Inflammatory Bowel Diseases

The exact cause of inflammatory bowel diseases (IBD) remains unknown. It is probable that these diseases are not due to a single cause and it is believed that the inflammation is triggered by a combination of different factors. For example, hereditary factors appear to play a key role. Although neither ulcerative colitis (UC) nor Crohn’s disease represents an inherited disease in the usual sense, it does appear that a person’s genes are responsible for a certain susceptibility (“genetic predisposition”).

Many risk factors have been discussed, including infections, special dietary habits and disorders of the immune system, including over reactive immune responses. More recently it has been found that gut bacteria (the microbiome) play a major role in the pathogenesis of IBD.

Read on to find out more about specific conditions.

Please consult your healthcare professional for further information

Ulcerative Colitis

Ulcerative Colitis

The exact cause of this disease remains unclear. It is most likely triggered by a complex interplay between environmental factors, such as infections caused by viruses or bacteria, changed dietary habits, disorders of the immune system operating on a background of a genetic predisposition or susceptibility and changes in the gut microbiome.

Symptoms and Disease Course

The term ulcerative colitis represents a condition in which inflammatory ulcerations develop on the inner lining of the colon, or large intestine. These ulcerations most frequently form first in the rectum; from there, the disease can spread in a continuous fashion to the lower segments of the colon. The inflammation is restricted to the superficial (inner) layers of the bowel wall.

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Diarrhoea, abdominal pain during defecation and blood and mucus in the faeces are the most common symptoms of ulcerative colitis. In more severe cases, patients may experience fever and weight loss due to the loss of protein into the bowel.

Many of those affected by ulcerative colitis feel that their physical performance is diminished and they complain of fatigue and loss of appetite. In rare cases, inflammation may occur elsewhere in the body, such as in the joints, eyes or in the liver. In some cases, primary sclerosing cholangitis (PSC), a cholestatic liver disease, may occur in parallel to ulcerative colitis.

Diagnosing ulcerative colitis

The first step is a complete physical examination during which the physician assesses the abdomen by touching and tapping on the abdominal wall. A rectal examination will be carried out. Laboratory examination of blood samples may reveal the presence of “inflammation markers” or other abnormalities. A valuable overview is provided by imaging the abdominal cavity with an ultrasound scanner. If ulcerative colitis is suspected, the physician will attempt to confirm the diagnosis through a colonoscopy.

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This procedure involves inserting a flexible optical instrument through the anus, which, as it is advanced higher into the colon, allows the examiner to directly inspect the colonic mucosal membrane. Inflammatory changes and ulcerations can be recognised and evaluated for their severity and localisation. It also allows small amounts of tissue (biopsies) to be taken for examination under the microscope.

In some cases diagnostic imaging, such as radiography (x-ray) or computerised tomography (CT or “CAT” scans), may be required.

Available treatments

Available treatments

Treatment goals include relieving symptoms, mucosal healing and preventing relapse. Mild to moderate disease flares may respond to mesalazine (5-aminosalicylic acid) as inflammation is often located at the lower end of the gastrointestinal tract it is sometimes useful to combine oral treatment in the form of tablets or granules with suppositories, enemas or foams.

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The drugs used to treat ulcerative colitis must continue to be taken, even after symptoms have resolved and patient is in remission. It has been shown that the long-term use of mesalazine is effective in preventing new disease flares. In more severe cases, patients may benefit from taking glucocorticoid (steroid) based drugs. If symptoms do not improve, or for more severe disease, your doctor may prescribe the treatment with medicines that have an effect on the immune system (immunosuppressants), such as azathioprine, 6-mercaptopurine (6-MP), cyclosporine or biologics / biosimilars (anti-TNF-α monoclonal antibodies).

Patients not responding to all the above medications can be offered surgery. This may involve partial or complete removal of the colon depending on the spread of disease. Surgical removal of the colon may result in cure for some patients with ulcerative colitis.

Crohn’s Disease

Crohn’s Disease

“Crohn’s disease” is named after the American gastroenterologist, Burrill B. Crohn, who first described this disease in the 1940’s. The exact cause of Crohn’s disease remains unclear. Besides a hereditary predisposition, it is probable that environmental factors play a role since Crohn’s disease is more frequent in the Western Countries than in the developing world.

Symptoms and Disease Course

Unlike ulcerative colitis, which is limited to the colon, Crohn’s disease can affect any part of the gastrointestinal tract from the mouth to the anus. It also differs from ulcerative colitis in that all layers of the intestinal wall may be affected by the inflammation. It is a disease that predominantly affects younger individuals aged 16 to 30 years. Symptoms of Crohn’s disease include abdominal pain, diarrhoea (up to 10-15 bowel movements per day in severe cases), weight loss and fever. Symptoms may begin slowly and insidiously. For this reason, the disease may not be recognized immediately. In fact, it may sometimes take years before Crohn’s disease is diagnosed: by this time, patients may develop other complications of the disease such as anal fistula formation (extension of an ulcer into deeper tissue that may communicate with the skin or internal organs) , or stricture (abnormal narrowing areas of the bowel).

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Other organs are also more frequently affected in patients with Crohn’s disease than are those with ulcerative colitis. These extraintestinal manifestations may include erythema nodosum, a painful, reddish-purple thickening of the skin, as well as recurring inflammation of the joints (arthritis) including spine, and eye inflammation as well.

Diagnosing Crohn’s disease

The first step is a complete physical examination at which the physician assesses the abdomen by touching and tapping on the abdominal wall. A rectal examination is done at this time. Laboratory examination of blood samples may reveal the presence of “inflammatory markers” or other abnormalities. A valuable overview is provided by imaging the abdominal cavity with an ultrasound scanner. If Crohn’s disease is suspected, the physician will attempt to confirm the diagnosis by means of colonoscopy. This procedure involves insertion of a flexible optical instrument through the anus, which when advanced higher into the colon, allows the examiner to directly inspect the colonic mucosal membrane. Inflammatory changes and ulcerations can be directly recognized and evaluated for their severity and localization. It also allows small amounts of tissue (biopsies) to be taken for examination under the microscope.

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In some cases diagnostic imaging, such as radiography (x-rays) or computerised tomography (CT or “CAT” scans), may be required.

Available treatments

Available treatments

Treatment goals include:

• Inducing remission (relieving symptoms and improving general wellbeing)
• Achieving complete mucosal healing (mucosa is the lining of the gut affected by the inflammatory processes of the disease)
• Maintaining remission and preventing relapse.

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Glucocorticoid (steroid) preparations are often required to treat an acute disease flare. There are two main types of steroids:

• Topical steroids (budesonide) which have a local anti-inflammatory effect in the colon
• Systemic steroids (prednisolone) show systemic anti-inflammatory effect throughout the body but are also known to cause many undesirable side effects

Budesonide is a well tolerated steroid treatment which works locally, at the site of inflammation in the gut. Budesonide formulations are designed to release the active drug in the lower small bowel (ileo-caecal region), which is the most common site of inflammation in Crohn’s disease (approx. 65% of patients). After producing the anti-inflammatory effect in the bowel, budesonide is absorbed and transported directly to the liver, where 90% of it is metabolized (broken down). Very little budesonide passes through the liver into the blood stream (about 10%), meaning that the patient is less likely to experience steroid side effects. This explains why patients taking budesonide report less side effects less frequently than those treated with conventional steroids.
According to European and National Guidelines, budesonide is the preferred first line treatment in mild to moderate ileo-caecal Crohn’s disease.

If remission cannot be induced by steroids (topical or systemic), the doctor may prescribe agents that suppress the immune system (immunosuppressants), such as azathioprine or methotrexate. Immunosuppressants support the anti-inflammatory effects of the corticosteroids and can help reduce their use. Finally, when no other agents successfully induce remission, biologics or biosimilar durgs may be tried (anti-TNF-α monoclonal antibodies).

Treatment with different drugs may postpone a new flare of disease, but cannot, in most cases, completely prevent disease recurrence.

Patients with Crohn’s disease may require surgery if complications such as fistula formation or stenosis occur. The principle surgical approach in these cases is one of bowel preservation, since surgical removal of inflamed bowel, unlike in some ulcerative colitis patients, does not lead to cure and inflammation may recur elsewhere in the gastrointestinal tract.

Patients with Crohn’s disease are subject to a number of deficiency syndromes. The absorption of nutrients including vitamins, minerals and proteins may be affected and these nutrients should be substituted using suitable food supplements.

During an acute flare, it may be necessary to supplement the essential nutrients by means of an intravenous infusions. In most cases, however, a special diet is not required. Due to a danger of malnutrition patients should make sure they are receiving a balanced diet.

Microscopic Colitis

Microscopic Colitis

The term microscopic colitis encompasses two different inflammatory disorders of the colon known as collagenous colitis and lymphocytic colitis. The cause of microscopic colitis remains unknown. Such factors as bacterial or viral infections, the long-term use of certain pain relievers called non-steroidal anti-inflammatory drugs (NSAIDs) and a genetic predisposition are under investigation. The number of new cases is about 10-30 cases per 100,000 persons each year. The total number of patients with the disease is estimated to be 100 per 100,000 persons in the population.

Symptoms and Disease Course

The clinical picture of both microscopic colitis disorders is dominated by chronic watery diarrhoea, sometimes accompanied by upper abdominal pain, fatigue and bloating and it is also known as the “watery diarrhoea syndrome”. The course of the disease can generally be described as benign and there is no increased risk of bowel cancer.

Diagnosing Microscopic Colitis

Women over the age of 40 years in particular presenting with these symptoms, are often misdiagnosed with the “irritable bowel syndrome” (IBS).

The diagnosis of microscopic colitis can only be made on the basis of serial biopsies taken along the entire length of the colon during the endoscopic examination and histological testing of the biopsies using correct staining techniques. The presence of a thickened layer of collagen (collagen band) in the deeper layers of the intestinal mucosa is characteristic for collagenous colitis. Lymphocytic colitis is characterized by an increased number of particular type of white blood cells called lymphocytes.

Available Treatments

Available Treatments

The treatment success rates in patients taking oral budesonide are reported to be high. In 80% of patients there is a significant reduction in the number of bowel movements, often with disappearance of the diarrhoea. This leads to a significant improvement in patients’ quality of life.