Digestive and Liver Disease 43S (2011) S293–S303

Chronic idiopathic inflammatory bowel diseases: The histology report

Matteo Cornaggia a,*, Monica Leutner b, Claudia Mescoli c, Giacomo Carlo Sturniolod,Renzo Gullotta e

On behalf of the “Gruppo Italiano Patologi Apparato Digerente (GIPAD)” and of the “Società Italianadi Anatomia Patologica e Citopatologia Diagnostica”/International Academy of Pathology,

Italian division (SIAPEC/IAP)aDepartment of Laboratory Medicine, Pathology Unit, Clinica S. Carlo, Paderno Dugnano, Italy

bS.C. Pathology Unit, University Hospital “Ospedale Maggiore della Carità”, Novara, ItalycDepartment of Diagnostic Medical Sciences & Special Therapies, Pathology Unit, University of Padova, Padova, Italy

dDepartment of Gastroenterology & Surgical Sciences, Gastroenterology Unit “R Farini”, University of Padova, Padova, ItalyeGastroenterology Unit, Clinica S. Carlo, Paderno Dugnano, Italy

Abstract

The incidence of chronic idiopathic inflammatory bowel diseases (IBD) is growing in western countries, making their histological diagnosisan everyday task for all pathologists.

Reviews from the literature strongly suggest that such diagnosis cannot be performed on the histological ground alone but requires aclinical-pathological approach.

Moreover, bewildering variations can be observed in the terminology employed to report either individual lesions or diagnostic categories.The aim of the present paper is to suggest a practical diagnostic algorithm summarizing the main data from the literature.Particular emphasis has been placed on minimum clinical information required and the accurate definition of individual lesions. Diagnostic

categories to employ and to avoid in daily practice have furthermore been stressed.© 2011 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

Keywords: Crohn’s disease; GIPAD report; Ulcerative colitis

1. Introduction

The diagnosis of chronic idiopathic inflammatory boweldiseases (IBD) requires a close correlation between morphol-

List of abbreviations: ALM, Adenoma-Like Mass; CD, Crohn’s disease;DALM, Dysplasia-Associated Lesion or Mass; IBD, chronic idiopathic in-flammatory bowel diseases; NOS, not otherwise specified; UC, ulcerativecolitis.* Correspondence to: Matteo Cornaggia, Department of LaboratoryMedicine, Pathology Unit, Clinica S. Carlo, Paderno Dugnano, Via Os-pedale 21, Paderno Dugnano, Milano, Italy. Tel: +39 02 99038283; fax: +3902 99030260.

E-mail address: cornaggia@clinicasancarlo.it (M. Cornaggia).

1590-8658/$ – see front matter © 2011 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

ogy, clinical features, endoscopic appearance, imaging andlaboratory data.

The microscopic picture, in fact, is often composed ofbasic lesions that can also be observed in other diseases andonly rarely appears to be pathognomonic.

The histopathological diagnosis is of paramount impor-tance in determining the choice of treatment, the prognosisand the follow-up.

The aim of the diagnosis is to:1. Differentiate IBD from other colitis.2. Differentiate ulcerative colitis (UC) from Crohn’s disease

(CD).3. Identify dysplastic lesions.

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2. Clinical indication for biopsy

A “gold standard” for IBD diagnosis has not yet beenestablished. In fact it is based on a combination of anamnesticdata, clinical evaluation, imaging and typical endoscopic andhistopathologic features.

Main indications leading to endoscopic investigation aresymptoms like chronic diarrhoea (loose stools lasting for6 weeks), hematochezia, abdominal pain, mucus discharge,unexplained systemic symptoms like fever and weight loss orvarious clinical signs like fistulae or extra-intestinal diseases(articular, cutaneous, ocular etc.) possibly associated withasymptomatic or attenuated IBD.

During colonoscopy it is always important to visualize theterminal ileum and to perform a complete biopsy sampling(see later paragraph) either in normal or in pathological areas.Histological examination is in fact mandatory to perform aconclusive IBD diagnosis.

In case of chronic diarrhoea with normal endoscopicappearance it is recommended that biopsies for microscopiccolitis identification (lymphocytic, collagenous) be performed:two in the ascending colon and two in the sigmoid colon.

3. Clinical data

As mentioned earlier, the clinical data are crucial forproper interpretation of the histopathological features [1–3].

The data should always be reported in the pathologyexamination request or submitted in separate form (Table 1).Sending a copy of the endoscopy report may be helpful,although in no way does it substitute correct and completecompilation of the pathology examination request, whichmust always include the precise case-specific opinion of thegastroenterologist.

It is mandatory for the pathologist, especially in newlydiagnosed cases, to obtain the main clinical data in order tovalidate the microscopic picture and to make a true clinico-pathological diagnosis. If sufficient clinical information is notavailable the diagnosis should only be descriptive.

Such information can be divided into the following cate-gories [3,4]:1. Clinical history.

Symptoms (features and duration): diarrhoea, hema-tochezia and fever.Presence of major extra-intestinal diseases.Current or previous therapy, with particular emphasis ontopic bowel therapies.

2. Laboratory data.Results of ongoing stool culture and faeces parasiteinvestigations, unspecific inflammatory serological markers(erythrocyte sedimentation test and C-reactive protein),anti-neutrophil cytoplasmic antibodies (ANCAs) and anti-saccharomyces cerevisiae antibodies (ASCAs).

3. Endoscopic appearance.Bowel tract examined (partial or total colonoscopy with orwithout terminal ileum visualization).

Table 1Clinical data form to be attached to the pathology examination request incases of suspected IBD

Description of the main lesions observed, with particularemphasis on continuous or segmental disease and thepresence of diverticula.

4. Imaging.Presence and morphology of lesions in tracts not exploredby endoscopy (jejunum, terminal ileum, bowel tract beyondstenotic portions).

4. Endoscopic sampling [4–7]

The diagnostic accuracy has been demonstrated to increasewith the number of biopsies performed and with the numberof bowel tracts sampled [3,5]. Therefore, it is mandatory toperform an extensive bioptic sampling, especially in the caseof newly diagnosed IBD, whereas sampling could be reducedin the follow-up examinations. It should also be noted thatCD is a trans-mural disease and that therefore the diagnosison endoscopic biopsies suffers from limitations and appearsmore difficult.

4.1. Optimal sampling for newly diagnosed IBD

Two biopsies should be performed in the terminal ileumand in each portion of the large bowel examined (caecum,

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ascending, transverse, descending, sigmoid colon and rectum)even if the mucosa appears endoscopically normal [3,8].

4.2. Minimum sampling during the follow-up

Two biopsies should be performed in all large bowel tractsshowing significant lesions and two biopsies in the rectum.

In case of discordance between the initial histologicaldiagnosis and the clinical course during the follow-up, itis mandatory to repeat a complete sampling (see previousparagraph) to settle the question.

It is also strongly recommended that a critical re-examination of previous biopsies is performed and writtenindications of this review provided in the final report.

4.3. Sampling for the detection of dysplasia in longstandingdisease (8–10 years duration) [9,10]

This is a highly controversial issue since indications in theliterature are very exacting and are often ignored in routinepractice. The protocol, in fact, recommends that two biopsiesbe performed every 10 cm of large bowel examined and anysuspicious lesion sampled.

5. Biopsy handling

The use of cellulose acetate films is highly recommendedbecause it allows proper mucosal sample orientation, whereasthe use of blotting paper should be discouraged owing tosample handling and possible artefacts.

Samples from each anatomical site should be adequate insize (presence of muscularis mucosae), carefully handled inorder to avoid crushing artefacts, immediately fixed in neutralbuffered formalin and unequivocally identified [6,7].

The diagnosis of IBD can be performed, in most cases,using sections stained with haematoxylin and eosin.

There is no gold standard rule concerning the number ofhistological sections to be examined although the diagnos-tic accuracy has been demonstrated to increase with serialsectioning, with particular reference to granuloma identifica-tion in CD [7]. Special staining techniques may help in thedifferential diagnosis (Table 2).

Table 2Special techniques for the differential diagnosis of IBD

• PAS for fungi identification.• Giemsa and Warthin-Starry for bacteria identification.• Masson Trichrome for basement membrane evaluation.• Ziehl Nielsen for mycobacteria identification.• Immunohistochemical reactions for T lymphocytes (CD3) and viral

antigen detection (cytomegalovirus and herpes virus).• PCR for mycobacteria identification and typifying.

6. Histologic individual lesions [1–3,11]

The diagnosis of IBD relies on the identification ofvariously intermingled individual histologic lesions (Table 3).These have been described since the first published papers,however their sensitivity and specificity have not yet beenestablished.

Particular emphasis should be placed on distinguishing“true lesions” from alterations caused by bowel prepara-tion and/or endoscopic trauma (Table 4) and from “minimalchanges” that fall within the normal colonic mucosa variabil-ity range.

Their precise and unequivocal identification is essential toavoid diagnostic mistakes. The diagnostic reproducibility ofbasic lesions, in fact, has been demonstrated to significantlyimprove using shared diagnostic criteria [5].

7. Normal colonic mucosa [1–3,11,12]

Normal colonic mucosa is characterized by a flat sur-face, parallel straight crypts homogeneously sized, regularlyaligned and spaced, less than 10% of which are branching(Figs. 1 and 2), and whose bottom reaches the muscularismucosae.

Table 3Individual histologic lesions in IBD

1. Mucosal architecture alterations1.1. Mucosal surface alterations1.2. Crypt distortion1.3. Atrophy

2. Epithelium breakings2.1. Erosions2.2. Ulcers2.3. Aphthous ulcers2.4. Pseudomembranes

3. Epithelium alterations3.1. Mucin depletion3.2. Paneth cell metaplasia3.3. Pseudopyloric metaplasia3.4. Dysplasia/Intraepithelial neoplasia

4. Inflammatory infiltration4.1. Neutrophil polymorphs4.2. Lymphoplasmacytic4.3. Basal plasma cell infiltration4.4. Granulation tissue-like inflammation4.5. Epithelioid granulomas4.6. Increase in lymphoid follicles

Table 4Alterations caused by bowel preparation and/or endoscopic trauma

• Epithelial sloughing• Acute haemorrhagic foci• Edema• Pseudolipomatosis• Decrease in intracellular mucus• Mitosis increase• Presence of occasional neutrophils in the surface epithelium, especially

above lymphoid follicles, and in the crypts (<1–2 neutrophils/crypt)

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Fig. 1. Normal colonic mucosa with parallel straight crypts.

Fig. 2. Normal colonic mucosa: mild irregularity could be due to imperfectbiopsy orientation.

The average normal crypt number is 7–8 per millimeter ofmucosal length although this value may decrease in the cecumand distal rectum.

Irregular architecture can be observed in correspondenceof lymphoid follicles, at the ileocecal valve and near to theappendiceal orifice.

The epithelium is composed of absorptive and goblet cellsin the upper-middle third, where occasional apoptosis can beseen, and of immature cells in the lower third, where mitosiscan be recognized.

Paneth cells can be observed throughout the right colon(up to splenic flexure). Lymphocytes and plasma cells arenormally present in the lamina propria. These are moreabundant in the cecum and show decreasing density from thesurface to the bottom of the crypts.

Throughout the right colon eosinophilic granulocytes arenormally present. Intraepithelial T lymphocytes can be ob-served and are considered normal up to a number of 20lymphocytes/100 enterocytes.

Lymphoid follicles also showing germinal centers andsometimes extending to the submucosa can be observed.

1. Mucosal architecture alterations [1,3,11]1.1. Mucosal surface alterations

Loss of the typical flat profile, showing fine irregu-larity or even a pseudovillous change (Fig. 3). Thesurface epithelium between crypts is composed ofenterocytes of different heights and arranged in smallgroups with a "lace-like" pattern (Fig. 4).

1.2. Crypt distortionLoss of parallelism of the crypts which show variablediameter and shape and irregular branching withdilatation up to cystic pattern (Fig. 5).

1.3. AtrophyReduction in the number of crypts (distance be-tween crypts greater than the diameter of one crypt)and/or shortening with increasing distance betweenthe bottom of the crypts and the muscularis mucosae(Fig. 6). This finding should be assessed in the ab-sence of moderate/severe inflammation in the laminapropria in order to avoid overestimation.

2. Epithelium breakings [1,3,11]2.1. Erosions

Small loss of surface epithelium with mild inflam-mation in the absence of underlying recognizable

Fig. 3. Mucosal surface alterations: pseudo-villous change.

Fig. 4. Mucosal surface alterations: “lace-like” pattern.

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Fig. 5. Mucosal architecture alterations: crypt distortion.

Fig. 6. Mucosal architecture alterations: atrophy.

granulation tissue. They can be coated with a mixtureof polymorphs, fibrin and necrotic cells (pseudomem-branes).

2.2. UlcersFull mucosal thickness breaks with recognizable un-derlying granulation tissue.

2.3. Aphthous ulcersLoss of surface epithelium with recognizable underly-ing lymphoid follicle (Fig. 7).

2.4. PseudomembranesVariable size accumulations of fibrin, mucus, poly-morphs and necrotic cells covering the surface epithe-lium. In severe cases it overlays one or more necroticcrypts and displays a typical "volcano-like" shape.

3. Epithelium alterations [1,3,11]3.1. Mucin depletion

Reduction in the number of goblet cells and/or in theirmucus content either in the crypts or in the surfaceepithelium.

3.2. Paneth cell metaplasiaThis consists of easily recognizable mature Panethcells (Fig. 8) and/or immature enterocytes, containingtypical supranuclear eosinophilic granules.

3.3. Pseudopyloric metaplasiaSubstitution of the crypt epithelium by a glandularepithelium resembling antral gastric glands.

Fig. 7. Epithelium breakings: aphthous ulcer.

Fig. 8. Epithelium alterations: Paneth cell metaplasia.

3.4. Dysplasia/intraepithelial neoplasia [13–15]The term dysplasia is synonymous with intraepithelialneoplasia, in accordance with World Health Orga-nization recommendations. The term should not beused in case of reparative and/or reactive alterations.Dysplasia is classified into low and high grade, as inother gastrointestinal tracts, according to:– architectural alterations such as gland fusion with

cribriform appearance or villous structure forma-tion

– cytological abnormalities such as nuclear stratifica-tion, loss of cell polarity, pleomorphism, abnormalnuclear/cytoplasmic ratio, nuclear hyperchroma-

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Fig. 9. Inflammatory infiltration: cryptitis.

Fig. 10. Inflammatory infiltration: cryptic abscess.

tism, increasing number and abnormal distributionof mitosis (upper third of the crypts) and presenceof atypical mitosis.

Dysplasia may arise in flat mucosa or in polypoidlesions. Polypoid lesions in IBD, unlike in a normalcolon, have been demonstrated to be associated withdifferent clinical risk according to their microscopiccharacteristics and should be distinguished into:– Dysplasia-Associated Lesion or Mass (DALM):

dysplastic lesions surrounded by flat mucosa wheredysplastic foci can be recognized. These lesionsare associated with an increased risk of developingor coexisting cancer.

– Adenoma-Like Mass (ALM): dysplastic lesionssurrounded by non dysplastic mucosa, which areassociated with a cancer risk similar to that ofsporadic adenomas.

4. Inflammatory infiltrations [1,3,11]4.1. Neutrophil polymorphs

The presence of neutrophilic polymorphs in thelamina propria, surface epithelium, crypt epithelium(cryptitis) and crypt lumina (cryptic abscess) definesdisease activity (Figs. 9 and 10).

Fig. 11. Inflammatory infiltration: basal plasma cell infiltration.

4.2. Lymphoplasmacytic cellsIncreasing number of plasma cells and lymphocytesin the lamina propria, which may be focal or diffuse.This is a critical parameter since the numerical rangeof lymphoid cells in normal mucosa has not yet beenclearly established in the literature. Its identification,therefore, appears certain only when dealing with amarked increase.

4.3. Basal plasma cell infiltrationPresence of a large number of plasma cells betweenthe bottom of the crypts and the muscularis mucosae(Fig. 11).

4.4. Granulation tissue-like inflammationArea of lymphoplasmacytic inflammation with abun-dant macrophages and displaying polymorph infiltra-tion and angiogenesis, similar to granulation tissuebut in areas without epithelium breakings.

4.5. Epithelioid granulomasVariable size collections of epithelioid cells (activatedhistiocytes with eosinophilic cytoplasm) sometimesassociated with multinucleated giant cells, localized inthe lamina propria and/or in the submucosa (Fig. 12).These should not be confused with "isolated giantcells" arranged around disrupted crypts.

4.6. Increase in lymphoid folliclesThe number of lymphoid follicles is considered ab-normal when higher than two follicles per millimetreof mucosa [1].

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Fig. 12. Inflammatory infiltration: multinucleated giant cells granuloma.

8. Diagnosis

The diagnosis of IBD is a complex procedure [3]. Often itcannot be performed easily and quickly but, on the contrary,requires patience, time and skill to recognize mistakes.

The diagnostic process can be summarized as follows:• Identification of bowel tracts with normal mucosa.• Identification of different individual lesions in each bowel

tract affected by disease.• Definition of disease as focal or diffuse (in biopsy speci-

mens of the same anatomical site).• Definition of disease as continuous or segmental (presence

of spared tracts).• Definition of disease as left or right colon predominant.• Evaluation of the terminal ileum.• Formulation of a diagnostic hypothesis.• Evaluation of the congruence between this hypothesis and

the clinical data.• Possible acquisition of additional clinical data.• Possible re-evaluation of previous biopsies.• Conclusive diagnostic statement.

Even if the microscopic features observed are rarelypathognomonic, nevertheless characteristic "pattern" for eachentity has been identified in the literature: the main differentialdiagnoses are summarized in Table 5.

9. Diagnostic categories [4]

9.1. Diagnostic

The term should only be used when dealing with adequatebiopsy sampling, complete clinical data, typical histologicalprofile and its congruence with clinical data.

It is in fact important to emphasize that erroneous positivediagnosis can produce long term medication and recruitmentof the patients in exacting follow-up protocols with highsocial costs.

Conversely, erroneous negative diagnosis causes the per-sistence of symptoms, or their quick reappearance, leading to

patient re-evaluation. A delayed correct diagnosis is normallyreached, though the patient will be exposed to a higher risk ofcomplications.

9.2. Highly suggestive

This category should be used when typical histologicalfeatures combine with incorrect and/or incomplete biopsysampling and/or insufficient clinical data and/or clinico-pathological discordance.

The caution described in the preceding paragraph shouldalso be applied in this diagnosis.

9.3. IBD NOS

The term should only be used when dealing with incom-plete biopsy sampling and little or no clinical data. Thisdiagnosis is based on a histopathological picture that does noteven allow a distinction to be made between UC and CD.

It should be used in a limited number of cases. In most ofthem it should be a temporary diagnosis, to be further workedup through subsequent histological examinations with correctand complete sampling and with full supportive clinicalinformation.

9.4. Healed disease

The term should never be used as diagnostic and mustalways be accompanied by the statement “highly suggestive”.The histological picture, in fact, is not specific and can alsobe observed in other diseases: therefore this diagnosis shouldonly be made if previous histological biopsies with activedisease are available.

The term identifies cases showing no significant increasein the number of lymphocytes and plasma cells in the laminapropria.

9.5. Disease activity

In daily practice it is appropriate to distinguish betweenquiescent and active disease. This distinction is based onthe identification of polymorphs between surface and/or cryptepithelial cells with variable epithelial damage [7].

Different methods to scale such parameter have beenproposed, however their poor reproducibility restricts theirapplication to clinical research.

9.6. Dysplasia/intraepithelial neoplasia

Must be divided into two grades: low and high.If the histological abnormalities observed appear insuffi-

cient to reach a definitive diagnosis, it is recommended thatthe term "indefinite for dysplasia" be used [13].

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Table 5Main clinical, gross and histological features in different type of colitis

Disease Clinical information Individual histologic lesions Gross lesion distribution Histological techniques

UC Diarrhoea.Rectal bleeding.

Mucosal surface alteration.Crypt distortion.Atrophy.Mucin depletion.Cryptitis and/or crypt abscesses.Diffuse lymphoplasmacellular infiltration in

the lamina propria.Basal plasma cell infiltration.

Ileal sparing.Diffuse lesions.Left colon involvement.

Haematoxylin and eosin.

CD Chronic diarrhoea.Abdominal pain.Fever.

Focal crypt distortion.Ulcers and/or aphtoid ulcers.Mucin depletion absent or weak.Pseudopyloric metaplasia.Focal cryptitis.Focal lymphoplasmacellular infiltration in

the lamina propria.Granulation tissue-like inflammation.Epithelioid granulomas.

Ileal involvement.Segmental lesions.Right colon involvement.Possible rectal sparing.

Haematoxylin and eosin.

Self limiting colitis/acute infectiouscolitis [12]

Acute diarrhoea.Rectal bleeding.Positive stool culture.

Normal architecture.Mucin depletion.Neutrophil polymorphs in the lamina

propria and intraepithelial (cryptitisand/or crypt abscesses).

Weak lymphoplasmacellular infiltrationdecreasing towards the crypt bottom.

Diffuse lesions. Haematoxylin and eosin.

Pseudomembranouscolitis [11]

Use of antibiotics. Pseudomembranous erosions with typical“volcano like” shape.

Diffuse lesions. Haematoxylin and eosin

Ischemic colitis [12] Rectal bleeding.Abdominal pain.

Variable according to the disease phase.Absence of chronic inflammation.Erosions.Pseudomembranes.Mucin depletion.Atrophy.Small crypts.Fibrinous microthrombi.

Focal lesions. Haematoxylin and eosin.

Mucosal prolapsesyndrome [12]

Constipation.Mucus discharge.Anorectal pain.

Crypt elongation with mucin depletion.Erosions.Pseudomembranes.Chronic ischemia-like lesions.Muscularis mucosae hyperplasia and

hypertrophy with smooth muscle locatedbetween crypts.

Rectal involvement Haematoxylin and eosin.

Radiation colitis[11,12]

Diarrhoea.Rectal bleeding.Previous radiotherapy.

Chronic ischemia-like lesions.Dilated mucosal vessels.Hyalinized arterioles.Mucosal oedema.Atypical “radiation fibroblasts”.

Focal lesions(corresponding to thebowel tract receivingradiation).

Haematoxylin and eosin.

Lymphocytic colitis[12,16]

Chronic diarrhoea lastingseveral months.

Drug assumption.Normal colonoscopy.

Increased intra-epithelial T lymphocytes(>15/100 enterocytes).

Diffuse lymphoplasmacellular infiltration.

Focal or diffuse lesions.Possible rectal sparing.

Haematoxylin and eosin.CD3 antibodies.

Collagenous colitis[12,16]

Chronic diarrhoea lastingseveral months.

Normal colonoscopy.Use of drugs.

Thick continuous sub-epithelial collagenousband (>10 μm).

Superficial epithelium damage.Lymphocytes and neutrophil polymorphs

granulocytes infiltrating superficialepithelium.

Focal or diffuse lesions.Possible recto-sigmoidsparing.

Haematoxylin and eosin.Masson’s trichrome.

Drug-induced colitis[17]

Use of nonsteroid anti-inflammatory drugs,chemotherapeuticagents and vasoactivedrugs.

Ischemic-like lesions.Microscopic colitis.IBD-like colitis.Graft versus host-like lesions.Cathartic colon lesions.

Focal or diffuse lesions Haematoxylin and eosin.

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Table 5 (continued)

Disease Clinical information Individual histologic lesions Gross lesion distribution Histological techniques

Diversion colitis[11,12]

Previous surgery creatinga blind intestinal loop.

Cryptitis and/or crypt abscesses.Diffuse lymphoplasmacellular infiltration.Lymphoid follicles hyperplasia.

Blind intestinal loop. Haematoxylin and eosin.

Diverticular disease-associated colitis[11,12]

Protean symptoms. Mild/severe lymphoplasmacellularinfiltration.

Cryptitis and/or crypt abscesses.Crypt distortion.Mucin depletion.

Bowel tracts affected bydiverticula.

Haematoxylin and eosin.

Eosinophilic colitis[12]

Diarrhoea.Rectal bleeding.Abdominal distension.Anorexia.Vomiting.

Rich eosinophilic granulocyte infiltrationin the absence of other lesions(>10 eosinophils/HPF).

Focal lesions.Prevailing left colon

involvement.

Haematoxylin and eosin.

Behçet syndrome[11]

Uveitis.Arthritis.Cutaneous lesions

(erythema nodosumand/or others).

Apthous stomatitis.Genital ulcers.

Deeply penetrating aphtoid ulcers.Submucosal small vessels vasculitis.

Ileo-cecal regioninvolvement.

Haematoxylin and eosin.

9.7. Diagnostic categories to be avoided [18]

9.7.1. Indeterminate colitisThe term was originally proposed for surgical cases

showing a histological picture typical of either UC or CDand it was later used in the same sense for biopsies. In suchcases it appears, on the contrary, more correct to use the term’chronic idiopathic inflammatory bowel disease NOS’.

9.7.2. Chronic colitisThis term has no scientific basis in that it does not identify

any clinical-pathological entity and is therefore wholly devoidof any clinical value. Its use must be absolutely banned.

10. Writing a report

According to the level of diagnostic certainty achieved,three different types of diagnosis can be written up.1. Unequivocal diagnosis (Table 6)

– Histopathological description (optional)1.– Type of observed disease: ulcerative colitis, Crohn’s

disease or chronic idiopathic inflammatory bowel NOS.– Assessment of disease activity.– Assessment of dysplasia.

2. Highly suggestive diagnosis (Table 6)– Histopathological description1.– Statement assessing the subjective grade of probability

supporting the diagnosis of the disease: ulcerative coli-

1Although the histopathological description may seem superfluous, it can beuseful in subsequent examinations to assess the "level of certainty," even ifthe slides are not available. It is therefore strongly recommended in cases ofhighly suggestive diagnosis.

Table 6Examples of histopathological report

Unequivocal diagnosis Highly suggestive diagnosis

• Histopathological description• Histopathological features

diagnostic for ulcerative colitis• Active disease• Dysplasia absent

• Histopathological description• Histopathological features highly

suggestive of Crohn’s disease• Active disease• Dysplasia absentNote: a complete sampling of theileo-colic mucosa should beperformed to validate the diagnosis.

tis, Crohn’s disease or chronic idiopathic inflammatorybowel NOS.

– Assessment of disease activity.– Assessment of dysplasia.– Explanatory note clarifying the causes preventing at-

tainment of a definitive diagnosis (incomplete samplingand/or insufficient clinical data).

3. Descriptive diagnosisThe mere description of histological findings should onlybe reserved to cases showing definitive abnormal micro-scopic features that, however, do not fit into any specificdisease entity.Its use should be restricted to cases where the pathologistwants to pass on the presence of abnormal findings thatneed further investigation.

11. Clinical impact of the histopathological diagnosis

Histological diagnosis, as previously stated, appears ofparamount importance in the diagnostic algorithm for patientswith clinical aspects highly suggestive for IBD.

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Table 7Histopathological diagnosis of IBD: its application in the clinico-therapeuticalgorithm

• Endoscopic typical lesions andunequivocal histopathologic diagnosis.

• Endoscopic typical lesions and highlysuggestive histopathologic diagnosis.

Specific therapy for IBD.

• Endoscopic typical lesions andnegative histopathologic diagnosis.

• Endoscopic typical lesions absent andunequivocal or highly suggestivehistopathologic diagnosis.

Clinico-endoscopic andhistopathologic follow-upwithout specific therapy forIBD.

• Endoscopic typical lesions absent andnegative histopathologic diagnosis.

Diagnosis of IBD unlikely:investigate different causes ofpatient symptoms.

However, it should be critically evaluated according tothe endoscopic appearance in order to establish a therapeuticstrategy.

Table 7 summarizes the main possible clinical implications.Two items of the histopathological report appear to be

particularly significant:• Disease activity: some data in the literature seem to

indicate that a higher relapse frequency is associatedwith cases exhibiting clinical-endoscopic remission stillshowing microscopic activity [19].

• Presence of dysplasia leading to relevant clinical treatmentsas summarized in Fig. 13 [20].

Acknowledgements

The authors wish to thank Mr. Alan Povall for revising themanuscript.

Fig. 13. Recommended algorithm for dysplasia treatment (modified from Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 8th ed. [20].)

Conflict of interest

The authors have no conflicts of interest to disclose.

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