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RISS 인기검색어
- 검색키워드
- 저자 : Wareeporn Disphanurat (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
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Peera Thienpaitoon,Wareeporn Disphanurat,Naree Warnnissorn 대한성형외과학회 2020 Archives of Plastic Surgery Vol.47 No.5
Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) has received increasing interest among plastic surgeons as a long-term complication of breast augmentation. Although the prognosis is usually good, mortality is a possible outcome. Most of the cases reported in the past two decades have been from the United States, Europe, and Australia, whereas cases of BIA-ALCL in Asia remain rare. Herein, we describe the first known case of BIA-ALCL in Thailand, in which a 32-year-old woman developed BIA-ALCL 3 years after breast augmentation using textured implants. The patient underwent bilateral removal of the implants and ipsilateral total capsulectomy. This case report—the first of its kind from Thailand—should increase awareness of BIA-ALCL among plastic surgeons in Asia. The true incidence of BIA-ALCL in Asia may be underreported.
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Klaewsongkram Jettanong,Buranapraditkun Supranee,Thantiworasit Pattarawat,Rerknimitr Pawinee,Tuchinda Papapit,Chularojanamontri Leena,Rerkpattanapipat Ticha,Chanprapaph Kumutnart,Disphanurat Wareeporn 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.6
Propose: The purpose of this study was to investigate panels of enzyme-linked immunospot assays (ELISpot) to detect drug-specific mediator releasing cells for confirming culprit drugs in severe cutaneous adverse reactions (SCARs). Methods: Frequencies of drug-induced interleukin-22 (IL-22)-, interferon-gamma (IFN-γ)-, and granzyme-B (GrB)-releasing cells were measured by incubating peripheral blood mononuclear cells (PBMCs) from SCAR patients with the culprit drugs. Potential immunoadjuvants were supplemented to enhance drug-induced mediator responses. Results: Twenty-seven patients, including 9 acute generalized exanthematous pustulosis (AGEP), 10 drug reactions with eosinophilia and systemic symptoms, and 8 Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) were recruited. The average frequencies of drug-induced IL-22-, IFN-γ-, and GrB-releasing cells were 35.5±16.3, 33.0±7.1, and 164.8±43.1 cells/million PBMCs, respectively. The sensitivity of combined IFN-γ/IL-22/GrB ELISpot was higher than that of IFN-γ ELISpot alone for culprit drug detection in all SCAR subjects (77.8% vs 51.9%, P < 0.01). The measurement of drug-induced IL-22- and IFN-γ releasing cells confirmed the culprit drugs in 77.8% of AGEP. The measurement of druginduced IFN-γ- and GrB-releasing cells confirmed the culprit drugs in 62.5% of SJS/TEN. Alpha-galactosylceramide supplementation significantly increased the frequencies of druginduced IFN-γ releasing cells. Conclusion: The measurement of drug-induced IFN-γ-releasing cells is the key for identifying culprit drugs. The additional measurement of drug-induced IL-22-releasing cells enhances ELISpot sensitivity to identify drug-induced AGEP, while the measurement of drug-induced GrB-releasing cells could have a role in SJS/TEN. ELISpot sensitivity might be improved by supplementary alpha-galactosylceramide.
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