WHAT IS IT?

A chronic inflammatory disease that can affect any part of the digestive system, from the mouth to anus. The patches of inflammation can range from only a few cm in length to a long distance along part of the gut.

As well as the inflammation affecting the lining of the bowel, it can also go deeper into the bowel wall, forming fistulas.

 

PATHOPHYSIOLOGY

Tissue of the gut is damaged by chronic inflammation from T-cell activation (lymphocyte WBC that plays a role in cell mediated immunity). They are activated by antigen presentation and due to defective regulation there is a large response of type 1 T helper cells. Th1 cytokines such as interleukin and TNF-alpha stimulate an

inflammatory response, and the inflammatory cells recruited by this then release substances which injure the intestine (including arachidionic acid metabolties, proteases, free radicals). Crohn disease begins with crypt inflammation and abscesses, which progress to small aphthoid ulcers. The mucosal lesions may develop into

deep longitudinal and transverse ulcers. Bowel obstruction can then occur due to thickening of the bowel wall, stricture formation, fibrosis, lymphedema. Abscesses occur often, as well as fistulas that penetrate into adjoining structures, including loops of the bowel or the bladder.

 

WHAT CAUSES IT?

Affects approximately 115,000 people in the UK. The exact cause is unknown, but it seems to be due to combination of environmental factors and genetic predisposition. More than 200 different genes have been identified that are more common in crohn’s sufferers. There is evidence that it runs in families, as 3 in 20 people with the condition have a close relative who also suffers, and identical twins have a 70% chance of developing it if the other twin has it.

In crohns disease, something seems to disrupt the immune system, which sends the protein called TNF-alpha (tumor necrosis factor) to kill all bacterial, regardless whether they are beneficial to the gut or not, which causes inflammation.

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Smoking causes an increased risk for crohn’s (where as it causes a lower risk for UC). They are twice as likely to develop the condition, and sufferers who smoke experience more severe symptoms.

Environmental factors are thought to be a cause, as a much larger number of cases occur in the developed parts of the world (UK and US) and a much lower number in the developing parts such as Africa and Asia. It has also become a lot more widespread since the 1950’s onwards. This suggests a cause may be associated with a modern western lifestyle.

2 theorys are the hygiene hypothesis (germ-free environments causes weak immune systems due to lack of exposure) and the cold-chain hypothesis (increased use od refrigerators in WW2).

 

SYMPTOMS

Symptoms vary from mild-severe, and patients may also have periods of remission, and relapses or flare-ups.

They include:

• Recurring diarrhoea

• Abdominal pain and cramping (especially after eating)

• Fatigue

• Weight loss

• Blood and mucous in faeces

• Anaemia

 

Less common symptoms are fever, nausea, vomiting, arthritis, mouth ulcers.

 

DIAGNOSIS

Blood tests : Measure levels of inflammation (such as C-reactive protein and Erythrocyte Sedimentation Rate) if you have an infection, whether your anaemic.

Stool samples may be taken to be checked for blood and mucous, can also be used to rule out parasitic infections (roundworm) or other infections.

Colonoscopy to see the level of inflammation inside the colon, a biopsy can also be taken during this. The tissue samples will then be examined under a microscope.

Wireless capsule endoscopy: involves swallowing a small capsule, that works its way down the small intestines, where it transmits images to a recording device which can then be examined.

MRE (magnetic resonance entergraphy) or CTE (computeristed tomography enterography) scans may be used.

Management/treatment

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DRUGS

• 5-aminosalicylic acids derivative agents (sulfasalazine)

• Coirtcosteriods (prednisolone/hydrocortisone)

• Immunosupressive agents (methotrexate)

• Monoclonal anitbodies (infliximab/adlimumab)

• Antibiotics (metronidazole/ciprofloxacin)

• Anti-diarrhael agents (loperamide)

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SURGERY

Although there is no surgical cure as the disease often progresses to different sections of the bowel, most patients will require surgical intervention:

• Resection of affected bowel

• Ileocolostomy, or proximal loop ileostomy

• Drainage of any septic foci

• Strictureplasty

• Colectomy