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1.
Curr Drug Targets ; 22(15): 1706-1715, 2021.
Article in English | MEDLINE | ID: mdl-33538671

ABSTRACT

BACKGROUND: The incidence of inflammatory bowel disease (IBD) continues to rise worldwide. Despite the advances in pharmacotherapy, the etiopathogenesis of Crohn's disease (CD) and ulcerative colitis (UC) remains underexplained. The migratory waves are a challenging setting to analyze the evolution of IBD prevalence and to infer its triggering factors. OBJECTIVE: Our study aimed to overview the literature regarding IBD prevalence and phenotype in first- and second-generation migrants Also, we aimed to summarize the migration history and to draw a possible correlation with IBD distribution. METHODS: A non-systematic review was performed following electronic (PubMed and Web of Science) and manual searches on relevant topics. RESULTS: Overall, first-generation migrants tend to maintain the IBD risk of the native country. On the following generation, the risk tends to converge to that of the destination country. Earlier age at migration modulates IBD risk, suggesting that the degree of exposure to environmental and socio-economic factors can be decisive for disease progression. In general, CD needs more time to reach a disease burden similar to that of the host country, indicating that UC may be more affected by nongenetic factors and genetic-nongenetic interactions. CONCLUSION: IBD phenotypes and natural history vary in migrants and according to ethnicity; however, the trends are not consensual among cohorts. Further studies are warranted to analyze the effect of genetic background and environmental risk factors in different ethnic groups, providing evidence to move towards the identification of at-risk individuals, prevention, and earlier diagnosis of IBD.


Subject(s)
Colitis, Ulcerative , Crohn Disease , Inflammatory Bowel Diseases , Transients and Migrants , Colitis, Ulcerative/diagnosis , Colitis, Ulcerative/epidemiology , Crohn Disease/epidemiology , Humans , Incidence , Inflammatory Bowel Diseases/epidemiology , Risk Factors
2.
Pharmacol Res Perspect ; 8(3): e00601, 2020 06.
Article in English | MEDLINE | ID: mdl-32476298

ABSTRACT

Recently, the gut microbiome has become an important field of interest. Indeed, the microbiome has been associated to numerous drug interactions and it is thought to influence the efficacy of pharmacologic treatments. Although statins are widely prescribed medications, there remains considerable variability in its therapeutic response. In this context, we aimed to investigate how statins modulate the gut microbiome and, reversely, how can the microbiome influence the course of anti-hypercholesterolemic treatment. We conducted a systematic review by searching four online databases, in accordance with PRISMA guidelines. Studies addressing gut microbiome changes following statin treatment and those assessing statins' response and associating it with patients' microbiome were included. Due to the limited number of results, we decided to include studies enrolling both humans and animals. We summarized information from three human and seven animal studies and aimed to assess the influence of gut microbiome composition on statin response (Outcome 1) and to evaluate the impact of statin treatment on the gut microbiome (Outcome 2). An association between a certain microbiome composition that promoted the lipid-lowering effect of statins was found. However, what kind of microorganisms and how they can exert this effect remains uncertain. Furthermore, statins might have a role in the modulation of the gut microbiome, but then again, it is still unknown whether this change is directly caused by the drug or another metabolic mechanism. Even though gut microbiota may have several potential therapeutic implications, its use as a personalized predictive biomarker requires further studies.


Subject(s)
Gastrointestinal Microbiome/drug effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Hypercholesterolemia/drug therapy , Animals , Humans , Hypercholesterolemia/microbiology , Lipids/blood
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