Puchitis
Patofizjologia i mechanizm

Pouchitis jest najczęstszym powikłaniem po proktokolektomii odtwórczej z zespoleniem jelitowo-odbytniczym (IPAA), występującym u około 50% pacjentów po operacji z powodu wrzodziejącego zapalenia jelita grubego (WZJG). Patogeneza pouchitis jest wieloczynnikowa i obejmuje dysbiozę mikrobioty jelitowej, zaburzenia bariery jelitowej (m.in. zwiększona ekspresja klaudyny-2), oraz dysfunkcję układu odpornościowego zarówno wrodzonego, jak i adaptacyjnego. Charakterystyczne są zmiany w ekspresji receptorów Toll-podobnych (TLR2, TLR3, TLR4, TLR5), zwiększona produkcja cytokin prozapalnych (TNF-α, IL-1β, IL-6, IL-8, IL-12) oraz aktywacja szlaku STAT1 i interferonu-γ. W błonie śluzowej zbiornika obserwuje się nacieki zapalne z udziałem komórek dendrytycznych i limfocytów T CD4+, co tłumaczy skuteczność terapii immunosupresyjnej, w tym inhibitorów integryny α4β7 (wedolizumab), inhibitorów TNF, IL-12/IL-23 oraz kinazy JAK-STAT3. Genetyczne predyspozycje, takie jak polimorfizmy w genach IL-1, TNF, TLR1 i NOD2/CARD15, również zwiększają ryzyko rozwoju pouchitis. Dysbioza charakteryzuje się m.in. wzrostem Clostridia i Staphylococcus aureus oraz zmniejszeniem Bacteroidetes i Faecalibacterium prausnitzii, co prowadzi do zwiększonej przepuszczalności jelitowej i zmniejszonej produkcji krótkołańcuchowych kwasów tłuszczowych, istotnych dla integralności błony śluzowej.

Patogeneza Pouchitis (Puchitis)

Pouchitis (puchitis) jest najczęstszym powikłaniem po proktokolektomii odtwórczej z zespoleniem jelitowo-odbytniczym (IPAA), występującym u ok. 50% pacjentów po operacji z powodu wrzodziejącego zapalenia jelita grubego (WZJG).1 Patogeneza tego schorzenia jest złożona i wieloczynnikowa, a mechanizmy leżące u podstawy rozwoju pouchitis wciąż nie są w pełni poznane.23

Dysbioza mikrobioty jelitowej

Zaburzenia składu mikrobioty jelitowej (dysbioza) odgrywają kluczową rolę w patogenezie pouchitis.45 Badania wykazały, że u pacjentów z pouchitis występuje zmniejszona różnorodność bakteryjna oraz zmieniona proporcja poszczególnych szczepów bakterii.6 Obserwuje się zwiększoną liczbę bakterii z rodzaju Clostridia w ostrej postaci pouchitis, podczas gdy w przewlekłej postaci obserwuje się wzrost ilości Staphylococcus aureus.7 Dodatkowo zauważono zwiększenie liczby Proteobacteria przy jednoczesnym zmniejszeniu Bacteroidetes i F. prausnitzii.8

Na rolę bakterii w patogenezie pouchitis wskazuje skuteczność antybiotykoterapii w leczeniu tego schorzenia.9 Kolonizacja przez patogenne mikroorganizmy prowadzi do:10

11

Zaburzenia odporności wrodzonej

U pacjentów z pouchitis po operacji z powodu WZJG obserwuje się zaburzenia w funkcjonowaniu układu odporności wrodzonej, które rzadziej występują u pacjentów operowanych z powodu rodzinnej polipowatości gruczolakowatej (FAP).12 Obejmują one:13

  • Dysfunkcję bariery jelitowej ze zwiększoną ekspresją klaudyny-2 w połączeniach ścisłych
  • Nieprawidłowe funkcjonowanie komórek dendrytycznych
  • Zwiększoną ekspresję defensyn
  • Zmiany w ekspresji receptorów Toll-podobnych (TLR), szczególnie TLR4
  • Zwiększoną ekspresję interferonu-γ
  • Aktywację szlaku STAT1 (sygnałowy przekaźnik i aktywator transkrypcji 1)

14

W patogenezie pouchitis obserwuje się zmniejszoną ekspresję TLR3 i zwiększoną ekspresję TLR5 w prawidłowym zbiorniku jelitowym, a także zwiększoną regulację ekspresji TLR2 w pouchitis i TLR4 zarówno w prawidłowym zbiorniku, jak i w pouchitis.15 Te zmiany w ekspresji receptorów rozpoznających wzorce molekularne (PRR) mogą prowadzić do nieprawidłowej odpowiedzi immunologicznej na mikrobiom zbiornika jelitowego.

Dysfunkcja odporności adaptacyjnej

W pouchitis obserwuje się zaburzenia funkcjonowania adaptacyjnej odpowiedzi immunologicznej.16 Zwiększona aktywacja komórek T CD4+ i produkcja interferonu gamma (IFN-γ) są charakterystyczne dla pouchitis.1718 Analiza wieloczynnikowa wykazała, że podwyższone poziomy mRNA IFN-γ są istotnie związane z wystąpieniem pouchitis (p=0,03).19

W patogenezie pouchitis obserwuje się zaburzenia równowagi pomiędzy interleukinem-8 a interleukinem-10.20 Dodatkowo stwierdzono zwiększoną ekspresję:2122

  • TNF-α (czynnik martwicy nowotworu alfa)
  • IL-1β (interleukina 1 beta)
  • IL-6 (interleukina 6)
  • IL-8 (interleukina 8)
  • IL-12 (interleukina 12)

2324

W błonie śluzowej zbiornika jelitowego u pacjentów z pouchitis obserwuje się nacieki zapalne, w tym zwiększony odsetek komórek dendrytycznych wykazujących ekspresję integryny β7, które odgrywają patogenną rolę w patogenezie pouchitis.25 Ta dysregulacja odpowiedzi immunologicznej może tłumaczyć skuteczność leków immunosupresyjnych, takich jak inhibitory integryny α4β7 (wedolizumab), inhibitory TNF, potencjalnie inhibitory IL-12 i IL-23 oraz inhibitory kinazy Janusowej (JAK)-STAT3 w leczeniu przewlekłego pouchitis.26

Czynniki genetyczne

Predyspozycje genetyczne odgrywają istotną rolę w patogenezie pouchitis.27 Zidentyfikowano kilka polimorfizmów genów związanych ze zwiększonym ryzykiem rozwoju pouchitis:28

  • Polimorfizm genu antagonisty receptora interleukiny-1 (IL-1) allel 2
  • Polimorfizm genu czynnika martwicy nowotworu (TNF) allel 2
  • Polimorfizmy w genach TLR1
  • Polimorfizmy w genach NOD2/CARD15

2930

Zaburzenia w szlaku sygnałowym NOD2 mogą przyczyniać się do rozwoju dysbiozy bakteryjnej, która była już wcześniej obecna i predysponowała osoby do rozwoju pouchitis.31 Badania wykazały również, że receptor interleukiny 17A jest odpowiedzialny za patogenezę pouchitis poprzez obniżoną regulację mikroRNA.32

Metaplazja okrężnicza

Zastój kału w zbiorniku jelitowym prowadzi do adaptacyjnych zmian nabłonka w kierunku nabłonka przypominającego okrężniczy.33 W zbiornikach u pacjentów z WZJG zmiany te są bardziej nasilone, nawet bez ostrego zapalenia.34 Metaplazja okrężnicza charakteryzuje się:35

  • Stępieniem kosmków jelitowych
  • Hiperplazją komórek krypt
  • Obecnością antygenów charakterystycznych dla nabłonka okrężnicy, takich jak ludzka tropomiozyna 5

36

Te zmiany mogą zwiększać ryzyko rozwoju pouchitis.37 Podobne zmiany w glikoproteinach mucyny występują w pouchitis, jak w WZJG. Zmienione glikoproteiny mogą być bardziej podatne na enzymatyczną degradację przez bakterie, co czyni barierę śluzową mniej odporną.38

Mechanizmy komórkowe i molekularne

Dysfunkcja bariery jelitowej

Zaburzenia funkcji bariery jelitowej odgrywają istotną rolę w patogenezie pouchitis.39 W biopsji błony śluzowej zbiornika jelitowego po proktokolektomii odtwórczej z powodu WZJG wykazano zwiększoną ekspresję klaudyny-2 oraz zaburzenia w funkcjonowaniu komórek dendrytycznych.40

Długotrwałe zapalenie może prowadzić do erozji wyściółki zbiornika, co skutkuje powstawaniem owrzodzeń, które mogą krwawić. Niektóre patogenne bakterie mogą również aktywnie uszkadzać barierę jelitową.41 Przewlekłe zapalenie może prowadzić do bliznowacenia zbiornika, co powoduje zwężenie ujścia i zmniejszenie przepływu krwi do zbiornika, co z kolei zaburza proces gojenia.42

Zaburzenia metabolizmu krótkołańcuchowych kwasów tłuszczowych

Pouchitis, podobnie jak aktywne WZJG, wiąże się z upośledzonym utlenianiem maślanu przez błonę śluzową jelita.43 Zmniejszenie produkcji krótkołańcuchowych kwasów tłuszczowych przyczynia się do rozwoju zapalenia w zbiorniku jelitowym.44 Kwasy te pełnią ważną funkcję w utrzymaniu integralności błony śluzowej i regulacji odpowiedzi immunologicznej.45

Mechanizmy prozapalne

W patogenezie pouchitis obserwuje się zwiększoną produkcję mediatorów zapalnych, w tym:46

  • Cytokin (IL-1, IL-6, IL-8)
  • Cząsteczek adhezyjnych (selektyna E, cząsteczka adhezji międzykomórkowej-1)
  • Czynnika aktywującego płytki krwi
  • Produktów kwasu arachidonowego (leukotrien B4, prostaglandyna E2)
  • Prozapalnych neuropeptydów
  • Białka zapalnego makrofagów 2 (MIP-2)
  • Metaloproteinaz macierzy (MMP-1, MMP-2, MMP-9)
  • MRP-14
  • Indukowalnej syntazy tlenku azotu

47

Zaburzenia równowagi między cytokinami prozapalnymi a immunoregulacyjnymi (IL-2, interferon-γ, IL-4, IL-10) są również obserwowane u pacjentów z pouchitis.48

Pouchitis jako choroba transmuralna

Nowsze koncepcje patogenezy pouchitis wskazują na możliwość, że jest to choroba transmuralna (obejmująca całą grubość ściany jelita) z potencjalnym udziałem komórek niebędących komórkami układu odpornościowego, w tym komórek podścieliska, w podtrzymywaniu zapalenia i dysfunkcji bariery jelitowej.49 Ta koncepcja zbliża pouchitis do modelu patogenezy choroby Leśniowskiego-Crohna, gdzie zapalenie obejmuje wszystkie warstwy ściany jelita.

Spektrum choroby zapalnej zbiornika

Pouchitis stanowi spektrum chorób o różnym przebiegu i patogenezie. Na podstawie odpowiedzi na leczenie można wyróżnić następujące postaci:5051

  • Ostra postać pouchitis reagująca na antybiotyki – gdzie główny mechanizm patogenetyczny związany jest z zaburzeniami mikrobioty
  • Przewlekła pouchitis zależna od antybiotyków (CADP) – gdzie pacjent wymaga ciągłego leczenia antybiotykami dla utrzymania remisji
  • Przewlekła pouchitis oporna na antybiotyki (CARP) – gdzie dominują mechanizmy immunologiczne, a nie dysbiotyczne

5253

Ta progresja sugeruje, że etiopatogeneza ewoluuje od zapalenia mediowanego przez mikroorganizmy do zapalenia przeważnie mediowanego przez mechanizmy immunologiczne.54

Pouchitis związana z IgG4

Podgrupa pacjentów z pouchitis wykazuje cechy procesu zapalnego związanego z immunoglobuliną G4 (IgG4), charakteryzującego się:5556

  • Zapaleniem zbiornika i odcinka jelita przed zbiornikiem
  • Obecnością autoprzeciwciał
  • Podwyższonym poziomem IgG4 w surowicy
  • Zwiększoną liczbą komórek wykazujących ekspresję IgG4 w błonie śluzowej zbiornika
  • Współwystępowaniem innych chorób autoimmunologicznych

5758

Pouchitis związana z IgG4 (definiowana jako zwiększona liczba infiltrujących komórek plazmatycznych IgG4-dodatnich) charakteryzuje się klinicznie zwiększoną częstością występowania przewlekłej pouchitis opornej na antybiotyki (CARP), a także współwystępowaniem z klinicznymi markerami procesu immunologicznego.59 Pacjenci z podwyższonym poziomem IgG4 w surowicy mieli znacząco wyższe podskale objawów PDAI (Pouchitis Disease Activity Index) w porównaniu do pacjentów z normalnym poziomem IgG4 w surowicy.60

Czynniki ryzyka pouchitis

Czynniki związane z chorobą podstawową

Pouchitis występuje znacznie częściej u pacjentów po proktokolektomii z powodu WZJG (do 60%) niż u pacjentów operowanych z powodu rodzinnej polipowatości gruczolakowatej (FAP) (0-10%).61 Sugeruje to, że podstawowa patogeneza WZJG może znacząco przyczyniać się do rozwoju pouchitis.62

Czynniki ryzyka związane z WZJG obejmują:6364

  • Rozległe WZJG i zapalenie boczne jelita krętego (backwash ileitis) przed kolektomią
  • Obecność pozajelitowych manifestacji choroby
  • Status osoby niepalącej
  • Polimorfizm genu antagonisty receptora IL-1
  • Obecność przeciwciał pANCA (przeciwciała przeciw cytoplazmie neutrofilów)

6566

W analizie wieloczynnikowej wskazano, że czynniki związane ze zwiększonym ryzykiem rozwinięcia przewlekłej pouchitis opornej na antybiotyki (CARP) to obecny status palenia (skorygowany współczynnik ryzyka 2,96; 95% CI 1,27-6,90; p=0,01) oraz wcześniejsze stosowanie leków biologicznych/małych cząsteczek (skorygowany współczynnik ryzyka 2,40; 95% CI 1,05-5,53; p=0,04).67

Ostre ciężkie WZJG

Ostre ciężkie WZJG (ASUC) w momencie kolektomii wiązało się ze zwiększonym prawdopodobieństwem wystąpienia ostrej pouchitis (HR 1,53 95% CI (1,06-2,22)).68 Jednocześnie starszy wiek w momencie kolektomii (HR 0,98 95% CI (0,97-0,99)) istotnie wiązał się ze zmniejszonym prawdopodobieństwem ostrej pouchitis, podczas gdy większa liczba leków biologicznych przed kolektomią (HR 1,30 95% CI (1,05-1,62)) wiązała się ze zwiększonym prawdopodobieństwem ostrej pouchitis.69

Pierwotne stwardniające zapalenie dróg żółciowych

Ryzyko rozwoju pouchitis jest zwiększone u pacjentów z pierwotnym stwardniającym zapaleniem dróg żółciowych (PSC). Dowody sugerują, że skumulowane ryzyko pouchitis po jednym, dwóch, pięciu i dziesięciu latach wynosi 15,5%, 22,5%, 36% i 45,5% u pacjentów bez PSC oraz 22%, 43%, 61% i 79% u pacjentów z jednoczesnym PSC.70

Etiologia pouchitis związanej z PSC pozostaje nieznana. Jednym z możliwych mechanizmów patofizjologicznych może być dysbioza w zbiorniku jelitowym.71

Leki przeciwzapalne niesteroidowe

Stosowanie niesteroidowych leków przeciwzapalnych (NLPZ) zwiększa ryzyko rozwoju pouchitis 3,24 razy (95% przedział ufności 1,71-6,13).72 NLPZ zostały zidentyfikowane jako jeden z czynników przyczyniających się do patogenezy pouchitis.73

Podobieństwa do nieswoistych chorób zapalnych jelit

Istnieje wiele podobieństw między pouchitis a chorobami zapalnymi jelit, takimi jak WZJG i choroba Leśniowskiego-Crohna.74 Podobnie jak w przypadku tych chorób, zapalenie błony śluzowej występujące w pouchitis jest zlokalizowane w obszarach o najwyższym stężeniu bakterii.75

Zarówno pouchitis, jak i choroba Leśniowskiego-Crohna:76

  • Są stanami zapalnymi, które mogą dotyczyć jelita cienkiego
  • Reagują na leczenie antybiotykami
  • Ulegają poprawie po odwróceniu strumienia kałowego

77

Co ważne, te metody leczenia nie są skuteczne w WZJG. Sugerowano, że pouchitis może stanowić nową, trzecią formę nieswoistych chorób zapalnych jelit (IBD).78 Różnice w odpowiedzi na leczenie obserwowane u pacjentów z pouchitis w porównaniu z WZJG i chorobą Leśniowskiego-Crohna mogą pasować do tej koncepcji.79

Interesującym aspektem pouchitis jest to, że występuje prawie wyłącznie u pacjentów z WZJG. Istnieją podobieństwa w zakresie prezentacji klinicznej i nieprawidłowości immunologicznych między pouchitis a WZJG, co sugeruje, że podgrupa pouchitis może faktycznie reprezentować nawrót choroby podobnej do WZJG w zbiorniku jelitowym.80 Dodatkowo, niektórzy pacjenci z pouchitis mają te same pozajelitowe manifestacje (takie jak artralgia i pierwotne stwardniające zapalenie dróg żółciowych) jak pacjenci z WZJG.81

Podsumowanie patogenezy

Patogeneza pouchitis jest złożona i obejmuje interakcję między różnymi czynnikami, w tym:8283

  • Genetyczną predyspozycją
  • Zmianami w mikrobiomie jelitowym (dysbiozą)
  • Zaburzeniami bariery jelitowej
  • Dysfunkcją układu immunologicznego (wrodzonego i adaptacyjnego)
  • Metaplazją okrężniczą błony śluzowej zbiornika
  • Czynnikami środowiskowymi (np. stosowaniem NLPZ)

8485

Obecne dowody sugerują, że interakcje między zmienionym składem i/lub ilością mikrobioty jelitowej (dysbioza), ze zmienionymi cechami błony śluzowej (metaplazja okrężnicza), w połączeniu z nieprawidłowościami wrodzonej i adaptacyjnej odporności błony śluzowej, odgrywają kluczową rolę w patogenezie pouchitis.86

Zrozumienie złożonych mechanizmów patogenetycznych pouchitis jest kluczowe dla opracowania skutecznych strategii terapeutycznych, szczególnie w przypadku przewlekłych postaci opornych na antybiotyki, gdzie mechanizmy immunologiczne mogą dominować nad dysbiozą w podtrzymywaniu stanu zapalnego.87

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  1. 26.04.2026
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Materiały źródłowe

  • #1 Gastroenterology Education and CPD for trainees and specialists » Pouchitis
    https://www.gastrotraining.com/category/inflammatory-bowel-disease/ulcerative-colitis/pouchitis
    Pouchitis is the inflammation of the ileal pouch reservoir. It is the most common long-term complication in patients with IPAA which significantly affects patients quality of life. It is estimated that approximately 50% of patients who have undergone IPAA surgery for UC will develop at least one episode of pouchitis. […] Pouchitis almost exclusively occurs in patients with underlying UC and is rarely seen in patients with FAP. Although the etiology and pathogenesis of pouchitis are not entirely clear, bulk of evidence points towards an abnormal mucosal immune response (innate and adaptive) to altered microflora in the pouch leading to acute and/or chronic inflammation.
  • #2 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Restorative proctocolectomy (RPC) with ileal pouch-anal anastomosis is the operation of choice for patients with ulcerative colitis. Pouchitis is the most common cause of pouch dysfunction. Although the pathogenesis of this disease is not well understood, bacteria have been implicated in the disease process. […] Similarly to UC and Crohns disease (CD) the mucosal inflammation that occurs in pouchitis is localized to the areas with the highest concentration of bacteria. There is a tenfold increased risk of pouchitis in patients who undergo RPC for UC compared with FAP. Therefore, it has been suggested that pouchitis represents reactivation of UC in the colonized small bowel of the pouch. […] The pathogenesis of PPI has not been studied. Ischaemia, CD and nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated in some cases, but where these factors have been excluded the pathogenesis is likely to be similar to that of pouchitis where bacteria are considered fundamental to the disease process.
  • #3 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    Pouchitis, the most common long-term complication of the procedure, involves a spectrum of disease processes with heterogeneous risk factors, clinical features, disease courses and prognoses. […] Dysbiosis has been implicated as a triggering factor for pouchitis, and concurrent infection with pathogens, such as Clostridium difficile, might contribute to disease relapse and exacerbation. […] Pouchitis comprises a spectrum of disease, ranging from antibiotic-responsive forms to antibiotic-refractory entities, which involve various aetiological and pathogenetic pathways and have differing clinical presentations, disease courses and prognoses. […] Dysbiosis (quantitative and/or qualitative alterations of the pouch microbiota) has a key role in the initiation and progression of pouchitis.
  • #4 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    Pouchitis, the most common long-term complication of the procedure, involves a spectrum of disease processes with heterogeneous risk factors, clinical features, disease courses and prognoses. […] Dysbiosis has been implicated as a triggering factor for pouchitis, and concurrent infection with pathogens, such as Clostridium difficile, might contribute to disease relapse and exacerbation. […] Pouchitis comprises a spectrum of disease, ranging from antibiotic-responsive forms to antibiotic-refractory entities, which involve various aetiological and pathogenetic pathways and have differing clinical presentations, disease courses and prognoses. […] Dysbiosis (quantitative and/or qualitative alterations of the pouch microbiota) has a key role in the initiation and progression of pouchitis.
  • #5 Microorganisms in the Pathogenesis and Management of Pouchitis | SpringerLink
    https://link.springer.com/chapter/10.1007/978-981-19-4800-8_14
    Pouchitis is the most frequent clinical complication following restorative proctocolectomy with ileal pouch anastomosis surgery to treat inflammatory bowel diseases. […] However, the role of microorganisms in the pathogenesis and management of pouchitis is gaining more attention as dysbiosis is frequently observed in pouchitis cases and most of the time treated with antibiotics. […] Colonization of pathogenic microbes in the pouch leads to an increase in gut permeability, more synthesis of pro-inflammatory factors, a decrease in the production of short-chain fatty acids, and a reduction in helpful host-microbiome diversity. […] The mechanism of action of beneficial bacteria in pouchitis treatment involves inhibition of entry and colonization of pathogenic bacteria by lowering pH of the lumen, production of antimicrobial compounds, and blocking the binding of pathogens.
  • #6 Key Focus Areas in Pouchitis Therapeutic Status: A Narrative Review
    https://ijms.sums.ac.ir/article_50229.html
    Pouchitis, as the most common complication after ileal pouch-anal anastomosis (IPAA), has an incidence from 7% to 46%. […] Although the etiology of pouchitis has remained unclear, the gut microbiome has been hypothesized as a key factor. In patients with pouchitis, there is a decrease in bacterial diversity and an altered abundance of pouch bacteria. […] Interleukin 17 receptor A is responsible for the pathogenesis of pouchitis through downregulation of microRNAs. […] The efficacy of antibiotic therapy for pouchitis can be due to the establishment of an antibiotic-resistant microbiome with low inflammatory potential, while this microbiome can cause resistance against colonization by bacteria that promote inflammation. […] In active pouchitis, a severe infiltration of the mucosa by immune cells happens and an increased proportion of mucosal dendritic cells expressing integrin 7 are noted that have a pathogenic role in the pathogenesis of pouchitis. […] NOD2 signaling pathway could contribute to intrinsic bacterial dysbiosis which was pre-existing and predisposed individuals to pouchitis.
  • #7 Pouchitis, a complication associated with the surgical treatment of ulcerative colitis. Diagnosis and treatment. Review
    http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-99572021000100065
    The exact pathophysiological mechanisms that cause pouchitis are unknown. However, it is more likely to be a multifactorial disease involving genetic predisposition, bacterial overgrowth and dysbiosis in the ileal pouch, among others. Recently, it has been found that in acute pouchitis cases there is an increase of species of the Clostridia genus and, reciprocally, its decrease is associated with response to antibiotic treatment. In contrast, in chronic pouchitis cases there is an increase in the amount of Staphylococcus aureus. Other factors involved in its development may include decreased short-chain fatty acids, nutritional deficiencies, ischemia or immune response alterations. In addition, other authors have considered that pouchitis may be a different inflammatory bowel disease and that several factors increase the risk of developing it. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) increases this risk 3.24 times (95 % confidence interval [CI] 1.71-6.13).
  • #8 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    The findings of the most recent study suggest that a reduction in bacterial diversity but not dysbiosis occurs in pouchitis and that UC RPC patients have a different, less-diverse microbiota with increased Proteobacteria and reduced Bacteroidetes and F. prausnitzii. […] Overall these findings suggest that the pathogenesis of pouchitis is similar to that of UC and CD and that either a reduction in bacterial diversity leads to stimulation of the immune system resulting in mucosal inflammation or that dysbiosis predisposes UC patients to pouchitis by increasing the likelihood of immune system stimulation.
  • #9 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Despite this there are several similarities between pouchitis and CD. Both are inflammatory conditions which can affect the small bowel, both respond to treatment with antibiotics and both improve with diversion of the faecal stream (importantly these treatments are not effective in UC). […] It has been suggested that pouchitis may represent a novel third form of inflammatory bowel disease (IBD). The differences in treatment response seen in pouchitis patients compared with UC and CD could be considered to fit with this. […] An abnormal host-microbial interaction has long been implicated in all forms of IBD including pouchitis. There is evidence from clinical practice to implicate bacteria in pouchitis. […] The results from culture-based studies of pouch microbiota using culture methods are varied and inconclusive. Advances in our understanding of gut microbiota following the introduction of molecular techniques have led to the realization that culture-based techniques are inadequate for the study of gut microbiota.
  • #10 Microorganisms in the Pathogenesis and Management of Pouchitis | SpringerLink
    https://link.springer.com/chapter/10.1007/978-981-19-4800-8_14
    Pouchitis is the most frequent clinical complication following restorative proctocolectomy with ileal pouch anastomosis surgery to treat inflammatory bowel diseases. […] However, the role of microorganisms in the pathogenesis and management of pouchitis is gaining more attention as dysbiosis is frequently observed in pouchitis cases and most of the time treated with antibiotics. […] Colonization of pathogenic microbes in the pouch leads to an increase in gut permeability, more synthesis of pro-inflammatory factors, a decrease in the production of short-chain fatty acids, and a reduction in helpful host-microbiome diversity. […] The mechanism of action of beneficial bacteria in pouchitis treatment involves inhibition of entry and colonization of pathogenic bacteria by lowering pH of the lumen, production of antimicrobial compounds, and blocking the binding of pathogens.
  • #11 Microorganisms in the Pathogenesis and Management of Pouchitis | SpringerLink
    https://link.springer.com/chapter/10.1007/978-981-19-4800-8_14
    Pouchitis is the most frequent clinical complication following restorative proctocolectomy with ileal pouch anastomosis surgery to treat inflammatory bowel diseases. […] However, the role of microorganisms in the pathogenesis and management of pouchitis is gaining more attention as dysbiosis is frequently observed in pouchitis cases and most of the time treated with antibiotics. […] Colonization of pathogenic microbes in the pouch leads to an increase in gut permeability, more synthesis of pro-inflammatory factors, a decrease in the production of short-chain fatty acids, and a reduction in helpful host-microbiome diversity. […] The mechanism of action of beneficial bacteria in pouchitis treatment involves inhibition of entry and colonization of pathogenic bacteria by lowering pH of the lumen, production of antimicrobial compounds, and blocking the binding of pathogens.
  • #12 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #13 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #14 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #15 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    The expression of Toll-like receptors (TLRs) is also altered, with a decreased expression of TLR3 and increased expression of TLR5 in normal ileal pouch, and an upregulation of TLR2 expression in pouchitis and upregulation of TLR4 in both normal pouch and pouchitis. […] An increased cytokine production of IL-1 beta, IL-6, IL-8 and TNF-alpha was seen in pouchitis. […] Risk factors that were identified to be associated with pouchitis include the following: extensive UC and backwash ileitis before colectomy; the presence of extraintestinal manifestations; non-smoker status; IL-1 receptor antagonist gene polymorphism; and the presence of pANCA (antineutrophil cytoplasmic antibodies). […] The treatment consists of controlling the concurrent autoimmune disorders and often requires immunosuppressive agents.
  • #16 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Dysregulated Adaptive Immunity A dysregulated immune response in chronic pouchitis is suggested by several studies and supported by the effectiveness of immunosuppressive treatments such as the α4β7 integrin inhibitor vedolizumab, tumor necrosis factor (TNF) inhibitors, potentially anti-interleukin (IL)-12 and -23 inhibitors, and Janus kinase (JAK)–STAT3 inhibitors. […] There is increased TNF expression in uninflamed UC pouches compared with FAP pouches and in patients with pouchitis. The role of the IL pathway is shown by increased expression of IL-1β, IL-6, IL-8, and IL-12 in pouchitis. […] Chronic pouchitis is a challenging and common complication of IPAA, with pathogenesis evolving from microbially mediated antibiotic-sensitive to antibiotic-resistant and immune-mediated processes.
  • #17 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    Concurrent infections (such as Clostridium difficile) and other triggering factors (such as NSAID use) should be identified and treated or eradicated. […] Pouchitis is associated with mucosal imbalance between interleukin-8 and interleukin-10. […] Pouchitis, similar to active ulcerative colitis, is associated with impaired butyrate oxidation by intestinal mucosa. […] The expression patterns of Toll-like receptors in the ileal pouch mucosa of postoperative ulcerative colitis patients. […] Increased state of activation of CD4 positive T cells and elevated interferon gamma production in pouchitis. […] Increased cytokine transcripts in pouchitis reflect the degree of inflammation but not the underlying entity. […] The bacteriology of pouchitis: a molecular phylogenetic analysis using 16S rRNA gene cloning and sequencing.
  • #18 The relationship between preoperative T helper cytokines in the ileal mucosa and the pathogenesis of pouchitis | BMC Gastroenterology | Full Text
    https://bmcgastroenterol.biomedcentral.com/articles/10.1186/s12876-020-01421-w
    Although the etiology of pouchitis remains unknown, inflammatory cytokines are significantly associated with the pathogenesis of pouchitis. […] The cytokine responses that characterize inflammatory bowel diseases (IBD) are key pathogenic components of the disease. […] In multivariate analysis, elevated IFN- messenger(m)RNA levels were significantly associated with pouchitis onset (p=0.03). […] IFN- expression in the normal ileal mucosa at the time of colectomy may be an important factor in the pathophysiology of pouchitis. […] Pouchitis is a heterogeneous disorder with a combination of various underlying case. […] Our data suggest that IFN- expression in the normal ileal mucosa at the time of colectomy may be an important factor in the pathophysiology of pouchitis.
  • #19 The relationship between preoperative T helper cytokines in the ileal mucosa and the pathogenesis of pouchitis | BMC Gastroenterology | Full Text
    https://bmcgastroenterol.biomedcentral.com/articles/10.1186/s12876-020-01421-w
    Although the etiology of pouchitis remains unknown, inflammatory cytokines are significantly associated with the pathogenesis of pouchitis. […] The cytokine responses that characterize inflammatory bowel diseases (IBD) are key pathogenic components of the disease. […] In multivariate analysis, elevated IFN- messenger(m)RNA levels were significantly associated with pouchitis onset (p=0.03). […] IFN- expression in the normal ileal mucosa at the time of colectomy may be an important factor in the pathophysiology of pouchitis. […] Pouchitis is a heterogeneous disorder with a combination of various underlying case. […] Our data suggest that IFN- expression in the normal ileal mucosa at the time of colectomy may be an important factor in the pathophysiology of pouchitis.
  • #20 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    Concurrent infections (such as Clostridium difficile) and other triggering factors (such as NSAID use) should be identified and treated or eradicated. […] Pouchitis is associated with mucosal imbalance between interleukin-8 and interleukin-10. […] Pouchitis, similar to active ulcerative colitis, is associated with impaired butyrate oxidation by intestinal mucosa. […] The expression patterns of Toll-like receptors in the ileal pouch mucosa of postoperative ulcerative colitis patients. […] Increased state of activation of CD4 positive T cells and elevated interferon gamma production in pouchitis. […] Increased cytokine transcripts in pouchitis reflect the degree of inflammation but not the underlying entity. […] The bacteriology of pouchitis: a molecular phylogenetic analysis using 16S rRNA gene cloning and sequencing.
  • #21 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Dysregulated Adaptive Immunity A dysregulated immune response in chronic pouchitis is suggested by several studies and supported by the effectiveness of immunosuppressive treatments such as the α4β7 integrin inhibitor vedolizumab, tumor necrosis factor (TNF) inhibitors, potentially anti-interleukin (IL)-12 and -23 inhibitors, and Janus kinase (JAK)–STAT3 inhibitors. […] There is increased TNF expression in uninflamed UC pouches compared with FAP pouches and in patients with pouchitis. The role of the IL pathway is shown by increased expression of IL-1β, IL-6, IL-8, and IL-12 in pouchitis. […] Chronic pouchitis is a challenging and common complication of IPAA, with pathogenesis evolving from microbially mediated antibiotic-sensitive to antibiotic-resistant and immune-mediated processes.
  • #22 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    The expression of Toll-like receptors (TLRs) is also altered, with a decreased expression of TLR3 and increased expression of TLR5 in normal ileal pouch, and an upregulation of TLR2 expression in pouchitis and upregulation of TLR4 in both normal pouch and pouchitis. […] An increased cytokine production of IL-1 beta, IL-6, IL-8 and TNF-alpha was seen in pouchitis. […] Risk factors that were identified to be associated with pouchitis include the following: extensive UC and backwash ileitis before colectomy; the presence of extraintestinal manifestations; non-smoker status; IL-1 receptor antagonist gene polymorphism; and the presence of pANCA (antineutrophil cytoplasmic antibodies). […] The treatment consists of controlling the concurrent autoimmune disorders and often requires immunosuppressive agents.
  • #23 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Dysregulated Adaptive Immunity A dysregulated immune response in chronic pouchitis is suggested by several studies and supported by the effectiveness of immunosuppressive treatments such as the α4β7 integrin inhibitor vedolizumab, tumor necrosis factor (TNF) inhibitors, potentially anti-interleukin (IL)-12 and -23 inhibitors, and Janus kinase (JAK)–STAT3 inhibitors. […] There is increased TNF expression in uninflamed UC pouches compared with FAP pouches and in patients with pouchitis. The role of the IL pathway is shown by increased expression of IL-1β, IL-6, IL-8, and IL-12 in pouchitis. […] Chronic pouchitis is a challenging and common complication of IPAA, with pathogenesis evolving from microbially mediated antibiotic-sensitive to antibiotic-resistant and immune-mediated processes.
  • #24 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    The expression of Toll-like receptors (TLRs) is also altered, with a decreased expression of TLR3 and increased expression of TLR5 in normal ileal pouch, and an upregulation of TLR2 expression in pouchitis and upregulation of TLR4 in both normal pouch and pouchitis. […] An increased cytokine production of IL-1 beta, IL-6, IL-8 and TNF-alpha was seen in pouchitis. […] Risk factors that were identified to be associated with pouchitis include the following: extensive UC and backwash ileitis before colectomy; the presence of extraintestinal manifestations; non-smoker status; IL-1 receptor antagonist gene polymorphism; and the presence of pANCA (antineutrophil cytoplasmic antibodies). […] The treatment consists of controlling the concurrent autoimmune disorders and often requires immunosuppressive agents.
  • #25 Key Focus Areas in Pouchitis Therapeutic Status: A Narrative Review
    https://ijms.sums.ac.ir/article_50229.html
    Pouchitis, as the most common complication after ileal pouch-anal anastomosis (IPAA), has an incidence from 7% to 46%. […] Although the etiology of pouchitis has remained unclear, the gut microbiome has been hypothesized as a key factor. In patients with pouchitis, there is a decrease in bacterial diversity and an altered abundance of pouch bacteria. […] Interleukin 17 receptor A is responsible for the pathogenesis of pouchitis through downregulation of microRNAs. […] The efficacy of antibiotic therapy for pouchitis can be due to the establishment of an antibiotic-resistant microbiome with low inflammatory potential, while this microbiome can cause resistance against colonization by bacteria that promote inflammation. […] In active pouchitis, a severe infiltration of the mucosa by immune cells happens and an increased proportion of mucosal dendritic cells expressing integrin 7 are noted that have a pathogenic role in the pathogenesis of pouchitis. […] NOD2 signaling pathway could contribute to intrinsic bacterial dysbiosis which was pre-existing and predisposed individuals to pouchitis.
  • #26 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Dysregulated Adaptive Immunity A dysregulated immune response in chronic pouchitis is suggested by several studies and supported by the effectiveness of immunosuppressive treatments such as the α4β7 integrin inhibitor vedolizumab, tumor necrosis factor (TNF) inhibitors, potentially anti-interleukin (IL)-12 and -23 inhibitors, and Janus kinase (JAK)–STAT3 inhibitors. […] There is increased TNF expression in uninflamed UC pouches compared with FAP pouches and in patients with pouchitis. The role of the IL pathway is shown by increased expression of IL-1β, IL-6, IL-8, and IL-12 in pouchitis. […] Chronic pouchitis is a challenging and common complication of IPAA, with pathogenesis evolving from microbially mediated antibiotic-sensitive to antibiotic-resistant and immune-mediated processes.
  • #27 Cellular and molecular mechanisms in the pathogenesis of pouchitis: more than just the microbiota | Gut
    https://gut.bmj.com/cgi/content/short/gutjnl-2024-334445v1?rss=1
    Pouchitis, defined as inflammation of the ileal pouch, is the most common complication following restorative proctocolectomy for refractory ulcerative colitis. […] This highlights the need for more effective treatment options and points to a more complex pathophysiology beyond the role of the pouch microbiome, similar to what is seen in inflammatory bowel disease. […] In this review, we outline the putative mechanisms of pouchitis, including genetic predisposition, microbiome alterations, dysfunction of the intestinal barrier and the immune system and review the available animal models of pouchitis. […] In addition, we introduce the concept of pouchitis as a possible transmural disease and discuss the potential role of non-immune cells, including stromal cells, in perpetuating inflammation and intestinal barrier dysfunction. […] We discuss future directions, implications for novel therapies and propose novel multicellular disease models that can better capture the complexity of pouchitis pathogenesis.
  • #28 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    The interactions between the pouch microbiota and host immune responses, innate and adaptive, play also significant role in pouchitis pathogenesis. […] Mucosal barrier dysfunction, with increased intestinal permeability, is also believed to play a role in pouchitis. […] The pathogenesis of pouchitis in these patients may be triggered by dysbiosis, leading to an altered mucosal immune response. […] Polymorphisms in the interleukin-1 receptor antagonist gene allele 2, tumor necrosis factor (TNF) allele 2, TLR 1 and NOD2/CARD15 have been associated with pouchitis. […] Different risk factors may be associated with the different types of pouchitis, suggesting different pathogenic pathways in the various forms of idiopathic pouchitis and secondary pouchitis. […] The pathogenesis of pouchitis in these patients may be triggered by dysbiosis, leading to an altered mucosal immune response.
  • #29 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    The interactions between the pouch microbiota and host immune responses, innate and adaptive, play also significant role in pouchitis pathogenesis. […] Mucosal barrier dysfunction, with increased intestinal permeability, is also believed to play a role in pouchitis. […] The pathogenesis of pouchitis in these patients may be triggered by dysbiosis, leading to an altered mucosal immune response. […] Polymorphisms in the interleukin-1 receptor antagonist gene allele 2, tumor necrosis factor (TNF) allele 2, TLR 1 and NOD2/CARD15 have been associated with pouchitis. […] Different risk factors may be associated with the different types of pouchitis, suggesting different pathogenic pathways in the various forms of idiopathic pouchitis and secondary pouchitis. […] The pathogenesis of pouchitis in these patients may be triggered by dysbiosis, leading to an altered mucosal immune response.
  • #30 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    The interleukin 1 receptor antagonist gene allele 2 as a predictor of pouchitis following colectomy and IPAA in ulcerative colitis. […] Risk factors for diseases of ileal pouch-anal anastomosis in patients with ulcerative colitis. […] Predictors of pouchitis after ileal pouch-anal anastomosis: a retrospective review. […] The efficacy and tolerability of AST-120 (spherical carbon adsorbent) in active pouchitis. […] Maintenance therapy with a probiotic in antibiotic-dependent pouchitis: experience in clinical practice.
  • #31 Key Focus Areas in Pouchitis Therapeutic Status: A Narrative Review
    https://ijms.sums.ac.ir/article_50229.html
    Pouchitis, as the most common complication after ileal pouch-anal anastomosis (IPAA), has an incidence from 7% to 46%. […] Although the etiology of pouchitis has remained unclear, the gut microbiome has been hypothesized as a key factor. In patients with pouchitis, there is a decrease in bacterial diversity and an altered abundance of pouch bacteria. […] Interleukin 17 receptor A is responsible for the pathogenesis of pouchitis through downregulation of microRNAs. […] The efficacy of antibiotic therapy for pouchitis can be due to the establishment of an antibiotic-resistant microbiome with low inflammatory potential, while this microbiome can cause resistance against colonization by bacteria that promote inflammation. […] In active pouchitis, a severe infiltration of the mucosa by immune cells happens and an increased proportion of mucosal dendritic cells expressing integrin 7 are noted that have a pathogenic role in the pathogenesis of pouchitis. […] NOD2 signaling pathway could contribute to intrinsic bacterial dysbiosis which was pre-existing and predisposed individuals to pouchitis.
  • #32 Key Focus Areas in Pouchitis Therapeutic Status: A Narrative Review
    https://ijms.sums.ac.ir/article_50229.html
    Pouchitis, as the most common complication after ileal pouch-anal anastomosis (IPAA), has an incidence from 7% to 46%. […] Although the etiology of pouchitis has remained unclear, the gut microbiome has been hypothesized as a key factor. In patients with pouchitis, there is a decrease in bacterial diversity and an altered abundance of pouch bacteria. […] Interleukin 17 receptor A is responsible for the pathogenesis of pouchitis through downregulation of microRNAs. […] The efficacy of antibiotic therapy for pouchitis can be due to the establishment of an antibiotic-resistant microbiome with low inflammatory potential, while this microbiome can cause resistance against colonization by bacteria that promote inflammation. […] In active pouchitis, a severe infiltration of the mucosa by immune cells happens and an increased proportion of mucosal dendritic cells expressing integrin 7 are noted that have a pathogenic role in the pathogenesis of pouchitis. […] NOD2 signaling pathway could contribute to intrinsic bacterial dysbiosis which was pre-existing and predisposed individuals to pouchitis.
  • #33 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #34 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #35
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Colonic metaplasia of the pouch mucosa seems to be a nonspecific adaptive response to the new luminal environment. […] Colonic metaplasia characterized by villous blunting, crypt cell hyperplasia, and colon epithelium-specific antigens such as human tropomyosin 5, may increase the risk for pouchitis. […] A similar alteration in mucin glycoproteins occurs in pouchitis as seen in UC. […] It is possible that the altered glycoproteins are more susceptible to enzymatic degradation by bacteria, making the mucus barrier less resistant. […] Additionally, some patients with pouchitis have the same extra-intestinal manifestations (such as arthralgia and primary sclerosing cholangitis or PSC) as those seen in patients with UC. […] Smoking tends to have a protective effect against the development of pouchitis as it does against UC.
  • #36
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Colonic metaplasia of the pouch mucosa seems to be a nonspecific adaptive response to the new luminal environment. […] Colonic metaplasia characterized by villous blunting, crypt cell hyperplasia, and colon epithelium-specific antigens such as human tropomyosin 5, may increase the risk for pouchitis. […] A similar alteration in mucin glycoproteins occurs in pouchitis as seen in UC. […] It is possible that the altered glycoproteins are more susceptible to enzymatic degradation by bacteria, making the mucus barrier less resistant. […] Additionally, some patients with pouchitis have the same extra-intestinal manifestations (such as arthralgia and primary sclerosing cholangitis or PSC) as those seen in patients with UC. […] Smoking tends to have a protective effect against the development of pouchitis as it does against UC.
  • #37
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Colonic metaplasia of the pouch mucosa seems to be a nonspecific adaptive response to the new luminal environment. […] Colonic metaplasia characterized by villous blunting, crypt cell hyperplasia, and colon epithelium-specific antigens such as human tropomyosin 5, may increase the risk for pouchitis. […] A similar alteration in mucin glycoproteins occurs in pouchitis as seen in UC. […] It is possible that the altered glycoproteins are more susceptible to enzymatic degradation by bacteria, making the mucus barrier less resistant. […] Additionally, some patients with pouchitis have the same extra-intestinal manifestations (such as arthralgia and primary sclerosing cholangitis or PSC) as those seen in patients with UC. […] Smoking tends to have a protective effect against the development of pouchitis as it does against UC.
  • #38
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Colonic metaplasia of the pouch mucosa seems to be a nonspecific adaptive response to the new luminal environment. […] Colonic metaplasia characterized by villous blunting, crypt cell hyperplasia, and colon epithelium-specific antigens such as human tropomyosin 5, may increase the risk for pouchitis. […] A similar alteration in mucin glycoproteins occurs in pouchitis as seen in UC. […] It is possible that the altered glycoproteins are more susceptible to enzymatic degradation by bacteria, making the mucus barrier less resistant. […] Additionally, some patients with pouchitis have the same extra-intestinal manifestations (such as arthralgia and primary sclerosing cholangitis or PSC) as those seen in patients with UC. […] Smoking tends to have a protective effect against the development of pouchitis as it does against UC.
  • #39 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    The interactions between the pouch microbiota and host immune responses, innate and adaptive, play also significant role in pouchitis pathogenesis. […] Mucosal barrier dysfunction, with increased intestinal permeability, is also believed to play a role in pouchitis. […] The pathogenesis of pouchitis in these patients may be triggered by dysbiosis, leading to an altered mucosal immune response. […] Polymorphisms in the interleukin-1 receptor antagonist gene allele 2, tumor necrosis factor (TNF) allele 2, TLR 1 and NOD2/CARD15 have been associated with pouchitis. […] Different risk factors may be associated with the different types of pouchitis, suggesting different pathogenic pathways in the various forms of idiopathic pouchitis and secondary pouchitis. […] The pathogenesis of pouchitis in these patients may be triggered by dysbiosis, leading to an altered mucosal immune response.
  • #40 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    Pouchitis is classified into either idiopathic (primary) or secondary, according to the cause. […] The etiology of primary or idiopathic pouchitis is not clearly defined but it is thought that dysbiosis plays an important role. Pouch construction determines local fecal stasis that leads to colonic metaplasia in the initial small bowel mucosa of the pouch that promotes an abnormal immune response in genetically predisposed organisms, which leads to inflammation; a similar mechanism that it is seen in UC. […] Similar with UC, physiopathology of idiopathic pouchitis involves an inadequate immune response to local microbiota in an organism with genetic susceptibility. […] Increased epithelial expression of the “pore forming” tight junction proteins claudin 2 and dendritic cells were identified in biopsy specimens from pouch mucosa after restorative proctocolectomy for UC.
  • #41 Pouchitis: What It Is, Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/15484-pouchitis
    Prolonged inflammation can cause erosion of the lining in your pouch, leading to ulcers, which may bleed. Some pathogenic bacteria may also actively erode your gut barrier. […] If your pouchitis never improved with antibiotics, or if it once did, but it no longer does, healthcare providers call this chronic antibiotic-resistant pouchitis (CARP). Your provider will begin by looking for possible overlooked causes, like a secondary infection, an autoimmune disease or a structural defect in your pouch. When theres no apparent cause, they treat chronic pouchitis like inflammatory bowel disease.
  • #42 Pouchitis: What It Is, Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/15484-pouchitis
    Some people become dependent on antibiotics known as chronic antibiotic-dependent pouchitis (CADP). And in some people, the antibiotics start to work less and less. This is called antibiotic-resistant pouchitis (CARP). […] Pouchitis is far more common in people who had proctocolectomy surgery to treat inflammatory bowel diseases, such as ulcerative colitis and Crohns disease. The mechanisms that caused this original disease may be affecting the pouch. […] Some bacterial infections are resistant to antibiotic treatment, like C. difficile. Repeat antibiotic use may also lead to non-pathogenic types of bacteria becoming resistant. This may contribute to the imbalance of bacteria in your pouch. […] Chronic inflammation can lead to scarring in your pouch. Scarring can cause the opening to narrow. It can also reduce blood flow to your pouch, which interferes with healing.
  • #43 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    Concurrent infections (such as Clostridium difficile) and other triggering factors (such as NSAID use) should be identified and treated or eradicated. […] Pouchitis is associated with mucosal imbalance between interleukin-8 and interleukin-10. […] Pouchitis, similar to active ulcerative colitis, is associated with impaired butyrate oxidation by intestinal mucosa. […] The expression patterns of Toll-like receptors in the ileal pouch mucosa of postoperative ulcerative colitis patients. […] Increased state of activation of CD4 positive T cells and elevated interferon gamma production in pouchitis. […] Increased cytokine transcripts in pouchitis reflect the degree of inflammation but not the underlying entity. […] The bacteriology of pouchitis: a molecular phylogenetic analysis using 16S rRNA gene cloning and sequencing.
  • #44 Microorganisms in the Pathogenesis and Management of Pouchitis | SpringerLink
    https://link.springer.com/chapter/10.1007/978-981-19-4800-8_14
    Pouchitis is the most frequent clinical complication following restorative proctocolectomy with ileal pouch anastomosis surgery to treat inflammatory bowel diseases. […] However, the role of microorganisms in the pathogenesis and management of pouchitis is gaining more attention as dysbiosis is frequently observed in pouchitis cases and most of the time treated with antibiotics. […] Colonization of pathogenic microbes in the pouch leads to an increase in gut permeability, more synthesis of pro-inflammatory factors, a decrease in the production of short-chain fatty acids, and a reduction in helpful host-microbiome diversity. […] The mechanism of action of beneficial bacteria in pouchitis treatment involves inhibition of entry and colonization of pathogenic bacteria by lowering pH of the lumen, production of antimicrobial compounds, and blocking the binding of pathogens.
  • #45 Microorganisms in the Pathogenesis and Management of Pouchitis | SpringerLink
    https://link.springer.com/chapter/10.1007/978-981-19-4800-8_14
    It also includes improving pouch mucosal and epithelial properties as high integrity, more short-chain fatty acid, and immunoregulation with more immunoglobulins and elevated cytokines. […] Microbial interventions such as probiotics, microbial restoration therapy, and fecal microbiota transplantation have great potential to reduce, suppress pouch inflammation, and relapse of pouchitis after antibiotic treatment.
  • #46
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Proinflammatory cytokines, such as TNF-, are released at a great extent in the inflamed mucosa by macrophages and monocytes, leading to tissue injury, and are considered to be involved in pouchitis as a secondary pathophysiologic mechanism. […] As in UC, the production of other inflammatory mediators including cytokines (such as IL-1, IL-6, and IL-8), cell adhesion molecules (such as E selectin and intercellular adhesion molecule-1), platelet-activating factor, lipoxygenase products of arachidonic acids (such as leukotriene B4 and prostaglandin E2), proinflammatory neuropeptides, macrophage inflammatory protein (MIP) 2, matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, MRP-14, and inducible nitric oxide, is also increased. […] Abnormalities in immunoregulatory cytokines such as IL-2, and interferon-, IL-4, and IL-10 are also seen in pouchitis.
  • #47
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Proinflammatory cytokines, such as TNF-, are released at a great extent in the inflamed mucosa by macrophages and monocytes, leading to tissue injury, and are considered to be involved in pouchitis as a secondary pathophysiologic mechanism. […] As in UC, the production of other inflammatory mediators including cytokines (such as IL-1, IL-6, and IL-8), cell adhesion molecules (such as E selectin and intercellular adhesion molecule-1), platelet-activating factor, lipoxygenase products of arachidonic acids (such as leukotriene B4 and prostaglandin E2), proinflammatory neuropeptides, macrophage inflammatory protein (MIP) 2, matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, MRP-14, and inducible nitric oxide, is also increased. […] Abnormalities in immunoregulatory cytokines such as IL-2, and interferon-, IL-4, and IL-10 are also seen in pouchitis.
  • #48
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Imbalance between proinflammatory and immunoregulatory cytokines has been described in patients with pouchitis. […] Abnormalities of T cells and other immune cells may not explain the whole mechanism of pouchitis. […] It is likely that such abnormalities are nonspecific and secondary in nature. […] Inconsistent results in the studies of immune cells and inflammatory mediators in pouchitis reflect the complexity in pathogenesis of the disease. […] There are few published studies addressing the interplay between microflora and mucosal immune system in pouchitis. […] Exposure of peripheral blood and lamina propria lymphocytes ex vivo to sonicated flora from pouchitis induces more intense proliferation as compared with sonicates from healthy pouches. […] In vitro pretreatment of the sonicate preparation of pouch flora with metronidazole abolishes the stimulating ability.
  • #49 Cellular and molecular mechanisms in the pathogenesis of pouchitis: more than just the microbiota | Gut
    https://gut.bmj.com/cgi/content/short/gutjnl-2024-334445v1?rss=1
    Pouchitis, defined as inflammation of the ileal pouch, is the most common complication following restorative proctocolectomy for refractory ulcerative colitis. […] This highlights the need for more effective treatment options and points to a more complex pathophysiology beyond the role of the pouch microbiome, similar to what is seen in inflammatory bowel disease. […] In this review, we outline the putative mechanisms of pouchitis, including genetic predisposition, microbiome alterations, dysfunction of the intestinal barrier and the immune system and review the available animal models of pouchitis. […] In addition, we introduce the concept of pouchitis as a possible transmural disease and discuss the potential role of non-immune cells, including stromal cells, in perpetuating inflammation and intestinal barrier dysfunction. […] We discuss future directions, implications for novel therapies and propose novel multicellular disease models that can better capture the complexity of pouchitis pathogenesis.
  • #50 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #51 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    Pouchitis, the most common long-term complication of the procedure, involves a spectrum of disease processes with heterogeneous risk factors, clinical features, disease courses and prognoses. […] Dysbiosis has been implicated as a triggering factor for pouchitis, and concurrent infection with pathogens, such as Clostridium difficile, might contribute to disease relapse and exacerbation. […] Pouchitis comprises a spectrum of disease, ranging from antibiotic-responsive forms to antibiotic-refractory entities, which involve various aetiological and pathogenetic pathways and have differing clinical presentations, disease courses and prognoses. […] Dysbiosis (quantitative and/or qualitative alterations of the pouch microbiota) has a key role in the initiation and progression of pouchitis.
  • #52 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #53 Pouchitis: What It Is, Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/15484-pouchitis
    Some people become dependent on antibiotics known as chronic antibiotic-dependent pouchitis (CADP). And in some people, the antibiotics start to work less and less. This is called antibiotic-resistant pouchitis (CARP). […] Pouchitis is far more common in people who had proctocolectomy surgery to treat inflammatory bowel diseases, such as ulcerative colitis and Crohns disease. The mechanisms that caused this original disease may be affecting the pouch. […] Some bacterial infections are resistant to antibiotic treatment, like C. difficile. Repeat antibiotic use may also lead to non-pathogenic types of bacteria becoming resistant. This may contribute to the imbalance of bacteria in your pouch. […] Chronic inflammation can lead to scarring in your pouch. Scarring can cause the opening to narrow. It can also reduce blood flow to your pouch, which interferes with healing.
  • #54 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Chronic pouchitis affects 13% to 17% of patients with ileal pouch–anal anastomosis and ulcerative colitis, and 20% with a history of acute pouchitis. […] Pathogenesis of chronic pouchitis can range from microbially mediated to more antibiotic-resistant and immune-mediated processes. […] Pathogenesis of Pouchitis […] Pouchitis is thought to result from disrupted innate immunity and a dysregulated adaptive immune response to altered pouch microbiota in susceptible hosts. It represents a disease spectrum, typically starting as acute antibiotic-responsive and then progressing to antibiotic-dependent and finally antibiotic-refractory disease. This progression suggests that etiopathogenesis evolves from microbially mediated inflammation to predominantly immune-mediated inflammation. […] Disrupted or Upregulated Innate Immunity Fecal stasis in the ileal pouch reservoir results in adaptive epithelial changes to a more colon-like mucosa. In UC pouches, these changes are more pronounced even without acute inflammation. Additionally, UC pouches exhibit disruptions in the innate immune system, which are less commonly observed with FAP pouches, including barrier dysfunction with increased claudin-2 tight junctions, aberrant dendritic cells, increased expression of defensins, Toll-like receptors such as TLR4, interferon-γ expression, and signal transducer and activator of transcription (STAT) 1 activation.
  • #55 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    Another possible cause of secondary pouchitis is the immune-mediated phenotype, which is associated with an inflammation of the pouch and of the pre-pouch ileum, positive autoantibodies, high serum levels of immunoglobulin (Ig) G4, an increase in Ig G4-expressing cells in the mucosa of the pouch and the association with other autoimmune conditions. […] The risk of developing pouchitis is increased in patients with primary sclerosing cholangitis. Evidence suggests that the cumulative risk of pouchitis at one, two, five and ten years is 15.5%, 22.5%, 36% and 45.5% in patients without PSC and 22%, 43%, 61% and 79% in patients with concomitant PSC. […] The etiology of PSC-associated pouchitis remains unknown. One possible physiopathological mechanism may involve pouch dysbiosis. […] The current review focuses on the therapeutic management of idiopathic pouchitis, including novel biologics and small molecules, and discusses the potential benefit of cellular therapies and mesenchymal-cell therapies as future treatment perspectives.
  • #56 Diagnosis and Management of IgG4-associated Pouchitis – Practical Gastro
    https://practicalgastro.com/2014/09/18/diagnosis-and-management-of-igg4-associated-pouchitis/
    While the exact role played by IgG4 in the pathogenesis of pouch dysfunction remains undefined, it is becoming clear that IgG4-associated pouchitis may have distinctive clinical characteristics and response to therapy. […] The identification of increased numbers of infiltrating IgG4-positive plasma cells in pouch biopsies appears to be associated with an increased propensity for refractoriness to antibiotic therapy. […] Thus, IgG4-associated pouchitis (as defined by an increased number of infiltrating IgG4-positive plasma cells) is characterized clinically by an increased incidence of CARP as well as a concurrence with clinical markers of an immune-mediated process. […] The presence of IgG4-expressing plasma cells in pouch biopsy specimens is relatively common in symptomatic IPAA patients.
  • #57 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    Another possible cause of secondary pouchitis is the immune-mediated phenotype, which is associated with an inflammation of the pouch and of the pre-pouch ileum, positive autoantibodies, high serum levels of immunoglobulin (Ig) G4, an increase in Ig G4-expressing cells in the mucosa of the pouch and the association with other autoimmune conditions. […] The risk of developing pouchitis is increased in patients with primary sclerosing cholangitis. Evidence suggests that the cumulative risk of pouchitis at one, two, five and ten years is 15.5%, 22.5%, 36% and 45.5% in patients without PSC and 22%, 43%, 61% and 79% in patients with concomitant PSC. […] The etiology of PSC-associated pouchitis remains unknown. One possible physiopathological mechanism may involve pouch dysbiosis. […] The current review focuses on the therapeutic management of idiopathic pouchitis, including novel biologics and small molecules, and discusses the potential benefit of cellular therapies and mesenchymal-cell therapies as future treatment perspectives.
  • #58 Diagnosis and Management of IgG4-associated Pouchitis – Practical Gastro
    https://practicalgastro.com/2014/09/18/diagnosis-and-management-of-igg4-associated-pouchitis/
    While the exact role played by IgG4 in the pathogenesis of pouch dysfunction remains undefined, it is becoming clear that IgG4-associated pouchitis may have distinctive clinical characteristics and response to therapy. […] The identification of increased numbers of infiltrating IgG4-positive plasma cells in pouch biopsies appears to be associated with an increased propensity for refractoriness to antibiotic therapy. […] Thus, IgG4-associated pouchitis (as defined by an increased number of infiltrating IgG4-positive plasma cells) is characterized clinically by an increased incidence of CARP as well as a concurrence with clinical markers of an immune-mediated process. […] The presence of IgG4-expressing plasma cells in pouch biopsy specimens is relatively common in symptomatic IPAA patients.
  • #59 Diagnosis and Management of IgG4-associated Pouchitis – Practical Gastro
    https://practicalgastro.com/2014/09/18/diagnosis-and-management-of-igg4-associated-pouchitis/
    While the exact role played by IgG4 in the pathogenesis of pouch dysfunction remains undefined, it is becoming clear that IgG4-associated pouchitis may have distinctive clinical characteristics and response to therapy. […] The identification of increased numbers of infiltrating IgG4-positive plasma cells in pouch biopsies appears to be associated with an increased propensity for refractoriness to antibiotic therapy. […] Thus, IgG4-associated pouchitis (as defined by an increased number of infiltrating IgG4-positive plasma cells) is characterized clinically by an increased incidence of CARP as well as a concurrence with clinical markers of an immune-mediated process. […] The presence of IgG4-expressing plasma cells in pouch biopsy specimens is relatively common in symptomatic IPAA patients.
  • #60 Diagnosis and Management of IgG4-associated Pouchitis – Practical Gastro
    https://practicalgastro.com/2014/09/18/diagnosis-and-management-of-igg4-associated-pouchitis/
    The natural history of IgG4-associated pouchitis has yet to be fully characterized. […] There is some evidence that IgG4-associated pouchitis is marked by a more severe clinical presentation: pouchitis patients with elevated serum IgG4 had significantly greater PDAI symptom sub-scores as compared to those with normal serum IgG4. […] A characteristic feature of AIP (as well as other IgG4-RD) is responsiveness to corticosteroid therapy. […] This may have implications for the treatment of IgG4-associated inflammation in intestinal sites, including in pouchitis. […] While the efficacy of corticosteroid therapy in this context has yet to be substantiated by large clinical studies, our group reported a case of IgG4-associated pouchitis that responded clinically to budesonide therapy. […] The presence of an IgG4-associated inflammatory process in the pouch, including in the setting of IgG4-RD, suggests that a B-cell targeting approach would be useful.
  • #61
    https://canadianibdtoday.com/article/view/1-1-2-narula
    Ileal pouch anal anastomosis (IPAA) is a surgical procedure conducted in patients with ulcerative colitis (UC) with medically refractory disease; in patients with the autosomal dominant inherited disease familial adenomatous polyposis (FAP); or in patients who have experienced dysplasia/colon cancer. […] A common complication from IPAA is pouchitis, which is characterized as an idiopathic non-specific inflammation within the created pouch resulting in symptoms including increased frequency of bowel movements and abdominal pain. […] Pouchitis is much more common in patients treated for UC (up to 60%) than in those receiving treatment for other indications (0-10%). This might be due to immune activation or dysbiosis in these patients.
  • #62 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    Restorative proctocolectomy with ileal-pouch anal anastomosis (IPAA) is the operation of choice for medically refractory ulcerative colitis (UC), for UC with dysplasia, and for familial adenomatous polyposis (FAP). […] The term pouchitis refers to nonspecific inflammation of the pouch and is a common complication in patients with IPAA; it occurs more often in UC patients than in FAP patients. This suggests that the pathogenetic background of UC may contribute significantly to the development of pouchitis. […] Based on the etiology we can sub-divide pouchitis into 2 groups: idiopathic and secondary. In idiopathic pouchitis the etiology and pathogenesis are still unclear, while in secondary pouchitis there is an association with a specific causative or pathogenetic factor. […] Current evidence suggests that the interactions of the altered composition and/or the quantity of the luminal microbiota (dysbiosis), with the altered characteristics of the mucosa (colonic metaplasia), in conjunction with abnormalities of innate and adaptive mucosal immunity, play a key role in the pathogenesis of pouchitis.
  • #63 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    The expression of Toll-like receptors (TLRs) is also altered, with a decreased expression of TLR3 and increased expression of TLR5 in normal ileal pouch, and an upregulation of TLR2 expression in pouchitis and upregulation of TLR4 in both normal pouch and pouchitis. […] An increased cytokine production of IL-1 beta, IL-6, IL-8 and TNF-alpha was seen in pouchitis. […] Risk factors that were identified to be associated with pouchitis include the following: extensive UC and backwash ileitis before colectomy; the presence of extraintestinal manifestations; non-smoker status; IL-1 receptor antagonist gene polymorphism; and the presence of pANCA (antineutrophil cytoplasmic antibodies). […] The treatment consists of controlling the concurrent autoimmune disorders and often requires immunosuppressive agents.
  • #64 Acute and chronic pouchitis—pathogenesis, diagnosis and treatment | Nature Reviews Gastroenterology & Hepatology
    https://www.nature.com/articles/nrgastro.2012.58
    The interleukin 1 receptor antagonist gene allele 2 as a predictor of pouchitis following colectomy and IPAA in ulcerative colitis. […] Risk factors for diseases of ileal pouch-anal anastomosis in patients with ulcerative colitis. […] Predictors of pouchitis after ileal pouch-anal anastomosis: a retrospective review. […] The efficacy and tolerability of AST-120 (spherical carbon adsorbent) in active pouchitis. […] Maintenance therapy with a probiotic in antibiotic-dependent pouchitis: experience in clinical practice.
  • #65 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    The expression of Toll-like receptors (TLRs) is also altered, with a decreased expression of TLR3 and increased expression of TLR5 in normal ileal pouch, and an upregulation of TLR2 expression in pouchitis and upregulation of TLR4 in both normal pouch and pouchitis. […] An increased cytokine production of IL-1 beta, IL-6, IL-8 and TNF-alpha was seen in pouchitis. […] Risk factors that were identified to be associated with pouchitis include the following: extensive UC and backwash ileitis before colectomy; the presence of extraintestinal manifestations; non-smoker status; IL-1 receptor antagonist gene polymorphism; and the presence of pANCA (antineutrophil cytoplasmic antibodies). […] The treatment consists of controlling the concurrent autoimmune disorders and often requires immunosuppressive agents.
  • #66 Pouchitis, a complication associated with the surgical treatment of ulcerative colitis. Diagnosis and treatment. Review
    http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-99572021000100065
    Similar to ulcerative colitis, smoking has been found to have a negative association and smoking cessation increases the risk of pouchitis, however this does not mean that people should start smoking to avoid developing it, as smoking has multiple harmful effects on humans and recently it has been reported that active smoking does not prevent the occurrence of this complication. When primary sclerosing cholangitis and UC occur concurrently, there is a higher risk of pouchitis than when UC occurs alone. High levels of perinuclear fluorescence pattern anti-neutrophil cytoplasmic antibody (p-ANCA) represent a risk of pouchitis of 8.5. According to a recent meta-analysis, the presence of p-ANCA was associated with increased risk of chronic pouchitis (Odds ratio [OR]: 1.8; 95 % CI: 1.2-2.6), but it was not associated with acute pouchitis. However, it should be noted that p-ANCA determination was performed after surgery in most of the studies included in said meta-analysis.
  • #67 Incidence, Risk Factors, and Outcomes of Chronic Antibiotic-Refractory Pouchitis in Korean Patients with Ulcerative Colitis
    https://www.gutnliver.org/journal/view.html?pn=ahead&uid=2240&vmd=Full
    Even though the remarkable development of many biologics and small molecule agents for patients with UC has reduced the rate of proctocolectomy with IPAA, the incidence rate of pouchitis within the first 2 years after IPAA has increased by 15% over 22 years in Western countries. Therefore, in order to reduce the significant clinical and economic burden of pouchitis, many studies have investigated optimal treatments for pouchitis, especially CARP, using biologics or small molecules. However, data and reports on CARP are still lacking in Asian populations. […] Patients developing CARP were less likely to use concomitant probiotics compared with the CADP group (29.0% vs 72.1%). In a multivariable analysis of 232 patients with IPAA, current smoking status (adjusted hazard ratio, 2.96; 95% CI, 1.27 to 6.90; p=0.01) and previous usage of biologics/small molecules (adjusted hazard ratio, 2.40; 95% CI, 1.05 to 5.53; p=0.04) were significantly associated with CARP development.
  • #68
    https://journals.lww.com/ajg/fulltext/2022/10002/s965_acute_severe_ulcerative_colitis_is_associated.965.aspx
    Pouchitis occurs in up to 80% of patients with ulcerative colitis (UC) after total proctocolectomy (TPC) with ileal pouch anal anastomosis (IPAA). The pathogenesis of pouchitis is thought to involve a complex interaction between the microbiome and mucosal immune system, and increasing data suggest a robust immune system may be associated with an increased risk of pouchitis. […] On multivariable analysis, older age at colectomy (HR 0.98 95% CI (0.97-0.99)) was significantly associated with a decreased probability of acute pouchitis, while ASUC (HR 1.53 95% CI (1.06-2.22)) and a greater number of biologics pre-colectomy (HR 1.30 95% CI (1.05-1.62)) were associated with an increased probability of acute pouchitis. […] ASUC at the time of colectomy was associated with an increased probability of acute pouchitis.
  • #69
    https://journals.lww.com/ajg/fulltext/2022/10002/s965_acute_severe_ulcerative_colitis_is_associated.965.aspx
    Pouchitis occurs in up to 80% of patients with ulcerative colitis (UC) after total proctocolectomy (TPC) with ileal pouch anal anastomosis (IPAA). The pathogenesis of pouchitis is thought to involve a complex interaction between the microbiome and mucosal immune system, and increasing data suggest a robust immune system may be associated with an increased risk of pouchitis. […] On multivariable analysis, older age at colectomy (HR 0.98 95% CI (0.97-0.99)) was significantly associated with a decreased probability of acute pouchitis, while ASUC (HR 1.53 95% CI (1.06-2.22)) and a greater number of biologics pre-colectomy (HR 1.30 95% CI (1.05-1.62)) were associated with an increased probability of acute pouchitis. […] ASUC at the time of colectomy was associated with an increased probability of acute pouchitis.
  • #70 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    Another possible cause of secondary pouchitis is the immune-mediated phenotype, which is associated with an inflammation of the pouch and of the pre-pouch ileum, positive autoantibodies, high serum levels of immunoglobulin (Ig) G4, an increase in Ig G4-expressing cells in the mucosa of the pouch and the association with other autoimmune conditions. […] The risk of developing pouchitis is increased in patients with primary sclerosing cholangitis. Evidence suggests that the cumulative risk of pouchitis at one, two, five and ten years is 15.5%, 22.5%, 36% and 45.5% in patients without PSC and 22%, 43%, 61% and 79% in patients with concomitant PSC. […] The etiology of PSC-associated pouchitis remains unknown. One possible physiopathological mechanism may involve pouch dysbiosis. […] The current review focuses on the therapeutic management of idiopathic pouchitis, including novel biologics and small molecules, and discusses the potential benefit of cellular therapies and mesenchymal-cell therapies as future treatment perspectives.
  • #71 Diagnosis and Medical Treatment of Acute and Chronic Idiopathic Pouchitis in Inflammatory Bowel Disease
    https://www.mdpi.com/1648-9144/60/6/979
    Another possible cause of secondary pouchitis is the immune-mediated phenotype, which is associated with an inflammation of the pouch and of the pre-pouch ileum, positive autoantibodies, high serum levels of immunoglobulin (Ig) G4, an increase in Ig G4-expressing cells in the mucosa of the pouch and the association with other autoimmune conditions. […] The risk of developing pouchitis is increased in patients with primary sclerosing cholangitis. Evidence suggests that the cumulative risk of pouchitis at one, two, five and ten years is 15.5%, 22.5%, 36% and 45.5% in patients without PSC and 22%, 43%, 61% and 79% in patients with concomitant PSC. […] The etiology of PSC-associated pouchitis remains unknown. One possible physiopathological mechanism may involve pouch dysbiosis. […] The current review focuses on the therapeutic management of idiopathic pouchitis, including novel biologics and small molecules, and discusses the potential benefit of cellular therapies and mesenchymal-cell therapies as future treatment perspectives.
  • #72 Pouchitis, a complication associated with the surgical treatment of ulcerative colitis. Diagnosis and treatment. Review
    http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-99572021000100065
    The exact pathophysiological mechanisms that cause pouchitis are unknown. However, it is more likely to be a multifactorial disease involving genetic predisposition, bacterial overgrowth and dysbiosis in the ileal pouch, among others. Recently, it has been found that in acute pouchitis cases there is an increase of species of the Clostridia genus and, reciprocally, its decrease is associated with response to antibiotic treatment. In contrast, in chronic pouchitis cases there is an increase in the amount of Staphylococcus aureus. Other factors involved in its development may include decreased short-chain fatty acids, nutritional deficiencies, ischemia or immune response alterations. In addition, other authors have considered that pouchitis may be a different inflammatory bowel disease and that several factors increase the risk of developing it. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) increases this risk 3.24 times (95 % confidence interval [CI] 1.71-6.13).
  • #73 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Restorative proctocolectomy (RPC) with ileal pouch-anal anastomosis is the operation of choice for patients with ulcerative colitis. Pouchitis is the most common cause of pouch dysfunction. Although the pathogenesis of this disease is not well understood, bacteria have been implicated in the disease process. […] Similarly to UC and Crohns disease (CD) the mucosal inflammation that occurs in pouchitis is localized to the areas with the highest concentration of bacteria. There is a tenfold increased risk of pouchitis in patients who undergo RPC for UC compared with FAP. Therefore, it has been suggested that pouchitis represents reactivation of UC in the colonized small bowel of the pouch. […] The pathogenesis of PPI has not been studied. Ischaemia, CD and nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated in some cases, but where these factors have been excluded the pathogenesis is likely to be similar to that of pouchitis where bacteria are considered fundamental to the disease process.
  • #74 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Despite this there are several similarities between pouchitis and CD. Both are inflammatory conditions which can affect the small bowel, both respond to treatment with antibiotics and both improve with diversion of the faecal stream (importantly these treatments are not effective in UC). […] It has been suggested that pouchitis may represent a novel third form of inflammatory bowel disease (IBD). The differences in treatment response seen in pouchitis patients compared with UC and CD could be considered to fit with this. […] An abnormal host-microbial interaction has long been implicated in all forms of IBD including pouchitis. There is evidence from clinical practice to implicate bacteria in pouchitis. […] The results from culture-based studies of pouch microbiota using culture methods are varied and inconclusive. Advances in our understanding of gut microbiota following the introduction of molecular techniques have led to the realization that culture-based techniques are inadequate for the study of gut microbiota.
  • #75 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Restorative proctocolectomy (RPC) with ileal pouch-anal anastomosis is the operation of choice for patients with ulcerative colitis. Pouchitis is the most common cause of pouch dysfunction. Although the pathogenesis of this disease is not well understood, bacteria have been implicated in the disease process. […] Similarly to UC and Crohns disease (CD) the mucosal inflammation that occurs in pouchitis is localized to the areas with the highest concentration of bacteria. There is a tenfold increased risk of pouchitis in patients who undergo RPC for UC compared with FAP. Therefore, it has been suggested that pouchitis represents reactivation of UC in the colonized small bowel of the pouch. […] The pathogenesis of PPI has not been studied. Ischaemia, CD and nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated in some cases, but where these factors have been excluded the pathogenesis is likely to be similar to that of pouchitis where bacteria are considered fundamental to the disease process.
  • #76 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Despite this there are several similarities between pouchitis and CD. Both are inflammatory conditions which can affect the small bowel, both respond to treatment with antibiotics and both improve with diversion of the faecal stream (importantly these treatments are not effective in UC). […] It has been suggested that pouchitis may represent a novel third form of inflammatory bowel disease (IBD). The differences in treatment response seen in pouchitis patients compared with UC and CD could be considered to fit with this. […] An abnormal host-microbial interaction has long been implicated in all forms of IBD including pouchitis. There is evidence from clinical practice to implicate bacteria in pouchitis. […] The results from culture-based studies of pouch microbiota using culture methods are varied and inconclusive. Advances in our understanding of gut microbiota following the introduction of molecular techniques have led to the realization that culture-based techniques are inadequate for the study of gut microbiota.
  • #77 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Despite this there are several similarities between pouchitis and CD. Both are inflammatory conditions which can affect the small bowel, both respond to treatment with antibiotics and both improve with diversion of the faecal stream (importantly these treatments are not effective in UC). […] It has been suggested that pouchitis may represent a novel third form of inflammatory bowel disease (IBD). The differences in treatment response seen in pouchitis patients compared with UC and CD could be considered to fit with this. […] An abnormal host-microbial interaction has long been implicated in all forms of IBD including pouchitis. There is evidence from clinical practice to implicate bacteria in pouchitis. […] The results from culture-based studies of pouch microbiota using culture methods are varied and inconclusive. Advances in our understanding of gut microbiota following the introduction of molecular techniques have led to the realization that culture-based techniques are inadequate for the study of gut microbiota.
  • #78 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Despite this there are several similarities between pouchitis and CD. Both are inflammatory conditions which can affect the small bowel, both respond to treatment with antibiotics and both improve with diversion of the faecal stream (importantly these treatments are not effective in UC). […] It has been suggested that pouchitis may represent a novel third form of inflammatory bowel disease (IBD). The differences in treatment response seen in pouchitis patients compared with UC and CD could be considered to fit with this. […] An abnormal host-microbial interaction has long been implicated in all forms of IBD including pouchitis. There is evidence from clinical practice to implicate bacteria in pouchitis. […] The results from culture-based studies of pouch microbiota using culture methods are varied and inconclusive. Advances in our understanding of gut microbiota following the introduction of molecular techniques have led to the realization that culture-based techniques are inadequate for the study of gut microbiota.
  • #79 The bacterial pathogenesis and treatment of pouchitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3002591/
    Despite this there are several similarities between pouchitis and CD. Both are inflammatory conditions which can affect the small bowel, both respond to treatment with antibiotics and both improve with diversion of the faecal stream (importantly these treatments are not effective in UC). […] It has been suggested that pouchitis may represent a novel third form of inflammatory bowel disease (IBD). The differences in treatment response seen in pouchitis patients compared with UC and CD could be considered to fit with this. […] An abnormal host-microbial interaction has long been implicated in all forms of IBD including pouchitis. There is evidence from clinical practice to implicate bacteria in pouchitis. […] The results from culture-based studies of pouch microbiota using culture methods are varied and inconclusive. Advances in our understanding of gut microbiota following the introduction of molecular techniques have led to the realization that culture-based techniques are inadequate for the study of gut microbiota.
  • #80
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    The greater stimulatory effect of sonicates from pouchitis suggests that certain microflora may predominantly present in inflamed pouch mucosa and these microflora may be potentially pathogenic in activation of local mononuclear cells. […] One of the most intriguing aspects of pouchitis is that it occurs almost exclusively in patients with underlying UC. […] Interestingly, there are similarities in terms of clinical presentations and immunological abnormalities between pouchitis and UC, suggesting that a subset of pouchitis may actually represent the recurrence of a UC-like disease in the ileal pouch. […] The theory of recurrent UC is supported by several lines of evidence. […] With the presence of stasis in the pouch, exposure to fecal contents and an increased microbial load could cause inflammatory changes leading to morphological alterations in the ileal pouch mucosa mimicking colon epithelia in UC.
  • #81
    https://www.wjgnet.com/1007-9327/full/v13/i42/5598.htm
    Colonic metaplasia of the pouch mucosa seems to be a nonspecific adaptive response to the new luminal environment. […] Colonic metaplasia characterized by villous blunting, crypt cell hyperplasia, and colon epithelium-specific antigens such as human tropomyosin 5, may increase the risk for pouchitis. […] A similar alteration in mucin glycoproteins occurs in pouchitis as seen in UC. […] It is possible that the altered glycoproteins are more susceptible to enzymatic degradation by bacteria, making the mucus barrier less resistant. […] Additionally, some patients with pouchitis have the same extra-intestinal manifestations (such as arthralgia and primary sclerosing cholangitis or PSC) as those seen in patients with UC. […] Smoking tends to have a protective effect against the development of pouchitis as it does against UC.
  • #82 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    Restorative proctocolectomy with ileal-pouch anal anastomosis (IPAA) is the operation of choice for medically refractory ulcerative colitis (UC), for UC with dysplasia, and for familial adenomatous polyposis (FAP). […] The term pouchitis refers to nonspecific inflammation of the pouch and is a common complication in patients with IPAA; it occurs more often in UC patients than in FAP patients. This suggests that the pathogenetic background of UC may contribute significantly to the development of pouchitis. […] Based on the etiology we can sub-divide pouchitis into 2 groups: idiopathic and secondary. In idiopathic pouchitis the etiology and pathogenesis are still unclear, while in secondary pouchitis there is an association with a specific causative or pathogenetic factor. […] Current evidence suggests that the interactions of the altered composition and/or the quantity of the luminal microbiota (dysbiosis), with the altered characteristics of the mucosa (colonic metaplasia), in conjunction with abnormalities of innate and adaptive mucosal immunity, play a key role in the pathogenesis of pouchitis.
  • #83 Cellular and molecular mechanisms in the pathogenesis of pouchitis: more than just the microbiota | Gut
    https://gut.bmj.com/cgi/content/short/gutjnl-2024-334445v1?rss=1
    Pouchitis, defined as inflammation of the ileal pouch, is the most common complication following restorative proctocolectomy for refractory ulcerative colitis. […] This highlights the need for more effective treatment options and points to a more complex pathophysiology beyond the role of the pouch microbiome, similar to what is seen in inflammatory bowel disease. […] In this review, we outline the putative mechanisms of pouchitis, including genetic predisposition, microbiome alterations, dysfunction of the intestinal barrier and the immune system and review the available animal models of pouchitis. […] In addition, we introduce the concept of pouchitis as a possible transmural disease and discuss the potential role of non-immune cells, including stromal cells, in perpetuating inflammation and intestinal barrier dysfunction. […] We discuss future directions, implications for novel therapies and propose novel multicellular disease models that can better capture the complexity of pouchitis pathogenesis.
  • #84 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    Restorative proctocolectomy with ileal-pouch anal anastomosis (IPAA) is the operation of choice for medically refractory ulcerative colitis (UC), for UC with dysplasia, and for familial adenomatous polyposis (FAP). […] The term pouchitis refers to nonspecific inflammation of the pouch and is a common complication in patients with IPAA; it occurs more often in UC patients than in FAP patients. This suggests that the pathogenetic background of UC may contribute significantly to the development of pouchitis. […] Based on the etiology we can sub-divide pouchitis into 2 groups: idiopathic and secondary. In idiopathic pouchitis the etiology and pathogenesis are still unclear, while in secondary pouchitis there is an association with a specific causative or pathogenetic factor. […] Current evidence suggests that the interactions of the altered composition and/or the quantity of the luminal microbiota (dysbiosis), with the altered characteristics of the mucosa (colonic metaplasia), in conjunction with abnormalities of innate and adaptive mucosal immunity, play a key role in the pathogenesis of pouchitis.
  • #85 Cellular and molecular mechanisms in the pathogenesis of pouchitis: more than just the microbiota | Gut
    https://gut.bmj.com/cgi/content/short/gutjnl-2024-334445v1?rss=1
    Pouchitis, defined as inflammation of the ileal pouch, is the most common complication following restorative proctocolectomy for refractory ulcerative colitis. […] This highlights the need for more effective treatment options and points to a more complex pathophysiology beyond the role of the pouch microbiome, similar to what is seen in inflammatory bowel disease. […] In this review, we outline the putative mechanisms of pouchitis, including genetic predisposition, microbiome alterations, dysfunction of the intestinal barrier and the immune system and review the available animal models of pouchitis. […] In addition, we introduce the concept of pouchitis as a possible transmural disease and discuss the potential role of non-immune cells, including stromal cells, in perpetuating inflammation and intestinal barrier dysfunction. […] We discuss future directions, implications for novel therapies and propose novel multicellular disease models that can better capture the complexity of pouchitis pathogenesis.
  • #86 Inflammatory pouch disease: The spectrum of pouchitis
    https://www.wjgnet.com/1007-9327/full/v21/i29/8739.htm
    Restorative proctocolectomy with ileal-pouch anal anastomosis (IPAA) is the operation of choice for medically refractory ulcerative colitis (UC), for UC with dysplasia, and for familial adenomatous polyposis (FAP). […] The term pouchitis refers to nonspecific inflammation of the pouch and is a common complication in patients with IPAA; it occurs more often in UC patients than in FAP patients. This suggests that the pathogenetic background of UC may contribute significantly to the development of pouchitis. […] Based on the etiology we can sub-divide pouchitis into 2 groups: idiopathic and secondary. In idiopathic pouchitis the etiology and pathogenesis are still unclear, while in secondary pouchitis there is an association with a specific causative or pathogenetic factor. […] Current evidence suggests that the interactions of the altered composition and/or the quantity of the luminal microbiota (dysbiosis), with the altered characteristics of the mucosa (colonic metaplasia), in conjunction with abnormalities of innate and adaptive mucosal immunity, play a key role in the pathogenesis of pouchitis.
  • #87 Navigating Chronic Pouchitis: Pathogenesis, Diagnosis, and Management – Gastroenterology & Hepatology
    https://www.gastroenterologyandhepatology.net/archives/january-2025/navigating-chronic-pouchitis-pathogenesis-diagnosis-and-management/
    Dysregulated Adaptive Immunity A dysregulated immune response in chronic pouchitis is suggested by several studies and supported by the effectiveness of immunosuppressive treatments such as the α4β7 integrin inhibitor vedolizumab, tumor necrosis factor (TNF) inhibitors, potentially anti-interleukin (IL)-12 and -23 inhibitors, and Janus kinase (JAK)–STAT3 inhibitors. […] There is increased TNF expression in uninflamed UC pouches compared with FAP pouches and in patients with pouchitis. The role of the IL pathway is shown by increased expression of IL-1β, IL-6, IL-8, and IL-12 in pouchitis. […] Chronic pouchitis is a challenging and common complication of IPAA, with pathogenesis evolving from microbially mediated antibiotic-sensitive to antibiotic-resistant and immune-mediated processes.