Analysis of Clinical and Histopathological Findings in Microscopic Colitis
Gozde TOPEL, Ebru CAKIR, Ilgin AYDIN, Fatma Husniye DILEK, Aysegul AKDER SARI
Department of Pathology, Izmir Katip Celebi University, Ataturk Training and Research Hospital, IZMIR, TURKEY
Keywords: Colitis, Microscopic colitis, Collagenous colitis, Lymphocytic colitis
Microscopic colitis is a chronic inflammatory disorder characterized by a triad of chronic diarrhea, endoscopy without significant
abnormality, and distinct histopathological features. Histopathologically, microscopic colitis is divided into 3 subtypes; collagenous colitis,
lymphocytic colitis, incomplete microscopic colitis. The main purpose of this study was to analyze the detailed clinicopathological parameters of
microscopic colitis cases in the Turkish population.
Material and Method: The clinicopathological parameters were evaluated in 53 microscopic colitis cases (37 collagenous colitis, 7 lymphocytic
colitis, 9 incomplete microscopic colitis) diagnosed between 2010 and 2019.
Results: All cases had lymphoplasmacytosis. The presence of ≥20 eosinophils/high power field in the lamina propria was remarkable in 75.7%,
57.1%, and 11.1% of collagenous colitis, lymphocytic colitis, and incomplete microscopic colitis cases, respectively. One of the striking findings
was the presence of concomitant Celiac disease in 29% of the lymphocytic colitis cases. In terms of drug use, proton pump inhibitors and
nonsteroidal anti-inflammatory drugs were the most commonly used drugs.
Conclusion: The mean age in our series is lower than the literature and a distinct male predominance was observed in lymphocytic colitis and
incomplete microscopic colitis, contrary to the literature. These suggest that susceptibility to microscopic colitis may differ between ethnic
groups. The presence of overt lymphoplasmacytosis, eosinophilic infiltration and epithelial damage are the microscopic features which should
alert the pathologist for the diagnosis of complete microscopic colitis. Given that microscopic colitis is a common treatable cause of chronic
diarrhea, awareness of the aforementioned histopathological features is of utmost importance for accurate diagnosis and not to miss incomplete
Microscopic colitis (MC) is a chronic inflammatory bowel
disorder characterized by a triad of chronic diarrhea,
endoscopy without significant abnormality, and distinct
histopathological features 1
. MC has been considered
to be a rare disease but currently it is diagnosed in about
10% of patients investigated by colonoscopy for chronic
. There is a female predominance with a
mean age of 65 years at diagnosis. Female preponderance
appears to be more pronounced in collagenous colitis
compared to lymphocytic colitis (female-to-male incidence
rate ratio 3.0 and 1.9, respectively) 4
. The exact etiology
of MC is unknown, but it is most likely multifactorial,
and infection, autoimmunity, smoking, drugs, mucosal
immunopathology, dysregulated collagen metabolism, and
genetics have been thought to play a role in the etiology 5-7
Three histological subtypes have been defined: collagenous
colitis (CC), lymphocytic colitis (LC), and incomplete
microscopic colitis (MCi) 1,8,9
. Lymphocytic colitis is described by an increased number of surface intraepithelial
lymphocytes (>20 intraepithelial lymphocytes (IELs)/100
enterocytes), and collagenous colitis by a thickened collagen
band (>10 μm) below the surface epithelium 1,10
is increased mixed inflammation in the lamina propria and
surface epithelial damage but only little crypt architectural
distortion, if any 1,11
. Incomplete and variant forms
disclosing less characteristic features have been described
by many different names such as borderline LC, minimal
CC, microscopic colitis not otherwise specified (MCnos),
paucicellular lymphocytic colitis, and MCi 1
differential diagnosis includes ulcerative colitis and
Crohns disease, infectious colitis, diverticular disease,
and amyloidosis in particular 12
. It may not be easy to
distinguish between non-specific inflammatory mucosal
changes and MC, especially the incomplete forms 9,13
Some patients with MC go into spontaneous remission.
Although antidiarrheals such as loperamide, diphenoxylate
or bismuth subsalicylate are used, the most promising evidence-based therapeutic option is currently budesonide,
a locally active corticosteroid 8
. Relapse following
treatment has been reported to be common in controlled
trials; however, the long-term course of MC and especially
MCi is not well-known 9,14
. Since incomplete forms are
reported to progress to MC in %30 of follow-up biopsies, it
is important to recognize these cases 15
. There are only
few studies in the English literature on histomorphological
features of MC and MCi in detail. The main purpose of
this study was to analyze the detailed histopathological and
clinical parameters of MC and MCi cases in the Turkish
The histopathological parameters were re-evaluated in 53
microscopic colitis cases (37 CC, 7 LC, 9 MCi) diagnosed
between January 2010 and December 2019. The study
protocol was approved by the institutional ethics committee
on January 21, 2021 (decision no: 0008). Clinical and
demographic data were retrieved from the hospital records.
We retrospectively reviewed all colon biopsies for each
patient and noted the biopsy indication and symptoms,
associated diseases, and the location and number of
biopsies obtained. Histopathological reviews were based
on hematoxylin and eosin (H&E) staining. In borderline
cases, CD3 immunostaining to evaluate the number of
intraepithelial lymphoctes and Masson Trichrome (MT)
to evaluate collagen density were also available for review.
All slides were re-evaluated by 2 pathologists; the presence of a subepithelial collagen band >10 μm in thickness and
>20 intraepithelial lymphocytes (IELs)/100 enterocytes
were considered diagnostic for CC and LC, respectively.
The presence of a subepithelial collagen band 5-10 μm in
thickness and/or 10-20 IELs/100 enterocytes were classified
as MCi 10.
Detailed histopathological examination for the following
parameters were carried out: the collagen band
thickness, presence of neutrophils, lymphoplasmacytes
and eosinophils in the lamina propria, intraepithelial
lymphocyte count, presence of crypt distortion, crypt
abscess, giant cell, granuloma and paneth cell metaplasia,
entrapment of erythrocytes and other cells in the
subepithelial collagen band, the evidence of the epithelial
damage as mucin depletion, vacuolization, sloughing of
the superficial mucosa and detachment of the surface
epithelium. Inflammatory infiltrate within the lamina
propria was scored as follows: lymphoplasmacytic
intensity was graded as mild and moderate/severe and
the location was categorized as superficial or superficial/
deep. Entrapment of cells was graded as slight/moderate/
severe. The number of eosinophils in the lamina propria
was grouped as 0-19, 20-49 and ≥50/HPF. Intraepithelial
lymphocyte count was grouped as 0-4, 5-9, 10-20, and
>20/100 enterocytes. The presence of IELs was evaluated
in areas without lymphoid aggregates, which are frequent in the colon and are associated with increased IELs
that would not in any way suggest lymphocytic colitis/
microscopic colitis. Subepithelial collagen band thickness
measurement was performed using the tools section of
the application (Olympus Labsens). Special care was taken
to avoid misinterpretation of a tangentially cut basement
membrane while measuring the collagen band thickness.
Biopsy sites were categorized as ascending colon, transverse
colon, descending colon and rectosigmoid colon. Multiple
endoscopic biopsies taken from 2-4 sites from the patients
were evaluated. Biopsies from the ceacum, ascending
colon, and transverse colon were classified as right-sided
and biopsies from the descending colon and rectosigmoid
as left-sided. The clinic data such as initial symptoms, the
association of other disease (celiac disease, helicobacter
pylori gastritis, gastrointestinal neoplasia), and drug
history were recorded.
Statistically, differences between groups for the categorical
clinicopathological variables were analyzed by the χ2 test,
using both Fisher's Exact test and the Fisher-Freeman-
Halton Exact test (SPSS version 22, IBM SPSS Inc., Armonk,
NY, USA). P<0.05 was considered statistically significant.
A total of 53 cases with the diagnosis of microscopic colitis
were included in the study.
Fifty one of the cases were diagnosed with microscopic
colitis in the initial biopsy, one case in the 3rd biopsy, and
the remaining case in the 4th biopsy. Thirty seven (70%)
cases were CC, seven (13%) cases were LC, and nine (17%)
cases were MCi with a mean age of 59 (22-87), 51 (27-83)
and 46 (24-72) years respectively. When patients were
divided into two groups according to age as ≤50 years
old and >50 years old, 73.0% of CCs, 42.9% of LCs, and
only 33.3% of MCi were found to be over 50 years of age.
Patients with CC were statistically significantly older (most
were >50 years of age) when compared to lymphocytic
colitis and incomplete microscopic colitis cases (p=0.045).
CC had a female predominance (n=26, 70.3%), while there
was a male predominance in LC (n=7, 100%) and MCi
(n=7, 77.8%). The gender difference between CC and
non-CC cases was statistically significant (p<0.001). The
concomitant disease and drug use history in MC cases are
summarized in Table I and the clinical features of MC and
MCi cases are summarized in Table II and Table III.
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|Table III: Clinical and histopathological features of collagenous colitis and non-collagenous colitis cases.
Biopsies were taken from 5 different sites in 15, 4 in 9, 3
in 19, and 2 different sites in 10 of 53 cases. The frequency
order of biopsy sites was the transverse colon, ceacumascending
colon, rectosigmoid colon and descending
colon, respectively. There was a predominance of right
colonic localization in 60% of CC and 77% of LC and left
colonic involvement in 60% of MCi cases. There were
multiple biopsy specimens in each case, and the distribution
according to all biopsy localizations was as follows; in CC:
ceacum - ascending colon (39%), transverse colon (24%),
descending colon (18%) and rectosigmoid colon (19%);
and in LC: transverse colon (44%), ceacum - ascending
colon (33%), with equal rates in the descending colon
and rectosigmoid colon (11%); and in MCi: rectosigmoid
colon (60%), descending colon (30%), transverse colon
(10%). All patients presented with chronic watery diarrhea.
Concomitant diseases were; Helicobacter pylori gastritis (n=7, 13%), Celiac disease (n=3, 6%), inflammatory bowel
disease (n=3, 6%; 2 cases were defined as ulcerative colitis),
autoimmune diseases (Hashimoto thyroiditis (n=2, 4%);
Sjogren disease (n=1, 2%); rheumatoid arthritis n=4, (8%);
Behçet disease (n=1, 2%)), coronary artery disease and
hypertension (n=12, 23%), diabetes mellitus (n=6, 11%).
Strikingly, 29% of LC cases had concomitant Celiac disease.
In terms of drug use history, PPIs (n=9, 17%) and NSAIDs
(n=8, 15%) were the most common medications. SSRI and
colchicine use was noted in one patient (2%). Notably, 8
out of 9 patients with a history of PPI use had CC (Table I).
The detailed histopathological features of MC and MCi
cases are summarized in Table II and Table III. All cases had lymphoplasmacytosis in the lamina propria which was
mild in 45.9% (17/37), 86% (6/7), 100% (9/9) of CC, LC and
MCi, respectively. Moderate/severe lymphoplasmacytosis
was present in more than half of CC (54.1%) while it
was observed in only 14% of LC and in none of the MCi.
The difference between the CC and non-CC cases was
statistically significant (p=0.002).
The majority of CC (n=36, 97.3%) and MCi (n=6,
66.7%) showed 5-20 IELs/100 enterocytes. All LC cases
showed >20 IELs/100 enterocytes (mean 33 IELs/100
enterocytes). In 97.3% of CCs, IEL was seen in the range
of 5-20/100 enterocytes and in 37.8% in the range of 10-
20/100 enterocytes. Intraepithelial lymphocyte count was
in the range of 10-19/100 enterocytes and the subepithelial collagen band was below 5 μm in one of the MCi cases in
which we described as lymphocytic type of incomplete
microscopic colitis. Intraepithelial lymphocyte count was
<10 in the other 8 cases that exhibited subepithelial collagen
band 5-10 μm in thickness and these were interpreted as
collagenous type MCi.
One of the remarkable findings was the presence of ≥20
eosinophils/1HPF in the lamina propria in 75.7% (28/37),
57.1% (4/7), 11.1% (1/9) of CC, LC, MCi, respectively and
the difference was statistically significant (p=0.008).
Sloughing of the superficial mucosa, flattening, vacuolization,
and loss of mucin in the surface epithelium were identified
in 73% (27/37), 51.4% (19/37), 65% (24/37), 62.2%
(23/39) of CC; 29% (2/7), 86% (6/7), 43% (3/7), 71% (5/7)
of LC while 33% (3/9), 11% (1/9), 22% (2/9), 33% (3/9) of
MCi, respectively. Epithelial damage with sloughing of the
superficial mucosa in CCs was significantly more frequent
than in lymphocytic and incomplete microscopic colitis
(p=0.014). Epithelial damage characterized as vacuolization
in MCi was lower than in CC and LC cases (p= 0.012).
Paneth cell metaplasia was observed in only CCs (n=6/37)
(not in LC or MCi). Crypt distortion, crypt abscess, giant
cell, granuloma, and ulceration were not identified in any
of the cases. Neutrophil leukocytes forming cryptitis were
present in only 3 of 37 (8.1%) CC cases, and in none of the
LC and MCi cases.
Entrapped erythrocytes and cells other than erythrocytes
in the subepithelial collagen band was observed in 91.9%
(34/37) and 54.1% (20/37) of CCs, respectively, but they
were significantly less common features for LC cases
(57.1% (4/7), 14.3% (1/7)) and MCi cases (55.6% (5/9), 0%
(0/9)), (p=0.006 and p=0.003), respectively.
The median collagen thickness was 25.1 μm (12.9-46.4) in
CCs, 3.91 μm (2.5-6.7) in LCs, and 8.24 μm (6.7-9.1) in MCi.
Among CC cases, when collagen thickness was classified as
<30 μm and ≥30 μm, sloughing of the superficial mucosa,
vacuolization and mucin loss were higher in patients
with a thickness ≥30 μm compared to those with collagen
thickness <30 μm (p=0.036, p=0.007, p=0.056).
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|Figure 1: Increased IEL/100 enterocytes, moderate
lymphoplasmocytosis and mild epithelial damage characterised
as mucin loss in LC case (H&E, x100).
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|Figure 3: Epithelial damage with sloughing of the superficial
mucosa and increased subepithelial collagen band thickness in
CC case (H&E, x100).
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|Figure 4: Masson Trichrome stain highlights increased
subepithelial collagen band thickness (x100).
Microscopic colitis (MC) is a chronic inflammatory bowel
disease defined by chronic watery diarrhea with normal
colonoscopy findings but with evidence of mucosal
inflammatory changes in colonic biopsies. Its incidence
is increasing and the quality of life in active MC patients
is poor but a proper treatment may help a lot of patients
to return to normal life. Biopsy findings are pivotal for the diagnosis of MC, and it is crucial for the pathologist
to be aware of MC and MCis diagnostic clues 7,11,13
This study provides detailed clinical and histopathological
findings in colonic biopsies obtained from patients
diagnosed with MC and MCi.
All patients had diarrhea at the time of MC diagnosis and
the diagnosis was based on both clinical and pathological
findings. Typically, MC is a disease of the elderly, with
an average age of approximately 65 years. However,
given that 25% of MC patients may present younger than
45 years, young patients with chronic diarrhea should
also be evaluated for the disease There is marked female
predominancy which is less notable in LC in comparison
to CC 6,8,11,16. The present study showed female
predominance in CC cases also but there was a distinct
male predominance in LC and MCi cases. The mean ages
of our CC, LC and MCi patients were 59 (22-87), 51 (27-83)
and 46 (24-72) years, respectively. The age distribution in
our series is consistent with the literature, but the mean age
at diagnosis is lower than the literature findings that report
the mean age of patients with CC and LC between 64-68
and 51-59 years, respectively 17-20. However, in another
Turkish population study, the mean age of diagnosis of LC
and CC was 45 (range: 27-68) and 60 years (range: 54-65
years) similar to our findings 21. The number of patients
with diagnosis of MC is increasing in Western, Eastern, as
well as Asian countries such as Japan and Korea. A possible
explanation for the increased frequency of MC might be the
increased use of colonoscopy during work-up investigation
of chronic diarrhea patients 22. Smoking might be the
culprit for the persistence of MC or it could amplify the risk
of developing MC at younger ages 23,24. On the other
hand, it is shown that the risk of MC might differ among
ethnic groups 22. The contrary findings in age and sex
distribution in the present study may also support ethnic
factors playing a role in the development of the disease.
The etiology of MC is unclear but is probably multifactorial
with contributing factors such as infection, smoking,
drugs, mucosal immunopathology, dysregulated collagen
metabolism (in CC), and genetics 6,7. According to the
literature, 20 to 60% of patients with lymphocytic colitis
and 17 to 40% of patients with collagenous colitis have coexistent
autoimmune diseases, such as rheumatoid arthritis,
collagen vascular diseases, or thyroid disorders, and there
is also a strong association with celiac disease 1. One of
the striking findings of our study was that 29% of LC cases
had concomitant celiac disease, and PPIs and NSAIDs
were the most commonly used drugs in terms of drug use
history. Eight out of 9 patients with a history of PPI use had CC. PPIs are shown to alter intestinal microbiota and
induce acid suppression along with increasing intercellular
permeability, which may contribute to disease given the
known tight junction dysfunction in MC 7.
Endoscopically normal colon with characteristic
histopathological findings form the diagnostic cornerstone
in MC. Histological key features are essential for the
diagnosis, for differentiating the 2 major subtypes -LC and
CC- and to avoid missing the diagnosis in MCi cases that
show only subtle changes 1,7. In MC, the morphologic
findings may be patchy and not continuous. To achieve an
accurate diagnosis, biopsies of the right and left colon are
recommended; if only the left colon is sampled, the diagnosis
of MC could be missed in up to 40% of the cases 1,7,17-19. Adequate sampling is important and may contribute
to the diagnosis of MC. In the present study, all cases had
multiple biopsies and the most distinct localization for CC
and LC was the right colon (60%, 77%), while for MCi it
was left colon (60%).
The cellularity in lamina propria is increased in both MC
and LC. We observed lymphoplasmacytosis in the lamina
propria at different levels in all CC, LC, MCi cases. The
grade of lymphoplasmacytosis was moderate/severe in 54%
of CC cases while moderate/severe density was infrequent
or absent in non-CC cases (14% of LC, 0% of MCi). The
significance of lamina propria inflammation was addressed
in a recent study in which the biopsies taken prior to an MC
diagnosis frequently showed an increased level of lymphoplasmacellular
infiltration 10. Therefore, the presence of
lymphoplasmacytosis is an important clue to search for the
other diagnostic criteria of MC and MCi while evaluating
a biopsy at low power. Cells other than lymphoplasmacytes
would be a component of lamina propria in MC cases.
One of the striking cell types is eosinophil leukocytes. It
is believed that eosinophilia may be evident in CC cases
when compared to LC 15,16. It has been reported that a
lower number of lamina propria eosinophils can be found
in LC than in CC 16. However, there are few reports on
this subject, and the increase in eosinophils in the lamina
propria is an important and unique finding of our study.
This may be explained by the increase in drug use, which
is blamed for the etiology of microscopic colitis, causing
an increase in eosinophils in the lamina propria. In the
present study, 75.7% of CCs had 20 or more eosinophil
leukocytes per high power field in the lamina propria, and
these rates were lower in LC (57.1%) and MCi (11.1%). The
acute inflammation is expected to be focal and mild, and
should not predominate within the inflammatory infiltrate,
as described earlier 1. Neutrophil leukocytes forming cryptitis were observed in the lamina propria in only 3
(8.1%) of our CC cases, and in none of the LC and MCi
The key histological feature of lymphocytic colitis is >20
IELs /100 enterocytes but an increased number of IEL is
also evident in CC but not to the same amount as LC. Most
of the time, the increase in the number of intraepithelial
lymphocytes is so obvious that there is no need for counting.
When there is doubt or the number of IELs is borderline,
manual counting should be performed and only the IELs
in the intercryptical areas should be taken into account 1.
Intraepithelial lymphocytosis (>5 IEL/100 surface epithelial
cells) was found to be present in 48% of the patients with
collagenous colitis, and a slightly thickened subepithelial
collagen band (5-10μm) accompanied 24% of the patients
with lymphocytic colitis 19. The thickness of the collagen
is not the same in different areas, and should be assessed
only in well-oriented sections. In CC, the thickness of the
collagen usually ranges from 10 to 30 μm 16. In our study,
in 97.3% of CCs, IEL was in the range of 5-20, and in 37.8%
in the range of 10-20 μm. Further subepithelial collagen
band thickness in the range of 5-10 μm in 28% of LC cases.
IEL was in the range of 10-20 in one of our MCi cases that we
commented as lymphocytic type of incomplete microscopic
colitis. A high IEL number despite under 20/100 enterocytes
may connect significant clinical and histological overlap
between lymphocytic and collagenous colitis and suggests
that these are two histological presentations of the same
disease entity 1. In our study, Masson Trichrome stain was
applied to all CC and MCi cases, and 86% (6/7) of LC cases,
while the CD3 stain was applied to 57% (4/7) of LC cases.
As per recent guidelines 1,6,10, histological diagnosis is
made on H&E sections but an immunohistochemical stain
(CD3) to demonstrate T-lymphocytes in LC and LCI and
connective tissue stain to reveal the subepithelial collagen
band in CC and CCi may be used if there is any doubt.
Damage of the surface epithelium is an important diagnostic
clue, especially in CC cases. In our study, epithelial damage
characterized by sloughing of the superficial mucosa and
vacuolization was more striking in CC cases than LC and
MCi cases, as reported in the literature. However, flattening
was observed more frequently in LC cases, which is contrary
to the literature 1. Epithelial damage with vacuolization
and mucin loss were significantly lower in MCis that show
less characteristic features than MC.
According to the literature, the degree of inflammation
does not correlate with the thickness of the collagen deposit
15. We found that epithelial damage characterized by
sloughing of the superficial mucosa, vacuolization and mucin loss were more common in patients with a thickness
≥30 μm compared to those with collagen thickness <30
μm. Entrapped erythrocytes in subepithelial collagen were
observed in 91.9% and cells other than erythrocytes were
observed in 54.1% of CC cases. This feature was not striking
in non-CC cases and could be used as a diagnostic clue in
the differential diagnosis of these entities.
Paneth cells are normally present in the right colon, and
when paneth cells are seen in the left colon and rectum
their presence indicates previous mucosal injury. Left-sided
paneth cells are frequently associated with ulcerative colitis
(UC), but they are not particularly specific. It is speculated
that paneth cell metaplasia may be a marker of CC which
is more refractory to therapy 16,20. We observed paneth
cell metaplasia in 16% of CC cases located in segments
other than the cecum/ascending colon but this feature was
not present in the LC and MCi cases.
We noticed that inflammatory bowel disease (6%) was
one of the concominant diseases in our study group. In
some small series of patients, microscopic colitis and
inflammatory bowel disease have been diagnosed at
different times which lead to the speculation that MC and
inflammatory bowel disease might be related to each other
and could represent end points of a spectrum of the same
disorder 1. In contrast to this opinion, there are studies
that claimed no obvious relation between MC and UC or
Crohns disease 9. Further studies are required to find out
if any relationship exists between these two entities.
The differential diagnosis of MC mainly includes NSAIDs
damage, acute infectious colitis, ischemic colitis, and
inflammatory bowel disease. In inflammatory bowel
disease there is a presentation of a younger patient
profile with bloody diarrhea and abnormal endoscopy.
Acute inflammation, cryptitis, crypt abscesses, marked
architectural distortion, and basal lymphoplasmacytosis
are also seen. In acute infectious colitis, there is diffuse,
marked polymorphonuclear leukocytes (PMN) and
infiltration of crypts and lamina propria, and there is no
IEL and increase in subepithelial collagen band thickness.
In NSAIDs damage ischemia-like changes, lamina propria
hyalinization, focal active colitis, focal cryptitis, and mild
increase in IELs are seen. When separating LC and CC
from each other, in lymphocyctic colitis there is greater
surface/crypt IELs than CC and there is no thickening of
subepithelial collagen 15.
In this study, clinical and diagnostic histopathologic parameters
have been analyzed for MC and MCi in detail.
The limitations of our study are the retrospective design, and the lack of regular clinical and endoscopic follow-up.
However, this is one of the largest series as an original article
reporting detailed clinical and histopathological characteristics
of MC and MCi cases in the Turkish population.
One of the striking points of our study was that 29% of LC
cases had concomitant celiac disease, and in terms of drug
use history PPI and NSAIDs were the most commonly used
drugs. The age distribution in our series is consistent with
the literature, but is lower than the general average, and
contrary to the literature a distinct male predominance in
LC and MCi cases were observed. The different findings
in age and sex in the present study may suggest the ethnic
factors role in the development of the disease. Another
important finding of our study was increased number of
eosinophils in the lamina propria, which may be explained
by the increase use of drugs. The presence of overt lymphoplasmacytosis,
increased eosinophils, and epithelial
damage should alert the pathologist for the diagnosis of
complete microscopic colitis. Collagenous colitis may also
demonstrate intraepithelial lymphocytosis although not
as much as LC. Given that microscopic colitis is a common
treatable cause of chronic diarrhoea, awareness of the
aforementioned histopathological features is utmost importance
for accurate diagnosis and also to avoid missing
hidden-incomplete cases. The constellation of clinical and
histological findings should enable the pathologist to reach
the accurate diagnosis in most cases.
Conflict of Interest
The authors declare no conflict of interest.
Concept: GT, EC, Design: GT, EC, Data collection or processing: GT,
EC, IA, Analysis or Interpretation: GT, EC, FHD, AAS, Literature
search: GT, EC, IA, FHD, Writing: GT, EC, Approval: EC, AAS.
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