Introduktion: Irritable Bowel Syndrome (IBS) är en vanlig kronisk mag- och tarmsjukdom. Sjukdomens olika symtom orsakas av en störning i mag- och tarmkanalen. Syfte: Litteraturstudiens syfte var att beskriva patienters upplevelse av att leva med IBS. Metod: Polit och Becks niostegsmodell användes i litteraturstudien. Litteratursökningen genomfördes i PubMed och CINAHL. En urvals- och kvalitetsgranskning är genomförd. Resultatet baserades på åtta kvalitativa och två kvantitativa artiklar. Resultat: Resultatet redovisades i tre teman existentiell upplevelse, upplevelser av hinder i vardagen och upplevelser av att hantera sjukdomen med tillhörande kategorier. Personer med IBS upplevde negativa känslor på grund av sjukdomens symtom i form av konstant oro och ångest relaterad till sjukdomens oförutsägbarhet. Sjukdomen var ett hinder för att utföra vardagliga aktiviteter. Ett undvikande beteende och en social isolering utvecklades. Personer med IBS använde sig av olika strategier för att hantera sjukdomen. De tyckte varken anhöriga eller hälso- och sjukvården förstod dem och upplevde att de inte fick tillräckligt med stöd. Något som däremot upplevdes givande för att hantera sjukdomen, var att få samtala och byta erfarenheter med andra människor med IBS. Slutsats: Personer med IBS upplever sig ha en försämrad livskvalité. Mer kunskap behövs om hur personer IBS upplever och hanterar vardagliga situationer och symtom. Detta för att upplevelserna och erfarenheterna kan föras vidare till andra personer med sjukdomen.

This thesis explores aspects pertinent to the phenotypic classification of paediatric patients with inflammatory bowel disease (IBD). In the current era it has never been more important to have rigourous phenotypic classification to facilitate genotype-phenotype correlation studies as well as to optimize design of clinical trials of emerging therapies, where frequently response may differ according to phenotype of disease. The first study examined the reliability of the Montreal Classification for classifying paediatric IBD patients. This is the first study exploring the reliability of phenotypic classification in a paediatric population. The reliability of assigning an overall diagnosis of type of IBD was good, but not excellent. Amongst Crohn’s disease patients, reliability of assigning disease behaviour was excellent, while the reliability of assigning disease location categories varied from fair to good. The percentage agreement when describing disease extent for ulcerative colitis was high. The second study described the evolution of disease phenotype in a cohort of paediatric IBD patients. Similar to observations in adult-onset IBD, disease location was found to be relatively stable, while Crohn’s disease behaviour evolves from an inflammatory to a stricturing and/or penetrating phenotype in 20% of patients by 5 years of follow-up. The final study explored the association between 2 polymorphisms in the NOD2 gene with the requirement for intestinal resection (a surrogate marker of complicated disease) in models that included and excluded disease duration. Although no difference was found, this may have been influenced by data quality, which was suboptimal. In conclusion, this thesis has demonstrated that imprecision exists in the phenotyping of paediatric IBD patients, in whom phenotypic characteristics evolve over time. It is pertinent that disease duration be considered in any study attempting to make phenotypic correlations.

This thesis explores aspects pertinent to the phenotypic classification of paediatric patients with inflammatory bowel disease (IBD). In the current era it has never been more important to have rigourous phenotypic classification to facilitate genotype-phenotype correlation studies as well as to optimize design of clinical trials of emerging therapies, where frequently response may differ according to phenotype of disease. The first study examined the reliability of the Montreal Classification for classifying paediatric IBD patients. This is the first study exploring the reliability of phenotypic classification in a paediatric population. The reliability of assigning an overall diagnosis of type of IBD was good, but not excellent. Amongst Crohn’s disease patients, reliability of assigning disease behaviour was excellent, while the reliability of assigning disease location categories varied from fair to good. The percentage agreement when describing disease extent for ulcerative colitis was high. The second study described the evolution of disease phenotype in a cohort of paediatric IBD patients. Similar to observations in adult-onset IBD, disease location was found to be relatively stable, while Crohn’s disease behaviour evolves from an inflammatory to a stricturing and/or penetrating phenotype in 20% of patients by 5 years of follow-up. The final study explored the association between 2 polymorphisms in the NOD2 gene with the requirement for intestinal resection (a surrogate marker of complicated disease) in models that included and excluded disease duration. Although no difference was found, this may have been influenced by data quality, which was suboptimal. In conclusion, this thesis has demonstrated that imprecision exists in the phenotyping of paediatric IBD patients, in whom phenotypic characteristics evolve over time. It is pertinent that disease duration be considered in any study attempting to make phenotypic correlations.

The gastrointestinal (GI) tract is subject to regulation by several neuronal networks, one of which is the sympathetic nervous system (SNS). Inflammatory bowel diseases (IBD), most importantly Crohn’s disease and ulcerative colitis, are chronic diseases of the GI tract that result in such functional symptoms as abdominal pain and diarrhea. These symptoms suggest an important role for dysregulation of the SNS in IBD, since this branch of the autonomic nervous system aids in regulation of blood flow, secretion and motility. Inflammatory cytokines that are elevated in the serum and tissue of IBD patients can have wide-ranging effects on neuronal function in vitro, and may be responsible for the functional alterations observed in vivo. With these neuronal alterations in mind, we hypothesized that interleukin-17, a novel cytokine with a central role in the pathogenesis of IBD, modulates the properties of sympathetic neurons innervating the gastrointestinal tract. Using electrophysiological techniques and Ca2+ imaging, we examined the effect of IL-17 on currents passing through voltage-gated Ca2+ channels in neurons from the superior mesenteric ganglion, which innervates the gut, and found that IL-17 inhibited these currents. In parallel, we found that IL-17 enhances the growth of sympathetic neurites in vitro. These effects depend upon activation of the nuclear factor κB (NF-κB) pathway, and do not appear to require glial cells. Therefore, dysregulated neural function during IBD may be due to direct effects of IL-17 on sympathetic neurons. / Thesis (Master, Physiology) -- Queen's University, 2009-09-03 11:33:53.63

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A piglet model of gastrointestinal inflammation (INF) and protein energy malnutrition (PEM) was developed to determine the mechanisms responsible for growth retardation and muscle wasting during inflammatory stress. Acute PEM decreased liver and plasma protein fractional synthesis rates (FSR), measured by stable isotope (2H3-leucine) incorporation. Conversely, both rates increased during PEM+INF at the expense of growth and muscle FSR. INF increased plasma protein synthesis by 77% in PEM without increasing its plasma concentration, demonstrating that the measurement of plasma protein concentration alone underestimates the metabolic impact of INF. INF during PEM results in a re-prioritization of amino acids from muscle protein synthesis and growth to hepatic synthesis of plasma proteins to support the acute phase response. This underscores the critical role of adequate protein-energy nutrition during inflammation in preventing muscle wasting and growth failure. This new piglet model can be applied to investigate nutritional and therapeutic interventions in inflammatory bowel disease.

Diss. (sammanfattning)--Linköping : Linköpings universitet, 2006. / Härtill 5 uppsatser.

Diss. (sammanfattning) Göteborg : Göteborgs universitet , 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Lund : Lunds universitet, 2006. / Härtill 4 uppsatser.