Autoimmunity and hernia mesh: fact or fiction?

BACKGROUND: There is an increasing number of patients following hernia surgery with implanted mesh reporting symptoms that could indicate autoimmune or allergic reactions to mesh. 'Allergy' to metals, various drugs, and chemicals is well recognised. However, hypersensitivity, allergy or autoimmunity caused by surgical mesh has not been proven by a scientific method to date. The aim of this study was twofold: to describe the pathophysiology of autoimmunity and foreign body reaction and to undertake a systematic review of surgical mesh implanted at the time of hernia repair and the subsequent development of autoimmune disease. METHODS: A systematic review using the PRISMA guidelines was undertaken. Pubmed (Medline), Google Scholar and Cochrane databases were searched for all English-written peer-reviewed articles published between 2000 and 2021. The search was performed using the keywords "hernia", "mesh", "autoimmunity", "ASIA", "immune response", "autoimmune response". RESULTS: Seven papers were included in the final analysis-three systematic reviews, three cohort studies and one case report. Much of the current data regarding the association of hernia mesh and autoimmunity relies on retrospective cohort studies and/or case reports with limited availability of cofounding factor data linked to autoimmune disease such as smoking status or indeed a detailed medical history of patients. Three systematic reviews have discussed this topic, each with a slightly different approach and none of them has identified causality between the use of mesh and the subsequent development of autoimmune disease. CONCLUSION: There is little evidence that the use of polypropylene mesh can lead to autoimmunity. A large number of potential triggers of autoimmunity along with the genetic predisposition to autoimmune disease and the commonality of hernia, make a cause and effect difficult to unravel at present. Biomaterials cause foreign body reactions, but a chronic foreign body reaction does not indicate autoimmunity, a common misunderstanding in the literature.

Surgical therapy of chronic lung allograft dysfunction.

Lung transplantation has become a standardized and widely accepted treatment modality for selected end-stage lung diseases. Many factors influ- ence the long-term survival of patients after lung transplantation. One of the most important is clearly the development of chronic lung allograft dysfunction (CLAD). This review summarizes current knowledge of the histopathology of CLAD and its clinical characteristics. It also describes lung re-transplantation as the only causal therapy, its possible complications, and outcomes in standard and high-urgency patients awaiting a suitable organ with extracorporeal membrane oxygenation support. Fundoplication is an important surgical modality potentially leading to an improvement of the patients' condition. The indications and outcomes of this surgical procedure are discussed in a separate chapter. In addition, several nonsurgical treatment options aimed at slowing the progression of CLAD are outlined, as well as ongoing research focused on extending the life of these patients.

The first lung retransplantation with “ECMO bridge” in the Czech Republic - case report.

During the last 23 years of the National Lung Transplant Program in the Czech Republic, more than 500 lung transplantations, 4 retransplantations and one lobar retransplantation have been performed. We present the case report of a female patient with cystic fibrosis who underwent her first bilateral lung transplantation in January 2020. Due to a chronic lung allograft dysfunction, the patient required ECMO support and retransplantation. For the first time in the Czech Republic, a lung retransplantation with “ECMO bridge to (re)transplantation” preoperative support was performed in April 2021. The patient was discharged 39 days after retransplantation in a stable condition. At the day 90 follow-up visit, the patient was in a generally good condition with satisfying spirometric functions.

SARS-CoV-2 viral load assessment in lung transplantation.

In the era of COVID-19 pandemic, organ transplantation programs were facing serious challenges. The lung transplantation donor pool was extremely limited and SARS-CoV-2 viral load assessment has become a crucial part of selecting an optimal organ donor. Since COVID-19 is a respiratory disease, the viral load is thought to be more important in lung transplantations as compared to other solid organ transplantations. We present two challenging cases of potential lung donors with a questionable COVID-19 status. Based on these cases, we suggest that the cycle threshold (Ct) value should always be requested from the laboratory and the decision whether to proceed with transplantation should be made upon complex evaluation of diverse criteria, including the nasopharyngeal swab and bronchoalveolar lavage PCR results, the Ct value, imaging findings and the medical history. However, as the presence of viral RNA does not ensure infectivity, it is still to be clarified which Ct values are associated with the viral viability. Anti-SARS-CoV-2 IgA antibodies may support the diagnosis and moreover, novel methods, such as quantifying SARS-CoV-2 nucleocapsid antigen in serum may provide important answers in organ transplantations and donor selections.

COVID-19 and the immune system.

A close interaction between the virus SARS-CoV-2 and the immune system of an individual results in a diverse clinical manifestation of the COVID-19 disease. While adaptive immune responses are essential for SARS-CoV-2 virus clearance, the innate immune cells, such as macrophages, may contribute, in some cases, to the disease progression. Macrophages have shown a significant production of IL-6, suggesting they may contribute to the excessive inflammation in COVID-19 disease. Macrophage Activation Syndrome may further explain the high serum levels of CRP, which are normally lacking in viral infections. In adaptive immune responses, it has been revealed that cytotoxic CD8+ T cells exhibit functional exhaustion patterns, such as the expression of NKG2A, PD-1, and TIM-3. Since SARS-CoV-2 restrains antigen presentation by downregulating MHC class I and II molecules and, therefore, inhibits the T cell-mediated immune responses, humoral immune responses also play a substantial role. Specific IgA response appears to be stronger and more persistent than the IgM response. Moreover, IgM and IgG antibodies show similar dynamics in COVID-19 disease.