Presentation about Inflammatory Bowel Disease (IBD), focused on pathologic diagnosis with a short introduction containing incidence, etiology and pathogenesis.

1. Inflammatory Bowel Disease (IBD)
Histopathology
Ferenc Pinter MD, PharmD, PhD
Surgical and Pathological Department
National Cancer Institute
Budapest, Hungary

3. Incidence
ECCO-EpiCom
2010 & 2011:
Crohns: 37%
UC: 53%
IBD unclassified: 10%
Eastern Europe:
11,3 / 100 000

4. Ulcerative Colitis Crohn’s Disease
Age-Specific Incidence of IBD *
Incidence in both CD and UC have 2 peaks
( in 3 rd and 6 th decades ).
10
0
2
4
6
8
0 20 40 60 80
10
0
2
4
6
8
0 20 40 60 80
Age (yrs) Age (yrs)

5. Etiology + Pathogenesis

6. Etiology: Smoking

7. Surgical therapy: UC vs. CD

8. Requirements for Dx
 ≥5 sites x ≥2 biopsies
• rectum  terminal ileum
• colonoscopy + ileoscopy
 2-3 tissue levels (step sections) x ≥5 serial sections
 Clinical information
• endoscopic findings
• age
• duration
• treatment
• comorbidities
• travel history

9. Macroscopy - Localisation
CDUC
Whole GI tractEspecially colonLocation
Skip lesionsDiffuseDistribution
Often involvedNo (except backwash ileitis)Ileum
RightLeftLeftRightColon
Typically sparedInvolved in >90%Rectum

10. Macroscopy – Mucosa & wall demage
CDUC
Aphtous,
confluent deep
SuperficialUlcers
+Mucosal atrophy
+Inflammatory polyps
+Cobblestone pattern
+ (except fulmimant colitis)Deep fissures
+ (except fulmimant colitis)Fistulae
NormalWall thickness
+Fat wrapping
+Strictures

11. Microscopy - Inflammation
CDUC
FocalDiffuse (proximally )
Acute/chronic
inflammation
Transmural
Transmucosal
(sometimes in submucosa)
Localisation
Transmural
Frequent in mucosa,
submucosa
Lymphoid aggregates
+ (except ruptured crypts)Granulomas
+ (except fulmimant colitis)Serositis
+Crypt abcesses

12. Microscopy – Mucosal architecture/epithelial abnormality
CDUC
FocalDiffuseCrypt architectural irregularity
FocalDiffuseCrypt epithelial polymorphs
+Mucin depletion
+Paneth cell metaplasia
+Neuronal hyperplasia
+Muscular hypertrophy
+Pyloric gland metaplasia

13. Microscopy – UC stages
 Early stage disease:
• focal/diffuse basal plasmacytosis
 Longstanding disease:
• crypt architectural irregularity
• lamina propria cellularity 
• continous  discontinous !!!
 Quiescent disease:
• crypt architectural irregularity
• crypt density 
• neutrophils 
• basal plasmacytosis 
Relapse

14. CD diagnosis
 Granulomas (not related to crypt injury)
 Focal chronic inflammation
 Focal crypt irregularity

15. CMV reactivation – Predictive value
Immunsupressive
therapy
CMV reactivation
UC: 10-57% CD: 0-30%Steroid-refr > steroid-resp
25-30% 0-10%
HE – sensitivity: 10-87% IHC – sensitivity: 93%

16. CRC
Risk factors:
IBD  Risk of
malignancy
• Young age
• Long disease duration
• Extensive large bowel involvement
• Primary sclerosing cholangitis
• Polypoid mucosal lesions
• Family history of CRC
p53 IHC+:
Dysplasia: 33-67%
CRC: 83-95%
Regenerating epithel:
occasional

17. Summary
 UC/CD  different therapy  differentiation is important
 Differentiation: - granuloma formation: +/-
- inflammation: focal/diffuse
- wall structure change: focal/diffuse
 Diagnostics is impacted by IBD stage (early/chronic/quiscent)
 Dysplasia is the most reliable marker of CRC risk.
This should be evaluated in areas with chronic inflammation and
confirmation by an independent expert GI pathologist is
recommended.