Publication: Association Between Secondary Botulinum Toxin A Treatment Failure in Cosmetic Indication and Anti-Complexing Protein Antibody Production
Issued Date
2020-01-01
Resource Type
ISSN
21909172
21938210
21938210
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2-s2.0-85085307229
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Mahidol University
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SCOPUS
Bibliographic Citation
Dermatology and Therapy. (2020)
Suggested Citation
Rungsima Wanitphakdeedecha, Watsachon Kantaviro, Panittra Suphatsathienkul, Ploypailin Tantrapornpong, Chadakan Yan, Chalermkwan Apinumtham, Yuttana Srinoulprasert Association Between Secondary Botulinum Toxin A Treatment Failure in Cosmetic Indication and Anti-Complexing Protein Antibody Production. Dermatology and Therapy. (2020). doi:10.1007/s13555-020-00397-5 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/56289
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Title
Association Between Secondary Botulinum Toxin A Treatment Failure in Cosmetic Indication and Anti-Complexing Protein Antibody Production
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Abstract
© 2020, The Author(s). Introduction: Botulinum toxin A (BoT/A) treatment failure (BTF) affects patients subjected to repeated BoT/A exposure for cosmetic indications. BoT/A’s general formulation contains core BoT/A and complexing proteins. BTF may be caused by antibody-induced treatment failure. Antibodies against core BoT/A can occur; however, anti-complexing protein antibodies have never been demonstrated, and tools for anti-complexing protein antibody detection have not been developed. The aim of this study was to evaluate immune involvement in BoT/A-nonresponsive patients. Methods: Patients suspected of nonresponsiveness to BoT/A for cosmetic indications were recruited. All volunteers were categorized as BoT/A-responsive or BoT/A-tolerant according to frontalis testing with onabotulinumtoxinA (onaA). Twenty-two BoT/A-tolerant volunteers were recruited separately for frontalis testing with incobotulinumtoxinA (incoA). Anti-BoT/A and anti-complexing protein antibodies were quantified by special ELISA using sera from blood sampled before and after frontalis testing. Results: Significantly higher levels of IgG against complexing protein were detected in onaA-tolerant sera but not in onaA-responders, leading to proposals that anti-complexing protein antibodies could cause onaA unresponsiveness. Some onaA-tolerant patients according to frontalis test with incoA were responsive to incoA. Newly developed absorption ELISA confirmed that incoA-responsive sera predominantly contained IgG against complexing proteins, whereas incoA-tolerant sera contained significant levels of IgG against core BoT/A. The presence of anti-complexing protein antibodies higher than 90.75% in sera of onaA-tolerant patients could respond to incoA. The ELISA technique might be employed as a tool to predict incoA responsiveness. Our frontalis testing after incoA treatment showed that anti-incoA IgG levels were not increased by incoA. Conclusions: BoT/A-exposed patients may develop antibodies against core botulinum toxin and complexing proteins. Our study is the first to demonstrate that anti-complexing protein antibodies cause BTF. High levels of antibodies against complexing proteins can cause onaA unresponsiveness, although some patients were still incoA-responsive. Our developed ELISA to detect anti-complexing protein antibodies can determine whether onaA-tolerant patients respond to incoA without incoA frontalis testing.