Introduction
Crohn disease is one of the inflammatory bowel disorders (IBD), the other being Ulcerative colitis.

IBD is a chronic disease characterized by alteration in mucosal immune response as a result of complex interactions between host immune system and intestinal flora. It is seen in genetically predisposed individuals.

IBD commonly presents in the second to third decades of life. However they can present at any age.
It is more common in the western world. The incidence in Asian population is now on the rise.

Pathogenesis
The pathogenesis of IBD is complex and involves interactions between the host immune system, gut microbiome and genetic factors.
There are many genetic polymorphisms associated with IBD, one of the most important being NOD2 polymorphism.
“Hygiene hypothesis” is also put forth which is related to the alteration in the gut flora.

Morphology Gross pathology
Crohn disease can involve any part of the gastrointestinal tract.
Site : Distal ileum, ileo-caecal valve and caecum are the common sites involved.
Skip lesions: The lesions tend to be multiple and sharply demarcated from the uninvolved mucosa. As a result there is normal appearing uninvolved mucosa in-between lesional, involved mucosa. This is referred to as “skip” lesions and helps us in differentiating Crohn disease from Ulcerative colitis which has a continuous involvement.

Strictures and Fissures and fistulas: Stricture formation is another feature that distinguishes Crohn disease from Ulcerative colitis. Due to transmural involvement, fissures are commonly seen in Crohn disease. With more extensive disease, fistulas and perforation can occur. Strictures are formed due to transmural oedema, inflammation, fibrosis and hypertrophy of muscularis propria.
Creeping fat: With extensive transmural involvement, mesenteric fat is seen over the serosal aspect which is referred to as “creeping fat”.
Aphthous ulcers: these are the earliest lesions which are superficial ulcers.
Serpentine/ Serpiginous ulcers: these are elongated ulcers seen along the long axis of intestine and are formed when multiple ulcers coalesce. The mucosa shows oedema and loss of folds.


Cobblestone appearance: it results from the patchy distribution of ulcers with intervening normal appearing mucosa.

Morphology Microscopy

In chronic disease, there is architectural distortion, basal plasmacytosis, pseudopyloric metaplasia, paneth cell metaplasia, fibrosis and hypertrophy of muscularis propria.

Cryptitis: Presence of neutrophils infiltrating the epithelium of crypts.
Crypt abscess: Aggregates of neutrophils within a crypt.
Abrupt transition between ulcer and normal mucosa is seen.


Granulomas: Non-necrotising granulomas composed of epithelioid histiocytes and lymphoctes are seen in about 35% cases of Crohn disease.

Clinical features
Most often the disease presents in an episodic manner with disease-free intervals of weeks to months.
Usual clinical features include abdominal pain, fever and diarrhoea.
Few patients present with severe, acute abdominal pain in right lower quadrant, fever and bloody diarrhoea mimicking acute appendicitis or intestinal perforation.
External factors like smoking, food products and emotional stress are known for causing disease activation.
Severe cases are associated with iron-deficiency anaemia, hypoalbuminemia and other nutritional deficiencies.

Extra-intestinal manifestations of Crohn disease
Uveitis
Sacro-ileitis
Ankylosing spondylitis
Erythema nodosum
Clubbing
Migratory polyarthritis
Primary sclerosing cholangitis
Pericholangitis

Treatment
Anti-inflammatory agents: like salicylates
Immunosuppressants: like steroids
Anti-TNF antibodies.
Surgery: in cases of strictures, fistulas, perforations, abscess,etc.

 

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