What is ulcerative colitis

Ulcerative colitis is a chronic (long lasting) disease that causes inflammation—irritation or swelling—and ulcers (sores) on the inner lining of the large intestine (colon) and rectum. Ulcerative colitis is a chronic inflammatory disease of the gastrointestinal (GI) tract, called inflammatory bowel disease (IBD). Inflammatory bowel disease (IBD) is more common in industrialized countries and in Western nations. The incidence is also increased in persons who live at higher latitudes ¹. Worldwide and in less developed nations, ulcerative colitis is more common than Crohn’s disease, whereas in some studies of U.S. populations, the incidence of the two disorders is almost equal ¹. Four percent of cases of inflammatory bowel disease cannot be characterized definitively as either Crohn’s disease or ulcerative colitis; these patients are said to have indeterminate colitis ².

Ulcerative colitis most often begins gradually and can become worse over time. Symptoms can be mild to severe. Most people have periods of remission—times when symptoms disappear—that can last for weeks or years.

Ulcerative colitis may affect as many as 907,000 Americans. The annual incidence of ulcerative colitis in the United States is between nine and 12 cases per 100,000 persons ¹. Men and women are equally likely to be affected (in contrast with Crohn’s disease, which has a higher incidence in women), and most people are diagnosed in their mid-30s. The disease can occur at any age (including infants) and older men are more likely to be diagnosed than older women.

While ulcerative colitis tends to run in families, researchers have been unable to establish a clear pattern of inheritance. Studies show that up to 20 percent of people with ulcerative colitis will also have a close relative with the disease. The disease is more common among white people of European origin and among people of Jewish heritage.

Ulcerative colitis can be debilitating and can sometimes lead to life-threatening complications. While it has no known cure, treatment can greatly reduce signs and symptoms of the disease and even bring about long-term remission.

Common Extraintestinal Manifestations of Ulcerative Colitis ³

Approximately one-third of patients with ulcerative colitis have extraintestinal manifestations, which may be present even when the disease is inactive.

• Arthritis (21%)
• Aphthous stomatitis (4%)
• Primary sclerosing cholangitis (4%)
• Uveitis (4%)
• Erythema nodosum (3%)
• Ankylosing spondylitis (2%)
• Pyoderma gangrenosum (2%)
• Psoriasis (1%)

Most people with ulcerative colitis receive care from a gastroenterologist, a doctor who specializes in digestive diseases. The goal of care is to keep people in remission long term.

Who is more likely to develop ulcerative colitis?

Ulcerative colitis can occur in people of any age. However, it is more likely to develop in people:

• between the ages of 15 and 30 ⁴
• older than 60 ⁵
• who have a family member with inflammatory bowel disease (IBD)
• of Jewish descent

Types of ulcerative colitis

Doctors often classify ulcerative colitis according to its location. Types of ulcerative colitis include:

• Ulcerative proctitis. Inflammation is confined to the area closest to the anus (rectum), and rectal bleeding may be the only sign of the disease. This form of ulcerative colitis tends to be the mildest. For approximately 30% of all patients with ulcerative colitis, the illness begins as ulcerative proctitis. Because of its limited extent (usually less than the six inches of the rectum), ulcerative proctitis tends to be a milder form of ulcerative colitis. It is associated with fewer complications and offers a better outlook than more widespread disease.
• Proctosigmoiditis. Inflammation involves the rectum and sigmoid colon (lower end of the colon). Signs and symptoms include bloody diarrhea, abdominal cramps and pain, and an inability to move the bowels in spite of the urge to do so (tenesmus). Moderate pain on the lower left side of the abdomen may occur in active disease.
• Left-sided colitis. Inflammation extends from the rectum up through the sigmoid and descending colon. Signs and symptoms include bloody diarrhea, abdominal cramping and pain on the left side, and unintended weight loss.
• Pancolitis. Pancolitis often affects the entire colon and causes bouts of bloody diarrhea that may be severe, abdominal cramps and pain, fatigue, and significant weight loss. Potentially serious complications include massive bleeding and acute dilation of the colon (toxic megacolon), which may lead to an opening in the bowel wall. Serious complications may require surgery.
• Acute severe ulcerative colitis. This rare form of colitis affects the entire colon and causes severe pain, profuse diarrhea, bleeding, fever and inability to eat.

Complications of ulcerative colitis

Possible complications of ulcerative colitis include:

• Severe bleeding
• A hole in the colon (perforated colon)
• Severe dehydration
• Liver disease (rare)
• Primary sclerosing cholangitis
• Bone loss (osteoporosis)
• Inflammation of your skin, joints and eyes
• An increased risk of colon cancer
• A rapidly swelling colon (toxic megacolon)
• Increased risk of blood clots in veins and arteries.

Fertility

The chances of a woman with ulcerative colitis becoming pregnant aren’t usually affected by the condition. However, infertility can be a complication of surgery carried out to create an ileo-anal pouch.

This risk is much lower if you have surgery to divert the small intestine through an opening in your abdomen (an ileostomy).

Pregnancy

The majority of women with ulcerative colitis who decide to have children will have a normal pregnancy and a healthy baby.

However, if you’re pregnant or planning a pregnancy you should discuss it with your care team. If you become pregnant during a flare-up, or have a flare-up while pregnant, there’s a risk you could give birth early (premature birth) or have a baby with a low birthweight.

For this reason, doctors usually recommend trying to get ulcerative colitis under control before getting pregnant.

Most ulcerative colitis medications can be taken during pregnancy, including corticosteroids, most 5-ASAs and some types of immunosuppressant medication.

However, there are certain medications (such as some types of immunosuppressant) that may need to be avoided as they’re associated with an increased risk of birth defects.

In some cases, your doctors may advise you to take a medicine that isn’t normally recommended during pregnancy. This might happen if they think the risks of having a flare-up outweigh the risks associated with the medicine.

Osteoporosis

People with ulcerative colitis are at an increased risk of developing osteoporosis, when the bones become weak and are more likely to fracture.

This isn’t directly caused by ulcerative colitis, but can develop as a side effect of the prolonged use of corticosteroid medication. It can also be caused by the dietary changes someone with the condition may take – such as avoiding dairy products, if they believe it could be triggering their symptoms.

If you’re thought to be at risk of osteoporosis, the health of your bones will be regularly monitored. You may also be advised to take medication or supplements of vitamin D and calcium to strengthen your bones.

Primary sclerosing cholangitis

Primary sclerosing cholangitis, where the bile ducts become progressively inflamed and damaged over time, is a rare complication of ulcerative colitis. Bile ducts are small tubes used to transport bile (digestive juice) out of the liver and into the digestive system.

Primary sclerosing cholangitis doesn’t usually cause symptoms until it’s at an advanced stage. Symptoms can include:

• fatigue (extreme tiredness)
• diarrhea
• itchy skin
• weight loss
• chills
• a high temperature (fever)
• yellowing of the skin and the whites of the eyes (jaundice)

There’s currently no specific treatment for primary sclerosing cholangitis, although medications can be used to relieve some of the symptoms, such as itchy skin. In more severe cases, a liver transplant may be required.

Toxic megacolon

Toxic megacolon is a rare and serious complication of severe ulcerative colitis, where inflammation in the colon causes gas to become trapped, resulting in the colon becoming enlarged and swollen.

This is potentially very dangerous as it can cause the colon to rupture (split) and cause infection in the blood (septicaemia).

The symptoms of a toxic megacolon include:

• abdominal (tummy) pain
• a high temperature (fever)
• a rapid heart rate

Toxic megacolon can be treated with fluids, antibiotics and steroids given intravenously (directly into a vein). If medications don’t improve the conditions quickly then surgical removal of the colon (known as a colectomy) may be needed.

Treating symptoms of ulcerative colitis before they become severe can help prevent toxic megacolon.

Bowel cancer

People who have ulcerative colitis have an increased risk of developing bowel cancer (cancer of the colon, rectum or bowel), especially if the condition is severe or involves most of the colon. The longer you have ulcerative colitis, the greater the risk.

People with ulcerative colitis are often unaware they have bowel cancer as the initial symptoms of this type of cancer are similar. These include:

• blood in the stools
• diarrhea
• abdominal pain

Therefore, you’ll usually have regular check-ups to look for signs of bowel cancer from about 10 years after your symptoms first develop.

Check-ups will involve examining your bowel with a colonoscope – a long, flexible tube containing a camera – that’s inserted into your rectum. The frequency of the colonoscopy examinations will increase the longer you live with the condition, and will also depend on factors such as how severe your ulcerative colitis is and if you have a family history of bowel cancer. This can vary between every one to five years.

To reduce the risk of bowel cancer, it’s important to:

• eat a healthy, balanced diet including plenty of fresh fruit and vegetables
• take regular exercise
• maintain a healthy weight
• avoid alcohol and smoking

Taking aminosalicylates as prescribed can also help reduce your risk of bowel cancer.

Ulcerative colitis causes

The exact cause of ulcerative colitis is unknown. Researchers believe the following factors may play a role in causing ulcerative colitis:

• Overactive intestinal immune system

Scientists believe one cause of ulcerative colitis may be an abnormal immune reaction in the intestine. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. Researchers believe bacteria or viruses can mistakenly trigger the immune system to attack the inner lining of the large intestine. This immune system response causes the inflammation, leading to symptoms.

• Genes

Ulcerative colitis sometimes runs in families. Research studies have shown that certain abnormal genes may appear in people with ulcerative colitis. Genetic factors have a role in ulcerative colitis. Having a sibling with ulcerative colitis increases the risk of developing the disease 4.6-fold, and the relative risk of one monozygotic twin having the disease is 95 times higher if the other twin is affected ⁶. However, researchers have not been able to show a clear link between the abnormal genes and ulcerative colitis.

• Environment

Some studies suggest that certain things in the environment may increase the chance of a person getting ulcerative colitis, although the overall chance is low.  Nonsteroidal anti-inflammatory drugs ⁵, antibiotics ⁵ and oral contraceptives ⁷ may slightly increase the chance of developing ulcerative colitis. A diet high in refined sugar, fat, and meat increases the risk, whereas a diet rich in vegetables reduces the risk ¹, ⁸. Infection with nontyphoid Salmonella or Campylobacter is associated with an eight to 10 times higher risk of developing ulcerative colitis in the following year ⁹. The risk diminishes with time, but is still present up to 10 years later. The intestinal bacterial flora of patients with inflammatory bowel disease has been shown to be markedly abnormal, but this finding has not yet led to therapeutic interventions ¹⁰.

The hygiene hypothesis states that excessive hygiene habits in Western industrialized nations prevent children from normal exposure to bacterial and helminthic antigens, thereby changing immune system responsiveness. Epidemiologic data provide indirect evidence for this theory, in the same way that they do for asthma and allergies ¹.

Some people believe eating certain foods, stress, or emotional distress can cause ulcerative colitis. Emotional distress does not seem to cause ulcerative colitis. A few studies suggest that stress may increase a person’s chance of having a flare-up of ulcerative colitis. Also, some people may find that certain foods can trigger or worsen symptoms.

Risk factors for ulcerative colitis

Ulcerative colitis affects about the same number of women and men. Risk factors may include:

• Age. Ulcerative colitis usually begins before the age of 30. But, it can occur at any age, and some people may not develop the disease until after age 60.
• Race or ethnicity. Although whites have the highest risk of the disease, it can occur in any race. If you’re of Ashkenazi Jewish descent, your risk is even higher.
• Family history. You’re at higher risk if you have a close relative, such as a parent, sibling or child, with the disease.

Ulcerative colitis signs and symptoms

The symptoms a person experiences can vary depending on the severity of the inflammation and where it occurs in the intestine. When symptoms first appear, most people with ulcerative colitis have mild to moderate symptoms and about 10 percent of people can have severe symptoms, such as frequent, bloody bowel movements (hematochezia); fevers; and severe abdominal cramping ⁵.

The most common signs and symptoms of ulcerative colitis are diarrhea with blood or pus and abdominal pain and cramping.

Other signs and symptoms include:

• an urgent need to have a bowel movement (tenesmus)
• inability to defecate despite urgency
• feeling tired
• nausea or loss of appetite
• weight loss
• fever
• anemia—a condition in which the body has fewer red blood cells than normal
• rectal pain
• rectal bleeding — passing small amount of blood with stool
• in children, failure to grow

Less common symptoms include:

• joint pain or soreness
• eye irritation
• certain rashes.

Symptoms of ulcerative colitis flare-up

Some people may go for weeks or months with very mild symptoms, or none at all (known as remission), followed by periods where the symptoms are particularly troublesome (known as flare-ups or relapses).

During a ulcerative colitis flare-up, some people with ulcerative colitis also experience symptoms elsewhere in their body. For example, some people develop:

• painful and swollen joints (arthritis)
• mouth ulcers
• areas of painful, red and swollen skin
• irritated and red eyes

In severe cases, defined as having to empty your bowels six or more times a day, additional symptoms may include:

• shortness of breath
• a fast or irregular heartbeat
• a high temperature (fever)
• blood in your stools becoming more obvious

In most people, no specific trigger for flare-ups is identified, although a gut infection can occasionally be the cause. Stress is also thought to be a potential factor.

Ulcerative colitis diagnosis

The onset of symptoms can be sudden or gradual ¹¹. The presence of anemia, thrombocytosis (too many platelets in blood), or hypoalbuminemia (the level of albumin in the blood is abnormally low) may suggest inflammatory bowel disease, but most patients with ulcerative colitis will not have these abnormalities ¹². C-reactive protein (CRP) level and erythrocyte sedimentation rate are relatively insensitive for detecting ulcerative colitis and should not be relied on to exclude inflammatory bowel disease. At the time of diagnosis, fewer than one-half of patients with ulcerative colitis have abnormal findings on these tests ¹³.

Endoscopic biopsy is used to confirm the diagnosis ¹⁴.

Elevated fecal calprotectin and lactoferrin levels have been proven sensitive for the detection of inflammatory bowel disease, but using these tests to exclude patients from endoscopic examination delays diagnosis in 6 to 8 percent of patients ¹³. Tests for perinuclear antineutrophil cytoplasmic antibodies and anti– Saccharomyces cerevisiae antibodies are often positive in patients with ulcerative colitis, and can help distinguish the condition from Crohn’s disease in those with indeterminate histology ¹³. Approximately one-third of patients with ulcerative colitis have extraintestinal manifestations, which may be present even when the disease is inactive.

A health care provider diagnoses ulcerative colitis with the following:

• Medical and family history
• Physical exam
• Lab tests
• Endoscopies of the large intestine
• X-ray. If you have severe symptoms, your doctor may use a standard X-ray of your abdominal area to rule out serious complications, such as a perforated colon.
• CT scan. A CT scan of your abdomen or pelvis may be performed if your doctor suspects a complication from ulcerative colitis. A CT scan may also reveal how much of the colon is inflamed.
• Computerized tomography (CT) enterography and magnetic resonance (MR) enterography. Your doctor may recommend one of these noninvasive tests if he or she wants to exclude any inflammation in the small intestine. These tests are more sensitive for finding inflammation in the bowel than are conventional imaging tests. MR enterography is a radiation-free alternative.

The health care provider may perform a series of medical tests to rule out other bowel disorders, such as irritable bowel syndrome, Crohn’s disease, or celiac disease, that may cause symptoms similar to those of ulcerative colitis.

Lab Tests

A health care provider may order lab tests to help diagnose ulcerative colitis, including blood and stool tests.

• Blood tests. A blood test involves drawing blood at a health care provider’s office or a lab. A lab technologist will analyze the blood sample. A health care provider may use blood tests to look for:
  • anemia
  • inflammation or infection somewhere in the body
  • markers that show ongoing inflammation
  • low albumin, or protein—common in patients with severe ulcerative colitis
• Stool tests. A stool test is the analysis of a sample of stool. A health care provider will give the patient a container for catching and storing the stool at home. The patient returns the sample to the health care provider or to a lab. A lab technologist will analyze the stool sample. Health care providers commonly order stool tests to rule out other causes of GI diseases, such as infection.

Endoscopies of the Large Intestine

Endoscopies of the large intestine are the most accurate methods for diagnosing ulcerative colitis and ruling out other possible conditions, such as Crohn’s disease, diverticular disease, or cancer. Endoscopies of the large intestine include:

• Colonoscopy. A colonoscopy can show irritated and swollen tissue, ulcers, and abnormal growths such as polyps––extra pieces of tissue that grow on the inner lining of the intestine. If the gastroenterologist suspects ulcerative colitis, he or she will biopsy the patient’s colon and rectum. A biopsy is a procedure that involves taking small pieces of tissue for examination with a microscope.
• Flexible sigmoidoscopy. Flexible sigmoidoscopy is a test that uses a flexible, narrow tube with a light and tiny camera on one end, called a sigmoidoscope or scope, to look inside the rectum, the sigmoid colon, and sometimes the descending colon. In most cases, a patient does not need anesthesia. The health care provider will look for signs of bowel diseases and conditions such as irritated and swollen tissue, ulcers, and polyps.

Ulcerative colitis treatment

Ulcerative colitis treatment usually involves either drug therapy or surgery.

Several categories of drugs may be effective in treating ulcerative colitis. The type you take will depend on the severity of your condition. The drugs that work well for some people may not work for others, so it may take time to find a medication that helps you. In addition, because some drugs have serious side effects, you’ll need to weigh the benefits and risks of any treatment.

Figure 1. Ulcerative colitis treatment (recommended treatment approach)

[Source ¹⁵]

ACTIVE DISEASE

For active disease distal to the descending colon, topical 5-aminosalicylic acid (5-ASA), including suppository and enema formulations, is the preferred treatment ¹⁶. Topical 5-ASA is more effective than oral 5-ASA or topical corticosteroid foams or enemas. Suppositories are effective for proctitis, whereas enemas are effective for disease that reaches as proximally as the splenic flexure ¹⁶. Topical mesalamine enemas, a common formulation of 5-ASA, induce remission in 72 percent of cases of active, left-sided ulcerative colitis within four weeks ¹⁷. Corticosteroid foams are also effective, although less so than 5-ASA. However, they may be easier to administer and more comfortable to retain ¹⁶. Oral 5-ASA is effective and may be preferred by patients who have difficulty with irritation or retaining topical formulations.18 A combination of oral and topical 5-ASA is superior to either formulation alone and should be used when other treatments are ineffective ¹⁸.

Oral 5-ASA is effective for mild to moderate active ulcerative colitis extending proximal to the sigmoid colon ¹⁹. If oral 5-ASA is ineffective, the addition of topical 5-ASA can be more effective than oral treatment alone ²⁰. A short-term course of oral corticosteroids may be effective if the disease does not respond to combination 5-ASA therapy, or for patients in whom a more rapid response is desired ²¹. Infliximab (Remicade), an intravenously administered monoclonal antibody to tumor necrosis factor-α, is effective for corticosteroid-refractory disease ²². A recent meta-analysis of studies of azathioprine (Imuran) for treatment of active ulcerative colitis showed no statistically significant effect ²³.

Patients with severe to fulminant disease can be divided into those who require urgent hospitalization and those who may receive a trial of outpatient treatment. Signs and symptoms that suggest the need for urgent hospitalization include severe pain, abdominal or colonic distension, gastrointestinal bleeding, and toxicity (e.g., fever, tachycardia, leukocytosis, anemia). In patients who do not require urgent hospitalization, a trial of maximal dosage combined oral/topical 5-ASA therapy is recommended in conjunction with oral corticosteroids. If symptoms do not improve and the patient still does not require urgent hospitalization, the addition of infliximab as outpatient therapy is another option ¹⁵.

For patients who do not improve on maximal outpatient medical management or who have signs of toxicity, hospital admission and administration of intravenous corticosteroids reduce morbidity and mortality ²⁴. If intravenous corticosteroids are ineffective after three to five days, intravenous cyclosporine (Sandimmune) or infliximab increases remission rates ²⁵.

For patients who do not improve with the addition of cyclosporine or infliximab, there is evidence that switching to the other agent may decrease the risk of colectomy; however, this is associated with an increased risk of infectious complications, and the decision should be individualized ²⁵. For patients with severe acute or chronic colitis who do not improve with medical therapy, surgical proctocolectomy is the next step. Proctocolectomy with ileal pouch-anal anastomosis is most common; however, permanent ileostomy is also an option. Other indications for surgery are exsanguinating hemorrhage, perforation, or carcinoma ¹⁵. A recent systematic literature review showed that 12 months after surgery, health-related quality of life and health status are equivalent to that in the general population ²⁶. Despite the potential benefits of surgery, complications are a concern. Colectomy is associated with a 54 percent reoperation rate for postsurgical complications ²⁷. Pouchitis (inflammatory disease of the ileal pouchanal anastomosis pouch of unknown etiology) is also common ²⁷.

MAINTENANCE

Once remission is induced, the same agent is usually used to maintain remission. 5-ASA suppositories and enemas are effective for maintenance of distal disease ²⁸. Oral 5-ASA is effective for extensive colitis.21 As with active disease, combined oral/topical therapy is more effective in maintaining remission than either agent alone ²⁹. Corticosteroids are not effective in maintaining remission and have potentially serious adverse effects with long-term use ³⁰. They should not be used for maintenance therapy. Azathioprine is an option for patients who require corticosteroids or cyclosporine for induction of remission or in whom remission is not adequately maintained with 5-ASA. However, it usually takes several months before it reaches full effect ³¹. For patients in whom remission was induced using infliximab, the same agent may be continued as maintenance therapy ²².

Ulcerative colitis medications

While no medication cures ulcerative colitis, many can reduce symptoms.

The goals of medication therapy are:

• inducing and maintaining remission
• improving the person’s quality of life

Many people with ulcerative colitis require medication therapy indefinitely, unless they have their colon and rectum surgically removed.

Table 1. Ulcerative Colitis medications 

Medication (form)	Dosage for active disease	Maintenance dosage	Adverse effects
Sulfasalazine (Azulfidine; oral)	4 to 6 g per day in 4 divided doses	2 to 4 g per day	Headache,† interstitial nephritis, nausea, vomiting
5-Aminosalicylic acid (oral)	2 to 4.8 g per day in 3 divided doses‡	1.2 to 2.4 g per day	Interstitial nephritis
5-Aminosalicylic acid (suppository)	1,000 mg once per day	500 mg once or twice per day	Anal irritation, discomfort
5-Aminosalicylic acid (enema)	1 to 4 g per day	2 to 4 g daily to every third day	Difficulty retaining, rectal irritation
Hydrocortisone (enema)	100 mg	Not recommended	Difficulty retaining, rectal irritation
Hydrocortisone (10% foam)	90 mg once or twice per day	Not recommended	Rectal irritation
Prednisone (oral)	40 to 60 mg per day until clinical improvement, then taper by 5 to 10 mg per week	Not recommended	Adrenal suppression, bone disease,§ cataracts, cushingoid features, glaucoma, impaired wound healing, infections, metabolic abnormalities, peptic ulcers, psychiatric disturbances
Methylprednisolone (Solu-Medrol; IV)	40 to 60 mg per day	Not recommended
Infliximab (Remicade; IV)	5 to 10 mg per kg on weeks 0, 2, and 6	5 to 10 mg per kg every 4 to 8 weeks	Increased risk of infection and lymphoma, infusion reaction
Azathioprine (Imuran; oral)	Not recommended	1.5 to 2.5 mg per kg per day||	Allergic reactions, bone marrow suppression, infection, pancreatitis
Cyclosporine (Sandimmune; IV)	2 to 4 mg per kg per day	Not recommended	Infection, nephrotoxicity, seizures
Lactobacillus GG (oral)	Not recommended	18 × 109 viable bacteria per day	Minimal
Escherichia coli Nissle 1917 (Mutaflor¶; oral)	Not recommended	2.5 to 25 × 109 viable bacteria per day	Minimal

Anti-inflammatory drugs

Anti-inflammatory drugs are often the first step in the treatment of ulcerative colitis. They include:

• 5-aminosalicylates. Examples of this type of medication include sulfasalazine (Azulfidine), mesalamine (Asacol HD, Delzicol, others), balsalazide (Colazal) and olsalazine (Dipentum). Which one you take, and whether it is taken by mouth or as an enema or suppository, depends on the area of your colon that’s affected.
• Corticosteroids. These drugs, which include prednisone and hydrocortisone, are generally reserved for moderate to severe ulcerative colitis that doesn’t respond to other treatments. Due to the side effects, they are not usually given long term.

Immune system suppressors

These drugs also reduce inflammation, but they do so by suppressing the immune system response that starts the process of inflammation. For some people, a combination of these drugs works better than one drug alone.

Immunosuppressant drugs include:

• Azathioprine (Azasan, Imuran) and mercaptopurine (Purinethol, Purixan). These are the most widely used immunosuppressants for treatment of inflammatory bowel disease. Taking them requires that you follow up closely with your doctor and have your blood checked regularly to look for side effects, including effects on the liver and pancreas.
• Cyclosporine (Gengraf, Neoral, Sandimmune). This drug is normally reserved for people who haven’t responded well to other medications. Cyclosporine has the potential for serious side effects and is not for long-term use.
• Infliximab (Remicade), adalimumab (Humira) and golimumab (Simponi). These drugs, called tumor necrosis factor (TNF) inhibitors, or biologics, work by neutralizing a protein produced by your immune system. They are for people with severe ulcerative colitis who don’t respond to or can’t tolerate other treatments.
• Vedolizumab (Entyvio). This medication was recently approved for treatment of ulcerative colitis for people who don’t respond to or can’t tolerate other treatments. It works by blocking inflammatory cells from getting to the site of inflammation.

Other medications

You may need additional medications to manage specific symptoms of ulcerative colitis. Always talk with your doctor before using over-the-counter medications.

He or she may recommend one or more of the following:

• Antibiotics. People with ulcerative colitis who run fevers will likely take antibiotics to help prevent or control infection.
• Anti-diarrheal medications. For severe diarrhea, loperamide (Imodium) may be effective. Use anti-diarrheal medications with great caution and after talking with your doctor, because they may increase the risk of toxic megacolon (enlarged colon).
• Pain relievers. For mild pain, your doctor may recommend acetaminophen (Tylenol, others) — but not ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve), and diclofenac sodium (Voltaren), which can worsen symptoms and increase the severity of disease.
  Iron supplements. If you have chronic intestinal bleeding, you may develop iron deficiency anemia and be given iron supplements.

Surgery

Surgery can often eliminate ulcerative colitis. But that usually means removing your entire colon and rectum (proctocolectomy).

In most cases, this involves a procedure called ileal pouch anal anastomosis. This procedure eliminates the need to wear a bag to collect stool. Your surgeon constructs a pouch from the end of your small intestine. The pouch is then attached directly to your anus, allowing you to expel waste relatively normally.

In some cases a pouch is not possible. Instead, surgeons create a permanent opening in your abdomen (ileal stoma) through which stool is passed for collection in an attached bag.

Cancer surveillance

Patients with ulcerative colitis have an increased risk of colorectal cancer. You will need more-frequent screening for colon cancer because of your increased risk. The recommended schedule will depend on the location of your disease and how long you have had it.

If your disease involves more than your rectum, you will require a surveillance colonoscopy every one to two years. Additionally, random biopsies spaced at regular intervals throughout the colon are recommended every one to two years during screening colonoscopies. Patients with proctitis or proctosigmoiditis do not seem to be at increased risk of cancer ¹⁵. You will need a surveillance colonoscopy beginning as soon as eight years after diagnosis if the majority of your colon is involved, or 15 years if only the left side of your colon is involved.

Foods to avoid with ulcerative colitis

Sometimes you may feel helpless when facing ulcerative colitis. But changes in your diet and lifestyle may help control your symptoms and lengthen the time between flare-ups.

There’s no studies have suggested that diet can either cause or treat ulcerative colitis and there is no specific diet that patients with ulcerative colitis should follow, though it is advisable to eat a balanced diet ³³. Likewise, there is no convincing evidence that ulcerative colitis results from food allergies. But certain foods and beverages can aggravate your signs and symptoms, especially during a flare-up.

It can be helpful to keep a food diary to keep track of what you’re eating, as well as how you feel. If you discover that some foods are causing your symptoms to flare, you can try eliminating them. Here are some suggestions that may help:

Foods to limit or avoid

• Limit dairy products. Many people with inflammatory bowel disease find that problems such as diarrhea, abdominal pain and gas improve by limiting or eliminating dairy products. You may be lactose intolerant — that is, your body can’t digest the milk sugar (lactose) in dairy foods. Using an enzyme product such as Lactaid may help as well.
• Limit fiber, if it’s a problem food. If you have inflammatory bowel disease, high-fiber foods, such as fresh fruits and vegetables and whole grains, may make your symptoms worse. If raw fruits and vegetables bother you, try steaming, baking or stewing them.

In general, you may have more problems with foods in the cabbage family, such as broccoli and cauliflower, and nuts, seeds, corn and popcorn.
Avoid other problem foods. Spicy foods, alcohol and caffeine may make your signs and symptoms worse.

Low-residue diet

Temporarily eating a low-residue or low-fiber diet can sometimes help improve symptoms of ulcerative colitis during a flare-up. These diets are designed to reduce the amount and frequency of the stools you pass.

Examples of foods that can be eaten as part of a low-residue diet include:

• white bread
• refined (non-wholegrain) breakfast cereals, such as cornflakes
• white rice, refined pasta and noodles
• cooked vegetables (but not the peel, seeds or stalks)
• lean meat and fish
• eggs

If you’re considering trying a low-residue diet, make sure you talk to your care team first.

Other dietary measures

• Eat small meals. You may find you feel better eating five or six small meals a day rather than two or three larger ones.
• Drink plenty of liquids. Try to drink plenty of fluids daily. Water is best. Alcohol and beverages that contain caffeine stimulate your intestines and can make diarrhea worse, while carbonated drinks frequently produce gas.
• Talk to a dietitian. If you begin to lose weight or your diet has become very limited, talk to a registered dietitian.

Ulcerative colitis diet

In studies involving people with chronic inflammatory bowel diseases (IBD) like Crohn’s disease and ulcerative colitis, the anti-Inflammatory diet (IBD-AID) has been used as an adjunct dietary therapy for the treatment of inflammatory bowel diseases (IBD) ³⁴. The goal of the anti-Inflammatory diet (IBD-AID) is to assist with a decreased frequency and severity of flares, obtain and maintain remission in people with inflammatory bowel diseases (IBD). Dysbiosis, or altered bacterial flora, is one of the theories behind the development of anti-Inflammatory diet (IBD-AID), in that certain carbohydrates in the lumen of the gut provide pathogenic bacteria a substrate on which to proliferate ³⁵, ³⁶.

The anti-Inflammatory diet (IBD-AID) has five basic components:

1. The first of which is the modification of certain carbohydrates, (including lactose, and refined or processed complex carbohydrates)
2. The second places strong emphasis on the ingestion of pre- and probiotics (e.g.; soluble fiber, leeks, onions, and fermented foods) to help restore the balance of the intestinal flora ³⁷, ³⁸, ³⁹
3. The third distinguishes between saturated, trans, mono- and polyunsaturated fats ⁴⁰, ⁴¹,
4. The fourth encourages a review of the overall dietary pattern, detection of missing nutrients, and identification of intolerances.
5. The last component modifies the textures of the foods (e.g.; blenderized, ground, or cooked) as needed (per patient symptomology) to improve absorption of nutrients and minimize intact fiber.

The phases indicated in Table 2 are examples of the modification of texture complexity, so that dietitian and patient can expand the diet as the patient’s tolerance and absorption improves. Some sensitivities common to many patients (not just those with IBD), are eased through supplementation of digestive enzymes or avoidance. A senior dietitian advised the patient and either family or spouse regarding the details of the diet during regular clinic visits. Patients taking supplements (probiotics, vitamin/minerals, omega-3 fatty acids) were advised to continue or discontinue, depending on the needs of the individual and the dietary intake ⁴².

The anti-Inflammatory diet (IBD-AID) consists of lean meats, poultry, fish, omega-3, eggs, particular sources of carbohydrate, select fruits and vegetables, nut and legume flours, limited aged cheeses (made with active cultures and enzymes), fresh cultured yogurt, kefir, miso and other cultured products (rich with certain probiotics) and honey. Prebiotics, in the form of soluble fiber (containing beta-glucans and inulin, such as bananas, oats, blended chicory root, and flax meal) are suggested. In addition, the patient is advised to begin at a texture phase of the diet matching with symptomology, starting with phase one if in an active flare. Many patients require foods to be softened and textures mechanically altered by pureeing the foods, and avoiding foods with stems and seeds when starting the diet (see phases 1–3 of Table 2), as intact fiber can be problematic for those with strictures and highly active mucosal inflammation. Some patients will require lifelong avoidance of intact fiber. Food irritants are not limited to intact fiber, but may include certain foods, processing agents and flavorings to which IBD patients may be reactive.

Table 2. The Anti-Inflammatory Diet (IBD-AID) Food Phase chart

Phase type	Phase I	Phase II	Phase III	Phase IV
	Soft, well-cooked or cooked then pureed foods, no seeds	Soft Textures: well-cooked or pureed foods, no seeds, choose floppy or tender foods	May still need to avoid stems, choose floppy greens or other greens depending on individual tolerance	If in remission with no strictures
Vegetables	Butternut Squash, Pumpkin, Sweet Potatoes, Onions	Carrots, Zucchini, Eggplant, Peas, Snow peas, Spaghetti squash, Green beans, Yellow beans, Microgreens (2 week old baby greens), Watercress, Arugula, Fresh flat leaf parsley and cilantro, Seaweed, Algae	Butter lettuce, Baby spinach, Peeled cucumber, Olives, Leeks Bok Choy, Bamboo shoots, Collard greens, Beet greens, Sweet peppers, Kale, Fennel bulb	Artichokes, Asparagus, Tomatoes, Lettuce, Brussels sprouts, Beets, Cabbage, Kohlrabi, Rhubarb, Pickles, Spring onions, Water chestnuts, Celery, Celeriac, Cauliflower, Broccoli, Radish, Green pepper, Hot pepper
	Pureed vegetables: Mushrooms, Phase II vegetables (pureed)	Pureed vegetables: all except cruciferous	Pureed vegetables: all from Phase IV, Kimchi
Fruits	Banana, Papaya, Avocado, Pawpaw	Watermelon (seedless), Mangoes, Honeydew, Cantaloupe, May need to be cooked: Peaches, Plums, Nectarines, Pears, (Phase III fruits are allowed if pureed and seeds are strained out)	Strawberries, Cranberries, Blueberries, Apricots, Cherries, Coconut, Lemons, Limes, Kiwi, Passion fruit, Blackberries, Raspberries, Pomegranate (May need to strain seeds from berries)	Grapes, Grapefruit, Oranges, Currants, Figs, Dates, Apples (best cooked), Pineapple, Prunes
Meats and fish	All fish (no bones), Sardines (small bones ok), Turkey and ground beef, Chicken, Eggs	Scallops	Lean cuts of Beef, Lamb, Duck, Goose	Shrimp, Prawns, Lobster
Non dairy unsweetened	Coconut milk, Almond milk, Oat milk, Soy milk
Dairy, unsweetened	Yogurt, Kefir	Farmers cheese (dry curd cottage cheese), Cheddar cheese	Aged cheeses
Nuts/Oils/Legumes/Fats	Miso (refrigerated), Tofu, Olive oil, Canola oil, Flax oil, Hemp oil, Walnut oil, Coconut oil	Almond flour, Peanut flour, Soy flour, Sesame oil, Grapeseed oil, Walnut oil, Pureed nuts, Safflower oil, Sunflower oil	Whole nuts, Soybeans, Bean flours, Nut butters, Well-cooked lentils (pureed), Bean purees (e.g. hummus)	Whole beans and lentils
Grains	Ground flax or Chia Seeds (as tolerated)	Steel cut oats (well-cooked as oatmeal)	Rolled well-cooked oats
Spices	Basil, Sage, Oregano, Salt, Nutmeg, Cumin, Cinnamon, Turmeric, Saffron, Mint, Bay leaves, Tamari (wheat free soy sauce), Fenugreek tea, Fennel tea, Vanilla	Dill, Thyme, Rosemary Tarragon, Cilantro, Basil, Parsley	Mint, Ginger, Garlic (minced), Paprika, Chives, Daikon, Mustard	Wasabi, Tamarind, Horseradish, Fenugreek, Fennel
Sweeteners	Stevia, Maple syrup, Honey (local), Unsweetened fruit juice	Lemon and lime juice
Misc.	Capsule or liquid supplements, Cocoa powder	Baking powder (no cornstarch), Baking soda, Unflavored gelatin	Ghee, Light mayonnaise, Vinegar	Ketchup (sugar free), Hot sauce (sugar free)

[Source ³⁴]

Stress relief

Although stress doesn’t cause inflammatory bowel disease, it can make your signs and symptoms worse and may trigger flare-ups.

Successfully managing stress levels may reduce the frequency of symptoms. The following advice may help:

To help control stress, try:

• Exercise. Even mild exercise can help reduce stress, relieve depression and normalize bowel function. Talk to your doctor about an exercise plan that’s right for you.
• Biofeedback. This stress-reduction technique helps you reduce muscle tension and slow your heart rate with the help of a feedback machine. The goal is to help you enter a relaxed state so that you can cope more easily with stress.
• Regular relaxation and breathing exercises. An effective way to cope with stress is to perform relaxation and breathing exercises. You can take classes in yoga and meditation or practice at home using books, CDs or DVDs.

Emotional impact

Living with a long-term condition that is as unpredictable and potentially debilitating as ulcerative colitis can have a significant emotional impact.

In some cases, anxiety and stress caused by ulcerative colitis can lead to depression. Signs of depression include feeling very down, hopeless and no longer taking pleasure in activities you used to enjoy. If you think you might be depressed, contact your doctor for advice.

You may also find it useful to talk to others affected by ulcerative colitis, either face-to-face or via the internet. Crohn’s and Colitis Foundation ⁴³ is a good resource, with details of local support groups and a large range of useful information on ulcerative colitis and related issues.

Alternative medicine

Many people with digestive disorders have used some form of complementary and alternative therapy.

Some commonly used therapies include:

• Herbal and nutritional supplements. The majority of alternative therapies aren’t regulated by the FDA. Manufacturers can claim that their therapies are safe and effective but don’t need to prove it. What’s more, even natural herbs and supplements can have side effects and cause dangerous interactions. Tell your doctor if you decide to try any herbal supplement.
• Probiotics. Researchers suspect that adding more of the beneficial bacteria (probiotics) that are normally found in the digestive tract might help combat the disease ⁴⁴. Lactobacillus GG and Escherichia coli Nissle 1917 (Mutaflor) have been shown to be as effective as 5-ASA for maintenance therapy ⁴⁵, ⁴⁶. Although research is limited, there is some evidence that adding probiotics along with other medications may be helpful, but this has not been proved.
• Fish oil. Fish oil acts as an anti-inflammatory, and there is some evidence that adding fish oil to aminosalicylates may be helpful, but this has not been proved.
• Aloe vera. Aloe vera gel may have an anti-inflammatory effect for people with ulcerative colitis, but it can also cause diarrhea.
• Acupuncture. Only one clinical trial ⁴⁷ has been conducted regarding its benefit. The procedure involves the insertion of fine needles into the skin, which may stimulate the release of the body’s natural painkillers.
• Turmeric. Curcumin, a compound found in the spice turmeric, has been combined with standard ulcerative colitis therapies in clinical trials. There is some evidence of benefit, but more research is needed.
• Wheatgrass has also shown some effectiveness in reducing symptoms of active disease ⁴⁸.

1. Talley NJ, Abreu MT, Achkar JP, et al.; American College of Gastroenterology IBD Task Force. An evidence-based systematic review on medical therapies for inflammatory bowel disease. Am J Gastroenterol. 2011;106(suppl 1):S2–S25.[↩][↩][↩][↩][↩]
2. Herrinton LJ, Liu L, Lewis JD, Griffin PM, Allison J. Incidence and prevalence of inflammatory bowel disease in a Northern California managed care organization, 1996–2002. Am J Gastroenterol. 2008;103(8):1998–2006.[↩]
3. Vavricka SR, Brun L, Ballabeni P, et al. Frequency and risk factors for extraintestinal manifestations in the Swiss inflammatory bowel disease cohort. Am J Gastroenterol. 2011; 106(1):113.[↩]
4. Inflammatory bowel disease (IBD). Centers for Disease Control and Prevention www.cdc.gov/ibd[↩]
5. Shanahan F. Ulcerative colitis. In: Hawkey CJ, Bosch J, Richter JE, Garcia-Tsao G, Chan FKL, eds. Textbook of Clinical Gastroenterology and Hepatology. 2nd ed. Oxford: Wiley-Blackwell; 2012: 355–371.[↩][↩][↩][↩]
6. Bengtson MB, Aamodt G, Vatn MH, Harris JR. Concordance for IBD among twins compared to ordinary siblings—a Norwegian population-based study. J Crohns Colitis. 2010;4(3):312–318.[↩]
7. Ko Y, Butcher R, Leong RW. Epidemiological studies of migration and environmental risk factors in the inflammatory bowel diseases. World Journal of Gastroenterology. 2014;20(5):1238–1247.[↩]
8. Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol. 2011;106(4):563–573.[↩]
9. Jess T, Simonsen J, Nielsen NM, et al. Enteric Salmonella or Campylobacter infections and the risk of inflammatory bowel disease. Gut. 2011;60(3):318–324.[↩]
10. Noor SO, Ridgway K, Scovell L, et al. Ulcerative colitis and irritable bowel patients exhibit distinct abnormalities of the gut microbiota. BMC Gastroenterol. 2010;10:134.[↩]
11. Sawczenko A, Sandhu BK. Presenting features of inflammatory bowel disease in Great Britain and Ireland. Arch Dis Child. 2003;88(11):995–1000.[↩]
12. Solem CA, Loftus EV Jr, Tremaine WJ, Harmsen WS, Zinsmeister AR, Sandborn WJ. Correlation of C-reactive protein with clinical, endoscopic, histologic, and radiographic activity in inflammatory bowel disease. Inflamm Bowel Dis. 2005;11(8):707–712.[↩]
13. Lewis JD. The utility of biomarkers in the diagnosis and therapy of inflammatory bowel disease. Gastroenterology. 2011;140(6):1817–1826.e2.[↩][↩][↩]
14. Turkay C, Kasapoglu B. Noninvasive methods in evaluation of inflammatory bowel disease: where do we stand now? An update. Clinics (Sao Paulo). 2010;65(2):221–231.[↩]
15. Kornbluth A, Sachar DB; Practice Parameters Committee of the American College of Gastroenterology. Ulcerative colitis practice guidelines in adults. Am J Gastroenterol. 2010;105(3):501–523.[↩][↩][↩][↩]
16. Marshall JK, Thabane M, Steinhart AH, Newman JR, Anand A, Irvine EJ. Rectal 5-aminosalicylic acid for induction of remission in ulcerative colitis Cochrane Database Syst Rev. 2010;(1):CD004115.[↩][↩][↩]
17. Cohen RD, Woseth DM, Thisted RA, Hanauer SB. A meta-analysis and overview of the literature on treatment options for left-sided ulcerative colitis and ulcerative proctitis. Am J Gastroenterol. 2000;95(5):1263–1276.[↩]
18. Safdi M, DeMicco M, Sninsky C, et al. A double-blind comparison of oral versus rectal mesalamine versus combination therapy in the treatment of distal ulcerative colitis. Am J Gastroenterol. 1997;92(10):1867–1871.[↩]
19. Ford AC, Achkar JP, Khan KJ, et al. Efficacy of 5-aminosalicylates in ulcerative colitis: systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):601–616.[↩]
20. Marteau P, Probert CS, Lindgren S, et al. Combined oral and enema treatment with Pentasa (mesalazine) is superior to oral therapy alone in patients with extensive mild/moderate active ulcerative colitis: a randomised, double blind, placebo controlled study. Gut. 2005;54(7):960–965.[↩]
21. Ford AC, Bernstein CN, Khan KJ, et al. Glucocorticosteroid therapy in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):590–599.[↩]
22. Ford AC, Sandborn WJ, Khan KJ, Hanauer SB, Talley NJ, Moayyedi P. Efficacy of biological therapies in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):644–659.[↩][↩]
23. Khan KJ, Dubinsky MC, Ford AC, Ullman TA, Talley NJ, Moayyedi P. Efficacy of immunosuppressive therapy for inflammatory bowel disease: a systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):630–642.[↩]
24. Turner D, Walsh CM, Steinhart AH, Griffiths AM. Response to corticosteroids in severe ulcerative colitis: a systematic review of the literature and a meta-regression. Clin Gastroenterol Hepatol. 2007;5(1):103–110.[↩]
25. Leblanc S, Allez M, Seksik P, et al.; GETAID. Successive treatment with cyclosporine and infliximab in steroid-refractory ulcerative colitis. Am J Gastroenterol. 2011;106(4):771–777.[↩][↩]
26. Heikens JT, de Vries J, van Laarhoven CJ. Quality of life, health-related quality of life and health status in patients having restorative proctocolectomy with ileal pouch-anal anastomosis for ulcerative colitis: a systematic review. Colorectal Dis. 2012;14(5):536–544.[↩]
27. Loftus EV Jr, Delgado DJ, Friedman HS, Sandborn WJ. Colectomy and the incidence of postsurgical complications among ulcerative colitis patients with private health insurance in the United States. Am J Gastroenterol. 2008;103(7):1737–1745.[↩][↩]
28. Hanauer S, Good LI, Goodman MW, et al. Long-term use of mesalamine (Rowasa) suppositories in remission maintenance of ulcerative proctitis. Am J Gastroenterol. 2000;95(7):1749–1754.[↩]
29. d’Albasio G, Pacini F, Camarri E, et al. Combined therapy with 5-ami-nosalicylic acid tablets and enemas for maintaining remission in ulcerative colitis: a randomized double-blind study. Am J Gastroenterol. 1997;92(7):1143–1147.[↩]
30. Regueiro M, Loftus EV Jr, Steinhart AH, Cohen RD. Medical management of left-sided ulcerative colitis and ulcerative proctitis: critical evaluation of therapeutic trials. Inflamm Bowel Dis. 2006;12(10):979–994.[↩]
31. Khan KJ, Dubinsky MC, Ford AC, Ullman TA, Talley NJ, Moayyedi P. Efficacy of immunosuppressive therapy for inflammatory bowel disease: a systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):630–642.[↩]
32. Ulcerative Colitis. Am Fam Physician. 2013 May 15;87(10):699-705. https://www.aafp.org/afp/2013/0515/p699.html[↩]
33. Ulcerative Colitis. http://patients.gi.org/topics/ulcerative-colitis/[↩]
34. Olendzki BC, Silverstein TD, Persuitte GM, Ma Y, Baldwin KR, Cave D. An anti-inflammatory diet as treatment for inflammatory bowel disease: a case series report . Nutrition Journal. 2014;13:5. doi:10.1186/1475-2891-13-5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896778/[↩][↩]
35. Vermeire S, Schreiber S, Sandborn WJ, Dubois C, Rutgeerts P. Correlation between the Crohn’s disease activity and Harvey-Bradshaw indices in assessing Crohn’s disease severity. Clin Gastroenterol Hepatol. 2010;8:357–363. doi: 10.1016/j.cgh.2010.01.001. https://www.ncbi.nlm.nih.gov/pubmed/20096379[↩]
36. Bosscher D, Breynaert A, Pieters L, Hermans N. Food-based strategies to modulate the composition of the intestinal microbiota and their associated health effects. J Physiol Pharmacol. 2009;60(Suppl 6):5–11. https://www.ncbi.nlm.nih.gov/pubmed/20224145[↩]
37. Jia W, Whitehead RN, Griffiths L, et al. Is the abundance of Faecalibacterium prausnitzii relevant to Crohn’s disease? Ross F, ed. Fems Microbiology Letters. 2010;310(2):138-144. doi:10.1111/j.1574-6968.2010.02057.x. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2962807/[↩]
38. McFarland LV. Systematic review and meta-analysis of Saccharomyces boulardii in adult patients. World Journal of Gastroenterology : WJG. 2010;16(18):2202-2222. doi:10.3748/wjg.v16.i18.2202. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2868213/[↩]
39. Lorea Baroja M, Kirjavainen PV, Hekmat S, Reid G. Anti-inflammatory effects of probiotic yogurt in inflammatory bowel disease patients. Clinical and Experimental Immunology. 2007;149(3):470-479. doi:10.1111/j.1365-2249.2007.03434.x. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219330/[↩]
40. Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol. 2011;106:563–573. doi: 10.1038/ajg.2011.44. https://www.ncbi.nlm.nih.gov/pubmed/21468064[↩]
41. Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutrition reviews. 2010;68:280–289. doi: 10.1111/j.1753-4887.2010.00287.x. https://www.ncbi.nlm.nih.gov/pubmed/20500789[↩]
42. Olendzki BC, Silverstein TD, Persuitte GM, Ma Y, Baldwin KR, Cave D. An anti-inflammatory diet as treatment for inflammatory bowel disease: a case series report. Nutrition Journal. 2014;13:5. doi:10.1186/1475-2891-13-5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896778/[↩]
43. Crohn’s & Colitis Foundation. http://www.crohnscolitisfoundation.org/what-are-crohns-and-colitis/what-is-ulcerative-colitis/[↩]
44. Mallon P, McKay D, Kirk S, Gardiner K. Probiotics for induction of remission in ulcerative colitis. Cochrane Database Syst Rev. 2007;(4):CD005573.[↩]
45. Zocco MA, dal Verme LZ, Cremonini F, et al. Efficacy of Lactobacillus GG in maintaining remission of ulcerative colitis. Aliment Pharmacol Ther. 2006;23(11):1567–1574.[↩]
46. Kruis W, Fric P, Pokrotnieks J, et al. Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine. Gut. 2004;53(11):1617–1623.[↩]
47. Joos S, Wildau N, Kohnen R, et al. Acupuncture and moxibustion in the treatment of ulcerative colitis: a randomized controlled study. Scand J Gastroenterol. 2006;41(9):1056–1063.[↩]
48. Ben-Arye E, Goldin E, Wengrower D, Stamper A, Kohn R, Berry E. Wheat grass juice in the treatment of active distal ulcerative colitis: a randomized double-blind placebo-controlled trial. Scand J Gastroenterol. 2002;37(4):444–449.[↩]