This is the first investigation, to the best of our knowledge, to underscore the correlates of refractory and NOD within the bariatric context. Further studies are recommended as such information could be valuable for patient selection, prognostic scoring, and outcome monitoring.

The most common complication of silicone breast implants is capsular contracture (massive scar formation around the implant). We postulate that capsular contracture is always a sequel to inflammatory processes, with both innate and adaptive immune mechanisms participating. In general, fibroblasts and macrophages have been used as cell types to evaluate in vitro the biocompatibility of breast implant surfaces. Moreover, also T cells have been found at the implant site at the initial stage of fibrous capsule formation. However, only few studies have addressed the influence of surfaces with different textures on T-cell responses. The aim of the present study was to investigate the immune response of human peripheral blood mononuclear cells (PBMC) to commercially available silicone breast implants in vitro. PBMC from healthy female blood donors were cultured on each silicone surface for 4 days. Proliferation and phenotype of cultured cells were assessed by flow cytometry. Cytokine levels were determined by multiplex and real-time assay. We found that silicone surfaces do not induce T-cell proliferation, nor do they extensively alter the proportion of T cell subsets (CD4, CD8, naïve, effector memory). Interestingly, cytokine profiling identified matrix specific differences, especially for IL-6 and TNF-α on certain surface topographies that could lead to increased fibrosis.

Diabetes response was confirmed, however with more refractory cases than in bariatric controls, whereas high proportions of NOD occurred. Such dichotomous pattern seems unusual albeit consistent with previous studies.

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Diabetes regression rate was 94.3% at 5 years and 84.7% at around 8 years. In responsive patients, both BMI and biochemical indices normalized in the first 2 years and followed a stable path thereafter. Nonoperative treatment was unable to reduce HbA1c, glucose, or WBC count, and HbA1c was a clear prognostic marker of persistent disease in surgical cases. Further studies emphasizing the metabolic and inflammatory signature of obesity-related diabetes are worthwhile.