A comparative radiographic and pathological study of intestinal vaso-architecture in Crohn's disease and in ulcerative colitis

Brahme, Folke; Lindström, C

doi:10.1136/gut.11.11.928

Cited by 117 publications

(59 citation statements)

References 12 publications

(22 reference statements)

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“…Vascular changes in IBD were noted as early as 1954 and throughout the late 1950s and 1960s; however, descriptions of these vascular changes and the interpretations of what they meant varied widely (8,78,125,164). In 1970, Brahme and Lindstrom (21) reported increases in vascularity in active Crohn's disease which they showed by radiography of vascular castings. Recent forays into human and experimental colitis have further indicated an important role for the microvasculature in IBD (58,79,85).…”

Section: Ibd Pathogenesismentioning

confidence: 99%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

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Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

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Section: Ibd Pathogenesismentioning

confidence: 99%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

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“…Thus, vascular injury and diminished blood flow will result in tissue hypoxia and damage of epithelial cells. 5 Anatomical and functional vascular changes in UC have been noted some time ago 6,7 and confirmed recently. 8 In early stages of UC, angiographic studies have demonstrated tortuous, dilated vessels, abnormal distribution, and small luminal irregularities in the peripheral branches.…”

mentioning

confidence: 99%

“…In contrast, advanced UC lesions demonstrated reduced vessel diameter, decreased vascular density, and diminished blood flow in the involved segments. 6,7 Hatoum et al 9 found in UC patients decreased vasodilatory capacity in chronically inflamed mucosa, which was associated with high levels of oxidative stress. A study of trinitrobenzene sulfonic acid (TNBS)-induced UC showed decreased colonic capillary blood flow in acute stage.…”

mentioning

confidence: 99%

Early endothelial damage and increased colonic vascular permeability in the development of experimental ulcerative colitis in rats and mice

Tolstanova

Deng

French

et al. 2012

Laboratory Investigation

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The role of endothelial damage and increased vascular permeability (VP) in the pathogenesis of ulcerative colitis (UC) has not been investigated. We examined using functional, morphologic, and molecular biologic studies whether and to what extent the endothelial barrier dysfunction precedes enhanced epithelial permeability (EP) and the development of mucosal lesions during the early stages of experimental UC. We showed that in rats with iodoacetamide (IA)-induced UC increased colonic VP occurs early (ie, 2.6-fold increase at 15 min, Po0.01) preceding changes in epithelial barrier permeability. EP was unchanged at 15 and 30 min after IA administration and was increased 1.9-fold at 1 h and 6.7-fold at 2 h (both Po0.001) after IA. In the dextran sodium sulfate-induced slowly developing UC, colonic VP was significantly increased in 2 days (Po0.05) and EP only in 4 days (Po0.05). Mucosal endothelial injury led to hypoxia (Po0.05) of colonic surface epithelial cells 30 min after IA administration that was associated with increased expressions of transcription factors hypoxia-inducible factor-1a and early growth response-1. Electron and light microscopy demonstrated areas of colonic mucosa with perivascular edema covered by intact layer of surface epithelial cells in both rat and mouse models of UC. This is the first demonstration in four models of UC that endothelial damage, increased colonic VP, perivascular edema, and epithelial hypoxia precede epithelial barrier dysfunction that is followed by erosions, ulceration, and inflammation in UC. KEYWORDS: endothelial damage; epithelial permeability; hypoxia; inflammatory bowel disease; ulcerative colitis; vascular permeability Ulcerative colitis (UC) is characterized by chronic, recurrent ulcers and inflammation of the colonic mucosa. It has been postulated that impaired epithelial barrier function, resulting in penetration of bacteria and other antigens into the mucosa, is one of the major factors of UC pathogenesis.

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“…Inflammatorisk tarmsykdom er assosiert med nydanning av blodkar og økt blodtilfør-sel i veggen til de betente tarmsegmentene (28). Fargedoppler kan brukes til å vurdere kartetthet semikvantitativt (fig 6) og er til en viss grad assosiert med sykdomsaktivitet (29,30).…”

Section: Behandlingsovervåkning Og Sykdomsaktivitetunclassified

Transabdominal ultrasonografi ved inflammatorisk tarmsykdom

Naevdal¹,

Nylund²,

Gilja³

2010

Tidsskriftet

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SammendragBakgrunn. Transabdominal ultrasonografi er de siste 15 årene blitt brukt i økende grad til å vurdere pasienter med inflammatorisk tarmsykdom. Ved Medisinsk avdeling, Haukeland universitetssykehus utføres om lag 300 slike undersøkelser årlig. Artikkelen gir en oversikt over bruk av ultrasonografi ved ulcerøs kolitt og Crohns sykdom.Materiale og metode. Artikkelen er basert på ikke-systematiske søk i PubMed samt materiale fra vårt eget litteraturarkiv.Resultater. Ved Crohns sykdom ses ofte strukturendringer i og fortykkelse av tarmveggen med transabdominal ultrasonografi. Ved ulcerøs kolitt er strukturen ofte bevart, sykdommen begrenset til tykktarmen og veggen lett eller moderat fortykket. Sensitiviteten og spesifisiteten for å oppdage inflammatorisk tarmsykdom ligger rundt henholdsvis 85 % og 95 %. For Crohns sykdom alene er tilsvarende funn 88 % og 93 %. Hos pasienter med komplisert Crohns sykdom er transabdominal ultrasonografi best til påvisning av stenoser (sensitivitet 74-100 %, spesifisitet 91-100 %) og noe dårligere til å påvise fistler (sensitivitet 71 %, spesifisitet 96 %) og abscesser (sensitivitet 81 %, spesifisitet 93 %). Lokal hyperemi i tarmveggen taler for aktiv inflammasjon og kan påvises med fargedoppler.Fortolkning. Transabdominal ultrasonografi er nyttig ved primaerutredning og oppfølging av pasienter med inflammatorisk tarmsykdom. At klinikerne selv utfører undersøkelsen, gir potensielt mer effektiv og billigere primaerutredning og oppfølging av pasienter med inflammatorisk tarmsykdom.Insidensen og prevalensen for Crohns sykdom og ulcerøs kolitt er høy i Skandinavia, Storbritannia og Nord-Amerika, og økende i andre land med vestlig livsstil (1). Transabdominal ultrasonografi av tarm er en ikkeinvasiv, lett tilgjengelig undersøkelsesmeto-de som de siste 15 årene er blitt benyttet i diagnostikk av inflammatorisk tarmsykdom. I motsetning til en del andre undersøkelses-metoder, som CT, MR og røntgen av tynntarm med sonde, kan klinikeren selv utføre ultrasonografi og bruke metoden til å undersøke sine «egne» pasienter. Ved Medisinsk avdeling, Haukeland universitetssykehus er ultralydundersøkelser av pasienter med inflammatorisk tarmsykdom inkludert i den daglige rutinen, på linje med endoskopiundersøkelser. Årlig utfører vi ca. 300 undersøkelser på denne typen pasienter.I denne artikkelen ønsker vi å belyse hvordan ultrasonografi kan anvendes til å vurdere pasienter med inflammatorisk tarmsykdom. Hovedfokus er Crohns sykdom, men ulcerøs kolitt blir også omtalt. Materiale og metodeArtikkelen er basert på en gjennomgang av artikler i vårt eget litteraturarkiv, noen relevante referanser hentet fra disse artiklene og våre egne erfaringer med ultrasonografi ved inflammatorisk tarmsykdom. Det er også gjort ikke-systematiske litteratursøk i PubMed, som resulterte i et skjønnsmessig utvalg av artikler. PasientforberedelserUltralydundersøkelser av pasienter med inflammatorisk tarmsykdom krever vanligvis ingen forberedelser. Det er en fordel om pasienten møter fastende (> 4 timer) slik at det blir...

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A comparative radiographic and pathological study of intestinal vaso-architecture in Crohn's disease and in ulcerative colitis

Cited by 117 publications

References 12 publications

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Early endothelial damage and increased colonic vascular permeability in the development of experimental ulcerative colitis in rats and mice

Transabdominal ultrasonografi ved inflammatorisk tarmsykdom

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