Ulcerative Colitis Blog

I am pleased to welcome you to the AGA Institute Ulcerative Colitis Weblog. The blog offers a unique opportunity for us to have an informal discussion of topics related to ulcerative colitis. While there are certain topics which I plan to cover, much of the dialogue will be directed by your comments and questions, so I look forward to hearing from you. Both Dr. McGreal and I will be posting weekly and we will address as many topics as possible. The goal is to advise and inform regarding this common and complex disease. We will, however, avoid making case specific recommendations regarding care, since optimal medical care can only be provided through a close relationship with a physician who has had an opportunity to review the patient’s entire case.

There are several questions we hear commonly from patients (not to mention family, friends, and absolute strangers). Here are a just a few:

1) What causes ulcerative colitis and why did I get it?

2) Is there any particular diet I should follow that could improve my symptoms?

3) How will ulcerative colitis affect my ability to have children?

4) Are all of these medications I am taking safe?

5) How long will I need to continue taking medication?

6) What is my risk of colon cancer?

These will act as a starting point for our dialogue. I look forward to your comments and questions, which will direct the route we will follow.

Welcome to the AGA Institute Ulcerative Colitis Weblog. This weblog has been created as an interactive resource for patients with ulcerative colitis (UC) to share their comments and questions about living life with inflammatory bowel disease (IBD). Our goal is to provide a forum where individuals can obtain factual, reliable information about UC while also feeling free to share their own insights into the disease. As a physician, I have found that some of the most valuable information I have learned has been taught to me by my patients. Based upon the comments and questions generated by patients on this site, we will be creating weekly postings to address the issues and topics that are of interest to those with UC.

With the summer season in full swing, many patients in the office have had questions about how manage their UC while enjoying the summer sun and traveling. Some tips for keeping healthy this summer:

1) Stay well hydrated especially during outdoor activities and long car/plane trips.

2) Medications such as prednisone, sulfasalazine, certain antibiotics, and methotrexate can
be associated with increased sensitivity to the sun. Wear sunblock with a minimum sun
protection factor (SPF) of 15.

3) Airline travel which involves sitting for long periods puts people at risk of developing blood
clots in the legs known at deep venous thromboses (DVTs). Patients with IBD have an
increased risk of developing clots due to the disease itself. It is recommended
that during long trips you move your legs by flexing your ankles or marching your
knees to promote circulation.

4) If you are traveling to a location with a high rate of gastrointestinal infections (ie;
Mexico, Central America), speak with your doctor about taking an antibiotic to prevent
travelers’ diarrhea or at least one to have on hand in the event you get sick. Remember that
some antibiotics can cause problems for patients with IBD, so it is best to discuss what the
appropriate medicine to take with you may be ahead of time.

5) Be careful about consuming fresh fruits and vegetables from street vendors that may
harbor bacteria like E. coli and can cause illness. Drink bottled water when traveling to
locations with high rates of gastrointestinal infections.

6) If you are going abroad to exotic locations such as Africa or parts of Southeast Asia which
require vaccinations prior to travel speak with your doctor. In general, most vaccines are safe
for patients with IBD, but certain “live agent” vaccines may be contraindicated for patients on
immune suppression.

I join Dr. Schwartz in looking forward to our discussions together this year.

One of the most common questions posed by patients about their disease is: Why did I get UC?

Our current understanding is that inflammatory bowel disease (IBD) develops in genetically susceptible individuals when they are exposed to an environmental trigger that sets off an exuberant inflammatory cascade. Although most people with a new diagnosis of IBD do not have a family history, there is compelling evidence for a genetic contribution to this disease, further supported by the discovery of genes associated with IBD in the last five years. Approximately 5-25% of patients with IBD report having a family member who also has IBD (either Crohn’s disease or UC). Siblings of patients with UC are 5-15 times more likely to develop IBD than individuals without an affected brother or sister. Studies of identical twins have shown that if one twin has UC, there is a 10-20% probability of the other twin also developing UC. With regard to fraternal twins, however, the risk is the same as that for non-twin siblings. If one parent has UC, the chance of his/her child developing IBD is about 5%. In the special instance that both parents have IBD, the likelihood of their children having IBD increases to about 30% by age 28. Research has shown that there is concordance (similarity) of disease type among family members. That is, within families with one or more family members affected by IBD, individuals are likely to have the same form of disease as one another (Crohn’s disease or UC). Some studies have suggested that individuals with a family history of IBD may have earlier disease onset compared to individuals without affected family members.

Other factors influencing genetic risk include ethnic/racial background. The highest rates of IBD are found in Caucasian individuals, especially those of Jewish heritage. Among Jewish sub-groups, Ashkenazi Jews have a 2 to 9 fold greater prevalence over non-Jewish counterparts. African Americans and Asians are believed to have a lower risk of IBD, although there appears to be a trend towards growing prevalence rates in these populations.

While investigators have identified a handful of genes which may play a role in UC, no single gene alone has been established as a cause. Research has shown that the genetics of IBD are complex, most likely involving interactions of multiple genes and environmental factors. It is hoped that a better understanding of the interplay between genes and the environment will help identify what triggers IBD and how we may either prevent or treat it more effectively.

The causes of ulcerative colitis are not yet known, but complex associations have been identified. As Dr. McGreal described, the role of genetics has been carefully studied, and exposures to infections, toxins, and foods have also been investigated.

Race/Ethnicity
It had been assumed for some time that whites were at a much higher risk of UC than blacks or Hispanics. However this conclusion has been called into question, and may have falsely arisen because natural history studies of UC had been performed in areas with very few minorities, such as Rochester, MN, Manitoba, Canada, and Scandinavia. Recent data has shown that the UC rates for blacks and Hispanics is more similar to whites than previously thought.

Socioeconomic Status
UC is predominantly a disease of the developed world, and even in underdeveloped nations it is more common in people of higher socioeconomic status. Some experts theorize that UC is caused by an infection. While people exposed to lots of germs during their youth develop tolerance to such “infections”, those not exposed until an older age may develop a vigorous unregulated immune response, and the disease we call “UC”.

Foods
There is no consistent evidence that any particular food, such as milk, carbohydrates, or alcohol, causes UC or UC flares, although many people with and without UC have symptoms caused by consuming certain foods, such as dairy, a result of lactose intolerance. Likewise, there is not conclusive evidence that a restricted diet can cure the disease or adequately control it long term.

Tobacco
Cigarette smoking plays a significant role in the development of UC. Smoking decreases the risk of ulcerative colitis by about 50%, but quitters have a jump in risk to almost twice the risk of the general population. Some former smokers with UC who do not respond well to medicines have an impressive response when they restart smoking (although we avoid recommending this for obvious reasons). Nicotine therapy with patches, pills and enemas has not been effective and limited by side effects, suggesting that the protective effect of smoking cigarettes may be a chemical other than nicotine.

Appendectomy
Patients who undergo appendectomy have a low rate of UC. While the removal of the appendix may decrease the amount of immune tissue in the intestine, appendectomy may be a marker of some other, unidentified, factor, which puts this group at lower risk.

While I do not recommend that we do away with indoor plumbing, start smoking, or have elective appendectomies just to decrease UC risk, it is one of many reasons that kids may use to justify a romp in the mud.

What is ulcerative colitis and how is it different from other types of colitis?

Colitis is a general term referring to inflammation of the colon. It is derived from col = colon, and itis = inflammation. There are several types of colitis, such as infectious, ulcerative, and microscopic. While all involve inflammation of the colon, they each have a different underlying cause. By analogy, you can liken this to arthritis (arth = joint and itis = inflammation) which is an umbrella term describing inflammation of the joints. Similar to colitis, there are many different forms of arthritis, such as osteoarthritis and rheumatoid arthritis. Therefore, you can think of colitis as an all-encompassing word that describes any type of inflammation of the colon.

UC is a specific form of colitis in which the body’s immune system becomes overactive and does not respond to normal signals to turn off inflammatory responses. The continued cascade of immune factors released in the body primarily targets the colon resulting in inflammation of that particular organ. It is for this reason you may hear people describe UC as an autoimmune disorder, or as the immune system attacking the colon. The cornerstone of UC treatment is medication which suppresses the overactive immune system, dampening it to a normal level of regulation.

UC is differentiated from other types of colitis such as infectious and microscopic colitis based upon patient history, laboratory tests, colonoscopy results, and pathology studies. Prior to making a diagnosis of UC, your doctor may perform blood tests, stool examinations, and endoscopies with tissue biopsies to help him or her sort out what type of colitis you have. It is important to distinguish the various types of colitis from one another as their treatments and prognoses are very different.

One of the first issues when a patient presents with symptoms suggestive of inflammatory bowel disease is to determine whether there is UC or Crohn disease (CD). There are many similarities and differences between UC and CD. There are also times when they cannot even be distinguished.

We are still learning about the underlying genetics and disease process of UC and CD, but the clinical signs, symptoms, and histopathology are well described.

Here are some of the key differences between UC and CD:

1. UC only affects the colon, while CD can involve any part of the gastrointestinal tract from the mouth to the anus. Most commonly, CD affects the terminal ileum (distal small intestine) and/or colon, less often proximal small bowel (5%), and <5% of patients have upper GI involvement (stomach/esophagus).

2. UC typically involves, and is most severe in, the rectum. There is circumferential and continuous involvement moving proximally. The severity of inflammation decreases more proximally until there is a transition to normal tissue. CD tends to spare the rectum and often has patchy involvement throughout the colon and small intestine with normal intervening mucosa.

3. The ulcers of UC are typically superficial, while those of CD, though usually superficial, are more likely to extend deeper and can even erode through the entire bowel wall.

4. Many patients with CD will develop strictures, fistulas, and abscesses in the abdomen or the anorectum. Since UC is not a transmural disease these complications are quite rare.

5. UC is strongly associated with primary sclerosing cholangitis (PSC), a disease causing strictures of the bile ducts in the liver. While only 5% of patients with UC have PSC, 50% of patients with PSC have UC. CD tends to cause kidney stones due to altered intestinal handling of oxalate.

Despite these differences, UC and CD are both autoimmune diseases, overactive immune responses against self. About 10% of the time CD can be difficult, or even impossible, to distinguish from UC, but does that even matter?