef | Web of Science | Medline9
Krueger JG . The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol 2002;46:1-23
CrossRef | Web of Science | Medline10
Grakoui A ,Bromley SK ,Sumen C , et al. The immunological synapse: a molecular machine controlling T cell activation. Science 1999;285:221-227
CrossRef | Web of Science | Medline11
Kuypers TW ,Roos D . Leukocyte membrane adhesion proteins LFA-1, CR3 and p150,95: a review of functional and regulatory aspects. Res Immunol 1989;140:461-486
CrossRef | Medline12
Dustin ML ,Springer TA . Lymphocyte function-associated antigen-1 (LFA-1) interaction with intercellular adhesion molecule-1 (ICAM-1) is one of at least three mechanisms for lymphocyte adhesion to cultured endothelial cells. J Cell Biol 1988;107:321-331
CrossRef | Web of Science | Medline13
Werther WA ,Gonzalez TN ,O'Connor SJ , et al. Humanization of an anti-lymphocyte function-associated antigen (LFA)-1 monoclonal antibody and reengineering of the humanized antibody for binding to rhesus LFA-1. J Immunol 1996;157:4986-4995
Web of Science | Medline14
Krueger GG . Selective targeting of T cell subsets: focus on alefacept -- a remittive therapy for psoriasis. Expert Opin Biol Ther 2002;2:431-441
CrossRef | Web of Science | Medline15
Krueger J ,Gottlieb A ,Miller B ,Dedrick R ,Garovoy M ,Walicke P . Anti-CD11a treatment for psoriasis concurrently increases circulating T-cells and decreases plaque T-cells, consistent with inhibition of cutaneous T-cell trafficking. J Invest Dermatol 2000;115:333-333
CrossRef | Web of Science | Medline16
Gottlieb A ,Krueger JG ,Bright R , et al. Effects of administration of a single dose of a humanized monoclonal antibody to CD11a on the immunobiology and clinical activity of psoriasis. J Am Acad Dermatol 2000;42:428-435
CrossRef | Web of Science | Medline17
Papp K ,Bissonnette R ,Krueger JG , et al. The treatment of moderate to severe psoriasis with a new anti-CD11a monoclonal antibody. J Am Acad Dermatol 2001;45:665-674
CrossRef | Web of Science | Medline18
Gottlieb AB ,Krueger JG ,Wittkowski K ,Dedrick R ,Walicke P ,Garovoy M . Psoriasis as a model for T-cell-mediated disease: immunobiologic and clinical effects of treatment with multiple doses of efalizumab, an anti-CD11a antibody. Arch Dermatol 2002;138:591-600
CrossRef | Web of Science | Medline19
Wei LJ ,Lachin J . Properties of the urn randomization in clinical trials. Control Clin Trials 1988;9:345-364[Erratum, Control Clin Trials 1989;10:126a.]
CrossRef | Medline20
Ashcroft DM ,Wan Po AL ,Williams HC ,Griffiths CEM . Clinical measures of disease severity and outcome in psoriasis: a critical appraisal of their quality. Br J Dermatol 1999;141:185-191
CrossRef | Web of Science | Medline21
Gottlieb AB . Psoriasis. Dis Manag Clin Outcomes 1998;1:195-202
CrossRef22
Krueger GG ,Papp KA ,Stough DB ,Loven KH ,Gulliver WP ,Ellis CN . A randomized, double-blind, placebo-controlled phase III study evaluating efficacy and tolerability of 2 courses of alefacept in patients with chronic plaque psoriasis. J Am Acad Dermatol 2002;47:821-833
CrossRef | Web of Science | Medline23
Krueger GG ,Feldman SR ,Camisa C , et al. Two considerations for patients with psoriasis and their clinicians: what defines mild, moderate, and severe psoriasis? What constitutes a clinically significant improvement when treating psoriasis? J Am Acad Dermatol 2000;43:281-285
CrossRef | Web of Science | Medline24
Heydendael VMR ,Spuls PI ,Opmeer BC , et al. Methotrexate versus cyclosporine in moderate-to-severe chronic plaque psoriasis. N Engl J Med 2003;349:658-665
Full Text | Web of Science | Medline25
Crandall WV ,Mackner LM . Infusion reactions to infliximab in children and adolescents: frequency, outcome and a predictive model. Aliment Pharmacol Ther 2003;17:75-84
CrossRef | Web of Science | Medline26
Sandborn WJ ,Hanauer SB . Antitumor necrosis factor therapy for inflammatory bowel disease: a review of agents, pharmacology, clinical results, and safety. Inflamm Bowel Dis 1999;5:119-133
CrossRef | Web of Science | Medline
- Citing Articles (213)
Citing Articles
1
A. Bellizzi, C. Nardis, E. Anzivino, D. M. Rodìo, D. Fioriti, M. Mischitelli, F. Chiarini, V. Pietropaolo. (2012) Human polyomavirus JC reactivation and pathogenetic mechanisms of progressive multifocal leukoencephalopathy and cancer in the era of monoclonal antibody therapies. Journal of NeuroVirology
CrossRef2
K. Reich, A.D. Burden, J.N. Eaton, N.S. Hawkins. (2011) Efficacy of biologics in the treatment of moderate to severe psoriasis: a network meta-analysis of randomized controlled trials. British Journal of Dermatologyno-no
CrossRef3
Amanda Robinson, Marisa Kardos, Alexandra B. Kimball. (2011) Physician Global Assessment (PGA) and Psoriasis Area and Severity Index (PASI): Why do both? A systematic analysis of randomized controlled trials of biologic agents for moderate to severe plaque psoriasis. Journal of the American Academy of Dermatology
CrossRef4
Marie-Nathalie Beaudoin, Philip G. Zimbardo. (2011) A medical issue affecting the diagnosis of mood, attention and autistic disorders: a closer look at celiac disease and gluten sensitivity. Health Psychology Review1-19
CrossRef5
M. Inzinger, B. Heschl, W. Weger, A. Hofer, F.J. Legat, A. Gruber-Wackernagel, H. Tilz, W. Salmhofer, F. Quehenberger, P. Wolf. (2011) Efficacy of psoralen plus ultraviolet A therapy vs. biologics in moderate to severe chronic plaque psoriasis: retrospective data analysis of a patient registry. British Journal of Dermatology 165:3, 640-645
CrossRef6
Nina Pilat, Mohamed H. Sayegh, Thomas Wekerle. (2011) Costimulatory pathways in transplantation. Seminars in Immunology 23:4, 293-303
CrossRef7
Sachin Kedar, Joseph R. Berger. (2011) The Changing Landscape of Progressive Multifocal Leukoencephalopathy. Current Infectious Disease Reports 13:4, 380-386
CrossRef8
M. L. Ford, C. P. Larsen. (2011) Transplantation Tolerance: Memories That Haunt Us. Science Translational Medicine 3:86, 86ps22-86ps22
CrossRef9
L. Morell, J.M. Carrascosa, C. Ferrándiz, M. García-Bustinduy, E. Fonseca, G. Carretero, E. Daudén, S.E. Marrón, J.L. López-Estebaranz, M. Ferrán, M. Sánchez-Regaña, C. Muñoz-Santos, I. Belinchón, Luis Puig. (2011) Perfil clínico y curso evolutivo de los pacientes tratados con efalizumab tras la suspensión de su autorización por la EMEA. Estudio observacional y multicéntrico. Actas Dermo-Sifiliográficas 102:5, 354-364
CrossRef10
Saveria Pastore, Valentina Mariani, Daniela Lulli, Emanuela Gubinelli, Desanka Raskovic, Serena Mariani, Andrea Stancato, Chiara de Luca, Alessandra Pecorelli, Giuseppe Valacchi, Alla I. Potapovich, Vladimir A. Kostyuk, Liudmila G. Korkina. (2011) Glutathione peroxidase activity in the blood cells of psoriatic patients correlates with their responsiveness to Efalizumab. Free Radical Research 45:5, 585-599
CrossRef11
Eduardo J. Villablanca, Barbara Cassani, Ulrich H. von Andrian, J. Rodrigo Mora. (2011) Blocking Lymphocyte Localization to the Gastrointestinal Mucosa as a Therapeutic Strategy for Inflammatory Bowel Diseases. Gastroenterology 140:6, 1776-1784.e5
CrossRef12
Ramin Ghazizadeh, Mamiko Tosa, Mohammad Ghazizadeh. (2011) Clinical Improvement in Psoriasis With Treatment of Associated Hyperlipidemia. The American Journal of the Medical Sciences 341:5, 394-398
CrossRef13
K. Setoguchi, A. D. Schenk, D. Ishii, Y. Hattori, W. M. Baldwin, K. Tanabe, R. L. Fairchild. (2011) LFA-1 Antagonism Inhibits Early Infiltration of Endogenous Memory CD8 T Cells into Cardiac Allografts and Donor-Reactive T Cell Priming. American Journal of Transplantation 11:5, 923-935
CrossRef14
Smriti Raychaudhuri. 2011. Biologics. , 147-163.
CrossRef15
Marina Talamonti, Giulia Spallone, Alessandro Di Stefani, Antonio Costanzo, Sergio Chimenti. (2011) Efalizumab. Expert Opinion on Drug Safety 10:2, 239-251
CrossRef16
Robert Weissert. (2011) Progressive multifocal leukoencephalopathy. Journal of Neuroimmunology 231:1-2, 73-77
CrossRef17
L. Morell, J.M. Carrascosa, C. Ferrándiz, M. García-Bustinduy, E. Fonseca, G. Carretero, E. Daudén, S.E. Marrón, J.L. López-Estebaranz, M. Ferrán, M. Sánchez-Regaña, C. Muñoz-Santos, I. Belinchón, Luis Puig. (2011) Clinical Characteristics and Disease Course in Patients Treated With Efalizumab Following Suspension of Marketing Authorization by the European Medicines Agency: A Multicenter Observational Study. Actas Dermo-Sifiliográficas (English Edition) 102:5, 354-364
CrossRef18
M. Talamonti, M. Teoli, E. Botti, G. Spallone, S. Chimenti, A. Costanzo. (2011) Patients with Moderate to Severe Plaque Psoriasis: One Year after the European Medicines Agency Recommendation of Efalizumab Suspension. Dermatology 222:3, 250-255
CrossRef19
Prakash Manikwar, Paul Kiptoo, Ahmed H. Badawi, Barlas Büyüktimkin, Teruna J. Siahaan. (2011) Antigen-specific blocking of CD4-specific immunological synapse formation using BPI and current therapies for autoimmune diseases. Medicinal Research Reviewsn/a-n/a
CrossRef20
Igal Ifergan, Hania Kebir, Simone Terouz, Jorge I. Alvarez, Marc-André Lécuyer, Steve Gendron, Lyne Bourbonnière, Ildiko R. Dunay, Alain Bouthillier, Robert Moumdjian, Adriano Fontana, Arsalan Haqqani, Armelle Klopstein, Marco Prinz, Rubèn López-Vales, Thomas Birchler, Alexandre Prat. (2011) Role of Ninjurin-1 in the migration of myeloid cells to CNS inflammatory lesions. Annals of Neurologyn/a-n/a
CrossRef21
Vasileios C. Kyttaris. 2011. Biologic Agents in the Treatment of Systemic Lupus Erythematosus. , 1109-1117.
CrossRef22
Idelberto R. Badell, Maria C. Russell, Peter W. Thompson, Alexandra P. Turner, Tim A. Weaver, Jennifer M. Robertson, Jose G. Avila, Jose A. Cano, Brandi E. Johnson, Mingqing Song, Frank V. Leopardi, Sarah Swygert, Elizabeth A. Strobert, Mandy L. Ford, Allan D. Kirk, Christian P. Larsen. (2010) LFA-1–specific therapy prolongs allograft survival in rhesus macaques. Journal of Clinical Investigation 120:12, 4520-4531
CrossRef23
Joseph R. Berger. (2010) Progressive Multifocal Leukoencephalopathy and Newer Biological Agents. Drug Safety 33:11, 969-983
CrossRef24
Dermot Cox, Marian Brennan, Niamh Moran. (2010) Integrins as therapeutic targets: lessons and opportunities. Nature Reviews Drug Discovery 9:10, 804-820
CrossRef25
Mandy E Schram, Phyllis I Spuls, Jan D Bos. (2010) Off-label use of efalizumab in dermatology. Expert Review of Dermatology 5:5, 535-547
CrossRef26
Wai Y. Sun, Stuart M. Pitson, Claudine S. Bonder. (2010) Tumor Necrosis Factor-Induced Neutrophil Adhesion Occurs Via Sphingosine Kinase-1-Dependent Activation of Endothelial α5β1 Integrin. The American Journal of Pathology 177:1, 436-446
CrossRef27
Hongyan Wang, Daina Lim, Christopher E. Rudd. (2010) Immunopathologies linked to integrin signalling. Seminars in Immunopathology 32:2, 173-182
CrossRef28
O. Baniandrés, A. Pulido, C. Silvente, R. Suárez, P. Lázaro. (2010) Evolución clínica de los pacientes psoriásicos tratados con efalizumab al suspender el fármaco. Actas Dermo-Sifiliográficas 101:5, 421-427
CrossRef29
Manjula REDDY, Gisela TORRES, Thomas McCORMICK, Colleen MARANO, Kevin COOPER, Newman YEILDING, Yuhua WANG, Charles PENDLEY, Uma PRABHAKAR, Jackson WONG, Cuc DAVIS, Stephen XU, Carrie BRODMERKEL. (2010) Positive treatment effects of ustekinumab in psoriasis: Analysis of lesional and systemic parameters. The Journal of Dermatology 37:5, 413-425
CrossRef30
O. Barreiro, P. Martin, R. Gonzalez-Amaro, F. Sanchez-Madrid. (2010) Molecular cues guiding inflammatory responses. Cardiovascular Research 86:2, 174-182
CrossRef31
T. Hautz, B. Zelger, J. Grahammer, C. Krapf, A. Amberger, G. Brandacher, L. Landin, H. Müller, M. P. Schön, P. Cavadas, A. W. P. Lee, J. Pratschke, R. Margreiter, S. Schneeberger. (2010) Molecular Markers and Targeted Therapy of Skin Rejection in Composite Tissue Allotransplantation. American Journal of Transplantation 10:5, 1200-1209
CrossRef32
Torello Lotti, Sergio Chimenti, Andreas Katsambas, Jean-Paul Ortonne, Louis Dubertret, Daiana Licu, Jan Simon. (2010) Efficacy and Safety of Efalizumab in Patients with Moderate-to-Severe Plaque Psoriasis Resistant to Previous Anti-Psoriatic Treatment: Results of a Multicentre, Open-label, Phase IIIb/IV Trial. Archives of Drug Information 3:1, 9-18
CrossRef33
Honglin Wang, Julia von Rohrscheidt, Jan Roehrbein, Thorsten Peters, Anca Sindrilaru, Daniel Kess, Klaus T Preissner, Karin Scharffetter-Kochanek. (2010) Extracellular Adherence Protein of Staphylococcus aureus Suppresses Disease by Inhibiting T-Cell Recruitment in a Mouse Model of Psoriasis. Journal of Investigative Dermatology 130:3, 743-754
CrossRef34
María Denise Takahashi, Edgardo Néstor Chouela, Gladys Leon Dorantes, Ana Maria Roselino, Jesùs Santamaria, Miguel Angel Allevato, Tania Cestari, Maria Eugenia Manzanera de Aillaud, Fernando Miguel Stengel, Daiana Licu. (2010) Efalizumab in the Treatment of Scalp, Palmoplantar and Nail Psoriasis: Results of a 24-Week Latin American Study. Archives of Drug Information 3:1, 1-8
CrossRef35
Rubén Queiro, Mercedes Alperi, Sara Alonso, José Luis Riestra, Javier Ballina. (2010) Determinants of psoriatic arthritis in patients with psoriasis. Expert Review of Dermatology 5:1, 67-77
CrossRef36
Seung-Woong Lee, Jong-Sun Chang, Ju-Hwan Lim, Min-Seok Kim, Su-Jin Park, Hyung-Jae Jeong, Min-Soo Kim, Woo-Song Lee, Mun-Chual Rho. (2010) Quinolone Alkaloids from Evodiae fructus Inhibit LFA-1/ICAM-1-mediated Cell Adhesion. Bulletin of the Korean Chemical Society 31:1, 64-68
CrossRef37
Griffiths, Christopher E.M., Strober, Bruce E., van de Kerkhof, Peter, Ho, Vincent, Fidelus-Gort, Roseanne, Yeilding, Newman, Guzzo, Cynthia, Xia, Yichuan, Zhou, Bei, Li, Shu, Dooley, Lisa T., Goldstein, Neil H., Menter, Alan, . (2010) Comparison of Ustekinumab and Etanercept for Moderate-to-Severe Psoriasis. New England Journal of Medicine 362:2, 118-128
Full Text38
Dafna D. Gladman. 2010. Management of Psoriatic Arthritis. , 55-69.
CrossRef39
M. Amin Arnaout. (2009) Integrin beta 2. AfCS-Nature Molecule Pages
CrossRef40
Fernando M. Stengel, Valeria Petri, Gladys A.M. Campbell, Gladys Leon Dorantes, Magdalina López, Ricardo L. Galimberti, Raúl P. Valdez, Lucia F. de Arruda, Mario Amaya Guerra, Edgardo N. Chouela, Daiana Licu, . (2009) Control of Moderate-to-Severe Plaque Psoriasis with Efalizumab: 24-Week, Open-Label, Phase IIIb/IV Latin American Study Results. Archives of Drug Information 2:4, 71-78
CrossRef41
Peter Foley, Michael Freeman, Kurt Gebauer, Dedee Murrell, Stephen Shumack, Christopher Tyson, George Varigos. (2009) Long-term efalizumab therapy for patients with moderate-to-severe, chronic plaque psoriasis: results from an Australian expanded access program. International Journal of Dermatology 48:12, 1376-1384
CrossRef42
Young-Min Hyun, Craig T. Lefort, Minsoo Kim. (2009) Leukocyte integrins and their ligand interactions. Immunologic Research 45:2-3, 195-208
CrossRef43
Yang Wang, Dan Li, Dan Jones, Roland Bassett, George E. Sale, Jahan Khalili, Krishna V. Komanduri, Daniel R. Couriel, Richard E. Champlin, Jeffrey J. Molldrem, Qing Ma. (2009) Blocking LFA-1 Activation with Lovastatin Prevents Graft-versus-Host Disease in Mouse Bone Marrow Transplantation. Biology of Blood and Marrow Transplantation 15:12, 1513-1522
CrossRef44
Danielle Levine, Alice Gottlieb. (2009) Evaluation and Management of Psoriasis: An Internist's Guide. Medical Clinics of North America 93:6, 1291-1303
CrossRef45
A.J. Blasco, P. Lázaro, C. Ferrándiz, A. García-Díez, J. Liso. (2009) Eficiencia de los agentes biológicos en el tratamiento de la psoriasis moderada-grave. Actas Dermo-Sifiliográficas 100:9, 792-803
CrossRef46
Gustavo Helguera, Tracy R. Daniels, José A. Rodríguez, Manuel L. Penichet. 2009. Monoclonal Antibodies, Human, Engineered. .
CrossRef47
D Pathirana, AD Ormerod, P Saiag, C Smith, PI Spuls, A Nast, J Barker, JD Bos, G-R Burmester, S Chimenti, L Dubertret, B Eberlein, R Erdmann, J Ferguson, G Girolomoni, P Gisondi, A Giunta, C Griffiths, H Hönigsmann, M Hussain, R Jobling, S-L Karvonen, L Kemeny, I Kopp, C Leonardi, M Maccarone, A Menter, U Mrowietz, L Naldi, T Nijsten, J-P Ortonne, H-D Orzechowski, T Rantanen, K Reich, N Reytan, H Richards, HB Thio, P van de Kerkhof, B Rzany. (2009) European S3-Guidelines on the systemic treatment of psoriasis vulgaris. Journal of the European Academy of Dermatology and Venereology 23, 1-70
CrossRef48
F. Prignano, F. Ricceri, L. Pescitelli, G. Buggiani, M. Troiano, F. Zanieri, S. Rossari, T. Lotti. (2009) Comparison of body weight and clinical-parameter changes following the treatment of plaque psoriasis with biological therapies. Current Medical Research and Opinion 25:9, 2311-2316
CrossRef49
Daniele Focosi, Fabrizio Maggi, Elisabetta Andreoli, Letizia Lanini, Luca Ceccherini-Nelli, Mario Petrini. (2009) The role of bone marrow cells for JCV pathogenicity. Journal of Clinical Virology 45:3, 230-231
CrossRef50
Philip J Mease. (2009) Psoriatic arthritis assessment and treatment update. Current Opinion in Rheumatology 21:4, 348-355
CrossRef51
F. Prignano, F. Zanieri, S. Milani, T. Lotti. (2009) Switch from etanercept to efalizumab in a psoriatic patient with HCV infection: a case report. Dermatologic Therapy 22:4, 386-390
CrossRef52
Carl G. Gahmberg, Susanna C. Fagerholm, Susanna M. Nurmi, Triantafyllos Chavakis, Silvia Marchesan, Mikaela Grönholm. (2009) Regulation of integrin activity and signalling. Biochimica et Biophysica Acta (BBA) - General Subjects 1790:6, 431-444
CrossRef53
L. Puig, E. Roé, X. García-Navarro, F. Corella, A. Alomar. (2009) Efalizumab treatment of psoriasis vulgaris: a cohort study in outpatient clinical practice. Clinical and Experimental Dermatology 34:4, 469-475
CrossRef54
L. Puig, J.M. Carrascosa, E. Daudén, J.L. Sánchez-Carazo, C. Ferrándiz, M. Sánchez-Regaña, M. García-Bustinduy, X. Bordas, J.C. Moreno, J.M. Hernanz, S. Laguarda, V. García-Patos. (2009) Directrices españolas basadas en la evidencia para el tratamiento de la psoriasis moderada a grave con agentes biológicos. Actas Dermo-Sifiliográficas 100:5, 386-413
CrossRef55
Anna L. Chien, James T. Elder, Charles N. Ellis. (2009) Ustekinumab. Drugs 69:9, 1141-1152
CrossRef56
Mandy L. Ford, Christian P. Larsen. (2009) Translating costimulation blockade to the clinic: lessons learned from three pathways. Immunological Reviews 229:1, 294-306
CrossRef57
Wenjun Ouyang, Ellen Filvaroff, Yan Hu, Jane Grogan. (2009) Novel therapeutic targets along the Th17 pathway. European Journal of Immunology 39:3, 670-675
CrossRef58
Zhengguang Zhang, Jochen Schmitt, Gottfried Wozel, Wilhelm Kirch. (2009) Behandlung der Plaque-Psoriasis mit Biologics. Medizinische Klinik 104:2, 125-136
CrossRef59
Dafna D. Gladman. (2009) Psoriatic arthritis. Dermatologic Therapy 22:1, 40-55
CrossRef60
Xinaida T. Lima, Elizabeth M. Seidler, Hermênio C. Lima, Alexandra B. Kimball. (2009) Long-term safety of biologics in dermatology. Dermatologic Therapy 22:1, 2-21
CrossRef61
Paolo F Fabene, Graciela Navarro Mora, Marianna Martinello, Barbara Rossi, Flavia Merigo, Linda Ottoboni, Simona Bach, Stefano Angiari, Donatella Benati, Asmaa Chakir, Lara Zanetti, Federica Schio, Antonio Osculati, Pasquina Marzola, Elena Nicolato, Jonathon W Homeister, Lijun Xia, John B Lowe, Rodger P McEver, Francesco Osculati, Andrea Sbarbati, Eugene C Butcher, Gabriela Constantin. (2008) A role for leukocyte-endothelial adhesion mechanisms in epilepsy. Nature Medicine 14:12, 1377-1383
CrossRef62
Jesús Rivera-Nieves, Gezahegn Gorfu, Klaus Ley. (2008) Leukocyte adhesion molecules in animal models of inflammatory bowel disease. Inflammatory Bowel Diseases 14:12, 1715-1735
CrossRef63
E. Y. Choi, E. Chavakis, M. A. Czabanka, H. F. Langer, L. Fraemohs, M. Economopoulou, R. K. Kundu, A. Orlandi, Y. Y. Zheng, D. A. Prieto, C. M. Ballantyne, S. L. Constant, W. C. Aird, T. Papayannopoulou, C. G. Gahmberg, M. C. Udey, P. Vajkoczy, T. Quertermous, S. Dimmeler, C. Weber, T. Chavakis. (2008) Del-1, an Endogenous Leukocyte-Endothelial Adhesion Inhibitor, Limits Inflammatory Cell Recruitment. Science 322:5904, 1101-1104
CrossRef64
James G Krueger, Hans D Ochs, Piyush Patel, Ellen Gilkerson, Emma Guttman-Yassky, Wolfgang Dummer. (2008) Effect of Therapeutic Integrin (CD11a) Blockade with Efalizumab on Immune Responses to Model Antigens in Humans: Results of a Randomized, Single Blind Study. Journal of Investigative Dermatology 128:11, 2615-2624
CrossRef65
Darryl P. Toth, Kim Papp, David Gratton. (2008) Long-term efficacy of up to 15 months’ efalizumab therapy in patients with moderate-to-severe chronic plaque psoriasis. Dermatologic Therapy 21, S6-S14
CrossRef66
Benedetta Belloni, Christian Andres, Markus Ollert, Johannes Ring, Martin Mempel. (2008) Novel immunological approaches in the treatment of atopic eczema. Current Opinion in Allergy and Clinical Immunology 8:5, 423-427
CrossRef67
Jessica R Philpott, Philip B Miner. (2008) Antisense inhibition of ICAM-1 expression as therapy provides insight into basic inflammatory pathways through early experiences in IBD. Expert Opinion on Biological Therapy 8:10, 1627-1632
CrossRef68
Heinz Wiendl. (2008) Idiopathic inflammatory myopathies: Current and future therapeutic options. Neurotherapeutics 5:4, 548-557
CrossRef69
Kim A. Papp. (2008) Monitoring biologics for the treatment of psoriasis. Clinics in Dermatology 26:5, 515-521
CrossRef70
Michael P. Schön. (2008) Efalizumab in the treatment of psoriasis: mode of action, clinical indications, efficacy, and safety. Clinics in Dermatology 26:5, 509-514
CrossRef71
Alexa B. Kimball, Thomas S. Kupper. (2008) Future perspectives/quo vadis psoriasis treatment? Immunology, pharmacogenomics, and epidemiology. Clinics in Dermatology 26:5, 554-561
CrossRef72
J. Schmitt, Z. Zhang, G. Wozel, M. Meurer, W. Kirch. (2008) Efficacy and tolerability of biologic and nonbiologic systemic treatments for moderate-to-severe psoriasis: meta-analysis of randomized controlled trials. British Journal of Dermatology 159:3, 513-526
CrossRef73
Yi-Yang Yvonne Li, Thomas M. Zollner, Michael P. Schön. (2008) Targeting leukocyte recruitment in the treatment of psoriasis. Clinics in Dermatology 26:5, 527-538
CrossRef74
D. Thaçi. (2008) Long-term data in the treatment of psoriasis. British Journal of Dermatology 159, 18-24
CrossRef75
Leona Yip, Shannon Harrison, Peter Foley. (2008) From biologic to biologic to biologic: Lessons to learn for erythrodermic and recalcitrant chronic plaque psoriasis. Australasian Journal of Dermatology 49:3, 152-155
CrossRef76
Kristian Reich. (2008) Keynote lecture: psoriasis update. Expert Review of Dermatology 3:4s, S3-S9
CrossRef77
Seung Woong Lee, Young Kook Kim, Koanhoi Kim, Hyun Sun Lee, Jung Ho Choi, Woo Song Lee, Chang-Duk Jun, Jee Hun Park, Jeong Min Lee, Mun-Chual Rho. (2008) Alkamides from the fruits of Piper longum and Piper nigrum displaying potent cell adhesion inhibition. Bioorganic & Medicinal Chemistry Letters 18:16, 4544-4546
CrossRef78
A.K. Brimhall, L.N. King, J.C. Licciardone, H. Jacobe, A. Menter. (2008) Safety and efficacy of alefacept, efalizumab, etanercept and infliximab in treating moderate to severe plaque psoriasis: a meta-analysis of randomized controlled trials. British Journal of Dermatology 159:2, 274-285
CrossRef79
Iskandarsyah, Bimo A. Tejo, Usman S. F. Tambunan, Gennady Verkhivker, Teruna J. Siahaan. (2008) Structural Modifications of ICAM-1 Cyclic Peptides to Improve the Activity to Inhibit Heterotypic Adhesion of T cells. Chemical Biology & Drug Design 72:1, 27-33
CrossRef80
Jie Zhao, Qi Qi, Yong Yang, Hong-Yan Gu, Na Lu, Wei Liu, Wei Wang, Lei Qiang, Ling-Bo Zhang, Qi-Dong You, Qing-Long Guo. (2008) Inhibition of α4 integrin mediated adhesion was involved in the reduction of B16-F10 melanoma cells lung colonization in C57BL/6 mice treated with Gambogic acid. European Journal of Pharmacology 589:1-3, 127-131
CrossRef81
William Huang, Kelly M. Cordoro, Sarah L. Taylor, Steven R. Feldman. (2008) To test or not to test? An evidence-based assessment of the value of screening and monitoring tests when using systemic biologic agents to treat psoriasis. Journal of the American Academy of Dermatology 58:6, 970-977
CrossRef82
Julia M. Kwan, Amy M. Reese, John P. Trafeli. (2008) Delayed autoimmune hemolytic anemia in efalizumab-treated psoriasis. Journal of the American Academy of Dermatology 58:6, 1053-1055
CrossRef83
S. Boulinguez. (2008) Actualité du psoriasis aux Journées de Dermatologie de Paris 2007. Annales de Dermatologie et de Vénéréologie 135, S276-S280
CrossRef84
Manuelle Viguier, Pascal Richette, François Aubin, Marie Beylot-Barry, Morad Lahfa, Christophe Bedane, Franck Delesalle, Marie-Aleth Richard-Lallemand, Emmanuel Delaporte, Louis Dubertret, Thomas Bardin, Hervé Bachelez. (2008) Onset of psoriatic arthritis in patients treated with efalizumab for moderate to severe psoriasis. Arthritis & Rheumatism 58:6, 1796-1802
CrossRef85
Erin G Harper, Eric L Simpson, Rodd H Takiguchi, Miranda D Boyd, Stephen E Kurtz, Antony C Bakke, Andrew Blauvelt. (2008) Efalizumab Therapy for Atopic Dermatitis Causes Marked Increases in Circulating Effector Memory CD4+ T Cells That Express Cutaneous Lymphocyte Antigen. Journal of Investigative Dermatology 128:5, 1173-1181
CrossRef86
Kristian Reich, Rodney Sinclair, Graeme Roberts, Christopher E. M. Griffiths, Maggie Tabberer, Jonathan Barker. (2008) Comparative effects of biological therapies on the severity of skin symptoms and health-related quality of life in patients with plaque-type psoriasis: a meta-analysis. Current Medical Research and Opinion 24:5, 1237-1254
CrossRef87
R.J.B. Driessen, M.A.M. Berends, J.B. Boezeman, P.C.M. van de Kerkhof, E.M.G.J. de Jong. (2008) Psoriasis treatment with etanercept and efalizumab: clinical strategies influencing treatment outcome. British Journal of Dermatology 158:5, 1098-1106
CrossRef88
C. Leonardi, A. Menter, T. Hamilton, I. Caro, B. Xing, A.B. Gottlieb. (2008) Efalizumab: results of a 3-year continuous dosing study for the long-term control of psoriasis. British Journal of Dermatology 158:5, 1107-1116
CrossRef89
Emma Guttman-Yassky, Yulia Vugmeyster, Michelle A Lowes, Francesca Chamian, Toyoko Kikuchi, Mark Kagen, Patricia Gilleaudeau, Edmund Lee, Brisdell Hunte, Kathy Howell, Wolfgang Dummer, Sarah C Bodary, James G Krueger. (2008) Blockade of CD11a by Efalizumab in Psoriasis Patients Induces a Unique State of T-Cell Hyporesponsiveness. Journal of Investigative Dermatology 128:5, 1182-1191
CrossRef90
Alan Menter, Alice Gottlieb, Steven R. Feldman, Abby S. Van Voorhees, Craig L. Leonardi, Kenneth B. Gordon, Mark Lebwohl, John Y.M. Koo, Craig A. Elmets, Neil J. Korman, Karl R. Beutner, Reva Bhushan. (2008) Guidelines of care for the management of psoriasis and psoriatic arthritis. Journal of the American Academy of Dermatology 58:5, 826-850
CrossRef91
Christina Weigert, Martin Röcken, Kamran Ghoreschi. (2008) Interleukin 4 as a potential drug candidate for psoriasis. Expert Opinion on Drug Discovery 3:3, 357-368
CrossRef92
TF Tsai, MT Liu, YH Liao, D Licu. (2008) Clinical effectiveness and safety experience with efalizumab in the treatment of patients with moderate-to-severe plaque psoriasis in Taiwan: results of an open-label, single-arm pilot study. Journal of the European Academy of Dermatology and Venereology 22:3, 345-352
CrossRef93
Carlos Cabanas, María Mittelbrunn, Francisco Sanchez-Madrid. (2008) Integrin alpha L. AfCS-Nature Molecule Pages
CrossRef94
Tiffani Hamilton, Alan Menter, Ivor Caro, Peter Compton, Jeffrey Sobell, Kim A Papp. (2008) Safety of Efalizumab Therapy in Patients with Moderate to Severe Psoriasis. Drug Safety 31:8, 715-726
CrossRef95
D. Firmin, A.M. Roguedas, G. Lemasson, J.F. Abgrall, L. Misery. (2008) Eczematous Dermatosis and Thrombocytosis Induced by Efalizumab: Two New Side Effects. Dermatology 217:3, 203-206
CrossRef96
J.M. Carrascosa. (2008) Estrategias para optimizar el tratamiento con efalizumab. Actas Dermo-Sifiliográficas 99, 37-50
CrossRef97
J.L. Sánchez Carazo, L. Martínez Casimiro, V. Alegre de Miguel. (2008) Es necesario el control de la psoriasis a largo plazo. Actas Dermo-Sifiliográficas 99, 29-36
CrossRef98
Rajat Varma, Jennifer A Cafardi, Wendy Cantrell, Craig Elmets. (2008) Safety and Efficacy of Subcutaneously Administered Efalizumab in Adults with Moderate-to-Severe Hand and Foot Psoriasis. American Journal of Clinical Dermatology 9:2, 105-109
CrossRef99
E. Daudén, M.J. Oñate. (2008) Efalizumab: ¿un tratamiento seguro para una enfermedad crónica?. Actas Dermo-Sifiliográficas 99, 18-28
CrossRef100
Benjamin Leader, Quentin J. Baca, David E. Golan. (2008) Protein therapeutics: a summary and pharmacological classification. Nature Reviews Drug Discovery 7:1, 21-39
CrossRef101
J.C. Moreno Giménez, M. Galán Gutiérrez, R. Jiménez Puya. (2008) Eficacia de efalizumab a corto y largo plazo. Actas Dermo-Sifiliográficas 99, 9-17
CrossRef102
Yoshinori Umezawa. (2008) TNF.ALPHA. inhibitors treatments for Psoriasis. Inflammation and Regeneration 28:1, 27-30
CrossRef103
Kamran Ghoreschi, Christina Weigert, Martin Röcken. (2007) Immunopathogenesis and role of T cells in psoriasis. Clinics in Dermatology 25:6, 574-580
CrossRef104
Paolo Gisondi, Giampiero Girolomoni. (2007) Biologic therapies in psoriasis: A new therapeutic approach. Autoimmunity Reviews 6:8, 515-519
CrossRef105
Ivan Valeryevich Shirinsky, Valery Stepanovich Shirinsky. (2007) Efficacy of simvastatin in plaque psoriasis: A pilot study. Journal of the American Academy of Dermatology 57:3, 529-531
CrossRef106
Helena Yusuf-Makagiansar, Tatyana V. Yakovleva, Bimo A. Tejo, Karen Jones, Yongbo Hu, Gennady M. Verkhivker, Kenneth L. Audus, Teruna J. Siahaan. (2007) Sequence Recognition of ?-LFA-1-derived Peptides by ICAM-1 Cell Receptors: Inhibitors of T-cell Adhesion. Chemical Biology & Drug Design 70:3, 237-246
CrossRef107
Olga Barreiro, Hortensia de la Fuente, María Mittelbrunn, Francisco Sánchez-Madrid. (2007) Functional insights on the polarized redistribution of leukocyte integrins and their ligands during leukocyte migration and immune interactions. Immunological Reviews 218:1, 147-164
CrossRef108
C. Bedini, F. Nasorri, G. Girolomoni, O. de Pità, A. Cavani. (2007) Antitumour necrosis factor-? chimeric antibody (infliximab) inhibits activation of skin-homing CD4+ and CD8+ T lymphocytes and impairs dendritic cell function. British Journal of Dermatology 157:2, 249-258
CrossRef109
C. Kleinschnitz, S.G. Meuth, B.C. Kieseier, H. Wiendl. (2007) Multiple-Sklerose-Update zur Pathophysiologie und neuen immuntherapeutischen Ansätzen. Der Nervenarzt 78:8, 883-911
CrossRef110
Alexander Nast, Ina B. Kopp, Matthias Augustin, Kirstin-Benita Banditt, Wolf-Henning Boehncke, Markus Follmann, Markus Friedrich, Matthias Huber, Christina Kahl, Joachim Klaus, Joachim Koza, Inga Kreiselmaier, Johannes Mohr, Ulrich Mrowietz, Hans-Michael Ockenfels, Hans-Dieter Orzechowski, Jörg Prinz, Kristian Reich, Thomas Rosenbach, Stefanie Rosumeck, Martin Schlaeger, Gerhard Schmid-Ott, Michael Sebastian, Volker Streit, Tobias Weberschock, Berthold Rzany. (2007) Evidence-based (S3) guidelines for the treatment of psoriasis vulgaris. JDDG 5:s3, 1-119
CrossRef111
F. Vincenti, R. Mendez, M. Pescovitz, P. R. Rajagopalan, A. H. Wilkinson, K. Butt, D. Laskow, D. P. Slakey, M. I. Lorber, J. P. Garg, M. Garovoy. (2007) A Phase I/II Randomized Open-Label Multicenter Trial of Efalizumab, a Humanized Anti-CD11a, Anti-LFA-1 in Renal Transplantation. American Journal of Transplantation 7:7, 1770-1777
CrossRef112
Manju Chacko, Jeffrey M Weinberg. (2007) Efalizumab. Dermatologic Therapy 20:4, 265-269
CrossRef113
Alan Menter, Tiffani K. Hamilton, Darryl P. Toth, Hoi M. Leung, Graham Wetherill, Brian Hennessey, Marvin Garovoy, Paul Kwon, David M. Pariser, . (2007) Transitioning patients from efalizumab to alternative psoriasis therapies: findings from an open-label, multicenter, Phase IIIb study. International Journal of Dermatology 46:6, 637-648
CrossRef114
A. Nast, I. Kopp, M. Augustin, K. B. Banditt, W. H. Boehncke, M. Follmann, M. Friedrich, M. Huber, C. Kahl, J. Klaus, J. Koza, I. Kreiselmaier, J. Mohr, U. Mrowietz, H. M. Ockenfels, H. D. Orzechowski, J. Prinz, K. Reich, T. Rosenbach, S. Rosumeck, M. Schlaeger, G. Schmid-Ott, M. Sebastian, V. Streit, T. Weberschock, B. Rzany. (2007) German evidence-based guidelines for the treatment of Psoriasis vulgaris (short version). Archives of Dermatological Research 299:3, 111-138
CrossRef115
Argentina Leon, Alain Nguyen, Julie Letsinger, John Koo. (2007) An attempt to formulate an evidence-based strategy in the management of moderate-to-severe psoriasis: a review of the efficacy and safety of biologics and prebiologic options. Expert Opinion on Pharmacotherapy 8:5, 617-632
CrossRef116
C. Ferrándiz, J.M. Carrascosa. (2007) Managing moderate-to-severe psoriasis with efalizumab: experience at a single Spanish institute. British Journal of Dermatology 156:s2, 24-29
CrossRef117
N. Selenko-Gebauer, F. Karlhofer, G. Stingl. (2007) Efalizumab in routine use: a clinical experience. British Journal of Dermatology 156:s2, 1-6
CrossRef118
Juan Jorge Manriquez, Maria Francisca Villouta, Hywel C. Williams. (2007) Evidence-based dermatology: Number needed to treat and its relation to other risk measures. Journal of the American Academy of Dermatology 56:4, 664-671
CrossRef119
Knud Kragballe. (2007) Efalizumab in the treatment of chronic plaque psoriasis: experiences from the largest psoriasis treatment centre in Denmark. British Journal of Dermatology 156:s2, 7-11
CrossRef120
Jeffrey P. Callen. (2007) Complications and Adverse Reactions in the Use of Newer Biologic Agents. Seminars in Cutaneous Medicine and Surgery 26:1, 6-14
CrossRef121
Krueger, Gerald G., Langley, Richard G., Leonardi, Craig, Yeilding, Newman, Guzzo, Cynthia, Wang, Yuhua, Dooley, Lisa T., Lebwohl, Mark, . (2007) A Human Interleukin-12/23 Monoclonal Antibody for the Treatment of Psoriasis. New England Journal of Medicine 356:6, 580-592
Full Text122
Onur Boyman, Curdin Conrad, Giulia Tonel, Michel Gilliet, Frank O. Nestle. (2007) The pathogenic role of tissue-resident immune cells in psoriasis. Trends in Immunology 28:2, 51-57
CrossRef123
Rodd Takiguchi, Susan Tofte, Brenda Simpson, Erin Harper, Andrew Blauvelt, Jon Hanifin, Eric Simpson. (2007) Efalizumab for severe atopic dermatitis: A pilot study in adults. Journal of the American Academy of Dermatology 56:2, 222-227
CrossRef124
Stephanie Diamantis, Mark Lebwohl. 2007. Dermatologic Management of Psoriasis. , 114-121.
CrossRef125
Luis R. Espinoza. 2007. Historical Aspects of the Disease. , 4-10.
CrossRef126
Thomas M. Zollner, Khusru Asadullah, Michael P. Schön. (2007) Targeting leukocyte trafficking to inflamed skin - still an attractive therapeutic approach?. Experimental Dermatology 16:1, 1-12
CrossRef127
2007. Management of Psoriatic Arthritis. , 97-113.
CrossRef128
Philip Mease. (2006) Infliximab (Remicade) in the treatment of psoriatic arthritis. Therapeutics and Clinical Risk Management 2:4, 389-400
CrossRef129
Philip Mease. (2006) Current Treatment for Psoriatic Arthritis and Other Spondyloarthritides. Rheumatic Disease Clinics of North America 32, 11-20
CrossRef130
Arisa Ortiz, Paul S. Yamauchi. (2006) A Treatment Strategy for Psoriasis: Transitioning From Systemic Therapy to Biologic Agents. SKINmed 5:6, 285-290
CrossRef131
Carlo Pincelli, Eric Henninger, Florence Casset-Semanaz. (2006) The incidence of arthropathy adverse events in efalizumab-treated patients is low and similar to placebo and does not increase with long-term treatment: pooled analysis of data from Phase III clinical trials of efalizumab. Archives of Dermatological Research 298:7, 329-338
CrossRef132
Alexander Nast, Ina B. Kopp, Matthias Augustin, Kirstin-Benita Banditt, Wolf-Henning Boehncke, Markus Follmann, Markus Friedrich, Matthias Huber, Christina Kahl, Joachim Klaus, Joachim Koza, Inga Kreiselmaier, Johannes Mohr, Ulrich Mrowietz, Hans-Michael Ockenfels, Hans-Dieter Orzechowski, Jörg Prinz, Kristian Reich, Thomas Rosenbach, Stefanie Rosumeck, Martin Schlaeger, Gerhard Schmid-Ott, Michael Sebastian, Volker Streit, Tobias Weberschock, Berthold Rzany. (2006) S3-Leitlinie zur Therapie der Psoriasis vulgaris. Journal der Deutschen Dermatologischen Gesellschaft 4, S1-S126
CrossRef133
Wolfram Sterry, Georg Stingl, Richard G.B. Langley, Hugh Zacharie, Morad Lahfa, Alberto Giannetti, Carlos Ferrándiz, Rodney Sinclair, Jean-Hilaire Saurat, . (2006) CLinical Experience Acquired with Raptiva
(CLEAR) trial in patients with moderate-to-severe plaque psoriasis: results from extended treatment in an international, Phase III, placebo-controlled trial. JDDG 4:11, 947-956
CrossRef134
J Sibilia. (2006) Psoriasis: skin and joints, same fight?. Journal of the European Academy of Dermatology and Venereology 20:s2, 56-72
CrossRef135
Michael R Lee, Alan J Cooper. (2006) Biologic agents in psoriasis. Australasian Journal of Dermatology 47:4, 217-230
CrossRef136
Peter Vanderslice, Darren G Woodside. (2006) Integrin antagonists as therapeutics for inflammatory diseases. Expert Opinion on Investigational Drugs 15:10, 1235-1255
CrossRef137
Philip Mease. (2006) Management of psoriatic arthritis: The therapeutic interface between rheumatology and dermatology. Current Rheumatology Reports 8:5, 348-354
CrossRef138
Wendy A. Myers, Alice B. Gottlieb, Philip Mease. (2006) Psoriasis and psoriatic arthritis: clinical features and disease mechanisms. Clinics in Dermatology 24:5, 438-447
CrossRef139
Nikolai Tsankov, Ivan Grozdev. (2006) Efalizumab for psoriasis. Expert Review of Dermatology 1:4, 503-513
CrossRef140
V. Descamps. (2006) Efalizumab. Annales de Dermatologie et de Vénéréologie 133:8-9, 666-678
CrossRef141
Daniel Bock, Sandra Philipp, Gerhard Wolff. (2006) Therapeutic potential of selectin antagonists in psoriasis. Expert Opinion on Investigational Drugs 15:8, 963-979
CrossRef142
Yi-Yang Yvonne Li, H Daniel Perez, Thomas M Zollner. (2006) Fatalities in natalizumab treatment - a 'no go for leukocyte recirculation approaches?. Expert Opinion on Therapeutic Targets 10:4, 489-499
CrossRef143
L. Dubertret, W. Sterry, J.D. Bos, S. Chimenti, S. Shumack, C.G. Larsen, N.H. Shear, K.A. Papp, . (2006) CLinical experience acquired with the efalizumab (RaptivaR) (CLEAR) trial in patients with moderate-to-severe plaque psoriasis: results from a phase III international randomized, placebo-controlled trial. British Journal of Dermatology 155:1, 170-181
CrossRef144
PCM van de Kerkhof. (2006) Consistent control of psoriasis by continuous long-term therapy: the promise of biological treatments. Journal of the European Academy of Dermatology and Venereology 20:6, 639-650
CrossRef145
Seitetsu Go, Audrey Fleischmann, Olivier Lantz, C??lia Cretolle, Nicole Brousse, Nadine Cerf-Bensussan, Sabine Sarnacki. (2006) Anti-LFA-1 Antibody Postpones T-cell Receptor Triggering While Preserving Generation of Regulatory T Cells in T-cell Receptor Anti-HY Transgenic Mice. Transplantation 82:1, 119-126
CrossRef146
J. Pfeffer, R. Kaufmann, W.-H. Boehncke. (2006) Psoriasis-SCID-Maus-Modell. Der Hautarzt 57:7, 603-609
CrossRef147
Kim A. Papp. (2006) The long-term efficacy and safety of new biological therapies for psoriasis. Archives of Dermatological Research 298:1, 7-15
CrossRef148
Paul Hasler. (2006) Biological therapies directed against cells in autoimmune disease. Springer Seminars in Immunopathology 27:4, 443-456
CrossRef149
Neil John McHugh. (2006) Treatments for psoriatic arthritis. Future Rheumatology 1:3, 331-338
CrossRef150
Sanjay M Rajpara, Anthony D Ormerod, Pick N Woo. (2006) Biological treatments for psoriasis. Therapy 3:3, 425-436
CrossRef151
Christopher P. Stowell. (2006) Therapy With Immunoglobulin. Journal of Infusion Nursing 29:Supplement, S29-S44
CrossRef152
Kim A. Papp, Reni Bressinck, Scott Fretzin, Bernard Goffe, Steven Kempers, Kenneth B. Gordon, Ivor Caro, Patricia A. Walicke, Xiaolin Wang, Alan Menter, . (2006) Safety of efalizumab in adults with chronic moderate to severe plaque psoriasis: A phase IIIb, randomized, controlled trial. International Journal of Dermatology 45:5, 605-614
CrossRef153
William D Tutrone, Jeffrey M Weinberg. (2006) Biological therapy for psoriasis: infliximab, etanercept, adalimumab, efalizumab and alefacept. Expert Review of Dermatology 1:2, 207-216
CrossRef154
Marinos C. Dalakas. (2006) Therapeutic targets in patients with inflammatory myopathies: Present approaches and a look to the future. Neuromuscular Disorders 16:4, 223-236
CrossRef155
Noah Scheinfeld. (2006) Efalizumab: a review of events reported during clinical trials and side effects. Expert Opinion on Drug Safety 5:2, 197-209
CrossRef156
Drew W Miller, Steven R Feldman. (2006) Cost-effectiveness of moderate-to-severe psoriasis treatment. Expert Opinion on Pharmacotherapy 7:2, 157-167
CrossRef157
Lily Yi Li, Angela K Brimhall, Alan Menter. (2006) Systemic therapy for moderate-to-severe psoriasis. Expert Review of Dermatology 1:1, 77-92
CrossRef158
Daniel J. Pearce, Andrew A. Nelson, Alan B. Fleischer, Rajesh Balkrishnan, Steven R. Feldman. (2006) The cost‐effectiveness and cost of treatment failures associated with systemic psoriasis therapies. Journal of Dermatological Treatment 17:1, 29-37
CrossRef159
Jose L S??nchez Carazo, Laura Mahiques Santos, Vicente Oliver Martinez. (2006) Safety of Etanercept in Psoriasis. Drug Safety 29:8, 675-685
CrossRef160
Kenneth B. Gordon, Alice B. Gottlieb, Craig L. Leonardi, Boni E. Elewski, Andrea Wang, Angelika Jahreis, Ralph Zitnik. (2006) Clinical response in psoriasis patients discontinued from and then reinitiated on etanercept therapy. Journal of Dermatological Treatment 17:1, 9-17
CrossRef161
Stephen Tyring, Alice Gottlieb, Kim Papp, Ken Gordon, Craig Leonardi, Andrea Wang, Deepa Lalla, Michael Woolley, Angelika Jahreis, Ralph Zitnik, David Cella, Ranga Krishnan. (2006) Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial. The Lancet 367:9504, 29-35
CrossRef162
Yves Poulin, Kim A. Papp, Wayne Carey, Wayne Gulliver, Aditya K. Gupta. (2005) A favourable benefit/risk ratio with efalizumab: A review of the clinical evidence. Journal of Cutaneous Medicine and Surgery 9:S1, 10-17
CrossRef163
David M. Pariser, Kenneth B. Gordon, Kim A. Papp, Craig L. Leonardi, Paul Kwon, Peter G. Compton, Amy Chen Rundle, Patricia A. Walicke, Mark Lebwohl. (2005) Clinical Efficacy of Efalizumab in Patients With Chronic Plaque Psoriasis: Results From Three Randomized Placebo-Controlled Phase III Trials: Part I. Journal of Cutaneous Medicine and Surgery 9:6, 303-312
CrossRef164
Kim A. Papp, Charles Camisa, Stephen P. Stone, Ivor Caro, Xiaolin Wang, Peter Compton, Patricia A. Walicke, Alice B. Gottlieb. (2005) Safety of Efalizumab in Patients with Moderate to Severe Chronic Plaque Psoriasis: Review of Clinical Data. Part II. Journal of Cutaneous Medicine and Surgery 9:6, 313-323
CrossRef165
Richard G. Langley, Vincent Ho, Charles Lynde, Kim A. Papp, Yves Poulin, Neil Shear, Jack Toole, Catherine Zip. (2005) Recommendations for incorporating biologicals into management of moderate to severe plaque psoriasis: individualized patient approaches. Journal of Cutaneous Medicine and Surgery 9:S1, 18-25
CrossRef166
Roberto Gonzalez-Amaro, Maria Mittelbrunn, Francisco Sanchez-Madrid. (2005) Therapeutic anti-integrin (alpha4 and alphaL) monoclonal antibodies: two-edged swords?. Immunology 116:3, 289-296
CrossRef167
M. de Groot, M.A. de Rie, J.D. Bos. (2005) Dermatitis during efalizumab treatment in a patient with psoriasis vulgaris. British Journal of Dermatology 153:4, 843-844
CrossRef168
Kristian Reich, Frank O Nestle, Kim Papp, Jean-Paul Ortonne, Robert Evans, Cynthia Guzzo, Shu Li, Lisa T Dooley, Christopher EM Griffiths. (2005) Infliximab induction and maintenance therapy for moderate-to-severe psoriasis: a phase III, multicentre, double-blind trial. The Lancet 366:9494, 1367-1374
CrossRef169
W-H. Boehncke, F.R. Ochsendorf, S. Noll, M. Urban, A. Popp, D. Waldherr, J. Haunschild, T. Litzenburger. (2005) Efficacy of the fully human monoclonal antibody MOR102 (#5) against intercellular adhesion molecule 1 in the psoriasis-severe combined immunodeficient mouse model. British Journal of Dermatology 153:4, 758-766
CrossRef170
Richard G.B. Langley, Wayne P. Carey, Elyse S. Rafal, Stephen K. Tyring, Ivor Caro, Xiaolin Wang, Graham Wetherill, Kenneth B. Gordon. (2005) Incidence of infection during efalizumab therapy for psoriasis: Analysis of the clinical trial experience. Clinical Therapeutics 27:9, 1317-1328
CrossRef171
C.H. Smith, A.V. Anstey, J.N.W.N. Barker, A.D. Burden, R.J.G. Chalmers, D. Chandler, A.Y. Finlay, C.E.M. Grifitths, K. Jackson, N.J. McHugh, K.E. McKenna, N.J. Reynolds, A.D. Ormerod, . (2005) British Association of Dermatologists guidelines for use of biological interventions in psoriasis 2005. British Journal of Dermatology 153:3, 486-497
CrossRef172
Valencia D. Thomas, F. Clarissa Yang, Joseph C. Kvedar. (2005) Biologics in psoriasis: A quick reference guide. Journal of the American Academy of Dermatology 53:2, 346-351
CrossRef173
Chee M. Ng, Amita Joshi, Russell L. Dedrick, Marvin R. Garovoy, Robert J. Bauer. (2005) Pharmacokinetic–Pharmacodynamic–Efficacy Analysis of Efalizumab in Patients with Moderate to Severe Psoriasis. Pharmaceutical Research 22:7, 1088-1100
CrossRef174
M. Hahn, T. Schulz. (2005) Gesundheitsökonomische Aspekte der Psoriasistherapie. Der Hautarzt 56:6, 576-580
CrossRef175
A.B. Gottlieb, C.E.M. Griffiths, V.C. Ho, M. Lahfa, U. Mrowietz, D.F. Murrell, J-P. Ortonne, G. Todd, R. Cherill, I. Marks, S. Emady-Azar, C.F. Paul, . (2005) Oral pimecrolimus in the treatment of moderate to severe chronic plaque-type psoriasis: a double-blind, multicentre, randomized, dose-finding trial. British Journal of Dermatology 152:6, 1219-1227
CrossRef176
Schön, Michael P., Boehncke, W.-Henning, . (2005) Psoriasis. New England Journal of Medicine 352:18, 1899-1912
Full Text177
Hywel C. Williams, Robert S. Stern. (2005) Prospective Clinical Trial Registration. Journal of Investigative Dermatology 124:5, viii-x
CrossRef178
R. Weller. (2005) U.S. experience of immunomodulators in the treatment of psoriasis. British Journal of Dermatology 152:4, 817-818
CrossRef179
Michael P Schön, Ralf J Ludwig. (2005) Lymphocyte trafficking to inflamed skin – molecular mechanisms and implications for therapeutic target molecules. Expert Opinion on Therapeutic Targets 9:2, 225-243
CrossRef180
L. Naldi, C.E.M. Griffiths. (2005) Traditional therapies in the management of moderate to severe chronic plaque psoriasis: an assessment of the benefits and risks. British Journal of Dermatology 152:4, 597-615
CrossRef181
Marika Merinen, Heikki Irjala, Marko Salmi, Ilkka Jaakkola, Arno Hänninen, Sirpa Jalkanen. (2005) Vascular Adhesion Protein-1 Is Involved in Both Acute and Chronic Inflammation in the Mouse. The American Journal of Pathology 166:3, 793-800
CrossRef182
Jennifer Clay Cather, Alan Menter. (2005) Efalizumab: continuous therapy for chronic psoriasis. Expert Opinion on Biological Therapy 5:3, 393-403
CrossRef183
Melissa A Magliocco. (2005) Emerging drugs for moderate-to-severe psoriasis. Expert Opinion on Emerging Drugs 10:1, 35-52
CrossRef184
Sompong Wattanasin, Joerg Kallen, Stewart Myers, Qin Guo, Michael Sabio, Claus Ehrhardt, Rainer Albert, Ulrich Hommel, Gisbert Weckbecker, Karl Welzenbach, Gabriele Weitz-Schmidt. (2005) 1,4-Diazepane-2,5-diones as novel inhibitors of LFA-1. Bioorganic & Medicinal Chemistry Letters 15:4, 1217-1220
CrossRef185
Shigetoshi Sano, Keith Syson Chan, Steve Carbajal, John Clifford, Mary Peavey, Kaoru Kiguchi, Satoshi Itami, Brian J Nickoloff, John DiGiovanni. (2005) Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model. Nature Medicine 11:1, 43-49
CrossRef186
Jochen Schmitt, Gottfried Wozel. (2005) The Psoriasis Area and Severity Index Is the Adequate Criterion to Define Severity in Chronic Plaque-Type Psoriasis. Dermatology 210:3, 194-199
CrossRef187
Alice B. Gottlieb. (2005) Psoriasis: emerging therapeutic strategies. Nature Reviews Drug Discovery 4:1, 19-34
CrossRef188
Hervé Bachelez. (2005) Immunopathogenesis of psoriasis: Recent insights on the role of adaptive and innate immunity. Journal of Autoimmunity 25, 69-73
CrossRef189
V Schleyer, M Landthaler, R-M Szeimies. (2005) Novel pharmacological approaches in the treatment of psoriasis. Journal of the European Academy of Dermatology and Venereology 19:1, 1-20
CrossRef190
Brian J. Nickoloff, Brian K. Bonish, Frank O. Nestle. (2005) Viewpoint 2. Experimental Dermatology 14:1, 72-74
CrossRef191
Catharine L. Kauffman, Nancy Aria, Eiko Toichi, Thomas S. McCormick, Kevin D. Cooper, Alice B. Gottlieb, Daniel E. Everitt, Bart Frederick, Yaowei Zhu, Martin A. Graham, Charles E. Pendley, Mary Ann Mascelli. (2004) A Phase I Study Evaluating the Safety, Pharmacokinetics, and Clinical Response of a Human IL-12 p40 Antibody in Subjects with Plaque Psoriasis. Journal of Investigative Dermatology 123:6, 1037-1044
CrossRef192
Abdul B. Lodhi, John D. Carter, Joanne Valeriano, Frank B. Vasey. (2004) Can we classify psoriatic arthritis?. Seminars in Arthritis and Rheumatism 34:3, 571-572
CrossRef193
Emma Terricabras, Claudia Benjamim, Nuria Godessart. (2004) Drug discovery and chemokine receptor antagonists: eppur si muove!. Autoimmunity Reviews 3:7-8, 550-556
CrossRef194
Christine Della Croce, Vicky Kwan Wong, Mark G Lebwohl. (2004) Efalizumab in the treatment of psoriasis. Therapy 1:2, 197-202
CrossRef195
Maryann Mikhail, Noah S Scheinfeld. (2004) Therapy treatment options for psoriasis: topical and systemic. Therapy 1:2, 319-330
CrossRef196
Craig L. Leonardi. (2004) Efalizumab in the treatment of psoriasis. Dermatologic Therapy 17:5, 393-400
CrossRef197
Lyn Guenther, Richard G. Langley, Neil H. Shear, Robert Bissonnette, Vincent Ho, Charles Lynde, Eileen Murray, Kim Papp, Yves Poulin, Catherine Zip. (2004) Integrating Biologic Agents into Management of Moderate-to-Severe Psoriasis: A Consensus of the Canadian Psoriasis Expert Panel. Journal of Cutaneous Medicine and Surgery 8:5, 321-337
CrossRef198
Dafna D. Gladman. (2004) Psoriatic arthritis. Dermatologic Therapy 17:5, 350-363
CrossRef199
Andrew Y. Finlay, Jean-Paul Ortonne. (2004) Patient Satisfaction with Psoriasis Therapies: An Update and Introduction to Biologic Therapy. Journal of Cutaneous Medicine and Surgery 8:5, 310-320
CrossRef200
Douglas A Hale. (2004) Biological effects of induction immunosuppression. Current Opinion in Immunology 16:5, 565-570
CrossRef201
J. N. W. N. Barker. (2004) A review of recent journal highlights. Clinical and Experimental Dermatology 29:5, 579-581
CrossRef202
W. Sterry, J. Barker, W.-H. Boehncke, J.D. Bos, S. Chimenti, E. Christophers, M. De La Brassinne, C. Ferrandiz, C. Griffiths, A. Katsambas, K. Kragballe, C. Lynde, A. Menter, J.-P. Ortonne, K. Papp, J. Prinz, B. Rzany, J. Ronnevig, J.-H. Saurat, M. Stahle, F.M. Stengel, P. Van De Kerkhof, J. Voorhees. (2004) Biological therapies in the systemic management of psoriasis: International Consensus Conference. British Journal of Dermatology 151:s69, 3-17
CrossRef203
T. Kormeili, N.J. Lowe, P.S. Yamauchi. (2004) Psoriasis: immunopathogenesis and evolving immunomodulators and systemic therapies; U.S. experiences. British Journal of Dermatology 151:1, 3-15
CrossRef204
(2004) IMMUNE AND INFLAMMATORY DISORDERS. Nature Reviews Drug Discovery 3:7, S19-S22
CrossRef205
Francesca Chamian, James G Krueger. (2004) Psoriasis vulgaris: an interplay of T lymphocytes, dendritic cells, and inflammatory cytokines in pathogenesis. Current Opinion in Rheumatology 16:4, 331-337
CrossRef206
Brian J. Nickoloff, Frank O. Nestle. (2004) Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. Journal of Clinical Investigation 113:12, 1664-1675
CrossRef207
Jane Barry, Brian Kirby. (2004) Novel biologic therapies for psoriasis. Expert Opinion on Biological Therapy 4:6, 975-987
CrossRef208
Sylvia Marecki, Peter Kirkpatrick. (2004) Fresh from the pipeline: Efalizumab. Nature Reviews Drug Discovery 3:6, 473-474
CrossRef209
Sheila A Doggrell. (2004) Efalizumab for psoriasis?. Expert Opinion on Investigational Drugs 13:5, 551-554
CrossRef210
Kohzoh IMAI, Hiroki TAKAHASHI. (2004) Japanese Journal of Clinical Immunology 27:1, 1-6
CrossRef211
Motomu SHIMAOKA. (2004) Japanese Journal of Thrombosis and Hemostasis 15:4, 321-333
CrossRef212
Leonardi, Craig L., Powers, Jerold L., Matheson, Robert T., Goffe, Bernard S., Zitnik, Ralph, Wang, Andrea, Gottlieb, Alice B., . (2003) Etanercept as Monotherapy in Patients with Psoriasis. New England Journal of Medicine 349:21, 2014-2022
Full Text213
Kupper, Thomas S., . (2003) Immunologic Targets in Psoriasis. New England Journal of Medicine 349:21, 1987-1990
Full Text
