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- Mancina, Rosellina Margherita, et al.
(author)
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Ulcerative Colitis as an Independent Risk Factor for Hepatic Steatosis
- 2020
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In: Gastroenterology Nursing. - : Ovid Technologies (Wolters Kluwer Health). - 1042-895X. ; 43:4, s. 292-297
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Journal article (peer-reviewed)abstract
- Inflammatory bowel disease (IBD) is an inflammatory condition of the gastrointestinal tract encompassing Crohn disease and ulcerative colitis, often associated with extraintestinal manifestations. Nonalcoholic fatty liver disease represents one of the described inflammatory bowel disease-related liver diseases. To understand the IBD contribution to nonalcoholic fatty liver disease onset, we compared liver fat content and fibrosis between IBD patients and healthy controls integrating medical and nursing expertise (integrated nursing approach). A total of 95 patients and 53 healthy volunteers were recruited. Only nondiabetic and nonobese individuals were included in the study. Liver evaluation was performed by an experienced nurse using transient elastography. We found that IBD patients had higher liver fat content than the control group (p= .003). Bonferroni post hoc analyses revealed that patients with Crohn disease or ulcerative colitis had higher liver fat than the control group. We also found that ulcerative colitis was associated with more than a 4-fold increased risk for mild steatosis and 7-fold increased risk for moderate/severe steatosis independently from other risk factors such as glucose and body mass index. In conclusion, we showed for the first time that ulcerative colitis is an independent risk factor for hepatic steatosis measured by transient elastography.
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- Gupta, Rahul, et al.
(author)
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Element-resolved evidence of superdiffusive spin current arising from ultrafast demagnetization process
- 2023
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In: Phys. Rev. B. - : American Physical Society. ; 108:6
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Journal article (peer-reviewed)abstract
- Using element-specific measurements of the ultrafast demagnetization of Ru/Fe65Co35 hetero-structures, we show that Ru can exhibit a significant magnetic contrast (3% asymmetry) resulting from ultrafast spin currents emanating from the demagnetization process of the FeCo layer. We use this magnetic contrast to investigate how superdiffusive spin currents are affected by the doping of heavy elements in the FeCo layer. We find that the spin currents are strongly suppressed, and that the recovery process in Ru slows down by Re doping. This is in accordance with a change in interface reflectivity of spin currents as found by the superdiffusive spin transport model.
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- Mancina, Rosellina Margherita, et al.
(author)
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PNPLA3 148M Carriers with Inflammatory Bowel Diseases Have Higher Susceptibility to Hepatic Steatosis and Higher Liver Enzymes
- 2016
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In: Inflammatory Bowel Diseases. - : Oxford University Press (OUP). - 1078-0998. ; 22:1, s. 134-140
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Journal article (peer-reviewed)abstract
- Background: Inflammatory bowel diseases (IBD) are characterized by chronic relapsing inflammation of the gastrointestinal tract and encompass Crohn's disease and ulcerative colitis. IBD are often associated with extraintestinal manifestations affecting multiple organs including the liver. Increased levels of serum aminotransferases, possibly related to nonalcoholic fatty liver disease, constitute one of the most frequently described IBD-related liver diseases. The PNPLA3 I148M substitution is a major common genetic determinant of hepatic fat content and progression to chronic liver disease. The aim of this study was to investigate whether carriers of PNPLA3 148M allele with IBD have higher risk of liver steatosis and increase in transaminases levels. Methods: The PNPLA3 I148M (rs738409) genotype was performed by Taqman assays in 158 individuals from Southern Italy (namely, Catanzaro cohort) and in 207 individuals from Northern Italy (namely, Milan cohort) with a definite diagnosis of IBD. Demographic and clinical data and also alanine transaminase levels were collected for both cohorts. The Catanzaro cohort underwent liver evaluation by sonography and liver stiffness and controlled attenuation parameter measurements by transient elastography. Results: Here, we show for the first time that carriers of the PNPLA3 148M allele with IBD have a greater risk of hepatic steatosis (odds ratio, 2.9, and confidence interval, 1.1-7.8), higher controlled attenuation parameter values (P = 0.029), and increased circulating alanine transaminase (P = 0.035) in the Catanzaro cohort. We further confirm the higher alanine transaminase levels in the Milan cohort (P < 0.001). Conclusions: Our results show that PNPLA3 148M carriers with IBD have higher susceptibility to hepatic steatosis and liver damage.
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- Spagnuolo, R., et al.
(author)
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Multifaceted pathogenesis of liver steatosis in inflammatory bowel disease: a systematic review
- 2021
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In: European Review for Medical and Pharmacological Sciences. - 1128-3602. ; 25:18, s. 5818-5825
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Non-Alcoholic Fatty Liver Disease (NAFLD), as a hepatic manifestation of metabolic syndrome (MET)-related obesity, insulin resistance, dyslipidemia, and hypertension, is the main cause of chronic liver disease. Inflammatory Bowel Diseases (IBD). (Crohn's Disease (CD) and Ulcerative Colitis (UC)). are often associated with extraintestinal manifestations. Of these. NAFLD is one of the most frequently reported. To highlight the etiopathogenesis of NAFLD in IBD, we performed a systematic review emphasizing the relationship between NAFLD genetic alterations, metabolic syndrome, and drugs. MATERIALS AND METHODS: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement (PRISMA) criteria, we performed a systematic literature search on PubMed, Google Scholar, and Web of Science for literature updated from 2010 to 1 March 2021. Inclusion criteria for studies were observational design and Randomized Controlled Trials (RCTs); written in English; primary research only; based on adult patients, and human research only. RESULTS: We identified nine studies on the link between NAFLD and IBD. Among these, two described the genetic predisposition to NAFLD of patients with IBD. Four reported an association between MetS and NAFLD in IBD patients. Regarding medications, none of four studies included. detected a relationship between NAFLD onset and IBD treatment (corticosteroids, immunomodulators, methotrexate, or biologics). However, a retrospective study showed a protective effect of anti-TNF alpha therapies against altered liver enzymes. CONCLUSIONS: In this interplay between genetic, metabolic, drug, and inflammatory factors, the underlying pathogenic mechanisms behind NAFLD in IBD are still far from clear. Further studies are needed to better clarify the role of individual components influencing the development of NAFLD in IBD.
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- Spagnuolo, R., et al.
(author)
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Weight Gain and Liver Steatosis in Patients with Inflammatory Bowel Diseases
- 2019
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In: Nutrients. - : MDPI AG. - 2072-6643. ; 11:2
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Journal article (peer-reviewed)abstract
- Background and Aim: Most studies focused on the benefits of weight loss on hepatic steatosis and no studies have been specifically designed to assess the role of weight gain on the development of liver steatosis in patients affected by inflammatory bowel diseases. The aim of this study was to analyse the relation between weight change over time and liver steatosis in patients with inflammatory bowel diseases. Methods: We retrospectively evaluated a population of 89 ambulatory patients in clinical remission or affected by mild disease, as determined from disease activity indices, with at least one follow-up visit. Transient elastography was used to quantify liver steatosis. Results: A total of 49 individuals (55%) were overweight/obese at baseline. A significant difference in weight change was found between participants that improved, were stable and worsened, over a mean follow-up of four years. (-1.0 kg +/- 4; 2.5 kg +/- 6; and 5.4 kg +/- 5; respectively, p = 0.009). We found a greater probability of worsening in the hepatic fat content in individuals who gained more than 6% of body weight than in those gaining less than this value (log-rank (Mantel-Cox) (2) test = 9.85; df = 1; p = 0.002). Conclusions: A body weight gain of 6% increases the probability of deterioration in liver steatosis over a period of four years in patients with inflammatory bowel diseases. Weight gain prevention with lifestyle interventions may be the cornerstone treatment of these patients.
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