Original article
Pre-pouch ileitis: a disease of the ileum in ulcerative colitis
after restorative proctocolectomy
A. J. Bell*†, A. B. Price*, A. Forbes*, P. J. Ciclitira†, C. Groves* and R. J. Nicholls*
*St Mark’s Academic Institute, St Mark’s Hospital, Harrow and †Department of Gastroenterology, The Rayne Institute, St Thomas’ Hospital, London, UK
Received 22 May 2005; accepted 17 October 2005
Abstract
Objective Ileal inflammation in ulcerative colitis can
occur as backwash ileitis or prestomal ileitis. After
restorative proctocolectomy (RPC), ileal inflammation
may be present in the pouch (pouchitis) but inflamma-
tion proximal to the pouch in the neo-terminal ileum, so
called pre-pouch ileitis (PI), has also been observed. As
pouchitis is increasingly common and PI can mimic it,
our aim was to characterize this condition.
Subjects and methods A review of prospectively col-
lected data on 571 inflammatory bowel disease patients
undergoing follow-up after RPC in a single centre over
22 years was performed. The histology of biopsy material
was reviewed and staining for colonic mucosal phenotypic
changes was undertaken. It was not routine practice to
prospectively assess all patients for pre-pouch ileitis when
the database was constructed.
Results Of 19 patients with inflammation of the pre-
pouch neo-terminal ileum (NTI) identified three had
Introduction
Small bowel inflammation may occur in ulcerative colitis
(UC) as backwash ileitis. This resolves after conventional
proctocolectomy. After restorative proctocolectomy
(RPC), however, inflammation may occur in the ileal
reservoir as pouchitis. This appears to be related to the
original diagnosis of UC since pouchitis is exceedingly
rare in familial adenomatous polyposis (FAP) after RPC
[1]. A pre-operative diagnosis of concurrent UC has been
demonstrated in cases of pouchitis occurring in FAP
patients [2]. Some patients with UC undergoing RPC
develop ileal inflammation in the neo-terminal ileum
(NTI) proximal to the pouch. This appears to be a
condition distinct from pouchitis. The present study
Correspondence to: Dr A J Bell, Department of Gastroenterology, Weston-
Super-Mare General Hospital, Somerset, UK.
E-mail: andrew.bell@waht.swest.nhs.uk
402
doi:10.1111/j.1463-1318.2006.00954.
Crohn’s disease and one a NSAID stricture. The
remaining 15 had a characteristic diffuse inflammation
extending from the NTI-pouch junction proximally: pre-
pouch ileitis. The inflammation extended proximally for
up to 50 cm. Fistula formation was seen in only one.
Seven (47%) of 15 had pouchitis but only two had
suffered backwash ileitis pre-operatively. Seven responded
to medical therapy and four to surgery. The histological
appearances including staining for colonic phenotypic
change were similar in PI and pouchitis.
Conclusion Pre-pouch ileitis is uncommon. As the
patients’ previous diagnosis of UC was confirmed and
there was no radiological or histological evidence of
Crohn’s disease, PI appears to have a distinct pathogen-
esis from Crohn’s disease.
Keywords Pouch, pouchitis, ileitis, Crohn’s disease,
ulcerative colitis
sought to ascertain the clinical and pathological charac-
teristics of pre-pouch ileitis (PI) by analysis of a database
In addition, histochemical staining of mucins in
biopsies from the NTI was conducted since colonic
phenotypic change of the pouch ileum with the expres-
sion of colonic proteins [3] and colonic-type sulphomuc-
ins [4] has been shown to be associated with pouchitis in
some patients.
Subjects and methods
The records of 571 consecutive patients undergoing RPC
for IBD between July 1976 and May 1998 at a single
centre followed for a mean of 83 ± 58 months were
reviewed. Data on the appearance of the neo-terminal
ileum had not routinely been entered in the database. To
identify those with possible PI patients in whom any ileal
abnormality was recorded during follow-up were
identified. On review of the case-notes those with an

2006 Blackwell Publishing Ltd. Colorectal Disease, 8, 402–410
A. J. Bell et al.
abnormality related to localized sepsis or to adhesions,
those in whom endoscopic examination disproved the
presence of inflammation, and those with Crohn’s disease
or a strong suspicion of a drug-related stricture based on
histology and ⁄ or recorded drug history were excluded.
Histopathology
The slides of previous biopsies and surgical specimens
stained with haematoxylin and eosin were reviewed by a
single histopathologist (ABP) blinded as to their origin.
Nine of 15 patients who satisfied the inclusion criteria
had archived blocks of tissue available from both the NTI
and the pouch. Paraffin sections of these archived blocks
were cut and stained using the high iron-diamine method
of Spicer [5]. This stains small intestinal sialomucins blue
whilst colonic sulphomucins are stained brown or black.
All slides were examined blind by two observers at 100·
magnification. All stained cells in each of five fields were
counted for each biopsy and the number of blue-staining
cells as a percentage of the total stained cells was
recorded. The mean percentage was calculated. Where
the observers’ mean estimates varied by more than 10% all
stained cells in the section were counted.
Biopsies from pouches with (n ¼ 8) and without
(n ¼ 11) pouchitis were used for comparison. Pouchitis
was defined according to the criteria of Moskowitz et al.
[1].
Statistical analysis of histochemical staining was by
unpaired t-test and significant results remained so
following Bonferroni correction.
Results
Of the 571 patients, 15 had evidence of idiopathic
inflammation of the NTI. This was identified by radio-
logical contrast studies in eight patients, by endoscopy in
four, by CT scanning in one, and at surgery in one. Those
diagnosed by imaging who remained symptomatic all
went on to have the findings confirmed at endoscopy or
surgery. In one further patient the means of diagnosis was
not recorded. One patient had well-controlled coeliac
disease.
The median age of the 15 patients was 36 years
(range 16–58 years) and the median time from pouch
construction to diagnosis of NTI inflammation was
3 years (range 0.02–11 years). Eight (53%) patients
were female.
Four (27%) patients had an end ileostomy prior to
restorative surgery with two of these having ileo-rectal
anatomosis as an intermediate procedure. Pouch oper-
ations were recorded as two-stage in 14 of 15 patients
and one-stage in one with 1S, 4J and 10W pouch

2006 Blackwell Publishing Ltd. Colorectal Disease, 8, 402–410
Pre-pouch ileitis
configurations recorded. Only one operation was des-
cribed as difficult; and only one recorded the use of
staples.
Clinical features
Symptoms included frequency of defaecation (6 ⁄ 15,
40%), subacute obstruction (6 ⁄ 15, 40%), loose stool
(5 ⁄ 15, 33%), abdominal flatus or colic (5 ⁄ 15, 33%),
evacuation difficulty (3 ⁄ 15, 20%) and weight loss (1 ⁄ 15,
7%). One patient was asymptomatic. Symptoms were
those elicited during unstructured routine follow-up
interviews with clinicians.
All 15 had continuous disease from the NTI-pouch
junction for a distance of 1 cm to more than 50 cm
proximally becoming milder more proximally (Fig. 1a,b).
Three had disease limited to the pouch-NTI junction;
nine had narrowing of the lumen in the NTI and in two
of these there was a severe stricture. One had a fistula
from the NTI to the vagina. Distally, two had a pouch-
vaginal fistula and one of these two had an additional
track arising from the ileal pouch-anal anastomosis. As
these are recognized complications of pouch surgery they
were not taken as diagnostic of Crohn’s disease in these
latter two patients. The other key patient characteristics
are shown in Table 1.
Radiological features
In 10 of the patients, contrast studies of the NTI were
performed when inflammation was active. The radiologist
specifically suggested Crohn’s disease in two cases whilst
in another the report included deep ulceration and
cobblestone appearance. In the remaining seven patients,
varying degrees and combinations of ulceration, thicken-
ing of folds, nodularity, irregularity and strictures were
described. The length of abnormal bowel varied from 1
to 30 cm when assessed radiologically. Dilation of the
NTI was reported in one patient.
Histopathological features
In 14 patients the pre-operative histological diagnosis
based on the colectomy specimen was confirmed as UC.
In one other patient UC was confirmed on review
elsewhere. Examination of resection specimens and
biopsies revealed no characteristic features to distinguish
PI from pouchitis (Fig. 2).
The macroscopic appearance of the resection specimen
of the five patients undergoing surgical removal of the
pre-pouch ileum, was of severe ulcerating mucosal
disease, with or without a stricture distally, giving way
to shallower more patchy ulceration proximally.
403
Pre-pouch ileitis A. J. Bell et al.

Figure 1 (a–d) The endoscopic findings at variable distances into the NTI from the pouch in a typical UC case, (a) at 40 cm, (b) at
15 cm, (c) NTI-pouch junction, (d) pouch. (e) A typical contrast study. The 15 cm of ileum leading into the pouch is clearly abnormal
demonstrating fold thickening and superficial ulceration.

Table 1 Patient characteristics. which is a recognized cause of granulomata in inflamma-

Idiopathic PI
tory bowel disease not confined to Crohn’s disease [6]. In
(n ¼ 15) one case with a stricture, capillary ectasia was a striking
feature and was felt to be suggestive of ischaemia. Three
n⁄N (%) specimens, including this case, the case with fistulating
disease and one of the other cases undergoing resection,
Family history of IBD 2 ⁄ 12 (17%) demonstrated fibrosis in the submucosa but none showed
Smoker 2 ⁄ 14 (14%)
the characteristic aggregated transmural inflammation of
Anaemia 8 ⁄ 13 (62%)
Crohn’s disease. In four cases an increase in severity was
Co-existent pouchitis 7 ⁄ 15 (47%)
seen over a follow up period ranging from one to 10 years
Backwash ileitis in original specimen 2 ⁄ 11 (18%)
Extra-intestinal manifestations 4 ⁄ 15 (27%) and one of these subsequently developed a severe
Significant stricture distal 3 ⁄ 15 (20%) stricture.
to pouch at ileo-anal anastomosis
End ileostomy or ileo-rectal 4 ⁄ 11 (36%)
Histochemistry
anastomosis prior to reconstruction
High iron diamine–Alcian blue staining reveals small
Values are shown as: no. with characteristic ⁄ no. in whom pres-
bowel sialomucins as blue (Fig. 3a) and large bowel
ence or absence of characteristic was recorded (%).
sulphomucins as brown (Fig. 3b). Several sections of the
Histopathology of the NTI was available for 12 pouch and pre-pouch ileum showed a mixed pattern of
patients. Sections showed degrees of villous atrophy and staining (Fig. 3c,d). The biopsies from UC pouches
a mucosal chronic inflammatory cell infiltrate accompan- without pouchitis exhibited sialomucins only with no
ied by neutrophils in the epithelium and ulceration of positive staining for sulphomucins. In inflamed speci-
variable intensity. mens, showing pouchitis and ⁄ or pre-pouch ileitis there
Granulomata were seen in only one case. This finding was a greater frequency of staining for sulphomucins with
was, however, not taken as evidence of Crohn’s disease this being the predominant mucin produced in some
since it was related to inflammatory crypt-abscess damage cases (Fig. 4). This demonstrates a further similarity

404
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A. J. Bell et al. Pre-pouch ileitis

Figure 2 The histology of a healthy pouch ileum contrasted with that typical of pouchitis and PI in the same patient. (a) Healthy
pouch with intact villi. (b) Inflamed pouch mucosa with flattened villi, acute inflammatory cell infiltration of the epithelium and chronic
inflammatory cells in the mucosa. (c) Similar appearance in inflamed pre-pouch ileum with overlying ulcer slough.

Figure 3 Sections stained with HID-AB. Blue represents small bowel sialomucins; brown colonic sulphomucins. (a) Normal small
bowel staining in pouch. (b) Normal large bowel staining in rectum. (c, d) Mixed staining pattern in a case of pouchitis (c) and pre-
pouch ileitis (d).

between PI and pouchitis. The difference was significant
(P ¼ 0.011; SE diff ¼ 11.367) when PI staining was
compared with controls but did not reach significance
when pouchitis was compared with controls. (P ¼
0.0599).
Treatment
As multiple treatments were used a flow-chart is provided
for ease of interpretation (Fig. 5).
Two patients with no or insignificant symptoms
received no treatment and their condition remained the
same. Two underwent spontaneous remission. One went
straight to open stricturoplasty and improved.
The remaining 10 patients were treated medically
initially, or with endoscopic dilatation. Seven of these
later required surgical intervention. Five of these came to
resection for refractory symptoms and this proved to be
effective treatment for their symptoms in three, although
this entailed sequential resections for recurrence with an
eventual end ileostomy in one.
All of those undergoing endoscopic dilatation later
came to resection. Another of these 10 patients did not
respond either symptomatically or endoscopically to de-
functioning of the inflamed segment. Of the seven
symptomatic patients not undergoing curative resection,
two became dependent on immuno-suppressive therapy
with one of them having poor symptom control whilst

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Pre-pouch ileitis A. J. Bell et al.

Percentage of goblet cells staining for had endoscopic recurrence; one required intermittent
sialomucins antibiotics and regular catheterization to empty the
100
pouch; and one resolved spontaneously following short-
lived responses to antibiotics, mesalazine and topical
steroids. In the five patients having a pouch-preserving
resection the inflammation recurred in three at a mean of
50 nine months. In two patients receiving an end ileostomy
there was no recurrence.
The indications for the original colectomy with extent
of disease, findings, treatment and outcome are summar-
0
ized in Table 2.

Pre-pouch ileitis Pouchitis controls Healthy pouch controls
Figure 4 The percentage staining for small bowel mucins in
sections from 27 patients is shown. Where less than 100% the
remainder stained for colonic mucins. More patients in the
inflamed groups including PI and pouchitis produced colonic
mucins.
the other later came to resection for side-effects of
treatment. Two were controlled on regular antibiotics;
one was controlled on antibiotics following resection but
Discussion
Involvement of the small intestine in inflammatory bowel
disease usually indicates Crohn’s disease. The ‘backwash
ileitis’ seen in some colitics with continuous disease is an
exception [7]. After restorative proctocolectomy some
degree of inflammation often occurs in the ileo-anal
pouch: pouchitis. Pouchitis appears to arise almost
exclusively in patients with a previous diagnosis of UC,
and it has been argued that it may represent a form of UC
affecting the ileal mucosa. The prevalence of pouchitis is

15 Patients with idiopathic pre-pouch ileitis

11 with symptoms
Strictureplasty medical Rx or
requiring treatment
(1) : well endo. diln. (10)

Resection for Surgery for long-term

side-effects (1)+ : medical Rx antibiotics +/-
well failure (7) prn steroids (2);
resolved off-
treatment (1)

Endo. Resection for Defunctioning

resection symptoms (4) ileostomy (1)
(polyp) (1)

Medical Rx following
surgical Rx failure (3)

immuno
antibiotics +/- suppressants (1)
catheter (2)
Figure 5 Flow-chart of treatment.
Abbreviations used in flow-chart: endo,
endoscopic; diln, dilatation; Rx, treat-
well well (2)# well Symptoms (1) ment; + pouch resected; # pouch resected
Well
and short bowel syndrome in one.

406
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A. J. Bell et al. Pre-pouch ileitis

Table 2 Indication for colectomy with disease extent, NTI findings, treatment and outcome.

Aetiology Indication Extent Reports PI Treatment Outcome

Idiopathic Res ⁄ ref Left 20 cm of minor stricturing Dilatation + MTZ + CS, Recurred postresection on
and aphthae in NTI resection, later MTZ + CS treatment, later symptoms
resolved. Functioning pouch.
Idiopathic Res ⁄ ref n⁄a Extensive ulceration in NTI i ⁄ v CS + Aza, CS initially Recovered but excised for
and pouch, cobblestoning effective then excision of steroid-dependence with
and deep ulcers pouch and NTI required osteoporotic fracture;
with no recurrence never functional pouch.
No recurrence 9 year
postop. End ileostomy.
Idiopathic Res ⁄ ref Pan Major aphthae + NTI-pouch Mild, not treated Mild symptoms continue
inflammation with slight
stricture
Idiopathic Res ⁄ ref Pan Superficial aphthae in Antibiotics good short-term Fairly well with prn
final 25 cm of NTI ciprofloxacin and live yoghurt.
Idiopathic Res ⁄ ref Ext Moderate ileitis for > 50 cm Nil Never symptomatic
ex anum
Idiopathic HGD Pan No PI at 4 year postop; MTZ to good symptomatic Well, intermittent treatment.
10 cm at 14 year effect in 2 week.s
Idiopathic Emergency n⁄a 20 cm NTI stricture Predfoam; Pentasa p.o. no Obstructive signs and
with ulcers reduction in frequency but symptoms. Cramps slightly
no obstruction; then dilated; better after polyp out
later inflammatory polyp and Pentasa
(ball-valve) removed
Idiopathic Res ⁄ ref Left Irregular ulcerated stricture Po ⁄ pr steroids, 5- ASA Settled on medication initially.
for last 30 cm of NTI and Aza, Dilatation Recurrent flares & quickly
then resection recurred postresection.
of stricture Continuous medical therapy.
Idiopathic Res ⁄ ref Left apthae, granularity & linear Initially defunctioned for Defunctioning did not
ulcers for > 40 cm subacute obstruction; alter PI.
lessening proximally stoma taken down, Well, on treatment.
catheter and MTZ effective
Idiopathic Emergency n⁄a 3 cm stricture just proximal Stricturoplasty of pre-pouch . Reduced frequency and severity
to pouch stricture of colicky pain
Idiopathic Emergency n⁄a Fistula from thickened NTI Resection NTI. Recurred at No recurrence but
with dilatation above. new NTI. Resected with has short
pouch. Recurred pre-Kock bowel syndrome
pouch. Resected. ileostomy.
Idiopathic Res ⁄ ref Ext Nodular narrowing in Nil Spontaneous resolution
afferent loop
Idiopathic Res ⁄ ref Left Granular mucosa and Antibiotics and pentasa Spontaneous resolution
aphthae at NTI-pouch and topical steroids all later
junction briefly effective
Idiopathic HGD Pan Stenosis proximal to pouch Spontaneous resolution Discharged well
Idiopathic Res ⁄ ref Ext Severe inflammation in NTI, Stoma for 6 month. Symptoms Well 1 year. post,
5 years later continuous helped by defunctioning; later resection functioning
stricture above for recurred and resected after pouch.
some distance 5 years. MTZ helped.
NSAID n⁄a n⁄a Stricture above pouch Resection Well post resection.
(‘NSAID’) ‘NSAID stricture’
Crohn’s Emergency Pan Proximal anastomotic Excised. Proximal small Well 9 month. postop.
ulcers; major aphthae bowel lesion so ‘Crohn’s’ End ileostomy.
at 10 cm proximal to but possibly previous
this. Normal between. stoma site

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Pre-pouch ileitis
Table 2 (Continued)
Aetiology Indication Extent Reports
Crohn’s n⁄a Left 10 cm ulceration
‘typical of Crohn’s
disease’ pre-pouch
Crohn’s Res ⁄ ref Ext Stricture at NTI-pouch
junction; minor
aphthae above only
Abbreviations used in Table 2: Res ⁄ ref ¼ treatment resistant or refractory disease; HGD ¼ high grade dysplasia; Ext ¼ extensive
colitis; Left ¼ left-sided; MTZ ¼ metronidazole; CS ¼ corticosteroids; Aza ¼ azathioprine; n ⁄ a ¼ not available.
increasing and it has been called the third inflammatory
bowel disease. As a result the differential diagnoses in
patients with a pouch are assuming greater significance.
This study describes a group of patients who have
inflammation proximal to the pouch. Only about half of
these have concomitant pouchitis. The present study
sought to characterize the clinical and pathological
features of pre-pouch ileitis.
The endoscopic features had been interpreted as
Crohn’s disease and so were three of 10 contrast studies.
Histologically, however, all 15 patients were confirmed to
have had ulcerative colitis at the time of RPC. Further-
more in none of the 13 patients who had undergone
contrast radiology of the proximal bowel was there any
evidence of any other small bowel lesion. In contrast to
what would be expected in Crohn’s disease, less than 15%
of patients smoked and of the two patients having faecal
diversion one developed distal inflammation and the
other did not improve [8].
Inflammation can occur immediately proximal to an
ileostomy although this is less common than is inflam-
mation in a Kock or ileo-anal pouch. It has been
suggested that pouch inflammation is related to distal
stricturing [9] but this did not appear to apply to the neo-
terminal ileum as only three (20%) patients in the present
study had a significant distal stricture. All were due to
stenosis of the ileal pouch-anal anastomosis.
There was no correlation between PI and the original
extent of the disease or the presence of backwash ileitis,
which has been proposed as a predictor of pouchitis [10].
The indications for RPC in the 15 patients were no
different from those in a general UC population under-
going surgery [11]. A history of extra-intestinal manifes-
tations has been suggested to be a marker for aggressive
disease [12,13]. However, this was present in less than
30% of the patients and, although the numbers are small,
this rate was similar to that reported in the general
population of patients who have had an RPC for UC
408
A. J. Bell et al.
PI Treatment Outcome
Defunctioned. Crohn’s. New activity
PI gone by 3 month. elsewhere in small bowel
precluded further attempts at
reversal of ileostomy.
Dilatation; continued Crohn’s. End ileostomy.
symptoms. Excision.
[14]. In terms of response to treatment the picture is
similar to resistant pouchitis. Various treatments were
given but none was consistently effective.
Other unusual patterns of small bowel inflammation
in UC have been reported. Hallak et al. [15] published
a series of nine cases of ‘postcolectomy ileitis’ which
they observed in patients with and without UC. These
included two with inflammation proximal to an S-
pouch similar to the cases reported in the present
study. In an analysis of eight cases with Crohn’s-like
complications following RPC, Goldstein et al. [16]
described three patients with stricturing enteritis at the
pouch inlet. The authors suggested that a re-classifica-
tion of the diagnosis from UC to Crohn’s disease
should not be considered unless there was intestinal
disease distant from the pouch or there were irrefutable
changes of Crohn’s disease in biopsies or in the
excision specimen. While there were two cases with a
pouch-vaginal fistula in the present series, this is a
recognized complication of RPC and is not per se
strong evidence of Crohn’s disease [17].
Morphological changes of the small bowel including
variable villous atrophy have been observed in acute
colitis [18]. However, these have a tendency to resolve
after the acute attack has settled. In coeliac disease there is
an association with microscopic colitis. In such instance,
however, neutrophil infiltration of the epithelium is not
prominent and there may be a gluten sensitivity of the
large intestinal lymphoid tissue as it responds to a gluten-
free diet [19]. The continuous nature of the inflamma-
tion together with its length and histological appearance
make it highly unlikely that the cases reported here are
examples of the more unusual vasculitic-type [20] or
NSAID-induced enteropathy [21].
One weakness of the present study is that the recent
use of NSAIDs was not prospectively collected in the
database. In the light of a recent report in which the
authors found this to be the likely explanation for afferent

2006 Blackwell Publishing Ltd. Colorectal Disease, 8, 402–410
A. J. Bell et al.
limb ulcers proximal to the pouches of four patients with
histologically proven UC, it is clearly relevant [22].
However, it seems unlikely to explain the extensive
ulceration seen in the cases here reported.
Adaptation of the pouch ileal mucosa takes place as
it begins to be exposed to faeces in the reservoir [23–
25]. Colonic proteins and mucins are produced along-
side small intestinal ones [4]. Changes in mucins in the
ileal pouch mucosa are well-documented [3,4,23,26–
28] but the present study has shown for the first time
that such phenotypic changes can also occur more
proximally. Using histochemical techniques for mucin
identification and conventional histological assessment
no morphological difference between PI and pouchitis
was found. This suggests that PI, like pouchitis, is a
distinct disease of the ileum occurring in patients with
UC after RPC.
Some colonic phenotypic change may lead to the
ileum being threatened by disease processes normally
limited to the colon.
Alternatively, pouch configuration may adversely
influence vascularization or motility of the neo-terminal
ileum. In the present study PI developed more frequently
following construction of W pouches (3.4%) rather than J
(1.9%) or S (2.1%) pouches.
The present study suggests that the prevalence of pre-
pouch ileitis is approximately three per cent of patients
having RPC. This may be an underestimate because the
NTI is not routinely examined in patients who have had
RPC. In three studies of pouch mucosal changes in which
the NTI was also biopsied, inflammation was found in 1
(5%) of 20 subjects [28], 14 (13.5%) of 104 [29] and 8
(29%) of 28 [22].
Conclusion
Pre-pouch ileitis appears to be a disease of the ileum
distinct from Crohn’s disease occurring after construction
of an ileo-anal pouch in patients with ulcerative colitis.
Macroscopically, it is seen as continuous inflammation
lessening in intensity proximally. Histological changes are
the same as those seen in pouchitis and there is colonic
phenotypic change also. PI should be included in the
differential diagnosis of poor function after RPC, and
endoscopic examination of the neo-terminal ileum with
biopsies is essential when investigating the patient with
nonspecific symptoms including poor function.
Acknowledgements
Dr Bell was supported by The Henry Smith Charity and
The St Mark’s Hospital Foundation. Dr Kay Wilkinson
and Steve Rumbles maintain the database.

2006 Blackwell Publishing Ltd. Colorectal Disease, 8, 402–410
Pre-pouch ileitis
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