Open Journal of Gastroenterology, 2011, 1, 7-12
doi:10.4236/ojgas.2011.12002 Published Online November 2011 ( OJGas
Published Online November 2011 in SciRes.
The pathogenesis of primary pouchitis following ileal
pouch-anal anastomosis: a review of current hypotheses
Sally Bath1, Christian P. Selinger1,2, Rupert W. L. Leong1,3
1Concord Repatriation General Hospital, Gastroenterology and Liver Services, Hospital Road, Concord, Australia;
2Salford Royal Hospital, Department of Gastroenterology, Stott Lane, Salford, UK;
3The Faculty of Medicine, The University of New South Wales, Sydney, Australia.
Received 3 October 2011; revised 8 November 2011; accepted 19 November 2011.
Primary pouchitis is a common complication of ileal
pouch-anal anastomosis following proctocolectomy in
patients treated for ulcerative colitis (UC), but is un-
usual for those treated for familial adenomatous
polyposis (FAP). While a number of theories as to the
pathogenesis of this inflammatory condition have
been proposed, no single one has been wholly satis-
factory. Much research has been devoted to investi-
gating a link between the pathogenic factors involved
in UC, but not FAP, and those underlying pouchitis.
The contribution of sulfate-producing bacteria has
also been explored. The role of other intraluminal
factors, such as short chain fatty acids and unconju-
gated bile salts, has also been investigated. A unifying
theory of a multi-step process might explain the
pathogenesis of pouchitis, but further research is re-
quired to proof causation. It is likely that pouchitis
develops as a result of a combination of genetic, im-
munological, microbial and metabolic factors. Future
insight into the causes of pouchitis may eventually
allow for the development of more effective treat-
Keywords: Pouchitis; Ileo-Pouch Anal Anastomosis;
Prior to the development of the ileal pouch-anal anasto-
mosis technique (IPAA) patients requiring proctocolec-
tomy were mandated to have an end-ileostomy. IPAA
restore the continuity of the lower GI tract by creating a
pouch of ileal loops directly anastomosed to the anal
canal, and preserving the anal sphincter function. Re-
storative proctocolecto my followed by IPAA is currently
the treatment of choice in the surgical management of
refractory ulcerative colitis (UC) and familial adenoma-
tous polyposis (FAP) [1,2]. Epidemiological studies
show that at least 10% of patients with UC will undergo
proctocolectomy during the course of their illness [3].
IPAA has been fou nd to have a positive impact on global
quality of life score as it provides symptomatic relief
while preserving fecal continence [4,5]. However, the
procedure is associated with significant short and long-
term morbidity, including immediate post-operative com-
ations, pouch failure, small bowel obstruction, sexual
dysfunction, irritable pouch syndro me and pouchitis [2].
Of these, pouchitis is the most common long-term
complication, occurring at a rate of 48% at 10 years and
70% at 20 years in patients with UC [6]. For patients
who have had one episode of pouchitis, there is a 64%
risk of recurrence [2]. In FAP, pouchitis is uncommon
and approximated 5% in those treated with restorative
proctoco lectomy with pouch [7]. Overall similar rates of
adverse post-operative outcomes have been reported in
patients treated for UC and those treated for FAP [8].
There is however a marked difference in the risk of fis-
tulisation and pouchitis [8]. Pouchitis is significantly
more common in patients treated for UC than FAP, and
this observation has formed the basis for a number of
hypotheses of pathogenesis.
Pouchitis is an inflammatory condition of the ileal
reservoir that is formed during IPAA [9]. It occurs as a
single acute episode in a third of cases but most have
recurrent acute episodes or a chronic course of disease
[10]. Acutely, it can be distressing with symptoms of
increased stool frequency, urgency, nocturnal inconti-
nence and abdomino-pelvic pain, often accompanied by
fever, weight-loss and bloody stools [5]. In chronic cases,
pouchitis may be associated with reduced quality of life
and the need for further surgery [9]. Currently, there are
no consensus guidelines for diagnosis and in most cases
a combination of clinical signs and symptoms and pou ch
S. Bath et al. / Open Journal of Gastroenterology 1 (2011) 7-12
endoscopy are utilised. For research purposes, a number
of detailed, standardised diagnostic tools have been de-
veloped which incorporate clinical, endoscopic and his-
tological criteria. The most commonly used version is
the Pouchitis Disease Activity Index (see Ta bl e 1 ) [11].
The complexity of these scores highlights the multifac-
eted nature of pouchitis.
Secondary pouchitis is diagnosed in 20% - 30% of pa-
tients presenting with pouchitis [12]. In these cases a
specific causative factor is identified, for example Can-
dida infection, Clostridium difficile infection, radio-
therapy, chemotherapy, CMV infection or collagen depo-
sition. The remainder of patients present with primary
(idiopathic) pouchitis. To date, the pathogenesis of pri-
mary pouchitis has not been fully elucidated, but a
number of theories have been proposed. The aim of this
paper is to review the evidence for and against each of
these theories.
The management of pouchitis includes confirmation
and exclusion of other inflammatory conditions include-
ing Crohn’s disease recurrence and secondary pouchitis.
Both metronidazole and ciprofloxacin are effective in
treating acute pouchitis [13,14] and continuous mainte-
nance antibiotic therapy may be required for chronic
pouchitis. Rifaximin, an oral broad-spectrum non-ab-
sorbed antib iotic was found be useful in an open-labelled
maintenance study in the maintenance of remission [15].
For patients with chronic pouchitis in remission, the
probiotic VSL#3 consisting of strains of lactobacilli,
bidobacteria and Streptococcus salivarius subsp. ther-
mophilus significantly reduced recurrences of pouchitis
from 100% in the placebo group to 15% [16]. Topical
treatments using enemas may be effective. Resistant
cases may respond to immunosuppressive therapies and
infliximab has been used effectively in difficult-to-treat
cases [17]. Finally, surgical reconstruction and excision
may be required.
Following an IPAA, the section of ileum used to fashion
the fecal reservoir (pouch) takes on many of the histo-
logical features of colonic epithelium, probably as a re-
sult of prolonged fecal exposure [18]. These changes
may render the pouch susceptible to conditions that pri-
marily affect the colon. Thus, it has been suggested that
pouchitis is a recurrence of UC.
There is significant overlap between UC and pouchitis
at the clinical, endoscopic, histological and molecular
levels, suggesting a common mechanism of pathogenesis.
The characteristic endoscopic findings in pouchitis are
oedema, granularity, friability, loss of vascular pattern,
mucous exudates and superficial ulceration (see Table 1)
[11]. Clearly, there are commonalities between these
findings and the hallmarks of UC. At the molecular level,
Amasheh et al. [19] have demonstrated changes in the
expression of claudin-1 and claudin-2 in tissue taken from
Table 1. The pouchitis disease activity index. [10] Score range 0 - 18; >7 indicates pouchitis.
Criteria Score
Stool frequency Usual postoperative frequency 0
1 - 2 stools/day more than postoperative norm 1
3 or more stools /day more than po stoperative norm 2
Fecal urgenc y/abdominal cramps None 0
Occasional 1
Usual 2
Rectal bleeding None or rare 0
Present daily 1
Fever (temp erature > 37.8˚C) Absent 0
Present 1
Endoscopic inflammation Oedema 1
Granularity 1
Friability 1
Loss of vascular pattern 1
Mucous exudates 1
Ulceration 1
Acute histological inflamm ation Polymorphonuclear leukocyte infiltration None 0
Mild 1
Moderate and crypt abscess 2
Severe and crypt abscess 3
Ulceration per low field (mean) None 0
<25% 1
25% - 50% 2
>50% 3
opyright © 2011 SciRes. OJGas
S. Bath et al. / Open Journal of Gastroenterology 1 (2011) 7-12 9
patients suffering acute pouchitis. These proteins are
components of epithelial tight junctions and altered ex-
pression of these proteins increases epithelial permeabil-
ity via the paracellular route. Similar changes have been
demonstrated in UC [20].
While pouchitis is prevalent in patients with a history
of UC, it is very infrequently seen in those with a history
of FAP. A large meta-analysis of studies comparing
post-IPAA outcomes in UC and FAP patients found sig-
nificantly higher rates of pouchitis in the UC population
(OR 6.44; 95% CI: 3.21 - 12.93) [8]. These results cer-
tainly support the theory that the pathological mecha-
nisms underlying UC, but not FAP, may be responsible
for the development of pouchitis. That pouchitis is more
common in patients with a history of pancolitis than
those with left-sided colitis also len ds weight to this the-
ory [21]. Ta bl e 2 lists some of the differences between
UC and FAP in the risk of developing pouchitis.
Immunological features of pouchitis often mimic UC.
CD19 + Ki-67 + cells and CD138 + Ki-67 + cells are
increased in UC and represent immature plasma cells
with increased proliferative activities. Similar cell phe-
notypes are found in pouchitis mucosa suggesting UC-
derived abnormalities in the pathogenesis of pouchitis
[22]. Pouchitis also correlated with decreased defensin
expression in UC in addition to high expr ession of cyto-
kines as opposed to FAP pouches that had increased ex-
pression of hBD-1 beta-defensin and low cytokine levels
[23]. Toll-like receptors (TLR) are members of the pat-
tern recognition family important involved in innate
immunity. TLR-4 is specifically activated by lipopoly-
saccharide, an endotoxin produced by gram-negative
bacteria. TLR-4 expression was found to be increased in
pouches of UC patients in comparison with FAP patients,
even in the absence of clin ical or histological inflamma-
tion. This may result in increased intracellular pathway
activity following activation by bacterial products in UC
patients. [24] The observation that extraintestinal mani-
festations of UC often occur in parallel with pouchitis
provides further support to a theory of common immu-
nological pathogenesis. Lohmuller et al. [25] found that
in a population of 734 pa tients who had undergone IPAA
for UC, 53% of those with postoperative extraintestinal
manifestations developed pouchitis compared to 25% of
those without extraintestinal manifestations (P < 0.001).
Seven patients with preoperative extraintestinal mani-
festations that resolved after IPAA had concomitant re-
currence of the extraintestinal manifestations and acute
The most compelling refutation of this theory lies in
the role of antibio tics in the treatment of pouchitis. Short
courses of metronidazole and ciprofloxacin have tradi-
tionally been used in the treatment of acute cases [26]. It
has been shown that treatment of pouchitis with met-
ronidazole results in resolution of the characteristic his-
tological changes of the condition [18]. UC is not rou-
tinely responsive to antibiotic therapy. While there is
compelling evidence for a common pathogenesis be-
tween pouchitis and UC, the theory does not fully ac-
count for this discrepancy. Additionally, mucosal cyto-
kine alterations found in pouchitis may simply reflect
inflammatory activity independent to those underlying
CD or UC. That is, cytokine changes are the result of
inflammation rather than causative [27].
Pouchitis appears to correlate with the presence of
pouch dysbiosis. The efficacy of antibiotics in the
treatment of acute pouchitis strongly suggests that
Table 2. Pouchitis risk and association with restorative procto-colectomy for ulcerative colitis (UC) versus familial adenomatous
polyposis (FAP).
Pouchitis association with UC a s opposed to FAP
Epidemiology more common wit h U C
Clinical UC extraintestinal manifestations may occur in parallel with pouchitis
Endoscopic macroscopic and microscopic features of pouchitis are in common with inflammatory bowel diseases
Bacteria pouch dysbiosis and loss of microbial biodivers ity in culture and molecular identification similar to UC
increased hydrogen sulfide-producing and sulfate-reducing organisms
Immune serological markers (pANCA) similar to UC
increased immature plasma cells with increased proliferative activities similar to UC
cytokine and defensin changes may reflect underlying UC pathogenesis
increased toll-like receptor 4 expression in UC pouches
altered tight junction proteins
Mucosal increased sulphomucin in UC pouches
pANCA = Perinuclear anti-neutrophil cytoplasmic antibody.
opyright © 2011 SciRes. OJGas
S. Bath et al. / Open Journal of Gastroenterology 1 (2011) 7-12
bacteria play a role in the pathogenesis of the condi-
tion. Loss of biodiversity occurs in pouches of UC
patients but not in pouches following FAP. UC
pouches in contrast to FAP pouches, there was increase
in Proteobacteria (P = 0.019), decrease in Bacteroide-
tes (P = 0.001) and Faecalibacterium prausnitzii (P =
0.029). Furthermore, bacterial diversity was signifi-
cantly greater in UC non-pouchitis compared with UC
pouchitis (P = 0.009). [28] Mucosal Clostridiaceae spp
colony forming units were significantly increased in
patients with recurrent or chronic pouchitis compared
to those with no- or single-episode pouchitis (OR:14.
95% CI: 0.887 - 224.021; P = 0.045) [29]. VSL#3, a
probiotic, is effective in preventing relapse of chronic
pouchitis and may prevent episodes of acute pouchitis
[26]. Specific causative bacteria or differential bacte-
rial count were not identified in the faeces of patients
with or without pouchitis in another study [30]. How-
ever, negative findings may reflect older techniques in
defining the microbiome. Patients with pouchitis have
been found to have a greater anaerobe to aerobe ratio
than those without [30,31]. Thus, it may be qualitative
rather than quantitative differences in microflora that
lead to the development of pouchitis. More recently, a
role for sulfate-reducing bacteria has been proposed
[32,33]. These bacteria are native to the human colon
and produce hydrogen sulfide as a by-product of me-
tabolism. Hydrogen sulfide is believed to compete
with normal colonic metabolic substrates, leading to
disruption of colonocyte metabolism and injury to the
intestinal mucosa [32]. The quantity of hydrogen sul-
fide gas produced by the pouch contents of patients
with active pouchitis is significantly greater than that
produced by patients with no history of pouchitis and
those receiving antibiotic therapy. In patients with FAP,
the quantity of hydrogen sulfide produced is signifi-
cantly less than in any group of UC patients [32].
Duffy et al. [33] report that sulfate-reducing bacteria
are found in the pouches of patients with UC, but not
those with FAP. Thus, this theory accounts for a num-
ber of the observed features of pouchitis: the efficacy
of antibiotics, the lack of a single identifiable causa-
tive organism and the differences in incidence between
UC and FAP patients.
The chief argument against a bacterial theory of
pathogenesis is that there is no correlation between the
characteristic histological changes of pouchitis and fecal
aerobic or anaerobic coun ts [18]. Future studies examin-
ing the relationship between hydrogen sulfide production
and mucosal morphology will, no doubt, be valuable.
Pouch mucosal mucin characteristics appear to differ
between UC and FAP pouches. The expression of sul-
phomucin is increased in the mucous gel layer of UC
compared with FAP pouches. Differential mucin ex-
pression favours colonization by different organisms
and sulphomucin expression was associated with sul-
phate-reducing bacteria and increased chronic inflam-
mation [34].
Short-chain fatty acids (SCFAs) are produced by
anaerobic bacteria through the fermentation of dietary
fibre. They are the principle source of energy for
colonocytes and are important for mucosal homeosta-
sis. Clausen et al. [35] found that concentrations of
SCFAs in the faeces of patients with pouchitis are
lower than in those without pouchitis, albeit in a small
sample of patients. This finding has led to the hy-
pothesis that reduced availability of SCFAs in the ileal
pouch plays a role in the development of pouchitis.
However, this is unlike ly to be the pr imary mechan ism
responsible for pouchitis for a number of reasons.
Sandborn et al. [30] quan tified SCFA concen tration s in
the faeces of UC patients, both with and without
pouchitis, and FAP patients, finding no significant dif-
ferences between the groups. This finding calls into
question the role of SCFAs in the pathogenesis of
pouchitis. Furthermore, it highlights the fact that this
theory cannot account for the observed differences in
incidence of pouchitis between patients with UC and
FAP. Glutamine and butyrate suppositories have been
trialled as therapy for chronic pouchitis on the basis
that increasing concentrations of SCFAs in the pouch
may reduce epithelial permeability, leading to symp-
tomatic improvement. The clinical response rate in
small, uncontrolled studies has been very low [26],
further undermining this hypothesis.
Unconjugated bile acids are released from primary
bile salts by the actions of anaerobic bacteria. These
unconjugated bile acids are toxic to lipid membranes.
High levels of unconjugated bile acids have been
found in the feces of patients with ileal pouches, as
compared to those who have undergone conventional
ileostomy [36]. It has been suggested that this increase
may predispose to pouchitis but others have not con-
firmed these findings. As for SCFAs, the concentra-
tions of unconjugated bile acids are no different in UC
and FAP patients [30]. If bile acids were the primary
pathogenic factor, a similar incidence of pouchitis
would be expected in the two groups. Thus, it is
unlikely that bile acids are a major pathogenic factor in
the development of pouchitis.
None of the theories discussed above can explain the
development of pouchitis fully on its own merit. Cof-
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S. Bath et al. / Open Journal of Gastroenterology 1 (2011) 7-12 11
fey et al. [37] have proposed that pouchitis is the re-
sults of a multi-step process rather than anyone single
factor. Their unifying theory is based on the following
steps: First colonic metaplasia develops in the ileal
pouch, which is followed by the production of sul-
phomycin by the goblets cells. Sulphomycin then pro-
vides the basis for sulfate-reducing bacteria colonisa-
tion. Hydrogen sulfide production by sulfate-reducing
bacteria may cause apoptosis and reactive crypt cell
hyperplasia. Hydrogen sulphide will then also cause
infl ammat io n and asso c iated s ympto ms [37].
While the multi-step theory unifies current isolated
findings, it does not fully explain the pathogenesis. It
remains unclear why greater rates of colonic metapla-
sia occur in UC compare to FAP patients. So far only
an association between sulfate-reducing bacteria colo-
nisation and colonic metaplasia has been found and
any causality is speculative.
Understanding of the pathogenesis of primary pouchitis
remains incomplete. While a number of theories have
been proposed, no single one fully explains the histo-
logical findings and the efficacy of certain treatments.
The evidence for a shared pathological basis between
UC and pouchitis is compelling, but it can not explain th e
therapeutic benefit of antibiotics. There is mounting
evidence that sulfate-reducing bacteria play a major role
in the condition, while it seems unlikely that SCFAs or
bile acid concentrations are the chief pathological cul-
prits. Certainly it seems plausible that all of these factors
may contribute to the development of pouchitis, in the
context of unknown immunological factors unique to
patients with UC. The multi-step process theory pro-
posed by Coffey et al. aims to unify the current find ings.
Future studies may elicit a unifying link between the
single hypotheses and proof or disproof the proposed
multi-step model. Regardless, further investigation into
the pathogenesis of primary pouchitis is warranted in the
search for more efficacious treatments and preventative
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