1,,,Axial CTE image showing severe inflammatory changes in the terminal ileum: marked mucosal enhancement (solid arrow), wall thickening (arrow head), engorgement of vasa recta or comb sign (broken arrows). Luminal stenosis is also seen. This lesion was scored as CTE inflammation (3), fibrostenosis (1).Surgical specimen from the patient in Figure 1 showing severe inflammation with mild fibrosis (a stiletto is inserted into a fistula tract)…Microscopic view of a section of the specimen in Figure 2 showing severe mucosal and submucosal acute and chronic inflammation with architectural distortion on the left and ulcer on the right.Coronal CTE image of severe fibrostenoticileal disease with mild inflammation. Mild mucosal enhancement, no significant mural stratification, and severe luminal stenosis (solid arrow) are associated with marked prestenotic dilation (broken arrow) and absent comb sign. This lesion was classified as CTE inflammation (1), fibrostenosis (2).Microscopic view of a section of the specimen showed in Figure 4 showing chronic inflammatory infiltrates in the mucosa and submucosa with marked thickening of the bowel wall by fibrous tissue.
Inflammatory Bowel Disease(IBD) is
currently presumed to result from the
aggregate effect of inherited variants of
genes conferring risk of disease and
environmental factors affecting the
immune system, which combined lead to
an aberrant inflammatory response.
THE INFLAMMATORY CASCADE IN IBD
Inflammatory response is perpetuated by T-cell activation
Inflammatory cytokines, such as L-1, IL-6, and TNF, have diverse
effects on tissues.
They promote fibrogenesis, collagen production, activation of
tissue metalloproteinases, and the production of other
inflammatory mediators; they also activate the coagulation
cascade in local blood vessels.
REPLICATED GENETIC LOCI IN IBD
IBD Locus a
Chromosome Gene b
Defective immune regulation in IBD
It is associated with HLA,DR1/DQw5 and NOD2 genes Associate with HLA-DR2 polymorphism
and an abnormal T-cell response particularly,CD4+T
in IL-10 gene and an abnormal T-cell
cell (TH1 cells).
response particularly of CD4+ T cells
It is chronic granulomatous disease which can be
affect any part of the gut
DIFFERENT CLINICAL, ENDOSCOPIC, AND
Gross blood in stool
Significant perineal disease
Response to antibiotics
Recurrence after surgery
Small bowel significantly
Abnormal terminal ileum
Granuloma on biopsy
Colonoscopy is the procedure of choice
Sigmoidoscopy examines the colon up to the splenic flexure
and is currently used to exclude distal colonic inflammation or
obstruction in young patients not at significant risk for colon
cancer. For elusive capsule endoscopy, or the novel technique
of double-balloon enteroscopy.
• The earliest lesion in crohn’s is the
aphthous ulcer. Many such ulcers may
fuse together to form serpentine ulcer
• Grossly, involved bowel segment
typically has a rigid, strictured or
thickened wall with creeping fat.
• Full thickness of the intestine is
affected in the disease i.e there is
transmural inflammation. This causes
weakness in the wall there by leading
to fissure and fistula formation in
Crohn’s disease. Fibrosis is also
commoner in this type IBD. Perianal
fistula is the most common fistula
The disease involves the entire colon
(pancolitis )starting from the rectum
(retrograde involvement). There is
presence of regenrating mucosa which
projects in the lumen and is called
In extreme cases, there is involvement
of the nerve plexus in the muscularis
layer resulting in decrese in the motility
of the colon and increase in its size over
a period of time giving rise to “toxic
The characteristic feature of the disease
is mucosal damage continuously from
the rectum and extended proximally.
This may also lead to “backwash ileitis”.
This type of IBD is more commonly
associated with progression of the
development of cancer.
• There is patchy involvement of the
intestine which is known as presence
of “skip lesion”. The intervening area
between two affected portions is
absolutely normal. So, the mucosa
appears to be irregular which is
unknown as “cobblestone mucosa.”
• There is a presence of non-caseating
• Clinical features are intermittent
attacks of abdominal pain, blood in
stools, fever steatorrhoea and
megaloblastic anemia (the last two
features result because there is
impairment in the absorption of bile
acids and vitamin B12 respectively
from the ileum).
Screeing test is presence of ASCA . AB
formation is common against cell wall
of yeast , sacchromyces cerevisae in
patients with crohn’s disease.
• There is absence of granulomas.
Clinical features are : intermittent
attacks of abdominal pain, bloody
mucoid stools and fever.
There is presence of p-ANCA.