乳房植入疾病可能源于肥大细胞激活:病例对照回顾性分析

Èva S. Nagy, Mark Westaway, Suzanne Danieletto, Lawrence B. Afrin
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摘要

研究乳房假体植入疾病(BII)与肥大细胞活化综合征(MCAS)之间可能存在的联系,后者通常表现为各种组织中肥大细胞(MC)增多,并可能解释 BII 的症状。 植入物导致 BII 症状的机制尚不清楚,但 BII 和 MCAS 的症状特征严重重叠,因此有必要研究两者之间的潜在联系。 我们回顾性分析了 20 位接受植入物剥离和全帽切除术的植入物患者,其中 15 位术前自述有 BII(受试者组),5 位认为自己没有 BII(对照组 1 (CG1))。5 名预防性乳房切除术患者组成对照组 2(CG2)。受试者和对照组 1 患者在术前和术后多次填写 BII 症状问卷。通过 CD117 染色,确定了切除组织中肥大细胞计数(MCC)的平均值和最高值。 移植后 2 周的平均 BII 症状评分降低了 77%(P < 0.0001),9 个月后降低了 85%。分析表明,CG1 患者的 BII 也有类似改善。在CG2患者中,健康乳腺组织显示的平均和最大MCC分别为5.0/hpf和6.9/hpf。BII患者胶囊中的平均和最大MCC分别为11.7/hpf和16.3/hpf,而CG1患者的平均和最大MCC分别为7.6/hpf和13.3/hpf。所有组间比较均有显著差异(P < 0.0001)。 BII 患者种植体周围囊中的 MCCs 增加;一些种植患者似乎有未被发现的 BII。鉴于新抗原/异生物暴露通常会引发 MCAS 中的 MCs 功能失调,从而增加异常介质的表达,导致炎症和其他问题,因此似乎有必要进一步调查 BII 是否代表种植体驱动的原有 MCAS 的升级,以及 MCAS 诊断是否标志着 BII 的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Breast Implant Illness May Be Rooted in Mast Cell Activation: A Case-Controlled Retrospective Analysis
To investigate the possible association between breast implant illness (BII) and mast cell activation syndrome (MCAS), which often manifests increased mast cells (MCs) in assorted tissues and may explain BII symptoms. Mechanisms by which implants cause BII symptoms remain unclear, but BII and MCAS symptom profiles heavily overlap, warranting investigation of potential linkage. We retrospectively analyzed 20 implant patients who underwent explantation and total capsulectomy; 15 self-reported preoperatively they had BII (subject group); 5 felt they did not [control group 1 (CG1)]. Five prophylactic mastectomy patients constituted control group 2 (CG2). Subjects and CG1 patients completed BII symptom questionnaires preoperatively and multiple points postoperatively. With CD117 staining, average and maximum mast cell counts (MCCs) in resected tissues were determined. Mean BII symptom score 2 weeks postexplantation was reduced by 77% (P < 0.0001), and 85% by 9 months. Analysis suggested BII in CG1 patients, too, who improved similarly. Among CG2 patients, healthy breast tissue showed mean and maximum MCCs of 5.0/hpf and 6.9/hpf. Mean and maximum MCCs in capsules in BII patients were 11.7/hpf and 16.3/hpf, and 7.6/hpf and 13.3/hpf in CG1 patients. All intergroup comparisons were significantly different (P < 0.0001). MCCs in peri-implant capsules in BII patients are increased; some implanted patients appear to have unrecognized BII. Given that neoantigenic/xenobiotic exposures commonly trigger dysfunctional MCs in MCAS to heighten aberrant mediator expression driving inflammatory and other issues, further investigation of whether BII represents an implant-driven escalation of preexisting MCAS and whether an MCAS diagnosis flags risk for BII seems warranted.
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