Inflammatory Bowel Disease

1 What is Inflammatory Bowel Disease?

Inflammatory bowel disease is a term comprising two disease entities: Crohn disease and Ulcerative Colitis.

Both diseases have a large degree of overlap in terms of presentation, testing and treatment.

Both diseases are idiopathic disorders of

  • bowel associated with diarrhea,
  • bleeding,
  • weight loss,
  • fever,
  • and abdominal pain.

Both are accurately diagnosed with endoscopy and barium studies, “string sign” on small bowel follow through after barium meal in CD, and both are treated with anti-inflammatory medications such as mesalamine, azathioprine, and 6-mercaptopurine. Steroids are used for acute exacerbations of both diseases.

2 Symptoms

It is difficult to diagnose which form of inflammatory bowel disease a patient is suffering from because both Crohn’s Disease and ulcerative colitis cause similar symptoms.

Symptoms related to inflammation of the GI tract:

  • Diarrhea
  • Rectal bleeding
  • Urgent need to move bowels
  • Abdominal cramps and pain
  • Sensation of incomplete evacuation
  • Constipation (can lead to bowel obstruction)

General symptoms that may also be associated with IBD:

Both illnesses do have one strong feature in common. They are marked by an abnormal response by the body’s immune system. The immune system is composed of various cells and proteins. Normally, these protect the body from infection. In people with Crohn’s disease, however, the immune system reacts inappropriately.

However, in people suffering from IBD, the immune system reacts inappropriately, mistaking benign or beneficial cells and bacteria for harmful foreign substances. When this happens, your immune system can do harm to your gastrointestinal tract and produce the symptoms of IBD.

The extraintestinal manifestations of IBD are: episcleritis, scleritis, iritis, sclerosing cholangitis, joint pains and skin manifestations such as pyoderma gangrenosum or erythema nodosum. Crohn disease is more likely associated with a palapable abdominal mass because of granulomas in bowel wall that are transmural in nature.

This can leads to different loops of bowel being held together and inflamed forming a mass. The abdominal masses of CD can be palpated and can cause pain. CD is not necessarily continuous and one hallmark of the disorder is that there are skip lesions, or areas of normal tissue in between areas of disease.

Ulcerative Colitis is limited exclusively to the large bowel. It is exclusively a mucosal disease and although it can cause bleeding, UC does not cause fistula formation. UC has no skip lesions, no fistula formation and no oral and peri-anal involvement. UC is more likely to cause bloody diarrhea.

Both forms of IBD can lead to colon cancer after 8 to 10 years of involvement of the colon. If the CD does not lead to colonic involvement, then it will not lead to cancer. Complications of Crohn disease are calcium oxalate stones in kidney, diarrhea and cholesterol gall stones.

3 Causes

The exact cause of inflammatory bowel disease remains unknown.

IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors leading to immunological responses and inflammation in the intestine.

Microbiota

Alterations in enteral bacteria may contribute to inflammatory gut diseases. IBD-affected individuals have been found to have 30-50 percent reduced biodiversity of commensal bacteria, such as decreases in Firmicutes (namely Lachnospiraceae) and Bacteroidetes.

Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD-affected individuals are more likely to have been prescribed antibiotics in the 2-5 year period before their diagnosis than unaffected individuals.

The enteral bacteria can be altered by environmental factors, such as concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.

Breach of intestinal barrier

Loss of integrity of the intestinal epithelium plays a key pathogenic role in IBD. Changes in the composition of the intestinal microbiota are an important environmental factor in the development of IBD.

Detrimental changes in the intestinal microbiota induce an inappropriate (uncontrolled) immune response that results in damage to the intestinal epithelium.

Breaches in this critical barrier (the intestinal epithelium) allow further infiltration of microbiota that, in turn, elicits further immune responses. IBD is a multifactorial disease that is nonetheless driven in part by an exaggerated immune response to gut microbiota that causes defects in epithelial barrier function.

Diet

High protein intake, specifically animal protein via meat and fish consumption has been significantly associated with inflammatory bowel disease as well as ulcerative colitis.

There was no such association related to plant proteins in the prospective study consisting of over 65,000 patients over a 10-year period. Animal proteins have greater amounts of sulphur containing amino acids such as methionine, which the colonic micro flora accrues into hydrogen sulfide, resulting in the pathogenesis of IBD and ulcerative colitis.

Such bacteria-derived cell poisons in the form of hydrogen sulfide are specifically elaborated by animal or meat and fish intake, and not by plant foods.

Genetics

The genetic contribution is poorly understood and seems to arise from the small contribution of dozens of genes.

The 163 loci were related to 300 known genes. The functional enrichment analysis of this group of genes using gene ontology showed that there are many genes related with cytokine production, lymphocyte activation and the response to bacterial infection. In an effort to identify likely causal genes, a probabilistic causal gene network was constructed.

Here, a sub-network including NOD2, Il10 and CARD9 seems to indicate a close relationship between IBD and genes related with host interaction with bacteria. Of particular relevance is the presence of the gene HCK which seems to play an important role anti-inflammation.

4 Making a Diagnosis

Making a diagnosis of inflammatory bowel disease is done by performing several tests.

Tests

The diagnosis of an IBD is primarily made with non-laboratory tests, in particular, a biopsy is considered the gold standard for diagnosis and for distinguishing between ulcerative colitis and Crohns disease.

However, laboratory testing is an important tool for ruling out other causes of:

  • diarrhea,
  • abdominal pain,
  • and colitis.

These causes can include:

Laboratory Tests

Tests that may be ordered to rule out other causes of diarrhea and gastrointestinal inflammation include:

  • Stool culture to look for bacterial infection
  • O&P (Ova and parasite) to detect parasites
  • Clostridium difficile to detect toxin created by bacterial infection; may be seen following antibiotic therapy
  • Fecal occult blood to look for blood in the stool due to causes such as infection, inflammation, and cancers
  • Stool WBC to detect white blood cells in the stool, an indication of inflammation in the digestive tract
  • Anti-tissue transglutaminase (anti-tTG) and other tests for celiac disease 

Tests that are not specific for IBD but may be done to detect and evaluate the inflammation and anemia associated with IBD include:

  • ESR (erythrocyte sedimentation rate) to detect inflammation
  • CRP (C-reactive protein) to look for inflammation
  • CBC (complete blood count) to check for anemia

Tests that are not yet widely used but may be ordered fall into two groups: stool tests and antibody tests.

Stool tests

Two stool (fecal) tests are available that detect substances released by white blood cells. These test for:

  • Calprotectin
  • Lactoferrin

These substances are associated with inflammation and with disease activity, severity, and relapse. They may be used to help distinguish between IBD and non-inflammatory disorders and also to monitor IBD. These tests are gaining attention as they may prove to be more sensitive than the current test for stool WBC.

Antibody tests

Tests to detect antibodies that are frequently present in people who have IBD: one or more may sometimes be ordered to help distinguish between the two most common types of IBD, ulcerative colitis (UC) and Crohns disease (CD). They are not sensitive or specific enough to diagnose either condition, but they may give the doctor additional information. These biomarkers are not widely used clinically and their ultimate role has yet to be determined. They include:

  • pANCA (Perinuclear anti-neutrophil cytoplasmic antibody). More common with UC, it is found in about 50% of those with UC but only about 5% to 20% of those with CD.
  • ASCA (Saccharomyces cerevisiae antibodies), IgG and IgA. ASCA is more common with CD; it is found in about 40% to 50% of those with CD. ASCA IgG is found in about 20% of those with UC. ASCA IgA is found in less than 1% of those with UC.
  • Anti-CBir1 (Clostridium species antibodies). Found to be associated with about 50% of Crohns disease cases.
  • Anti-Omp C (Escherichia coli antibodies). Associated with rapidly progressing Crohns disease.
  • Anti-I-2 (Pseudomonas fluorescens antibodies)

Several of these markers may be ordered together in a panel and overall findings evaluated. An example includes ordering ASCA, pANCA, and Anti-Omp C together to help differentiate CD from UC.

Non-laboratory Tests

These tests are used to help diagnose and monitor UC and CD. They can be used to look for characteristic changes in the structure and tissues of the intestinal tract and to detect blockages. Care must be taken during an acute attack or flare-up of an IBD as there is a slight chance of perforating the bowel during testing.

  • X-ray (abdominal). Barium contrast dye allows an evaluation of the intestines.
  • Sigmoidoscopy. A slender tube is used to examine the last 2 feet of the colon.
  • Colonoscopy. A slender tube is used to examine the entire colon; it includes a light and camera and can be used to take biopsies.

A biopsy may be performed during endoscopy or colonoscopy in which tissue samples are evaluated for inflammation and abnormal changes in cell structures.

This test is considered the gold standard for diagnosis and for distinguishing CD from UC because of the characteristic changes that are seen.

5 Treatment

The goal of treatment for inflammatory bowel disease is to improve and maintain patients’ general well-being.

Treat acute disease:

  • Eliminate symptoms and minimize side effects and long-term adverse effects
  • Reduce intestinal inflammation and if possible heal the mucosa
  • Maintain corticosteroid-free remissions (decreasing the frequency and severity of recurrences and reliance on corticosteroids)
  • Prevent complications, hospitalization, and surgery
  • Maintain good nutritional status

Drugs in IBD management

Aminosalicylates — anti-inflammatory agents

This group includes:

  • 5-aminosalicylic acid (5-ASA),
  • mesalazine (U.S. Adopted Name mesalamine).

Useful both for treating colitis flare-ups and maintenance of remission.

Data on 5-ASA in CD remain limited

In patients with mild ileocecal or right-sided colonic CD who decline or cannot tolerate corticosteroids, or in whom corticosteroids are contraindicated, 5-ASA should be considered for a first presentation or a single inflammatory exacerbation in a 12-month period.

Do not offer 5-ASA for moderate to severe CD or exacerbations or for extensive small-bowel disease or disease with penetrating or fibrostenosing complications.

In CD, sulfasalazine and mesalazine/mesalamine are presumed to be mainly effective in disease affecting the colon. However, this has not been specifically studied.

Patients receiving sulfasalazine should take folic acid.

It is important to use adequate doses: 2.0–4.8 g/day for active disease, ≥ 2 g/day for maintenance. However, the evidence for a dose-response effect for 5-ASA beyond 2 g/day is weak.

Corticosteroids

These usually provide significant suppression of inflammation and rapid relief of symptoms.

Corticosteroids induce remission in patients with a first presentation or a single inflammatory exacerbation of CD within a 12-month period.

They have no role in the maintenance of remission.

Side effects limit (long-term) use.

Concurrent use of calcium and vitamin D is recommended, as well as monitoring of blood glucose and arterial blood pressure.

In patients with distal ileal, ileocecal, or right-sided CD who decline or cannot tolerate corticosteroids, or in whom they are contraindicated, budesonide should be considered for a first presentation or a single inflammatory exacerbation within a 12-month period.

Budesonide may have fewer side effects than conventional corticosteroids.

Do not offer budesonide for severe CD or exacerbations.

The route of administration depends on the location and severity of the disease:

  • Intravenous (methylprednisolone, hydrocortisone).
  • Oral (prednisone, prednisolone, budesonide, dexamethasone).
  • Rectal (enema, foam preparations, suppository).

Immune modifiers — Thiopurines

Thiopurines are no more effective than placebo for inducing remission of CD or UC; they are effective for maintenance of remission induced by corticosteroids.

Do not offer azathioprine or mercaptopurine for CD or UC if thiopurine methyltransferase activity (TPMT) is deficient. Use at a lower dose if TPMT activity is below normal.

If TPMT measurement is not available, the thiopurine dose should be escalated from 50 mg to the full dose while monitoring the blood count. Asians appear to require lower doses of thiopurine to achieve efficacy, and the full dosage is usually limited by the development of cytopenia.

The addition of azathioprine or mercaptopurine to conventional corticosteroids or budesonide should be considered, in order to induce remission of CD if there are two or more inflammatory exacerbations within a 1-year period, or if the corticosteroid dose cannot be tapered and eliminated. It may also be considered if there are predictors of poor outcome even at the time of diagnosis (age < 40, corticosteroids for first flare, perianal disease, smoking, perforating phenotypes).

Thiopurines are associated with low rates of serious infection, but should be monitored more closely in the elderly.

Thiopurines increase the risk of lymphoma, although the extent of the increase is debated. Their use is also associated with an increased risk of non melanoma skin cancer.

Thiopurines in particular are associated with macrophage activation syndrome (MAS), most likely by promoting viral reactivation through inhibition of natural killer and cytotoxic T cells.

Patients should be monitored for neutropenia if they are taking azathioprine or mercaptopurine, even if TPMT enzyme levels are normal.

Azathioprine is used in resource-poor countries in patients with CD and UC because it is cheap, available, and appears to be safe. Patients often cannot afford 5-ASA and use corticosteroids, and present with severe complications; azathioprine is a better choice than corticosteroids.

Thiopurine metabolite tests are not available in many countries, but where available can help explain the lack of response.

Immune modifiers — calcineurin inhibitors

Cyclosporine A (CSA) or tacrolimus in UC and tacrolimus in CD.

The tacrolimus level should be measured and a trough of 10–15 ng/L should be aimed for.

Use of CSA is limited to acute (corticosteroid-refractory) severe colitis.

Calcineurin inhibitors are reserved for special circumstances.

Use of CSA is limited almost exclusively to patients with acute severe colitis.

Use of tacrolimus in UC or CD in which other proven therapies have failed.

Calcineurin inhibitors should be discontinued within 6 months to limit nephrotoxicity, and alternative immunosuppressives such as azathioprine (AZA), 6-mercaptopurine (6-MP), or methotrexate (MTX) will therefore be required if CSA is being considered.

There is a high colectomy rate 12 months after the introduction of CSA.

After intravenous CSA, there should be a switch to oral therapy when a clinical response is achieved, and 6-MP, AZA, or MTX should be added.

Immune modifiers — methotrexate (MTX) in CD

Methotrexate is more effective than placebo for induction of remission of CD and for maintenance of remission induced by corticosteroids.

The addition of methotrexate to conventional corticosteroids or budesonide should be considered in order to induce remission of CD if patients cannot tolerate azathioprine or mercaptopurine, or in patients in whom TPMT activity is deficient if there are two or more inflammatory exacerbations within a 1-year period, or if the corticosteroid dose cannot be tapered.

Methotrexate should only be considered in order to maintain remission of CD in patients who needed methotrexate to induce remission, or who cannot tolerate or have contraindications to azathioprine or mercaptopurine — MTX should also be avoided in young women because of pregnancy issues.

Methotrexate is a good option if concomitant therapy with an anti-TNF agent is undertaken. It has been shown to not have any advantage over placebo in inducing and maintaining remission in persons with CD who have received high-dose corticosteroids and an induction and maintenance regimen with infliximab over 1 year. However, co-administration with methotrexate can reduce antibody formation to anti-TNF therapy, and this will likely increase the sustained response to the anti-TNF. It is considered that the likelihood of increasing the risk for lymphoma with methotrexate as a single or combination therapy is less than when thiopurines are used. This risk is considered to be small.

Co-administration of folic acid is recommended.

Hepatotoxicity with methotrexate treatment for IBD is typically mild and reversible on stopping the drug. Patients should be monitored for hepatotoxicity at initiation and during treatment with methotrexate.

Immune modifiers: uses

Can be used to reduce or eliminate corticosteroid dependence in patients with IBD.

Can be used in selected patients with IBD when 5-ASAs and corticosteroids are either ineffective or only partly effective.

Can be used to maintain remission in CD and in UC when 5-ASAs fail.

Can be used in for primary treatment of fistulas.

Are alternative treatments for CD relapses after corticosteroid therapy.

Can be used in for corticosteroid dependence, to maintain remission and allow withdrawal of corticosteroids.

Either thiopurines or methotrexate can be used concurrently with biologic therapy to enhance effectiveness and reduce the likelihood of antibody formation.

Anti-tumor necrosis factor (anti-TNF) agents

This may be the first-line therapy in patients who present with aggressive disease and in those with perianal CD.

Infliximab, adalimumab, and certolizumab have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of moderate to severe CD when there is an inadequate response to standard medications.

Infliximab and adalimumab show a better clinical response and better remission and mucosal healing than placebo, with no increase in adverse effects.

Infliximab, adalimumab, and certolizumab are effective in maintaining remission of CD induced by anti-TNF agents.

Infliximab (IFX) is used for rescue therapy in corticosteroid-refractory severe UC.

The effects of intravenous IFX treatment last for approximately 8 weeks; regular scheduled dosing leads to better remission rates than episodic therapy. When there is a suboptimal response, the dosage can be increased from 5 mg/kg to 10 mg/kg, or the interval can be reduced. Other dosage adjustments can be tailored to drug levels. Adalimumab and certolizumab are administered subcutaneously every 2 and 4 weeks, respectively. In the case of adalimumab, dosing can be increased to weekly if there is a suboptimal response.

Concomitant administration of immunomodulatory agents reduces the risk of infliximab antibody development and the risk of infusion reactions. It may be useful when administered with other anti-TNF agents, but this has not been formally tested — there is a concern, though, about the use of combined therapy (thiopurines + anti-TNF) in young male patients, because of the increased risk of hepatosplenic T cell lymphoma.

Infliximab is the only proven therapy in the treatment of fistulas, on the basis of adequately powered randomized controlled trials. Adalimumab is also useful for fistulas, but these data are only available from subgroups in larger CD studies not specifically designed to assess the fistula response.

Infliximab treatment reduces hospitalization and surgery rates in patients with IBD. This significantly reduces the costs associated with the disease.

There is only a small increase in malignancy in anti-TNF users.

The risk of lymphoma is very low, but this remains a concern. Other cancers may be increased, especially nonmelanoma skin cancers and possibly melanoma.

Treatment of IBD with infliximab, adalimumab, certolizumab, and golimumab significantly increases the risk of opportunistic infections in comparison with placebo.

The risk of minor and serious infections is of concern. Anti-TNF agents are associated with low rates of serious infection, but they are associated with opportunistic infections, including Mycobacterium tuberculosis, histoplasmosis, coccidiomycosis, and listeriosis. There is an increased risk of reactivation of latent TB and of hepatitis B, which is endemic in many parts of the developing world.

If treatments fail or the patients become intolerant of one anti-TNF agent, a second anti-TNF agent can be effective.

In patients treated with infliximab, infliximab antibodies lead to a 2–6-fold increase in the risk of infusion reactions.

Therapeutic drug monitoring (which includes both measurement of circulating drug levels and also measurement of antibodies to the drug) is more widely available for infliximab than any other anti-TNF. It can help determine the cause of a secondary loss of response and may be adopted in dose reduction strategies.

Adhesion molecule antagonists

Vedolizumab (an antibody to alpha 4-beta 7) has recently been approved for the treatment of UC and CD and is effective at both inducing and maintaining remission. It has few side effects and no known risk for malignancy.

Antibiotics

Metronidazole and ciprofloxacin are the most commonly used antibiotics in CD. Antibiotics are used to treat CD complications (perianal disease, fistulas, inflammatory mass, bacterial overgrowth in the setting of strictures).
There has never been an adequately sized randomized controlled trial proving the efficacy of metronidazole and/or ciprofloxacin in perineal fistulas, but these are typically first-line therapies. There is an increased risk for C. difficile–associated disease (CDAD), and patients presenting with a flare of diarrheal disease should be checked for C. difficile and other fecal pathogens.

There are no data showing that any antibiotics are effective in UC, but they are used in the setting of fulminant colitis.

Probiotics

IBD may be caused or aggravated by alterations in the gut flora.
While many patients may use probiotics, there is no evidence that they are effective in either UC or CD. VSL#3, which is a combination of eight probiotics, induces and maintains remission of UC, and may be as effective as 5-ASA.

However, no such benefit has been demonstrated for CD.

Symptomatic therapy and supplements

Antidiarrheals such as loperamide (Imodium) if colitis is not fulminant; cholestyramine if the patient has previously undergone ileal resection.

Analgesics such as acetaminophen, or even codeine if acetaminophen is insufficient. However, narcotic use should be avoided, as it is associated with increased mortality in patients with IBD.

Nutritional supplementation for those with malnutrition, or during periods of reduced oral intake.

Vitamin B12 replenishment for those with deficiency.

Vitamin D supplementation if the local area does not allow sun exposure for much of the year— and for patients on thiopurines who are using sunscreens.

Routine vitamin D and calcium supplementation for corticosteroid users.

Routine multivitamin supplementation for all.

For chronic iron-deficiency anemia, parenteral iron should be administered (either as weekly intramuscular shots or dosing with intravenous iron) if oral iron is not tolerated.

Surgery in CD

70–75% of CD patients require surgery at some point to relieve symptoms if drug treatment fails, or to correct complications although the incidence of surgery in CD is falling.

Surgery should be considered as an alternative to medical treatment early in the disease course for short-segment CD limited to the distal ileum.

Surgery is rarely curative in CD; the condition recurs frequently after surgery. However, surgery can lead to long-lasting remission in some patients with CD. After surgery, azathioprine and metronidazole should be considered for at least 3 months, as this has been shown to reduce recurrence.

Laparoscopic ileocecal resection has perioperative morbidity rates similar to or better than those with open surgery for treatment of CD. Convalescence is shorter with the laparoscopic approach, although the operating time is longer.

Balloon dilation may be useful in patients with a single stricture that is short, straight, and accessible by colonoscopy. It should be ensured that abdominal surgery is available to manage complications or failure of balloon dilation.
Surgical options are:

  • Drainage of abscesses
  • Segmental resection
  • Bowel-sparing stricturoplasty
  • Ileorectal or ileocolonic anastomosis
  • Ileocolic resection
  • Temporary diverting ileostomy/colostomy in severe perianal fistula
  • Laparoscopic ileocecal resection 

Surgery in UC

25–30% of UC patients may require surgery if medical treatment is not completely successful, or in the presence of dysplasia.

Surgical options are:

  • Total proctocolectomy plus permanent ileostomy.
  • Ileal pouch–anal anastomosis (IPAA).
  • Segmental resection can be considered for localized neoplasms in the elderly, or in patients with extensive co morbidity.

6 Prevention

The hereditary causes of inflammatory bowel disease (IBD) can’t be prevented. However, you may be able reduce your risk of developing IBD or prevent a relapse by:

  • eating healthy foods
  • exercising regularly
  • quitting smoking

IBD can cause some discomfort, but there are ways you can manage the disease and still live a healthy, active lifestyle.

7 Lifestyle and Coping

Lifestyle modifications are necessary in order to cope with inflammatory bowel disease.

The impact of diet on inflammatory activity in UC/CD is poorly understood, but dietary changes may help reduce symptoms:

  • During increased disease activity, it is appropriate to decrease the amount of fiber. Dairy products can be maintained unless not tolerated.
  • A low-residue diet may decrease the frequency of bowel movements.
  • A high-residue diet may be indicated in cases of ulcerative proctitis (disease limited to the rectum, where constipation can be more of a problem than diarrhea).

There are limited data suggesting that a reduction of dietary fermentable oligosaccharides, disaccharides, and monosaccharides and polyols (FODMAP) may reduce the symptoms of IBD.

Dietary or lifestyle changes may reduce inflammation in CD

A liquid diet, pre-digested formula, or nothing by mouth (NPO status) may reduce obstructive symptoms. Exclusive enteral nutrition can settle symptoms in inflammatory disease, especially in children; however, how it affects the inflammation is unknown, since relapse upon stopping enteral nutrition is common unless some other intervention has been undertaken.

It may affect the gut microbiome, which reverts to baseline once the enteral nutrition is stopped and the usual table diet is reinitiated.

Enteral nutrition should be considered as an alternative to conventional corticosteroids to induce remission of CD in children in whom there is a concern about growth or when immunosuppression is not appropriate —e.g., in difficult-to-control sepsis.

Smoking cessation benefits patients with CD in relation to their disease course and benefits UC patients from a general health point of view (smoking cessation is associated with flaring of UC).

Dietary fiber has potential efficacy for treatment of IBD. There is limited, weak evidence for efficacy of ispaghula in maintenance of remission of UC and germinated barley in active UC.

Reduction of stress and better stress management may improve symptoms or the patients’ approach to their disease. The assistance of a mental health worker may be useful, and attention to co morbid psychiatric illness is imperative.

8 Risks and Complications

There are several complications associated with inflammatory bowel disease.

Intestinal complications of UC

  • Perforation (rupture) of the bowel: Occurs when chronic inflammation and ulceration of the intestine weakens the intestinal wall to such an extent that a hole develops. This complication is potentially life-threatening, and generally linked to toxic mega colon. In Crohn’s disease, perforation may occur as a result of abscess or fistula.
  • Fulminant colitis: Affecting less than 10% of people with UC, fulminant colitis involves progressive inflammation and damage to the entire colon. When severe inflammation causes the colon to become extremely dilated and swollen, a condition called ileus (when the bowel is not moving) may develop — normal contractions of the intestine stop, and abdominal distension occurs. As the condition progresses, the colon becomes more distended (loses muscle tone and begins to expand). Abdominal X-rays reveal trapped gas inside the paralyzed sections of intestine. Fulminant colitis can occur suddenly.
  • Toxic megacolon: Most serious, but relatively rare, complication of IBD (potentially life-threatening), and most extreme form of fulminant colitis. The colon loses its ability to contract properly and move intestinal gas along. Abdominal distension and illness is severe, causing high fever, abdominal pain and tenderness, and a high white blood cell count. Immediate medical attention is essential to try and "decompress" the bowel and prevent rupture. Urgent surgery may be needed if there is no improvement or if the condition worsens.
  • Increased risk of colorectal cancer. There is an increased risk of colorectal cancer among people with IBD. About 5% to 8% of people with UC develop colorectal cancer within 20 years after diagnosis as compared to 3% to 6% for the general population, and the risk increases with duration and severity of disease. People with UC have a higher risk of colorectal cancer than those with Crohn's disease.

Intestinal complications of Crohn's disease

  • Intestinal obstruction: Most common complication of Crohn's disease. An obstruction is caused by inflammation and formation of scar tissue in the intestinal wall. The bowel becomes blocked from scar tissue causing a narrowed area also known as a stricture. Symptoms include an inability to eat, crampy abdominal pain, nausea, vomiting, and bloating. Medications may relieve some inflammatory obstructions by reducing the intestinal swelling. If the obstruction recurs frequently or is severe, surgery may be necessary.
  • Abscesses: Localized pus pocket caused by bacterial infection. May form in the intestinal wall, inside the abdomen or pelvis, or in areas next to inflamed intestine. Visible abscesses, such as those around the anus, look like boils and treatment often involves surgical drainage. Symptoms include fever, pain, swelling, and tenderness. Once the abscess is drained, symptoms usually resolve promptly. Antibiotics are usually given to help treat the infection.
  • Fistulas: Abnormal passages that connect different parts of the intestine, which are caused by deep sores or ulcers within the intestinal tract. Fistulas may also tunnel into the surrounding tissues of the bladder, vagina or skin. Fistulas affect about 30% of people with Crohn's disease, and often become infected. If small, antibiotics and other medical treatment may be adequate. Surgery may be needed for large or multiple fistulas, especially if they cause persistent symptoms.
  • Fissures: Tears or cracks in the lining of the anus. May be superficial or deep. Unlike fistulas, fissures are only in the anus area. Can cause mild-to-severe rectal pain and bleeding, particularly during and immediately after bowel movements. Generally treated with local care, including topical creams or sitz baths.
  • Malabsorption and malnutrition: Related to deficiencies in nutrients, such as proteins, vitamins and fats. Crohn's disease usually affects the small intestine, which is the part of the gut that absorbs most nutrients. Malabsorption and malnutrition usually do not develop unless the disease is extensive or presents for a long period of time. Medical treatment is usually effective in the replacement of nutrients.
  • Bile salt diarrhea: The ileum (lower end of the small intestine) is the part of the intestine most commonly involved in Crohn's disease. This is the principal area for intestinal absorption of bile acids/salts, compounds that help transport and absorb fats. If this absorption becomes deficient, fat malabsorption and diarrhea can result. An oral medicine called cholestyramine is usually prescribed.
  • Small intestinal bacterial overgrowth (SIBO): With SIBO, excessive amounts of bacteria are present in the small intestine. As a result, bacteria break down or digest food higher up than normal in the GI tract, which produces gas, abdominal pain, bloating and diarrhea. SIBO, which also may occur in UC, usually improves after a course of antibiotics.

Other parts of the body (systemic)

  • Anaemia (lack of iron): Loss of blood in the stool can result in anaemia. Inflammation can also inhibit the ability of the bone marrow cells to produce red blood cells, which can also result in anaemia. This can lead to fatigue and generally feeling run down.
  • Arthritis: Joint inflammation with swelling, redness and tenderness of one or more joints, most often the large joints. This is seen when the disease is active.
  • Arthralgias: Joint pain without swelling, most often in the small joints of the hands and feet. This is seen often in people with IBD. These arthralgias can occur at any stage of the condition.
  • Cancer: There is a small increased risk for cancer of the intestines especially in patients with ulcerative colitis. Some medical studies suggest that 5-aminosalicylic acid (5-ASA) may have a protective effect, but this is still unconfirmed.
  • Skin rash: Erythema nodosum is a type of skin rash that is made up of large (0.5 to 2 cm) blue-red, tender nodules. These are especially common on the shin and forearm.
  • Uveitis (inflammation of the iris): Uveitis is an inflammation of the inner muscles of the eye. The symptoms include pain in the eye (particularly in bright light), blurry vision, headache and redness in the white part of the eye. Should be treated promptly.
  • Effects on the liver: Quite rare. Inflammation can result in narrowing of the bile ducts in the liver. Results in itchy skin and tiredness. It is generally detected through blood tests.
  • Malabsorption and malnutrition (Crohn’s disease mostly): Crohn’s disease usually affects the small intestine, which is the part of the gut that absorbs most nutrients. Malabsorption and malnutrition (of proteins, vitamins, and fats) can develop in severe cases.

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