We conclude that routine setup and use of rapid autotransfusion devices may not be necessary in every patient undergoing routine aortofemoral bypass for occlusive disease. Furthermore, the possibility that some patients may undergo AAA repair with tube grafts without use of the Cell Saver may be deserving of further investigation.

Background. Breast implants are commonly placed postbreast cancer reconstruction, cosmetic augmentation, and gender-affirming surgery. Breast implant illness (BII) is a systemic complication associated with breast implants. Patients with BII may experience autoimmune symptoms including fatigue, difficulty concentrating, hair loss, weight change, and depression. BII is poorly understood, and the etiology is unknown. The purpose of this literature review is to characterize BII autoimmune disorders and determine possible causes for its etiology. Methods. The PubMed, Google Scholar, Embase, Web of Science, and OVID databases were interrogated from 2010 to 2020 using a query strategy including search term combinations of “implants,” “breast implant illness,” “autoimmune,” and “systemic illness.” Results. BII includes a spectrum of autoimmune symptoms such as fatigue, myalgias/arthralgias, dry eyes/mouth, and rash. A review of epidemiological studies in the past ten years exhibited evidence affirming an association between breast implants and autoimmune diseases. The most commonly recognized were Sjogren’s syndrome, rheumatoid arthritis, systemic sclerosis, chronic fatigue syndrome, and Raynaud’s syndrome. Explantation resulted in alleviation of symptoms in over 50% of patients, strengthening the hypothesis linking breast implants to BII. Studies have shown that silicone is a biologically inert material and unlikely to be the cause of these symptoms. This is supported by the fact that increased risk of autoimmune disease was also reported in patients with other implantable biomaterials such as orthopedic implants. Recent studies shed light on a possible role of bacterial biofilm and subsequent host-pathogen interactions as a confounding factor to this problem. Conclusion. BII could be dependent on biofilm infection and the microenvironment around the implants. The true pathophysiology behind these complaints must be further investigated so that alternative treatment regimens other than explantation can be developed. Translational significance of these studies is not limited to breast implants but extends to other implants as well.

Over 10 million women worldwide have breast implants for breast cancer/prophylactic reconstruction or cosmetic augmentation. In recent years, a number of patients have described a constellation of symptoms that are believed to be related to their breast implants. This constellation of symptoms has been named Breast Implant Illness (BII). The symptoms described include chronic fatigue, joint pain, muscle pain and a host of other manifestations often associated with autoimmune illnesses. In this work, we report that bacterial biofilm is associated with BII. We postulate that the pathogenesis of BII is mediated via a host-pathogen interaction whereby the biofilm bacteria Staphylococcus epidermidis interacts with breast lipids to form the oxylipin 10-HOME. The oxylipin 10-HOME was found to activate CD4+ T cells to Th1 subtype. An increased abundance of CD4+Th1 was observed in the breast tissue of BII subjects. The identification of a mechanism of immune activation associated with BII via a biofilm enabled pathway provides insight into the pathogenesis for implant-associated autoimmune symptoms.

No abstract

Purpose: Breast Implant Illness (BII) is patient-described constellation of symptoms that are believed to be related to their breast implant. The symptoms described include fibromyalgia, chronic fatigue and a host of other symptoms that are often associated with autoimmune illnesses. In this work, we report that bacterial biofilm associated with breast implant, metabolize fatty acid oleic acid present in the breast tissue milieu to oxylipins, one such oxylipin identified from this study is (10S)-hydroxy-(8E)-octadecenoic acid (10-HOME). We hypothesize that immunomodulatory effects of oxylipin 10-HOME produced by biofilm present on the implant could be correlated with BII pathogenesis. Methods: Capsulectomy and breast implants from clinically indicated procedures for patients requesting prosthetic removal were collected using clinical parameters outlined in previous studies, and questionnaire screened for the commonly reported symptoms associated with BII. Predictive variables included age, diabetes status, co-morbidities, nature and duration of implant. Scanning electron microscopy (SEM), Wheat Germ Agglutinin (WGA) and 16SrRNA sequencing were used for bacterial biofilm bacterial identification. 10-HOME was quantitated through targeted and untargeted lipidomic analyses using LC-MS-MS. Results: Sixty eight Implant, associated capsules and breast tissue specimen were collected for BII (n=46) and two control groups, group I, (non-BII, n=14) patients with breast implants, no BII symptoms. Group II (normal tissue, n = 8), patients without an implant, whose breast tissue was removed due to surgical procedures. Bacterial biofilm was detected through SEM in both BII and non BII cohorts. However, WGA analysis (quantitative analysis) indicated increased abundance of biofilm in the BII cohort (n=7, p=0.0036). 16SrRNA (genomic) sequencing identified increased abundance of Staphylococcus epidermidis (Fisher’s exact test, p<0.001) in the BII group (63.04%) compared to non-BII group (14.3%) and the normal group. The BII group was 9.8 times significantly more likely to have Staphylococcus epidermidis colonization compared to the non-BII group (p=0.003, logistic regression), compared to normal, it is 17.4 times significantly more likely to have Staphylococcus epidermidis (p=0.0021). Elevated levels of 10-HOME BII compared to non-BII samples, (p < 0.0001) were observed through mass spectrometry. Positive correlation was observed between bacterial abundance and concentration of 10-HOME in BII subjects (R2=0.88). Similar correlation was observed in BII subjects with Staphylococcus epidermidis (R2=0.77). Conclusion: This study investigated the biofilm hypothesis of breast implant illness through a host-pathogen interaction. The breast microenvironment led to formation of biofilm derived 10-HOME from host oleic acid. The study provides the first evidence of a possible correlation between bacterial biofilm and biofilm derived 10-HOM...