Explore the vast range of titles available.

Local antibiotic delivery strategies have been increasingly employed for the prevention of fracture-related infections (FRIs). The aim of this study is to evaluate the efficacy and safety of antibiotic-coated implants in the prevention of FRIs after surgical treatment in patients with increased infectious risk. A retrospective observational study has been conducted on patients with upper and lower limb fractures treated with internal fixation or prosthetic replacements, using a gentamicin coated nail (CN) and/or antibiotic-loaded hydrogel applied to the implant of choice (ALH). The study included 37 patients (20 M, 17 F), with a mean age of 63 years. The mean estimated preoperative infectious risk score was 6.4%. ALH was used in 27 cases, tibial CNs were implanted in 4 cases, and both were employed in 6 cases. The antibiotics used locally were gentamicin in 72.97% of cases (27 patients) and a combination of gentamicin + vancomycin in 27.03% of cases (10 patients). Mean follow-up was 32 months. Only one case (2.94%) showed onset of FRI at 5 months after surgery. Local antibiotic prophylaxis by coating resulted in a reduction in the incidence FRI, as compared to the estimated preoperative risk. The use of ALH allows for the choice of antibiotic; however, the application of antibiotics seems more nonuniform when applied to a nail.

In ulcerative colitis (UC), inflammation begins in the rectum and can extend proximally throughout the entire colon. The extension of inflammation is an important determinant of disease course, and may be limited by the action of regulatory T cells (Tregs). In this cross-sectional study, we evaluated the relationship between UC extension and the proportions of CD3+CD4+Foxp3+ and CD3+CD4+LAP+Foxp3-Tregs in the colonic lamina propria (LP) of 79 UC patients and 29 controls. The role of these cells in UC extension was also investigated in the murine oxazolone-induced colitis model. Patients: Disease extension was classified according to the Montreal classification. Where possible, endoscopic biopsies of involved and uninvolved tissue were obtained from UC patients. Mouse model: Colitis was induced by intrarectal oxazolone administration. Lamina propria mononuclear cells were isolated from patient biopsies and mouse colon tissue using enzymatic method and the percentage of CD3+CD4+Foxp3+ and CD3+CD4+LAP+Foxp3-cells evaluated by immunofluorescence. Confocal microscopy was applied for the visualization and quantification of CD4+LAP+ cells on tissue histological sections. In UC patients with distal colitis the proportion of LP CD3+CD4+Foxp3+ Tregs was significantly higher in inflamed tissue than uninvolved tissue. As opposite, the proportion of LP CD3+CD4+LAP+ Tregs was significantly higher in uninvolved tissue than involved tissue. Both LP CD3+CD4+Foxp3+ and LP CD3+CD4+LAP+ Tregs proportion in involved tissue was significantly higher than in controls irrespective of the extension of inflammation. In mice with oxazolone-induced distal colitis, treatment with LAP-depleting antibody was associated with the development of extensive colitis. Our findings suggest that CD3+CD4+LAP+Foxp3-Tregs limit the extension of inflammatory lesions in UC patients.

Background/Aims: In patients with colon cancer who undergo resection for potential cure, 40-60% have advanced locoregional disease (stage III). Those who are suitable for adjuvant treatment had a definite disease-free-survival benefit. The aim of the present study was to demonstrate whether the presence of desmoplasia influenced the mortality rate of stage III colorectal cancer (CRC) within 5 years from the surgery and adjuvant therapy. Patients and Methods: Sixty-five patients with stage III CRC underwent resection and adjuvant therapy. Qualitative categorization of desmoplasia was obtained using Ueno's stromal CRC classification. Desmoplasia was related to mortality using Spearman correlation and stratified with other histological variables (inflammation, grading) that concurred to the major determinant of malignancy (venous invasion and lymph nodes) using the Chi-square test. Result: The 5-year survival rate was 65% and the relapse rate was 37%. The mortality rate in patients with immature desmoplasia was 86%, 27% in intermediate desmoplasia, and 0% in mature desmoplasia (Spearman correlation coefficient: −0.572,P= 0.05). Conclusion: Immature desmoplasia appears to be associated with disease recurrence and mortality in stage III CRC patients.

The chronic inflammation of Crohn's disease is caused, at least in part, by repression of TGF-β1 signaling, which is caused by high levels of SMAD7. This trial shows that mongersen, an antisense inhibitor of SMAD7 mRNA, induces disease remission in some persons. Crohn’s disease is a chronic inflammatory illness that primarily affects the terminal ileum and right colon. Crohn’s disease–related inflammation is segmental and transmural, leading to various degrees of tissue damage. 1 At disease onset, most patients have inflammatory lesions, which become predominantly strictures or penetrating lesions over time. 2 , 3 Mucosal healing can be promoted with the use of immunosuppressive drugs and anti–tumor necrosis factor α (TNF- α ) antibodies; however, more than one third of patients do not have a response to these therapies. The efficacy of these drugs may also diminish over time, and they can increase a patient’s risk . . .

Systemic sclerosis (SSc) is characterized by skin/internal organ fibrosis, vasculopathy and autoimmunity. Chemokine (C-X-C motif) ligand 4 (CXCL4) is an SSc biomarker, predicting unfavorable prognosis and lung fibrosis. CXCL4 binds DNA/RNA and favors interferon (IFN)-α production by plasmacytoid dendritic cells (pDCs), contributing to the type I IFN (IFN-I) signature in SSc patients. However, whether CXCL4 is an autoantigen in SSc is unknown. Here, we show that at least half of SSc patients show consistent antibody reactivity to CXCL4. T-cell proliferation to CXCL4, tested in a limited number of patients, correlates with anti-CXCL4 antibody reactivity. Antibodies to CXCL4 mostly correlate with circulating IFN-α levels and are significantly higher in patients with lung fibrosis in two independent SSc cohorts. Antibodies to CXCL4 implement the CXCL4–DNA complex’s effect on IFN-α production by pDCs; CXCL4–DNA/RNA complexes stimulate purified human B-cells to become antibody-secreting plasma cells in vitro. These data indicate that CXCL4 is indeed an autoantigen in SSc and suggest that CXCL4, and CXCL4-specific autoantibodies, can fuel a harmful loop: CXCL4–DNA/RNA complexes induce IFN-α in pDCs and direct B-cell stimulation, including the secretion of anti-CXCL4 antibodies. Anti-CXCL4 antibodies may further increase pDC stimulation and IFN-α release in vivo, creating a vicious cycle which sustains the SSc IFN-I signature and general inflammation.

ObjectivesStudies aimed at establishing which characteristics of patients with ulcerative proctitis could be predictive of the extension of inflammation have failed to provide conclusive results. The aim of the study was to evaluate the prognostic role of clinical and therapeutic parameters in patients with proctitis.Patients and MethodsCase records of 138 patients with ulcerative proctitis were retrospectively evaluated. The following parameters were considered: gender; age at onset of disease; smoking habits; histologic severity of disease at onset; mean number of clinical relapses of disease per year; mean duration of oral and topical mesalazine treatment; and number of topical corticosteroid treatments per year.ResultsTwenty-eight patients were excluded from the analysis for different reasons. During follow-up, inflammation spread proximally in 33 of 110 patients (30%). Patients with extended proctitis showed a significantly higher number of relapses and a shorter duration of oral mesalazine treatment than patients with nonprogressive proctitis (p < 0.001 for both). The multivariate analysis also found that the mean duration of topical mesalazine treatment was longer in patients with extended proctitis.ConclusionsUlcerative proctitis patients with more frequent relapses who need a longer duration of topical therapy are at higher risk of extension of the disease, while a more prolonged oral mesalazine treatment period protects against the proximal spread of rectal inflammation.

Adalimumab (ADA) biosimilars have entered the therapeutic armamentarium of inflammatory bowel disease (IBD), allowing for the treatment of a greater number of patients for their reduced cost than the originator. However, comparative data on the efficacy and safety of the various ADA biosimilars remains scarce.We compare the efficacy and safety of ADA biosimilars SB5, ABP501, GP2017, and MSB11022 in treating IBD outpatients in a real-life Italian setting. A retrospective analysis was performed on consecutive IBD outpatients with complete clinical, laboratory, and endoscopic data. Clinical activity was measured using the Mayo score in ulcerative colitis (UC) and the Harvey-Bradshaw Index in Crohn's disease (CD). The primary endpoints were the following: (1) induction of remission in patients new to biologics and patients new to ADA but previously exposed to other anti-tumor necrosis factor agents or other biologics; (2) maintenance of remission in patients switched from the ADA originator to an ADA biosimilar; and (3) safety of various biosimilars. A total of 533 patients were enrolled according to the inclusion criteria: 162 patients with UC and 371 patients with CD. Clinical remission was obtained in 79.6% of patients new to biologics and 59.2% of patients new to ADA but not to other biologics; clinical remission was maintained in 81.0% of patients switched from the originator, and adverse events were recorded in 6.7% of patients. There was no significant difference between the 4 ADA biosimilars for each predetermined endpoint. Adalimumab biosimilars are effective and safe in IBD treatment, both in new patients and in patients switched from the ADA originator. No difference in efficacy and safety was found between ADA biosimilars.

Colonic lipomatous polyps are often an incidental finding during colonoscopy. Generally, these types of polyps can cause gastrointestinal bleeding when they are larger than 4 cm in size. Some case reports have documented the occurrence of overlying adenomatous formations in the apical portion, as well as ulcerated mucosa. There is currently no standardized endoscopic removal technique for their treatment. In this report, we present a case of a large and ulcerated lipoma causing rectorrhagia, which was successfully treated with endoscopic en-bloc resection and endoloop placement.

Illicit substances are widely used all over the world. Among them, crack cocaine results to be the most used drug for the fact that it can be taken in different ways, such as inhaled or intravenous. Pulmonary complications are well known in people snorting it, mostly due to contamination with other substances contained in the objects able to infuse the drug. Herein, we present a case of lung candida abscess related to nasal insufflation of cocaine in an abuser patient suffering from hepatitis C virus (HCV) and not immunocompromised.

In the last decades, the comprehension of the pathophysiology of bone metabolism and its interconnections with multiple homeostatic processes has been consistently expanded. The branch of osteoimmunology specifically investigating the link between bone and immune system has been developed. Among molecular mediators potentially relevant in this field, vitamin D has been recently pointed out, and abnormalities of the vitamin D axis have been described in both in vitro and in vivo models of inflammatory bowel diseases (IBD) and arthritis. Furthermore, vitamin D deficiency has been reported in patients affected by IBD and chronic inflammatory arthritis, thus suggesting the intriguing possibility of impacting the disease activity by the administration vitamin D supplements. In the present review, the complex interwoven link between vitamin D signaling, gut barrier integrity, microbiota composition, and the immune system was examined. Potential clinical application exploiting vitamin D pathway in the context of IBD and arthritis is presented and critically discussed. A more detailed comprehension of the vitamin D effects and interactions at molecular level would allow one to achieve a novel therapeutic approach in gastro-rheumatologic inflammatory diseases through the design of specific trials and the optimization of treatment protocols.