Introdução: O conhecimento da fisiopatogênese da Doença Inflamatória Intestinal (DII) tem evoluído nas últimas décadas. No entanto, apesar das terapias terem evoluído, 2/3 dos casos ainda necessitam de drogas alternativas e terapias de suporte. A busca constante de tratamentos alternativos e modalidades mais eficazes tem gerado algumas abordagens promissoras, tais como a utilização do oxigênio hiperbárico (HBO). O uso dessa terapia cresceu rapidamente nos anos 90 mostrando bons resultados e poucos efeitos colaterais sendo, posteriormente \"esquecida\" ante a eficácia apresentada pelo uso das terapias biológicas. Objetivos: Os objetivos deste trabalho foram avaliar os efeitos do tratamento com HBO em camundongos com colite induzida quimicamente pelo ácido 2,4,6 trinitro benzeno sulfônico 2,5% (TNBS), sobre a avaliação dos animais, a análise histológica, o perfil inflamatório através das citocinas IL-4, IL-10, IL-12, IL-13, IL-17, fator de necrose tumoral alfa (TNFalfa) e Interferon y e da atividade das enzimas antioxidantes superóxido dismutase (SOD), glutationa peroxidase (GPx) e glutationa redutase (GR) em intestino de camundongos. Metodologia: Camundongos machos foram divididos em 6 grupos. No grupo 1, a colite foi induzida por TNBS 2,5% + Etanol 35%, sendo chamado de grupo TNBS; o grupo 2 também recebeu TNBS 2,5% + Etanol 35% seguido do tratamento com o HBO, sendo chamado de grupo TNBS+HBO; o grupo 3 recebeu apenas o veículo etanólico a 35%, sendo chamado de grupo ÁLCOOL; o grupo 4 também recebeu o veículo etanólico a 35% associado ao HBO, sendo chamado de grupo ÁLCOOL+HBO; o grupo 5 recebeu apenas solução salina (NaCl 0,9%), sendo chamado de grupo SALINA; e o grupo 6 recebeu a solução salina associado ao HBO, sendo chamado de grupo SALINA+HBO. Durante o tratamento os animais foram avaliados diariamente. O tratamento com HBO foi realizado por 4 dias e, ao final, as amostras da porção final do intestino foram retiradas e armazenadas para análise histológica, enzimas antioxidantes e citocinas. Resultados: A avaliação mostrou que o HBO promoveu uma melhora significativa no quadro clínico desses animais. A aplicação do ácido 2,4,6 trinitro benzeno sulfônico nos animais do grupo TNBS resultou na perda de 12,71% do peso corpóreo dos animais após 24 horas e, ao final do período experimental uma perda de peso total de 14,63%. Por outro lado, os animais que também receberam 2,4,6 trinitro benzeno sulfônico associado ao tratamento com o HBO (TNBS+HBO) tiveram uma perda de apenas 7,52% nas primeiras 24 horas, apresentando uma recuperação de 5,58% de seu peso no final do período experimental. A avaliação do quadro histológico mostrou uma melhora significativa entre o grupo TNBS+HBO quando comparado com o grupo TNBS. O tratamento com HBO aumentou a atividade das enzimas antioxidantes SOD e GPx em todos os grupos, sendo somente significativo entre os grupos TNBS vs TNBS+HBO, não sendo observado diferença da GR entre os grupos. Com relação ao perfil inflamatório foi observado que o tratamento com o HBO promoveu a diminuição das citocinas pró-inflamatórias INFy, IL-12, IL-17 e TNF? e o aumento das citocinas anti-inflamatórias IL-4 e IL-10, e não houve alteração da IL-13. Em modelo experimental, esses dados representam, o potencial efeito anti-inflamatório e o do aumento das defesas antioxidantes enzimáticas promovido pelo HBO / Introduction: The Knowledge about the physiopathogenesis of inflammatory bowel disease (IBD) has evolved over the last decades. However, although therapies have improved, 2/3 of the cases still need alternative drugs and support therapy. The constant search for alternative treatments and more effective modalities has brought to light some promising strategies, as the use of hyperbaric oxygen (HBO). The use of such therapy surged rapidly in the 90´s showing good results and few side effects being, later on, \"forgotten\" due to the efficacy shown by the use of biological therapies. Objective: This study aimed to evaluate the effects of HBO treatment in mice with chemically induced colitis, using 2,4,6 trinitrobenzene sulfonic acid 2,5% (TNBS) over the evaluation of the animals, histological analysis, inflammatory profile through cytokines IL-4, IL-10, IL-12, IL-13, IL-17, TNF- alfa and interferon y, and also the activity of the antioxidant enzymes superoxide dismutase (SOD), gluthatione peroxidase (GPx) and gluthatione reductase (GR) in intestine of mice. Methodology: Male mice were divided into 6 groups, in group 1, colitis was induced by TNBS 2,5%+ Ethanol 35%, named as TNBS, group 2 also received TNBS 2,5%+ Ethanol 35% + HBO, named as TNBS+HBO, group 3 received only Ethanol 35%, named as ALCOHOL, group 4 received Ethanol 35% associated with HBO, named as ALCOHOL+HBO, group 5 received Saline (NaCl 0,9%), named as SALINE and group 6 received Saline combined with HBO, named as SALINE+HBO. During the treatment the animals were evaluated daily. The treatment with HBO was performed for 4 days and at the end, the samples of the final portion of the bowel were removed and stored for histological, antioxidant enzymes and cytokines analysis. Results: This study has shown that the HBO promoted a significant improve on these animals clinical status. The group which received TNBS showed a 12,71% body weight loss after 24 hours, and by the end of the experimental period the average weight loss was 14,63%. On the other hand, the animals treated with HBO showed only 7,52% weight loss during the first 24 hours, having recovered the weight lost in 5,58% by the end of the experimental period. The histological evaluation of the TNBS+HBO group presented a significant improvement when compared with TNBS group. The treatment with HBO increased the activity of the antioxidant enzymes SOD and GPx in all groups, being only significant among the groups TNBS vs TNBS+HBO, difference in the activity of GR was not observed among the groups. Regarding the inflammatory profile, it was observed that the treatment with HBO promoted the decrease of pro-inflammatory cytokines INFy, IL-12, IL-17 and TNFalfa, as well as the increase of anti-inflammatory cytokines IL-4 and IL-10, while IL-13 was not affected. These data represents, in experimental model, the potential anti-inflammatory effect and the increase of the enzymatic antioxidant defenses promoted by the HBO

Crohn's disease, a chronic inflammation of the bowel, is a multi-factorial condition where uncontrolled immune responses to luminal bacteria occur in genetically predisposed individuals. The first observable clinical signs are small ulcers that form at a specialised form of epithelium, follicle-associated epithelium (FAB). The FAB covers immune inductive sites, Peyer's patches, which function primarily as sensory areas that sample the externaI gut environment. Dendritic cells are one of the key cells that are involved in sensing luminal contents and orchestrating the gut immune system. The main aim of this thesis was to determine whether the barrier of the FAB is breached in Crohn's disease and if dysfunctional immune regulators, namely dendritic cells, playaroIe in initiating and/or maintaining the chronic intestinal inflammation. Using biopsies and surgical specimens, we were able to show that in Crohn's disease, there was an increased transmucosaI transport of Escherichia coli compared to specimens from ulcerative colitis and non-inflammatory bowel disease (IBD) controIs. Dendritic cells internalised a higher percentage of bacteria that had translocated across the FAB in the Crohn's samples. Furthermore, significantly higher concentrations of TNF-u was released upon bacterial stimulation by tissues from patients with Crohn's disease than in controIs. We went on to characterise the dendritic cells present in the Peyer's patches of patients with Crohn's disease. We found an accumulation of both immature and mature dendritic cells beneath the FAB, in the sub-epithelial dome (SED). Normally, mature dendritic cells migrate towards T cell-rich areas. However, we observed mature dendritic cells accumulating in the SED because they lacked the CCR7 migratory receptor. Furthermore, they were more prone to take-up bacteria, and produced TNF-α. To study the function of mucosal dendritic cells, we performed isolation experiments and mixed Iymphocyte reactions. Dendritic cells from both the ileum and blood of patients with active Crohn's had reduced capacity for inducing T cell proliferation than non-IBD controIs. Blood dendritic cells of patients in remission had normalised function that was similar to dendritic cells from healthy controls. The SAMPl/YitFc mice, considered an appropriate murine model for Crohn's disease, had an inherent permeability defect that increased with the chronicity of intestinaI inflammation. However unlike in human Crohn's disease, dendritic cells did not seem to playaroIe in murine ileitis. This thesis highlights the accumulation of the actively surveying dendritic cells that are prone to bacterial internalisation, and points to their possible different functional roles in active versus in-active disease; thereby confirming dendritic cells as one ofthe key components in the pathogenesis ofCrohn's disease.

En el patró fibroestenosant de la malaltia de Crohn els fibroblasts intestinals augmenten en número contribuint al desenvolupament de la fibrosi. Un dels principals promotors de la proliferació d’aquestes cèl•lules és el bFGF. En el present estudi la fracció rica en tocotrienol ha demostrat tenir efectes antiproliferatius en fibroblasts intestinals humans independentment de la procedència dels fibroblasts. Els tocotrienols redueixen tant la proliferació basal com la induïda per bFGF en fibroblasts. L’apoptosi de les cèl•lules efectores en el desenvolupament de la fibrosi sembla ser el principal mecanisme de la seva resolució. Els tocotrienols instauraren un procés complert d’apoptosi en els fibroblasts. A diferència del que passa amb la majoria d’agents proapoptòtics, els tocotrienols provoquen l’activació tant de la via extrínseca com de la via intrínseca de l’apoptosi ja que activa les caspases 8 i 9. Sorprenentment, l’addició de ciclosporina A (CsA), un conegut inhibidor de la via intrínseca de l’apoptosi, bloqueja completament el procés d’apoptosi induït per FRT. Això demostra que tot i l’activació de la caspasa 8 i per tant, de la via extrínseca, en el tractament amb tocotrienols la predominant és la via intrínseca. L’autofàgia té un paper molt rellevant en l’aclariment de cossos apoptòtics. Els tocotrienols han demostrat eficàcia en la inducció d’autofàgia en fibroblasts, ja que provoca la maduració de la proteïna LC3 i l’aparició de vacuoles autofàgiques en el citoplasma d’aquestes cèl•lules. Un cop més la CsA reverteix aquest procés, i per tant inhibeix l’autofàgia, demostrant que aquest procés requereix la participació de la mitocòndria. Les patologies que cursen amb desenvolupament de fibrosi estan associades a alts nivells de TGF-β que resulta en el reclutament de fibroblasts al lloc de la lesió i a un increment en la producció de matriu extracel•lular. A nivell intracel•lular, la fosforilació d’Smad3 és el pas clau que regula les accions del TGF-β. Els tocotrienols han mostrat eficàcia en la disminució dels nivells intracel•lulars d’Smad3 fosforilada induïda per TGF-β. La fosforilació d’Smad3 té efectes oposats en la regulació de l’expressió gènica. Regula positivament l’expressió de TIMP-1, en canvi, regula negativament l’expressió de MMP-3. Tot i ser efectes oposats en quant a expressió gènica, aquests dos fenòmens afavoreixen l’acumulació de matriu extracel•lular. L’exposició a tocotrienols fa que es reverteixi aquest estat profibrogènic ja que indueix l’expressió de MMP-3 però no afecta als nivells de TIMP-1. La síntesi de MEC i especialment la síntesi de COL1, COL3 i COL5 està incrementada en la fibrosi intestinal, aquest fet està directament relacionat amb l’activitat de TGF-β en la zona afectada. Els tocotrienols interfereixen en la síntesi de col•lagen. A més, els tocotrienols disminueixen la fosforilació d’Smad3 induïda per TGF-β, un fet clau en la síntesi de matriu extracel•lular. Aquests resultats permeten hipotetitzar un potencial antifibrogènic dels tocotrienols. Per a confirmar aquest potencial “in vivo” ens calia disposar d’un model experimental de fibrosi intestinal. A diferència del que succeeix amb la colitis, en la que es disposa d’un gran nombre de models animals, hi ha pocs models experimentals específicament dissenyats per a reproduir la fibrosi intestinal. Aquest fet, ha limitat molt el desenvolupament de noves estratègies de tractament antifibrogènic en l’intestí. Mitjançant l’administració intracolònica repetida a dosis baixes de l’haptè TNBS vam poder establir fibrosi intestinal en la rata de manera rellevant i reproduïble. En aquest model de fibrosi intestinal, els animals que van rebre la dosi més alta de tocotrienols provada en aquest estudi van mostrar nivells disminuïts en paràmetres que mesuren la inflamació, això és, es va disminuir l’índex d’activitat de la malaltia i la pèrdua de pes causada pel TNBS així com també va reduir l’expressió de TNF-α. / Excessive fibroblast expansion and extracellular matrix deposition are key events for the development of bowel stenosis in Crohn’s disease patients. Tocotrienols are vitamin E compounds with proven in vitro antifibrogenic effects on rat pancreatic fibroblasts. We aimed at investigating the effects of tocotrienols on human intestinal fibroblast proliferation, apoptosis, autophagy, and synthesis of ECM. Intestinal fibroblasts isolated from patients with Crohn’s disease were treated with tocotrienol-rich fraction from palm oil. Tocotrienols significantly reduced proliferation, enhanced cell death by promoting apoptosis and autophagy. Fibroblast apoptosis, but not autophagy, was prevented by the pan-caspase inhibitor zVAD-fmk, whereas both types of cell death were prevented when the mitochondrial permeability transition pore was blocked by cyclosporin A, demonstrating a key role of the mitochondria in these processes. TRF diminished procollagen type I and laminin γ production these cells. Transforming growth factor-β plays a key role in matrix deposition during fibrosis. Treatment of intestinal fibroblasts with tocotrienol rich fraction prevents Smad3 phosporylation induced by transforming growth factor-β and reduces collagen type 1 and 3 production by these cells. Besides, in a rat model of intestinal fibrosis, treatment with tocotrienols reduces diarrhea, rectal bleeding and weight loss, as well as levels of colonic tumor necrosis factor-α and vimentin expression demonstrating that this compound has anti-inflammatory effects in vivo.

Inflammatory bowel disease (IBD), comprises Crohn’s disease (CD) and ulcerative colitis (UC), and is a chronic relapsing inflammation of gastrointestinal tract without any known cause or cure. Currently, it is accepted that IBD is a result of a dysfunctional immune response to commensal bacteria in a genetically susceptible host, and that environmental factors can trigger the onset or reactivation of the disease. This thesis considers the possibility of a specific pathogenic agent as well as an imbalance in the composition of the normal microflora in the pathogenesis of IBD. Gut biopsy tissues were taken from a population-based case-control tissue bank held at the University of Manitoba. Automated ribosomal intergenic spacer analysis (ARISA) and terminal restriction fragment length polymorphisms (T-RFLP) were employed to assess the diversity of gut microbiota. The phylogenetic, virulence and biochemical characteristics of Escherichia coli isolated from IBD biopsies were examined using multi-locus sequence typing (MLST), DNA microarray technology and API 20E system. Utilizing ARISA and T-RFLP, a remarkable increase in the order of unclassified Clostridia was detected in inflamed tissues, particularly in CD patients (P < 0.05). Moreover, species richness and diversity were the highest in non-inflamed IBD biopsies. Culture-based quantification detected a significantly higher number of E. coli in IBD tissues (P < 0.05). Phylogenetic analysis revealed the tendency of E. coli isolated from IBD patients to be grouped into separate clonal clusters based on their allelic profiles (P = 0.02). A link was detected between uropathogenic E. coli (UPEC) CFT073 and strains isolated from IBD, with regards to gene distribution and virulence, using microarray technology. Amino acid substitutions N91S and S99N in FimH, the adhesive subunit of E. coli type I fimbria, were significantly associated to IBD (P < 0.05). This study demonstrated an increase in the microbial diversity of non-inflamed IBD tissues and suggested a recruitment phase of bacterial adherence and colonization, before the inflammation sets in. Furthermore, E. coli isolated from IBD tissues were distinct from commensal strains in both clonal and virulence characteristics and shared remarkable traits with extraintestinal pathogenic E. coli. Features involved in bacterial adhesion to epithelial cells may hold the key to E. coli pathogenesis in IBD.

Inflammatory bowel disease (IBD), comprises Crohn’s disease (CD) and ulcerative colitis (UC), and is a chronic relapsing inflammation of gastrointestinal tract without any known cause or cure. Currently, it is accepted that IBD is a result of a dysfunctional immune response to commensal bacteria in a genetically susceptible host, and that environmental factors can trigger the onset or reactivation of the disease. This thesis considers the possibility of a specific pathogenic agent as well as an imbalance in the composition of the normal microflora in the pathogenesis of IBD. Gut biopsy tissues were taken from a population-based case-control tissue bank held at the University of Manitoba. Automated ribosomal intergenic spacer analysis (ARISA) and terminal restriction fragment length polymorphisms (T-RFLP) were employed to assess the diversity of gut microbiota. The phylogenetic, virulence and biochemical characteristics of Escherichia coli isolated from IBD biopsies were examined using multi-locus sequence typing (MLST), DNA microarray technology and API 20E system. Utilizing ARISA and T-RFLP, a remarkable increase in the order of unclassified Clostridia was detected in inflamed tissues, particularly in CD patients (P < 0.05). Moreover, species richness and diversity were the highest in non-inflamed IBD biopsies. Culture-based quantification detected a significantly higher number of E. coli in IBD tissues (P < 0.05). Phylogenetic analysis revealed the tendency of E. coli isolated from IBD patients to be grouped into separate clonal clusters based on their allelic profiles (P = 0.02). A link was detected between uropathogenic E. coli (UPEC) CFT073 and strains isolated from IBD, with regards to gene distribution and virulence, using microarray technology. Amino acid substitutions N91S and S99N in FimH, the adhesive subunit of E. coli type I fimbria, were significantly associated to IBD (P < 0.05). This study demonstrated an increase in the microbial diversity of non-inflamed IBD tissues and suggested a recruitment phase of bacterial adherence and colonization, before the inflammation sets in. Furthermore, E. coli isolated from IBD tissues were distinct from commensal strains in both clonal and virulence characteristics and shared remarkable traits with extraintestinal pathogenic E. coli. Features involved in bacterial adhesion to epithelial cells may hold the key to E. coli pathogenesis in IBD.

Metabolic bone disease is a frequent complication of Crohn’s disease (CD) with the pathogenesis of reduced bone mass in CD reported to include body weight, disease severity, disease treatments and surgery, physical activity and nutritional status. To date, there have been no studies to examine the prevalence of osteopenia and osteoporosis in an Australian CD population. Similarly, the roles of disease state and treatment, lifestyle factors and the role of body composition in the development of bone loss in CD have not been examined in an Australian CD cohort to date. This thesis has sought, for the first time, to determine the prevalence and severity of bone loss in an Australian CD population and to examine the relationship between various clinical, genetic, lifestyle and treatment variables. The role of body composition in bone loss was assessed by close examination of the muscle-bone relationship by dual-energy X-ray absorptiometry (DXA) and the local muscle-bone unit by peripheral quantitative computed tomography (pQCT) so that informed targeted treatment strategies may be implemented. Study 1 assessed the prevalence of bone loss and both molecular and clinical risk factors for bone loss in a large Crohn’s disease population. Bone mineral density (BMD) data were combined with clinical information and correlated with single nucleotide polymorphisms within the TNF-α, interleukin-10, and NOD2/CARD15 genes. Study 2 examined the independent effects of body composition and muscle strength on regional and whole body BMD in a cohort of CD patients to determine their relative importance to bone strength in this population. Study 3 used pQCT for the first time in a CD population to assess the functional muscle-bone unit in order to determine if the high prevalence of low bone mass reported in CD patients is mediated by altered body composition, in particular muscle mass and strength. Study 1 revealed 45% of CD patients had previously been diagnosed with osteopenia and 18% with osteoporosis. Both the TNF-α “GT” haplotype and the -857 “CC” genotype showed strong associations with bone mineral density overall (p=0.003 and p=0.002, respectively). Body mass index (p=0.01) and previous bowel resection in females (p=0.03) were predictive of a higher spine bone density, whilst body mass index (p=0.003) and the effect of years since first bowel resection (p=0.02) remained independent predictors of proximal femur bone mineral density. When bone mineral density was assessed in Study 2, the prevalence of osteopenia and osteoporosis was 32% and 17%, respectively, with osteopenia more common at the hip and osteoporosis more common at the spine. In multiple regression analyses, appendicular muscle mass was an independent predictor of whole body and regional BMD while lean mass was an independent predictor at the hip. Neither grip strength nor fat mass were independently associated with BMD. Of the components of body composition, muscle mass was strongly associated with regional and whole body bone mineral density. When the muscle-bone unit was assessed using pQCT in Study 3 to further examine this relationship, CD patients demonstrated lower tibial shaft mass, tibial shaft cortical cross-sectional area, and proximal tibia bone mineral density than similarly aged healthy controls. CD subjects also had significantly lower areal bone mineral density by DXA than controls at the total body (P=0.038) and hip (P=0.019). There were no significant differences between groups for any of the muscle-bone indices assessed, such as bone mineral content/muscle cross-sectional area and bone cross sectional area / muscle strength. Together, these studies have demonstrated a high prevalence of metabolic bone disease in an Australian CD population. We were able to identify a novel protective association between a TNF-α haplotype and bone mineral density and also confirmed the importance of body mass index and intestinal resection on bone loss in this population. Furthermore, these studies indicated that lean mass, and more specifically muscle mass, was a significant independent predictor of regional and whole body BMD. Consequently, maintaining or increasing muscle mass in this patient population may have a positive effect on BMD and prevent the development of osteopenia and osteoporosis. Although only modest differences were found between CD patients and controls for areal BMD by DXA and some bone parameters by pQCT, there were no differences in indices of the muscle-bone unit. These results suggest that bone strength is adequate for muscle size and strength in our sample of male CD patients with well-controlled disease, inferring that no specific intervention is required to correct expected deficiencies in this relationship. Instead, an exercise training program introduced to this patient cohort should aim to maintain or increase bone mass through weight-bearing exercises as well as encourage the maintenance or increase in muscle mass.

No description available.

Sammanfattning:  Bakgrund: Inflammatory Bowel Disease, IBD är ett samlingsnamn för kroniska inflammatoriska tarmsjukdomar som består av Crohns sjukdom (CD) och ulcerös kolit (UC). Sjukdomen går i skov och har symtom som frekventa diarréer, feber, rektal blödning, buksmärtor och viktnedgång.  Syfte:Syftet med studien var att beskriva personers upplevelser av att leva med IBD samt att presentera vilken undersökningsgrupp som beskrivits i de inkluderade artiklarna. Metod: Studien var en litteraturstudie med deskriptiv design baserad på 10 artiklar med kvalitativ ansats. Artiklarna söktes i databaser CINAHL och PubMed.  Huvudresultat:Personer med IBD upplever att både de själva och omgivningen saknar kunskaper om sjukdomen. De känner oro och osäkerhet över läkemedelseffekter, sjukdomens utveckling och återfall. Personer som hade levt med IBD under många år har utvecklat strategier för att klara av olika situationer. Deltagarna i de inkluderade studier är vuxna män och kvinnor i olika åldrar som kommer från olika länder.  Slutsats:Personer med IBD beskriver flertal upplevelser av att leva med sjukdomen. Det framkommer att en stor del av personernas problem uppstår på grund av brister på kunskap om sjukdomen. Det leder till att de drabbade personerna har svårt att hantera sina dagliga sysselsättningar och har oro inför framtiden. Patienterna behöver få bra information och individanpassat stöd för att höja KASAM, utveckla egna strategier och hantera sjukdomen på ett bättre sätt. / Abstract Background:Inflammatory Bowel Disease, IBD is a collective name for chronic inflammatory bowel disease consisting of Crohn's disease (CD) and ulcerative colitis (UC). The disease is in episode and has symptoms such as frequent diarrhea, fever, rectal bleeding, abdominal pain and weight loss. Aim: The purpose of the study was to describe people's experiences of living with IBD and to present which research group described in the included articles. Method: The study was a literature study with descriptive design based on 10 articles with qualitative approach. Articles were searched from databases CINAHL and PubMed.  Main Results: People with IBD experience that both themselves and the environment lack knowledge about the disease. They feel anxiety and insecurity about drug effects, disease development and relapse. People who had been living with IBD for many years have developed strategies to cope with different situations. Participants in the included studies are adult men and women of different ages from different countries. Conclusions: People with IBD describe several experiences of living with the disease. It appears that a large part of the people's problems arise due to lack of knowledge about the disease. This means that the affected people are having difficulty managing their daily life and are worried about the future. Patients need to get good information and personalized support to raise KASAM, to develop their own strategies and manage the disease in a better way.

The thesis deals with the lifestyle of patients with chronic intestinal disease. The theoretical part contains topics of theoretical knowledge essential to the orientation in the issue. It describes the principles of a healthy lifestyle, the issue of chronic intestinal disease, especially Crohn's disease and ulcerative colitis as a disease of clinical manifestations, from diagnosis to treatment. An important chapter of the theoretical part of the work are the impacts of IBD on lifestyle at chronically ill patients. The empirical part deals with the qualitative research. For datas collecting was chosen and used the method of questioning with narrative interview technique. Methodology of narrative interview was expanded to include specific methods of collection datas, the life curve method. The content of each interpretation is the final report that summarizes the observed facts associated with answers to research questions. Significant elements of the interviews are recorded in tables. The aim of the thesis was to find out in what areas and how the selected people with chronic intestinal diseases have changed their lifestyle. To provide information to the public about the limitations of patients with chronic intestinal diseases that directly affect their everyday lives. Finally to assist society tolerance to constraints of patients with chronic intestinal disease.

Crohn's disease is a chronic inflammatory disease that affects the entire gastrointestinal tract in all its layers.The theoretical part deals with the characteristics of the disease, its causes, symptoms, complications, treatment and psychological aspects. It also touches on the needs of children and communication with a chronically ill child.At first, this work set out to achieve two goals: mapping the provision of nursing care to children with Crohn's disease in hospitals and determining the impact of Crohn's disease on the everyday life of a child. A third goal, gathering respondents' views on the possibilities of community nurses in collective institutions, was encountered during the research and was added.The empirical part was carried out using qualitative research method using semi-structured interviews both with health professionals working at pediatric wards, as well as children with Crohn's disease and their parents.Survey results show that children with Crohn's disease come in contact with health workers at various departments of health facilities. The most common early symptoms of Crohn's disease in children included abdominal pain, diarrhea with blood or mucus and failure to thrive. The most common areas affected were the gastrointestinal tract, the small intestine, the colon in one case and the rectum in another.Some workers did not know which tests or treatments their hospital prescribes to the children.They report pain as the main nursing challenge, but this did not reflect in nursing practice.In all departments, except one, there was no material on Crohn's disease, which would have been helpful to the workers.Interviews with children and parents, as well as with health workers confirmed that the disease has a socio-cultural impact on the child and those around it. The results of this diploma thesis were presented at three conferences and will be published.