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BACKGROUND: The coexistence of human immunodeficiency virus (HIV) infection and inflammatory bowel disease (IBD) is uncommon. Data on the impact of HIV on IBD course and its management is scarce. AIM: To describe the IBD phenotype, therapeutic requirements and prevalence of opportunistic infections (OI) in IBD patients with a coexistent HIV infection. METHODS: Case-control, retrospective study including all HIV positive patients diagnosed with IBD in the ENEIDA registry. Patients with positive HIV serology (HIV-IBD) were compared to controls (HIV seronegative), matched 1:3 by year of IBD diagnosis, age, gender and type of IBD. RESULTS: A total of 364 patients (91 HIV-IBD and 273 IBD controls) were included. In the whole cohort, 58% had ulcerative colitis (UC), 35% had Crohn's disease (CD) and 7% were IBD unclassified. The HIV-IBD group presented a significantly higher proportion of proctitis in UC and colonic location in CD but fewer extraintestinal manifestations than controls. Regarding treatments, non-biological therapies (37.4% vs. 57.9%; P=0.001) and biologicals (26.4% vs. 42.1%; P=0.007), were used less frequently among patients in the HIV-IBD group. Conversely, HIV-IBD patients developed more OI than controls regardless of non-biological therapies use. In the multivariate analysis, HIV infection (OR 4.765, 95%CI 2.48-9.14; P<0.001) and having ≥1 comorbidity (OR 2.445, 95%CI 1.23-4.85; P=0.010) were risk factors for developing OI, while CD was protective (OR 0.372, 95%CI 0.18-0.78;P=0.009). CONCLUSIONS: HIV infection appears to be associated with a less aggressive phenotype of IBD and a lesser use of non-biological therapies and biologicals but entails a greater risk of developing OI.
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BACKGROUND AND AIMS: The prevalence of the non-alcoholic fatty liver disease (NAFLD) in developed countries is up to 30% of the general population, and 50% of patients present type 2 diabetes mellitus (DM2). Fibrosis is the most important prognostic factor in NAFLD. The aim of this study was to search evidence for an early diagnosis of liver fibrosis in subjects with DM2 and to evaluate potential risk and protective factors. METHODS: This study was conducted among 160 diabetic patients with NAFLD proven biopsy. Anthropometric assessments, laboratory test, liver histological features and follow-up of a Mediterranean diet were evaluated. RESULTS: Diabetic patients with liver fibrosis showed a greater number of positive metabolic criteria than diabetic patients without liver fibrosis. Patients with hepatic fibrosis have a lower score on the PREDIMED test (9.0 (2.4) vs. 6.2 (2.3); p < 0.05). Diabetic patients with liver fibrosis showed higher glucose levels (delta: 10.1 (4.5) mg/dl), fasting insulin levels (delta: 3.1 (1.5) UI/L), HOMA-IR (delta: 2.1 (0.3) units) and HbA1c (delta: 0.6 (0.2)%). Non-invasive tests showed a higher score (non-alcoholic fatty liver disease fibrosis score and fibrosis-4) in liver fibrosis subjects than no liver fibrosis subjects. A logistic regression analysis adjusted by age, gender, HbA1c and body mass index showed independent significant direct association between liver fibrosis and homeostatic model assessment of insulin resistance as indicator of insulin resistance (odds ratio (OR) = 1.53: 95% confidence interval (CI): 1.1-2.2; p = 0.026) and inverse association with PREDIMED score as an indicator of adherence to Mediterranean diet (OR = 0.6; 95% CI: 0.4-0.8; p = 0.01). CONCLUSION: In patients with DM2, insulin resistance is an independent risk factor associated with liver fibrosis, and the adherence of a Mediterranean diet is a protective factor associated with absence of liver fibrosis.