Efficacy of omalizumab in patients with atopic dermatitis: A systematic review and meta-analysis
2016; Elsevier BV; Volume: 138; Issue: 6 Linguagem: Inglês
10.1016/j.jaci.2016.05.038
ISSN1097-6825
AutoresHsiao-Han Wang, Yu‐Chuan Li, Yu‐Chen Huang,
Tópico(s)Allergic Rhinitis and Sensitization
ResumoOmalizumab has been used to treat patients with atopic dermatitis (AD) with controversial results.1Makris M.P. Papadavid E. Zuberbier T. The use of biologicals in cutaneous allergies—present and future.Curr Opin Allergy Clin Immunol. 2014; 14: 409-416Crossref PubMed Scopus (11) Google Scholar Our objective was to perform a systematic review and meta-analysis to investigate the efficacy of omalizumab and the factors associated with better therapeutic results in patients with AD. The search included PubMed, MEDLINE, EmBase, and the Cochrane Library (Cochrane Database of Systematic Reviews, Database of Abstracts of Reviews of Effects, Cochrane Controlled Trials Register, and Health Technology Assessment Databases) from inception to November 30, 2015, using the search terms atopic dermatitis or eczema combined with omalizumab. Only human clinical studies written in English were included in this analysis. This literature search focused on randomized controlled trials (RCTs), comparative studies, and case series in which 3 or more patients with AD received omalizumab treatment. Review articles, single case reports, guidelines, consensus manuscripts, and correspondence were excluded. The primary outcome assessed was the clinical response of omalizumab in patients with AD. Data on the following measures were extracted: study design, sample size, trial duration, treatment regimen, and author's conclusion (Table I). For studies that provided the patients' raw data (detailed information for each patient), data on patients' age, sex, asthma history, pretreatment IgE concentration, pretreatment and posttreatment severity of eczema (using Severity Scoring of Atopic Dermatitis [SCORAD], Eczema Area and Severity Index [EASI], or Investigators' Global Assessment [IGA] scores), clinical response, adverse event, and treatment duration were collected (Table II). The dosing regimens were divided into 2 groups on the basis of total dosage of the month: 600 mg/month or more (eg, 300 mg omalizumab subcutaneously in 2-week intervals or 150 mg in a 1-week interval) or less than 600 mg/month (eg, 150 mg omalizumab subcutaneously in 2-week intervals or 300 mg in 3-week interval). We then performed multivariate logistic regression on the detailed data to evaluate the possible factors associated with an excellent clinical response. Values of P less than .05 were considered statistically significant. Statistical analysis was performed using PASW Statistics 18.0.Table ISummary of included studiesStudy (year)Study designSample size and classificationOmalizumab treatmentPrevious/concomitant therapyAuthor's conclusionKrathen and Hsu,2Krathen R.A. Hsu S. Failure of omalizumab for treatment of severe adult atopic dermatitis.J Am Acad Dermatol. 2005; 53: 338-340Abstract Full Text Full Text PDF PubMed Scopus (154) Google Scholar 2005Case series3 OMA450 mg OMA q2w for 4 moSystemic steroids and ISA/NANo subjective or objective improvementLane et al,3Lane J.E. Cheyney J.M. Lane T.N. Kent D.E. Cohen D.J. Treatment of recalcitrant atopic dermatitis with omalizumab.J Am Acad Dermatol. 2006; 54: 68-72Abstract Full Text Full Text PDF PubMed Scopus (171) Google Scholar 2006Case series3 OMA150-450 mg OMA q2w for 6 moSystemic steroids and ISA/antibiotics and topical agentsSuccessful treatment with OMAVigo et al,4Vigo P.G. Girgis K.R. Pfuetze B.L. Critchlow M.E. Fisher J. Hussain I. Efficacy of anti-IgE therapy in patients with atopic dermatitis.J Am Acad Dermatol. 2006; 55: 168-170Abstract Full Text Full Text PDF PubMed Scopus (120) Google Scholar 2006Case series7 OMA300 mg OMA q2w for 3-7 moSystemic steroid/NABeneficial effect in ADBelloni et al,E1Belloni B. Ziai M. Lim A. Lemercier B. Sbornik M. Weidinger S. et al.Low-dose anti-IgE therapy in patients with atopic eczema with high serum IgE levels.J Allergy Clin Immunol. 2007; 120: 1223-1225Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar2007Case series11 OMA150 mg OMA q2w for 5 mo (10 cycles)≥1 systemic steroid, Csa, UV and free for 6 wk/topical steroid onlyControversialSheinkopf et al,5Sheinkopf L.E. Rafi A.W. Do L.T. Katz R.M. Klaustermeyer W.B. Efficacy of omalizumab in the treatment of atopic dermatitis: a pilot study.Allergy Asthma Proc. 2008; 29: 530-537Crossref PubMed Scopus (125) Google Scholar 2008Case series21 OMA150 mg (n = 6), 300 mg (n = 15); q2-4w for 9-12 moNA/inhalers for asthma, oral antihistamines and topical agentsEffective for patients with AD and moderate to severe allergic asthmaAmrol,E2Amrol D. Anti-immunoglobulin E in the treatment of refractory atopic dermatitis.South Med J. 2010; 103: 554-558Crossref PubMed Scopus (32) Google Scholar 2010Case series3 OMA300-375 mg OMA q2w for 3 moSystemic steroid and ISA/oral antihistamines and topical agentsClinical improvement in patients with severe ADRamírez Del Pozo et al,E3Ramirez del Pozo M.E. Contreras Contreras E. López Tiro J. Gómez Vera J. Omalizumab (an anti-IgE antibody) in the treatment of severe atopic eczema.J Investig Allergol Clin Immunol. 2011; 21: 416-417PubMed Google Scholar 2011∗Studies without clinical response rate and data of individual patients.Case series11 OMANASystemic therapy/NAGeneral improvement in SCORAD and quality-of-life scoresHeil et al,6Heil P.M. Maurer D. Klein B. Hultsch T. Stingl G. Omalizumab therapy in atopic dermatitis: depletion of IgE does not improve the clinical course—a randomized, placebo-controlled and double blind pilot study.J Dtsch Dermatol Ges. 2010; 8: 990-998PubMed Google Scholar 2010∗Studies without clinical response rate and data of individual patients.RCT7 placebo, 13 OMA0.016 mg/kg/IgE (IU/mL) q4w for 4 moNA/topical hydrocortisone onlyOMA reduced IgE-related parameters without significant changes in clinical parameters. The therapeutic benefit of OMA might be seen more in acute AD than in chronic ADThaiwat and Sangasapaviliya,E4Thaiwat S. Sangasapaviliya A. Omalizumab treatment in severe adult atopic dermatitis.Asian Pac J Allergy Immunol. 2011; 29: 357-360PubMed Google Scholar 2011Case series3 OMA300 mg OMA q2-4w for 4 mo (8 cycles)Systemic steroids/NAImprovement in EASI and pruritic scores without adverse effectKim et al,E5Kim D.H. Park K.Y. Kim B.J. Kim M.N. Mun S.K. Anti-immunoglobulin E in the treatment of refractory atopic dermatitis.Clin Exp Dermatol. 2013; 38: 496-500Crossref PubMed Scopus (53) Google Scholar 2013Case series10 OMA300 mg OMA q2w for 4 mo (8 cycles)≥1 systemic steroid, Csa, UV and free for 6 wk/topical steroid onlyEvident clinical improvement after 2 mo of treatment. Maybe valuable for treatment-resistant AD with high IgEFernandez-Anton Martinez et al,E6Fernandez-Anton Martinez M.C. Leis-Dosil V. Alfageme-Roldan F. Paravisini A. Sánchez-Ramón S. Suárez Fernández R. Omalizumab for the treatment of atopic dermatitis.Actas Dermosifiliogr. 2012; 103: 624-628Crossref PubMed Scopus (31) Google Scholar 2012Case series8 OMA450 mg OMA q3w (n = 6), 300 mg q2w (n = 1), and 600 mg q3w (n = 1) for 3-18 moSystemic steroid and ISA/oral antihistamines and topical agentsOMA as a safe drug that can be useful for severe ADLacombe Barrios et al,E7Lacombe Barrios J. Begin P. Paradis L. Hatami A. Paradis J. Des Roches A. Anti-IgE therapy and severe atopic dermatitis: a pediatric perspective.J Am Acad Dermatol. 2013; 69: 832-834Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar 2013Case series7 OMA225-375 mg q2w for 12-67 mo. One dropout due to scheduling reasonCsa and ISA/oral antihistamines and topical agentsClinical improvement first after 3-6 mo. Mean SCORAD improvement of 45.6 at 12 mo and a mean IgE reduction of 60.5%Iyengar et al,7Iyengar S.R. Hoyte E.G. Loza A. Bonaccorso S. Chiang D. Umetsu D.T. et al.Immunologic effects of omalizumab in children with severe refractory atopic dermatitis: a randomized, placebo-controlled clinical trial.Int Arch Allergy Immunol. 2013; 162: 89-93Crossref PubMed Scopus (102) Google Scholar 2013RCT4 placebo, 4 OMA150-375 mg q2-4w for 6 moNA/cetirizine and topical agents (triamcinolone and pimecrolimus)Decrease in TSLP, TARC, and OX40 L but comparable clinical effect with the control groupHotze et al,8Hotze M. Baurecht H. Rodriguez E. Chapman-Rothe N. Ollert M. Fölster-Holst R. et al.Increased efficacy of omalizumab in atopic dermatitis patients with wild-type filaggrin status and higher serum levels of phosphatidylcholines.Allergy. 2014; 69: 132-135Crossref PubMed Scopus (79) Google Scholar 2014Case series20 OMA150-300 mg q2w for 7 mo (14 cycles)Systemic steroid/NAAll 8 responders were nonfilagrin carriers and showed a higher level of glycophospholipidsRomano et al,E8Romano C. Sellitto A. De Fanis U. Balestrieri A. Savoia A. Abbadessa S. et al.Omalizumab for difficult-to-treat dermatological conditions: clinical and immunological features from a retrospective real-life experience.Clin Drug Investig. 2015; 35: 159-168Crossref PubMed Scopus (26) Google Scholar 2015Case series3 OMA300-450 mg OMA q2w for 7, 18, and 42 mo. One dropoutSystemic steroids, Csa/topical steroid onlyOMA can be considered for refractory AD if total IgE level falls within the range of neutralization by the mAbCsa, Cyclosporin A; ISA, immunosuppressants; NA, no data available; OMA, omalizumab; TARC, thymus and activation-regulated chemokine; TSLP, thymic stromal lymphopoietin; q2w or q3w, in 2-wk or 3-wk interval; UV, ultraviolet light treatment.∗ Studies without clinical response rate and data of individual patients. Open table in a new tab Table IISummary of clinical and therapeutic data of patients with AD from included studiesStudyMean age (y)Baseline mean IgE (IU/mL)Baseline disease severity scores∗SCORAD, EASI, or IGA scores were specified.Posttreatment disease severityClinical response†Percentages of patients with excellent clinical response, satisfying clinical response, and no relevant clinical changes or deterioration (top-down order). (%)Major adverse event (%)Mean treatment duration (mo)Krathen and Hsu,2Krathen R.A. Hsu S. Failure of omalizumab for treatment of severe adult atopic dermatitis.J Am Acad Dermatol. 2005; 53: 338-340Abstract Full Text Full Text PDF PubMed Scopus (154) Google Scholar 200539.3 ± 7.617,613Severe‡Severity was defined as severe in the original study without mentioning the use of any specific scoring system.NA3 of 3 (100)0004Lane et al,3Lane J.E. Cheyney J.M. Lane T.N. Kent D.E. Cohen D.J. Treatment of recalcitrant atopic dermatitis with omalizumab.J Am Acad Dermatol. 2006; 54: 68-72Abstract Full Text Full Text PDF PubMed Scopus (171) Google Scholar 200611 ± 1.13,666.7Around 80% BSANA2 of 3 (66.6)1 of 3 (33.3)006Vigo et al,4Vigo P.G. Girgis K.R. Pfuetze B.L. Critchlow M.E. Fisher J. Hussain I. Efficacy of anti-IgE therapy in patients with atopic dermatitis.J Am Acad Dermatol. 2006; 55: 168-170Abstract Full Text Full Text PDF PubMed Scopus (120) Google Scholar 200631.6 ± 17.91,062.8IGA 2-4IGA 0-23 of 7 (42.9)2 of 7 (28.6)2 of 7 (28.6)03-7Belloni et al,E1Belloni B. Ziai M. Lim A. Lemercier B. Sbornik M. Weidinger S. et al.Low-dose anti-IgE therapy in patients with atopic eczema with high serum IgE levels.J Allergy Clin Immunol. 2007; 120: 1223-1225Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar 200736.8 ± 8.715,095.460.1 ± 13.346.2 ± 19.32 of 11 (18.2)4 of 11 (36.4)5 of 11 (27.3)05Sheinkopf et al,5Sheinkopf L.E. Rafi A.W. Do L.T. Katz R.M. Klaustermeyer W.B. Efficacy of omalizumab in the treatment of atopic dermatitis: a pilot study.Allergy Asthma Proc. 2008; 29: 530-537Crossref PubMed Scopus (125) Google Scholar 200842.9 ± 14.91,520.7Modified IGA 8.3 ± 4.1Modified IGA 2 ± 2.116 of 21 (76.2)5 of 21 (23.8)009-12Amrol,E2Amrol D. Anti-immunoglobulin E in the treatment of refractory atopic dermatitis.South Med J. 2010; 103: 554-558Crossref PubMed Scopus (32) Google Scholar 201018.7 ± 17.014,08374.2 ± 3.634.8 ± 18.51 of 3 (33.3)2 of 3 (66.6)003Thaiwat and Sangasapaviliya,E4Thaiwat S. Sangasapaviliya A. Omalizumab treatment in severe adult atopic dermatitis.Asian Pac J Allergy Immunol. 2011; 29: 357-360PubMed Google Scholar 201132.7 ± 8.7489.8EASI 10EASI 6.601 of 3 (33.3)2 of 3 (66.6)04Kim et al,E5Kim D.H. Park K.Y. Kim B.J. Kim M.N. Mun S.K. Anti-immunoglobulin E in the treatment of refractory atopic dermatitis.Clin Exp Dermatol. 2013; 38: 496-500Crossref PubMed Scopus (53) Google Scholar 201326.1 ± 5.51,704 to >5,00056.5 ± 8.442.2 ± 9.02 of 10 (20)5 of 10 (50)3 of 10 (30)04Fernandez-Anton Martinez et al,E6Fernandez-Anton Martinez M.C. Leis-Dosil V. Alfageme-Roldan F. Paravisini A. Sánchez-Ramón S. Suárez Fernández R. Omalizumab for the treatment of atopic dermatitis.Actas Dermosifiliogr. 2012; 103: 624-628Crossref PubMed Scopus (31) Google Scholar 201231.0 ± 15.19,169.1Severe‡Severity was defined as severe in the original study without mentioning the use of any specific scoring system.NA2 of 8 (25)0 (0)6 of 8 (75)1 (vasovagal)3-18Lacombe Barrios et al,E7Lacombe Barrios J. Begin P. Paradis L. Hatami A. Paradis J. Des Roches A. Anti-IgE therapy and severe atopic dermatitis: a pediatric perspective.J Am Acad Dermatol. 2013; 69: 832-834Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar 201311.6 ± 6.21,068 (218-1,890)77.1 ± 24.538.9 ± 27.26 of 7 (85.7)1 of 7 (14.3)006Iyengar et al,7Iyengar S.R. Hoyte E.G. Loza A. Bonaccorso S. Chiang D. Umetsu D.T. et al.Immunologic effects of omalizumab in children with severe refractory atopic dermatitis: a randomized, placebo-controlled clinical trial.Int Arch Allergy Immunol. 2013; 162: 89-93Crossref PubMed Scopus (102) Google Scholar 201310.6 ± 5.116,007 (7,520-35,790)75.4 ± 13.330.1 ± 9.81 of 4 (25)03 of 4 (75)029.3Hotze et al,8Hotze M. Baurecht H. Rodriguez E. Chapman-Rothe N. Ollert M. Fölster-Holst R. et al.Increased efficacy of omalizumab in atopic dermatitis patients with wild-type filaggrin status and higher serum levels of phosphatidylcholines.Allergy. 2014; 69: 132-135Crossref PubMed Scopus (79) Google Scholar 201423-76935.545.8 ± 15.140.5 ± 23.04 of 20 (20)4 of 20 (20)12 of 20 (60)07Romano et al,E8Romano C. Sellitto A. De Fanis U. Balestrieri A. Savoia A. Abbadessa S. et al.Omalizumab for difficult-to-treat dermatological conditions: clinical and immunological features from a retrospective real-life experience.Clin Drug Investig. 2015; 35: 159-168Crossref PubMed Scopus (26) Google Scholar 201520.3 ± 1.53,961.746.3 ± 3.514.3 ± 15.02 of 3 (66.6)1 of 3 (33.3)0022.3Overall total data (N = 103)30.2 ± 15.1 (N = 83)6,838 (N = 83)65.1 ± 17.1 (SCORAD)36.8 ± 20.9 (SCORAD)44 of 103 (42.7)26 of 103 (25.2)33 of 103 (32.1)13-29Data expressed as mean ± SD (if available) or percentage.Comparisons by ANOVA or the χ2 test.BSA, Body surface area; NA, no data available.∗ SCORAD, EASI, or IGA scores were specified.† Percentages of patients with excellent clinical response, satisfying clinical response, and no relevant clinical changes or deterioration (top-down order).‡ Severity was defined as severe in the original study without mentioning the use of any specific scoring system. Open table in a new tab Csa, Cyclosporin A; ISA, immunosuppressants; NA, no data available; OMA, omalizumab; TARC, thymus and activation-regulated chemokine; TSLP, thymic stromal lymphopoietin; q2w or q3w, in 2-wk or 3-wk interval; UV, ultraviolet light treatment. Data expressed as mean ± SD (if available) or percentage. Comparisons by ANOVA or the χ2 test. BSA, Body surface area; NA, no data available. An excellent clinical response was defined as a SCORAD reduction of more than 50%, or an EASI reduction of more than 75% or total clearance (improvement to IGA 0), or an improvement of 2-degree or more in IGA/modified IGA severity (eg, severe to mild). Satisfying clinical response was a SCORAD reduction between 25% and 50%, or an EASI reduction between 25% and 50%, or a 1-degree improvement in IGA/modified IGA severity (eg, moderate to mild). No relevant clinical change was defined by a reduction in SCORAD of less than 25% or in EASI of less than 50%, or identical IGA severity status. Deterioration after the treatment was defined as a SCORAD increase of more than 25%. Disease severity was defined as mild, moderate, or severe. SCORAD values ranged from 0 to 103 ( 50, severe AD). IGA scores ranged from 0 to 5 (0, clear; 1, almost clear; 2, mild; 3, moderate; 4, severe; 5, very severe). EASI scores ranged from 0 to 72 (0, clear; 0.1-1.0, almost clear; 1.1-7.0, mild; 7.1-21.0, moderate; 21.1-50.0, severe; 50.1-72.0, very severe). Modified IGA scores ranged from 0 to 18 (1-6, mild; 7-12, moderate; 13-18, severe). The clinical response and severity were defined as in each original study if no aforementioned scoring system was used. A total of 15 studies (2 RCTs and 13 case series with ≥3 cases included) were recruited (Table I) and 13 studies (103 patients) were analyzed (Table II). Most of the patients (60.5%) had severe AD at baseline. Seventy-six percent of the patients had a history of allergic asthma. Only 25% of the population displayed total serum IgE values of lower than 700 IU/mL and 43.4% of the patients showed IgE concentrations above 5000 IU/mL. Also, 66.7% of the patients were treated with 600 mg or more of omalizumab per month. Forty-three percent (n = 44 of 103) of the patients achieved excellent clinical response, while 27.2% of the patients showed satisfying results and 30.1% showed irrelevant clinical changes or even deterioration (Table II). Multivariate logistic regression on the 83 patients (12 studies) including all the detailed data showed that IgE serum concentrations of lower than 700 IU/mL were significantly associated with an excellent clinical response, compared with those with IgE concentrations of 700 to 5000 IU/mL (odds ratio, 12.3; 95% CI, 2.46-62.5) and more than 5000 IU/mL (odds ratio, 9.17; 95% CI, 1.83-45.5), respectively. Age, sex, baseline clinical disease severity, the history of concomitant asthma, and the use of 600 mg/month or more of omalizumab regimen showed no significant association with the clinical results associated with omalizumab use. Less than half of the patients with AD in our study had achieved marked clinical improvement after receiving omalizumab. The only 2 RCTs showed a decrease in TH2-mediated cytokines7Iyengar S.R. Hoyte E.G. Loza A. Bonaccorso S. Chiang D. Umetsu D.T. et al.Immunologic effects of omalizumab in children with severe refractory atopic dermatitis: a randomized, placebo-controlled clinical trial.Int Arch Allergy Immunol. 2013; 162: 89-93Crossref PubMed Scopus (102) Google Scholar and prominent changes in IgE-related immunologic parameters.6Heil P.M. Maurer D. Klein B. Hultsch T. Stingl G. Omalizumab therapy in atopic dermatitis: depletion of IgE does not improve the clinical course—a randomized, placebo-controlled and double blind pilot study.J Dtsch Dermatol Ges. 2010; 8: 990-998PubMed Google Scholar However, there was no significant clinical improvement after omalizumab and the clinical effects were comparable only with the control group.6Heil P.M. Maurer D. Klein B. Hultsch T. Stingl G. Omalizumab therapy in atopic dermatitis: depletion of IgE does not improve the clinical course—a randomized, placebo-controlled and double blind pilot study.J Dtsch Dermatol Ges. 2010; 8: 990-998PubMed Google Scholar, 7Iyengar S.R. Hoyte E.G. Loza A. Bonaccorso S. Chiang D. Umetsu D.T. et al.Immunologic effects of omalizumab in children with severe refractory atopic dermatitis: a randomized, placebo-controlled clinical trial.Int Arch Allergy Immunol. 2013; 162: 89-93Crossref PubMed Scopus (102) Google Scholar When initially approved for allergic asthma, omalizumab was indicated for patients with a serum IgE concentration of 30 to 700 IU/mL, and the highest dose was 750 mg/month. Recently, there is an extension of the omalizumab dosing table ranging from 150 to 1200 mg/month, according to the total IgE concentrations within a range between 30 and 1500 IU/mL.9Kornmann O. Watz H. Fuhr R. Krug N. Erpenbeck V.J. Kaiser G. Omalizumab in patients with allergic (IgE-mediated) asthma and IgE/bodyweight combinations above those in the initially approved dosing table.Pulm Pharmacol Ther. 2014; 28: 149-153Crossref PubMed Scopus (25) Google Scholar There is no recommended dosage for patients whose pretreatment serum total IgE concentrations or body weight is outside the limits of the dosing table. However, 75% of the patients with AD in this study had IgE concentrations far exceeding 700 IU/mL and individualized dosing was ineligible for these patients. The dosing regimens were rather arbitrary, ranging from 150 to 900 mg/month in the included studies, which might be insufficient for patients with extremely high IgE concentrations. The association of serum IgE concentrations of less than 700 IU/mL with more favorable clinical responses in this analysis might be explained by better IgE neutralization in patients with lower concentrations of IgE under fixed dosages.5Sheinkopf L.E. Rafi A.W. Do L.T. Katz R.M. Klaustermeyer W.B. Efficacy of omalizumab in the treatment of atopic dermatitis: a pilot study.Allergy Asthma Proc. 2008; 29: 530-537Crossref PubMed Scopus (125) Google Scholar However, the discrepant results of omalizumab in treating AD might be attributed to the complex immune dysregulation of AD other than IgE as the primary pathogenic mechanism. Hotze et al8Hotze M. Baurecht H. Rodriguez E. Chapman-Rothe N. Ollert M. Fölster-Holst R. et al.Increased efficacy of omalizumab in atopic dermatitis patients with wild-type filaggrin status and higher serum levels of phosphatidylcholines.Allergy. 2014; 69: 132-135Crossref PubMed Scopus (79) Google Scholar reported that none of the patients carrying a filaggrin mutation responded to therapy, whereas all responders were nonfilaggrin mutation carriers and characterized by the presence of high concentrations of glycerophospholipids, indicating that patients with primary skin barrier deficiency were less likely to benefit from an immunomodulatory treatment with anti-IgE. The limitations of this review included the fact that most of the existing articles were case series and the sample sizes with complete individual data were rather limited. The disease severity scoring systems also varied among the studies. Few studies provided comprehensive immunologic data that could allow systemic analysis. There was no concrete evidence of the overall effectiveness of omalizumab for AD from this meta-analysis and systematic review based on existing small-scale case series and RCTs. Forty-three percent of the patients with AD could achieve remarkable clinical response after omalizumab treatment. Potential therapeutic benefits might be seen in selected patients with lower serum concentrations of IgE. More RCTs should be performed to clarify the potential benefits in the subgroups of patients with AD. The optimal dosage of omalizumab for patients with AD with higher IgE levels should also be further studied.
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