Background Inhaled colistin (IC) is formally indicated to treat Pseudomonas aeruginosa bronchial infections in cystic fibrosis (CF) patients. In patients without CF it is not indicated and must be prescribed off-label if they have pseudomonas-infected bronchiectasis. Purpose To evaluate the way inhaled colistin is used, its effectiveness and economic impact for patients who do not have CF in our hospital. Materials and methods Retrospective study. 24 patients’medical records were evaluated. All of them were undergoing IC treatment for their PA colonised bronchiectasis for at least 6 months from January 2011 to January 2013 in our hospital. None of them was diagnosed with CF. Besides demographics, the frequency and duration of hospitalisation for respiratory exacerbations and emergency episodes were counted in each patient before and after colistin intensive treatment. These two values were considered as efficacy parameters. Data were compared using a student’s t test for paired samples. Regarding the cost analysis, only hospitalisation-related expenditure and inhaled colistin treatment costs were included. Neither concomitant antibiotic treatment, nor expenditure related to medical consultations were measured. Results 13 patients were female and mean age was 74.8. Mean treatment duration was 16.56 months and mean colistin expenditure was 7,504.44 € per patient. Average number of hospital admissions before treatment was 1.52 per patient with a mean duration of 8.37 days. These were reduced after treatment, with 0.79 hospitalisations per patient with a mean duration of 5.45 days. This generated savings of 1402.9 € per patient overall. The emergency episodes also decreased from 1.87 to 1.45. Although these differences showed clinical relevance, they did not reach statistical significance. Conclusions Though the limited sample size does not enable us to demonstrate the real difference, inhaled colistin may be considered a cost-effective option to treat patients with pseudomonas-infected bronchiectasis but no CF. No conflict of interest.

Background Anti-TNF drugs are safe during pregnancy in inflammatory bowel disease (IBD), but they cross the placenta most actively in the third trimester, and some guidelines still recommend stopping them during this period. There few data that examines the impact of anti-TNF discontinuation on the clinical course of IBD, so we aimed to explore the clinical outcomes of IBD pregnant patients who stopped anti-TNF at the third trimester. Methods We performed a retrospective, longitudinal study on female IBD patients receiving anti-TNF agents at our IBD clinic. We included IBD pregnant patients who discontinued the anti-TNF in the third trimester of pregnancy, and we matched these cases in a 1:1 ratio with non-pregnant female IBD patients by age, type of IBD, type of anti-TNF, duration of treatment, location, and behavior of IBD. Demographic and clinical variables were collected from 18 months before anti-TNF discontinuation and 12 months after discontinuation, and when available endoscopic indices (SES CD and UC). We determined whether subjects presented any adverse clinical outcome during the follow-up defined as development of disease flare, corticosteroid use, hospital admission, need for surgery, biologic dose escalation, or switch. Results We included 34 pregnant patients and 34 controls. Patients who stopped anti-TNF more frequently presented an adverse clinical outcome during the follow-up year when compared to the control group (47.1% vs. 23.5% p = 0.04) and flare activity (35, 3 vs. 11.8%, p = 0.02). We found no differences in escalation or biologic switch, hospital admission, or surgery between the subjects. We also found an association between the development of an adverse clinical outcome and anti-TNF monotherapy (p=0.009) and a higher SESCD in the previous year (p=0.017). In the multivariate analysis, anti-TNF monotherapy was the only independent factor for developing an adverse clinical outcome up to 1 year after anti-TNF discontinuation (OR: 3.47, CI 95%: 1.16–10.4, p=0.026). Conclusion In our cohort of female IBD patients on anti-TNF, monotherapy was independently associated with an adverse clinical outcome in the following year after anti-TNF discontinuation.

Background Fungi account for approximately 0.1% of the total microorganisms in the gut. Despite the vast body of literature on the bacterial component of the gut microbiota, little has been published on the fungal microbiota. Fungal-bacterial interactions may be significant in inflammatory bowel disease (IBD), with several lines of evidence linking fungi and IBD. Our study aimed to explore and compare the fungal and bacterial loads in fecal samples from different ulcerative colitis (UC) patients’ groups. Methods Using two qPCR systems to amplify the ITS2 sequence from fungi and the 16srRNA gene from bacteria, we characterized and compared fungal and bacterial loads in 3 groups: 1) UClr: UC patients in long-term remission (≥5 years of flare-free disease, clinical, endoscopic and histological remission at inclusion); 2) UCsr: UC patients in short-term remission (3 months in clinical remission at inclusion and previously more than one relapse/year); 3) UCfl: UC patients with active disease (CAI >4 at inclusion). We obtained two frozen fecal samples from all subjects, except for the UCfl group from which we obtained 1 sample at flare onset. Results were expressed in copies/g of feces. Results We included 87 UC patients, 29 in UClr, 20 in UCsr, and 38 in UCfl groups. Median age was 39 years, women comprised 52%. Fecal samples contained a significantly lower number of ITS2 gene copies (median 9.27E+05) than 16srRNA gene copies (median 4.28E+11). 16s rRNA gene copies were similar among the different groups with a median 3.88E+11 for UClr, median 5.29E+11 for UCsr, and median 4.315E+11 for UCfl patients (FDR p=0.65). In contrast, copies of ITS2 gene were increased in UCfl (median 1.95E+06) when compared to UClr (3.68E+04, FDR p=0.0036) but not significantly different to UCsr (5.24E+05 copies, FDR p=0.20). We analyzed the variation between samples over time; we compared the number of copies of ITS2 and 16s rRNA genes in fecal samples collected at two different time points: basal versus 8-weeks. We calculated overall fold changes that reflect stability over time. We found a trend for a more significant variation in the quantity of the ITS2 gene than the 16srRNA gene, but this was not significant. Analysis of the ITS2/16S rRNA ratio assessing the frequency of fungi compared to bacteria showed that this ratio was higher in UCfl (median 6.94E-06) when compared to UClr (median 2.63E-07, FDR p=0.0005) and UCsr patients (median 5.60E-07, FDR p=0.0072), there were no differences between UClr and UCsr patients. Conclusion Fungal abundance was increased in UC flare patients compared to UC patients in long remission, while there were no differences in bacterial abundance. This high number of fungi could be involved in the inflammatory response of UC patients.