7 research outputs found

    Thu0349 autologous fat grafting in the treatment of patients with systemic sclerosis: current experience and future prospects

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    none13nomixedSpinella, Amelia; Pignatti, Marco; Citriniti, Giorgia; Lumetti, Federica; Cocchiara, Emanuele; Palermo, Adalgisa; Sighinolfi, Gianluca; Pacchioni, Lucrezia; Zaccaria, Giovanna; Lusetti, Irene Laura; Santis, Giorgio De; Salvarani, Carlo; Giuggioli, DiliaSpinella, Amelia; Pignatti, Marco; Citriniti, Giorgia; Lumetti, Federica; Cocchiara, Emanuele; Palermo, Adalgisa; Sighinolfi, Gianluca; Pacchioni, Lucrezia; Zaccaria, Giovanna; Lusetti, Irene Laura; Santis, Giorgio De; Salvarani, Carlo; Giuggioli, Dili

    “Infections of scleroderma digital ulcers: a single center cohort retrospective study”

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    BACKGROUNDS: Systemic Sclerosis (SSc) is a complex autoimmune and up to fifty percent of patients develop digital ulcers. AIMS: Understand how much infections influence scleroderma digital ulcers’ healing. METHODS: We revised fifty consecutive patients with SSc-related DUs who referred to our Scleroderma Unit. Thirty-five of them who showed clear signs of DUs infection underwent to cutaneous swab and microbiological data collection. We performed 87 cutaneous swabs overall.  RESULTS: DUs were recurrent in 58% of the patients and multiple in 60% of patients. Fourty-four swabs (53%) were positive for Staphylococcus Aureus (13% Methicillin-Resistant), 9 were positive for Pseudomonas Aeruginosa (Pseudomonas A.) (10%), and then the others less frequently isolated. Twenty-fifth percent of patients needed hospitalization. CONCLUSIONS: Our data support a patient-tailored approached to DUs, particularly those infected. Self-hygiene and asepsis during dressing procedures are mandatory. Patient must be trained to avoid dangerous  behaviors and reduce the risk of infection

    Neutrophil-mediated mechanisms of damage and in vitro protective effect of colchicine in non-vascular Behçet's syndrome

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    Behçet’s syndrome (BS) is a systemic vasculitis with several clinical manifestations. Neutrophil hyperactivation mediates vascular BS pathogenesis, via both a massive reactive oxygen species (ROS) production and neutrophil extracellular traps (NETs) release. Here, we investigated neutrophil‐mediated mechanisms of damage in non‐vascular BS manifestations and explored the in‐vitro effects of colchicine in counteracting these mechanisms. NETs and intracellular ROS production was assessed in blood samples from 80 BS patients (46 with active non‐vascular BS, 34 with inactive disease) and 80 healthy controls. Moreover, isolated neutrophils were incubated for 1 h with an oxidating agent [2,2â€Č‐azobis (2‐amidinopropane) dihydrochloride; 250 nM] and the ability of pure colchicine pretreatment (100 ng/ml) to counteract oxidation‐induced damage was assessed. Patients with active non‐vascular BS showed remarkably increased NET levels [21.2, interquartile range (IQR) = 18.3–25.9 mU/ml] compared to patients with inactive disease (16.8, IQR = 13.3–20.2 mU/ml) and to controls (7.1, IQR = 5.1–8.7 mU/ml, p < 0.001]. Also, intracellular ROS tended to increase in active BS, although not significantly. In active non‐vascular BS, NETs correlated with neutrophil ROS production (p < 0.001) and were particularly increased in patients with active mucosal (p < 0.001), articular (p = 0.004) and gastrointestinal symptoms (p = 0.006). In isolated neutrophils, colchicine significantly reduced oxidation‐induced NET production and cell apoptosis, although not via an anti‐oxidant activity. Neutrophil‐mediated mechanisms might be directly involved in non‐vascular BS, and NETs, more than ROS, might drive the pathogenesis of mucosal, articular and intestinal manifestations. Colchicine might be effective in counteracting neutrophils‐mediated damage in BS, although further studies are needed
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