■为了研究乳房植入物疾病(BII)与肥大细胞活化综合征(MCAS)之间的可能关联,通常表现为各种组织中肥大细胞(MC)增加,并可能解释BII症状。
■植入物引起BII症状的机制尚不清楚,但是BII和MCAS症状特征严重重叠,保证对潜在联系的调查。
■我们回顾性分析了20例接受了移植和全囊切除术的植入物患者;15例自我报告术前有BII(受试者组);5例认为他们没有[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CG1患者在术前和术后多个点完成BII症状问卷。用CD117染色,确定切除组织中的平均和最大肥大细胞计数(MCC)。
■移植后2周平均BII症状评分降低77%(P<0.0001),到9个月,85%。分析提示CG1患者的BII,也是,他们也有类似的进步。在CG2患者中,健康乳腺组织显示平均和最大MCC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,CG1患者为7.6/hpf和13.3/hpf。所有组间比较均有显著差异(P<0.0001)。
■BII患者植入周围胶囊中的MCC增加;一些植入患者似乎未识别BII。鉴于新抗原/异种生物暴露通常会引发MCAS中功能失调的MC,以提高驱动炎症和其他问题的异常介质表达,进一步调查BII是否代表植入驱动的已有MCAS升级,以及MCAS诊断是否标志着BII的风险.
UNASSIGNED: 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.
UNASSIGNED: Mechanisms by which implants cause BII symptoms remain unclear, but BII and MCAS symptom profiles heavily overlap, warranting investigation of potential linkage.
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.