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Subject: Inflammatory Bowel Disease FAQ V3.0

This article was archived around: 20 May 2006 04:20:48 GMT

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All FAQs posted in: alt.support.crohns-colitis
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Archive-name: medicine/crohns-colitis-faq Posting-frequency: every two weeks Last-modified: 1997/3/15 Version: 3.0 URL: http://qurlyjoe.bu.edu/cduchome.html
Inflammatory Bowel Disease Frequently Asked Questions Version 3.0 This document was last modified on 3/15/1997 Introduction: ============ Alt.support.crohns-colitis was created in early 1994 as a forum where people suffering from ulcerative colitis, Crohn's Disease, and irritable bowel syndrome can share their everyday struggles with these illnesses, as well as discuss medicines, treatments, surgery, diet, health care providers, related illnesses, and anything else anyone can think of that relates to these diseases. In other words, this is the on-line equivalent of a support group, which means that no question is stupid and no condition embarrassing here. It also means we're all here to help each other out, so please be nice, be polite, and no flaming. Lastly, discussions of all types of medicine- conventional and alternative, Western and Eastern, your Aunt Harriet's home remedies, whatever- are welcome here. No one's figured out what causes these illnesses, no one's come up with a cure, and we need all the help we can get. If you have comments, suggestions, or corrections concerning the content of this FAQ, please contact me via email at khorgan@ucla.edu. Please do not send me email asking for help with your news reader (ask your system administrator) or to subscribe to a mailing list (I have no control over the usenet group or the IBDLIST mailing list) or anything unrelated to the content of this FAQ. Sorry. Copyright Notice: ================ Copyright 1997 by Kevin Horgan, M.D., Christopher Holmes and Michael Bloom. All rights reserved. See the end of this document for information on permission to use, copy and distribute. Disclaimer: ========== This FAQ is provided by the authors "as is". See end of document for complete disclaimer. Where to get this FAQ: ===================== This FAQ is posted twice a month to the alt.support.crohns-colitis, alt.answers, and news.answers newsgroups. It is also now archived at MIT and is available by anonymous ftp at rtfm.mit.edu and its mirrors (listed below). The file is, unfortunately, not found in a consistent place. It can be archived under the subject line of the post (Inflammatory_Bowel_Disease_FAQ_Vx.x) or under the archive name (crohn-colits-faq) note the misspelling. Some sites use UNIX compress so there may be a trailing .Z as well and you'll need a program to UN-compress it. Note that there are three other FAQ's, the Information Resources FAQ, the IBS FAQ and the Collagenous Colitis FAQ The Information Resources FAQ is also posted to alt.support.crohns-colitis twice a month and describes informational resources on IBD and IBS available either on the internet or elsewhere. It includes address and phone numbers of support organizations such as the Crohn's and Colitis Foundation of America (CCFA) and the United Ostomy Association (UOA), book titles and reviews, and WWW sites. The IBS FAQ deals with Irritable Bowel Syndrome, which has symptoms that can be similar to those of UC or CD. The Collagenous Colitis FAQ discusses a less typical form of IBD which also shares many of the symptoms of UC. For those with World Wide Web access, current versions of all these FAQs can be found at Bill Robertson's website, URL http://qurlyjoe.bu.edu/cduchome.html. Commonly-used abbreviations in this FAQ and on alt.support.crohns-colitis (a.s.c.-c): IBD inflammatory bowel disease- includes Crohn's Disease and ulcerative colitis IBS irritable bowel syndrome UC ulcerative colitis CD Crohn's Disease CCFA the Crohn's and Colitis Foundation of America CCFC Canadian Foundation for Ileitis and Colitis UOA the United Ostomy Association NSAID Non-steroidal, anti-inflammatory drug TPN Total parenteral nutrition GI Gastro-intestinal, i.e., pertaining to your digestive system ============================== 1.0 Digestive system primer 1.1 Q: What is Inflammatory Bowel Disease (IBD)? 1.1.1 Q: What is ulcerative colitis (UC)? 1.1.2 Q: What is Crohn's disease (CD)? 1.1.3 Q: What is ileitis? 1.1.4 Q: What is Crohn's colitis? 1.1.5 Q: What is ulcerative proctitis? 1.1.6 Q: What is Granulomatous colitis? 1.1.7 Q: What is Irritable Bowel Syndrome? 1.2 Q: What symptoms are experienced by IBD patients? 1.2.1 Q: What are extra-intestinal manifestations of these diseases? 1.2.2 Q: What other complications can occur? 1.2.3 Q: What is toxic megacolon? 1.2.4 Q: What are fistulas and abscesses? 1.2.5 Q: What are strictures? 1.2.6 Q: What is the cancer risk in IBD patients? Q: Are there other factors predisposing to the development of colon cancer? Q: Are there ways to reduce the risk of developing colon cancer? 1.3 Q: What are the causes of Crohn's disease and ulcerative colitis? 1.4 Q: Could IBD be an inherited condition? 1.5 Q: Who gets these diseases? 1.6 Q: Are there any factors that predispose to the development of UC and/or CD? 1.7 Q: Are there any factors that protect against the development of UC and/or CD? 1.8 Q: How is ulcerative colitis diagnosed? 1.8.1 Q: What are flexible sigmoidoscopy and colonoscopy? 1.9 Q: How is Crohn's disease diagnosed? 2.1 Q: What Drug therapies are used to treat IBD? 2.1.1 Q: What are 5-ASA Drugs? Q: What is Azulfidine? Q: What is Dipentum? Q: What is Asacol? Q: What is Salofalk? Q: What is Pentasa? Q: What is Balsalazide? Q: What is Rowasa? 2.1.2 What is Metronidazole? 2.1.3 Q: What is Ciprofloxacin? 2.1.4 Q: What is Clarithromycin (Biaxin)? 2.1.5 Q: What are adrenal corticosteroids (steroids), and when and why are they used? Q: What are the side effects from taking steroids? Q: What is meant by "Alternate Day Therapy"? What is Budesonide? What is ACTH? Q: What do steroids do to bones? Q: What should be done to minimize the damage done by steroids to bones when I am being treated for IBD? 2.1.6 Q: What are immunosuppressive drugs and when are they used? Q: What are Azathioprine and 6-MP? Q: What is Methotrexate? Q: What is Cyclosporine? 2.2 Q: Are any other drugs used to treat IBD? 2.2.1 Q: Are nicotine patches ever used to treat UC? 2.2.2 Q: What about antibodies against TNF (Tumor Necrosis Factor)? Q: What is Tumor Necrosis Factor or TNF? Q: Does TNF serve any useful function? Q: Is TNF important in IBD? just CD? what about UC? Q: What is this new anti-TNF treatment? Q: How does the anti-TNF treatment work? Q: Are there problems with the treatment? Q: What sort of patients are suitable candidates for treatment with anti-TNF antibody? Q: What are the alternatives available at present? 2.2.3 Q: What about Interleukin-10 (IL-10) therapy for CD? 2.2.4 Q: What about fish oil for therapy? 2.3 Q: Can different drugs be used together to treat IBD? 2.4 Q: Will I need to keep taking medications permanently? 3.1 Q: Drugs aren't working, what can surgery do for my UC? 3.1.1 Q: What's an ileostomy? 3.1.2 Q: What's a Continent Ileostomy? 3.1.3 Q: What's an Ileoanal Anastomosis, or Ileoanal Pull-Through? 3.2.4 Q: What can go wrong with these surgeries? 3.2 Q: Are there surgical treatments for Crohn's? 3.2.1 Q: What's a resection? 3.2.2 Q: After surgery for CD can anything be done to prevent it recurring again? 4.1 Q: What role does diet play in IBD? 4.1.1 Q: What is an elemental or astronaut diet? 4.1.2 Q: What is total parenteral nutrition? 4.1.3 Q: What is lactose intolerance? So what can I do about lactose intolerance? Q: So what can I do about lactose intolerance? 5.1 Q: What part does stress play in IBD? 5.2 Q: Can anything else cause a flare up? 6.1 Q: How can I make the most of my consultations with my physician? ============================================================================= 1.0 Digestive System Primer The Digestive System is a complex system of organs responsible for converting the food we eat into the nutrients which we require to fuel our metabolism. Here is a guide to the terminology used to describe the various components of the Digestive System. The Digestive System in essence consists of a long tube which connects the mouth to the anus. The term Gastrointestinal (GI) tract refers to the entire system. Once food leaves your mouth it enters the first part of the GI tract which is called the esophagus and then the stomach. The food passes relatively quickly into the stomach where it pauses and is churned up with acid into very small particles. It then passes into the small intestine which is about 20 feet long. The main function of the small intestine is to absorb nutrients from the food particles that arrive from the stomach. The food is digested with the assistance of secretions from the liver, gall bladder and pancreas. The term bowel is synomymous with intestine. The small intestine is therefore also referred to as small bowel. The small bowel has three parts; the part nearest the stomach is the duodenum, the next part is the jejunum and the third part that connects to the large intestine is the ileum. The last part of the ileum, known as the terminal ileum, is a frequent site of involvement in Crohn's disease. The large intestine is more frequently referred to as the colon. The first part of the colon is called the cecum and the appendix is found there. The main function of the colon is to absorb water from the processed food residue that arrives after the nutrients have been absorbed in the small intestine. The last part of the colon is the rectum which is a reservoir for feces. Feces are stored here until it is convenient for their expulsion and the sphincter muscles of the anus then relax. 1.1 Q: What is Inflammatory Bowel Disease? Inflammatory Bowel Disease (IBD) is an umbrella term referring to two chronic diseases that cause inflammation of the intestines: ulcerative colitis (UC) and Crohn's disease (CD). Though UC and CD are different diseases they do have features in common but there are important distinctions also. Frequently, the symptoms caused by UC and CD are similar. Both diseases are chronic and most frequently have their onset in early adult life. Some patients have alternating periods of relative health (remission) alternating with periods of disease (relapse or flare), while other patients have continuous symptoms from continued inflammation. Fortunately, as treatment has improved the proportion of people with continued symptoms appears to have diminished significantly . The severity of the diseases varies widely between individuals. Some suffer only mild symptoms, but others have severe and disabling symptoms. Some have a gradual onset of symptoms, some develop them suddenly. About half of patients have mild symptoms, the other half suffer frequent flare-ups. Medical science has not yet discovered a cause or cure, but numerous medications are now available to control symptoms with many more on the horizon. 1.1.1 Q: What is ulcerative colitis? Ulcerative colitis (UC) is an inflammatory disease of the large intestine, commonly called the colon. UC causes inflammation and ulceration of the inner lining of the colon and rectum. This inner lining is called the mucosa. Crohn's disease (CD) causes inflammation that extends into the deeper layers of the intestinal wall. The inflammation of UC is usually most severe in the rectal area with severity diminishing (at a rate that varies from patient to patient) toward the cecum, where the large and small intestine join. Significant deviations from this pattern may be a clue to the physician to suspect CD rather than UC. Such deviations may include either "skip areas" and/or "sparing of the rectum". Skip areas are patches of healthy tissue separating segments of diseased tissue. They are often seen in CD, but rarely in UC. Inflammation of the rectum is called proctitis. Inflammation of the sigmoid colon (located just above the rectum) is called sigmoiditis. Inflammation involving the entire colon is termed pan-colitis. The inflammation causes the colon to empty frequently resulting in diarrhea. As the lining of the colon is destroyed ulcers form releasing mucus, pus and blood. UC is relatively common in the western world and at least 250,000 in the United States alone have the disease. It occurs most frequently in people ages 15 to 30 although children and older people occasionally develop the disease. About 50% of patients are free of symptoms at any given time but the vast majority suffer at least one relapse in any 10 year period. Drug treatment is effective for about 70-80% of patients; surgery becomes necessary in the remaining 20-30%. 1.1.2 Q: What is Crohn's disease? Crohn's disease (CD) is an inflammatory process that can affect any portion of the digestive tract, but is most commonly seen (roughly half of all cases) in the last part of the small intestine otherwise called the terminal ileum and cecum. Altogether this area is also known as the ileocecal region. Other cases may affect one or more of: the colon only, the small bowel only (duodenum, jejunum and/or ileum), the anus, stomach or esophagus. In contrast with UC, CD usually doesn't affect the rectum, but frequently affects the anus instead. 1.1.3 Q: What is ileitis? This is CD of the ileum which is the third part of the small intestine. At one time, CD was thought to affect only the ileum, and for this reason the name "ileitis" was at one time synonymous with CD but now simply refers to CD of the ileum. 1.1.4 Q: What is Crohn's colitis? This is CD affecting part or all of the colon. This form comprises about 20% of all cases of CD. Various patterns are seen. In about half of these cases CD lesions may be seen throughout one continuous subsegment of the colon. In another quarter, skip areas are seen between multiple diseased areas. In the remaining quarter, the entire colon is involved, with no skip areas. Unlike UC, in which inflammation is usually confined to the inner mucosal surface, CD typically involves all layers of the affected tissues. 1.1.5 Q: What is ulcerative proctitis? Ulcerative proctitis is a form of UC that affects only the rectum. 1.1.6 Q: What is Granulomatous colitis? This is another name for Crohn's disease that affects the colon. 1.1.7 Q: What is Irritable Bowel Syndrome? This is *NOT* a variant of UC and Crohn's. UC and Crohn's disease are defined by the presence of inflammation in the intestine. There is no inflammation in the intestine in Irritable Bowel Syndrome. Irritable Bowel Syndrome (IBS) is also known as Functional Bowel Syndrome (FBS), Functional Bowel Disease (FBD) or spastic colon . Older terms for IBS are spastic or mucous colitis or even simply "colitis". These terms are no longer used because they cause people to confuse IBS with UC. IBS is characterized by a variety of symptom patterns which include diarrhea, constipation, alternating diarrhea/constipation and abdominal pain. Fever and/or bleeding are NOT features of IBS. IBS is much more common than CD or UC and many people with symptoms of IBS do not seek medical attention. Some patients with Crohns or UC can also have concurrent IBS. 1.2 Q: What symptoms are experienced by IBD patients? The most common symptom of both UC and CD is diarrhea, sometimes severe, that may require frequent visits to a toilet (in some cases up to 20 or more times a day). Abdominal cramps are often present, the severity of which may be correlated with the degree of diarrhea present. Blood may also appear in the stools, especially with UC. Fever, fatigue, and loss of appetite may accompany these symptoms (with consequent weight loss). At times, some UC and CD patients experience constipation during periods of active disease. In CD this can result from a partial obstruction usually of the small intestine. In UC constipation is most often a consequence of inflammation of the rectum (also known as proctitis); the colon has a nervous reaction and stasis of stool occurs upstream . Inflammation can affect gut nerves in such a way as to make the patient feel that there is stool present ready to be evacuated when there actually is not. That results in the symptom known as tenesmus where there is an uncomfortable urge to defecate but nothing comes out. The feeling of urgency to pass stool is a frequent consequence of proctitis also. Inability to retain stool is an extreme manifestation of urgency. It is important to bring these symptoms to the attention of your physician because they may improve dramatically with appropriate local therapy. Pain usually results from intestinal cramping or inflammation causing reflex irritability of the nerves and muscles that control intestinal contractions. Pain may also indicate the presence of severe inflammation or the development of a complication such as an abscess or a perforation of the intestinal wall. Generally, new onset pain or a significant change in the character of pain should be brought to the attention of your physician. The pain of CD is often in the lower right area of the abdomen. This is where the terminal ileum is located and pain there usually indicates inflammation of the terminal ileum. Location and intensity of abdominal pain vary from patient to patient, depending upon the location and type of disease in the affected tissues. Because of a phenomenon known as "referred pain", the location where pain is produced may not be the same as the location where it is experienced. 1.2.1 Q: What are extra-intestinal manifestations of these diseases? These are symptoms of IBD that occur outside of the digestive tract. Many IBD patients experience a wide variety of extra-intestinal manifestations of their disease. The most common is joint pain due to inflammation of the joints (arthritis). Others include various types of eye inflammation (iritis, conjunctivitis and episcleritis), skin inflammation (erythema nodosum and pyoderma gangrenosum) liver inflammation (hepatitis and sclerosing cholangitis). Other diseases and complications may be associated with IBD but less frequently. At present there is no satisfactory explanation for the occurence of these extra-intestinal complications of IBD. Some researchers consider them to be secondary to the primary disease, while others see both the extra-intestinal manifestations *and* the primary disease as symptoms of a "systemic" condition. Resolution of this will depend on clarification of the cause of IBD. 1.2.2 Q: What other complications can occur? Fatigue is the most common complication. Fever usually indicates active disease and/or a complication such as an abscess. Severe diarrhea, blood loss or infection can lead to rapid heartbeat and a drop in blood pressure. Continued loss of small amounts of blood in the stool (which may not be visible) may lead to anemia (reduced blood count); this may result in fatigue. CD frequently results in the development of fistulas which are abnormal connections between loops of intestine. These may even involve other organs such as the urinary bladder or open onto the skin. CD inflammation also frequently results in the formation of scar tissue with narrowed segments known as strictures. These strictures frequently cause bowel obstructions the symptoms of which will depend on the severity. The presence of a significant stricture is a common reason for surgery in CD. Hemorrhoid-like skin tags and anal fissures may also develop. Growth may be retarded in children with both forms of IBD and/or there may be a delay in the onset of puberty. 1.2.3 Q: What is toxic megacolon? Toxic megacolon is a severe dilation of the colon which occurs when inflammation spreads from the mucosa through the remaining layers of the colon. It is much more commonly a complication of UC though it can be seen occasionally in CD. The colon becomes paralyzed which can lead to it eventually bursting; this is known as a "perforation". Such perforation is a dire medical emergency with a 30% mortality rate. Many patients with toxic megacolon require surgery. Anyone with UC or CD serious enough to be at risk for toxic megacolon should be hospitalized and closely monitored. Warning signs include abdominal pain/tenderness, abdominal distention, fever, large numbers of stools with obvious blood and a rapid (more than 100/minute) pulse rate. Fortunately, this grave complication appears to be decreasing in frequency which probably reflects more effective treatment. Use of certain drugs (opiates, opioids and/or antispasmodics) may predispose to this complication. This is one of the reasons that these drugs should be used very carefully in both UC and CD. 1.2.4 Q: What are fistulas and abscesses? Fistulas are hollow tracts running from a part of one organ (such as the colon) to other organs, adjacent loops of bowel, and or the skin. They occur in CD as a result of deep ulceration. Fistulas between loops of bowel can interfere with nutrient absorption. This is especially true for fistulas between the small and large bowel. Fistulas can also become infected forming abscesses. Abscesses are collections of pus that may be accompanied by significant pain, and which can become life threatening emergencies. Simple treatment of abscesses resulting from fistulas can sometimes be accomplished via a procedure called "incision and drainage" (I/D), in which an incision is made, through which the abscess is drained. However this procedure does not deal with the underlying fistula which gave rise to the problem. Accordingly, a more elaborate procedure, known as a fistulectomy, is usually necessary for more definitive treatment. Fistulas are relatively common in CD patients and are very rare in patients with UC. 1.2.5 Q: What are strictures? Patients with CD in the small intestine may develop bowel obstructions which can result in severe cramps and vomiting. These obstructions can result from narrowing of the intestine due to inflammation as well as from scar tissue (stricture) from healed lesions. If the obstruction is a consequence of inflammation then it can usually be relieved by medical therapy such as steroids. However if the obstruction is due to a fibrous stricture then surgical resection may be necessary. In others, it may be possible to clear some of these obstructions via a technique known as stricturoplasty, which attempts to expand the narrowed segment of the intestine. Strictures can also occur in the large intestine, but are much less common. 1.2.6 Q: What is the cancer risk in IBD patients? For patients who have had UC longer than ten years, the risk of colon cancer is greater than that for comparable people without UC. There is data that suggests a risk of 5-10% at that point increasing to a range between 15 and 40% after 30 years, depending upon the particular study one looks at. If only the rectum and lower (sigmoid) colon are involved, the risk of cancer is not significantly increased. Patients that exhibit dysplasia (pre-cancerous changes in cells that can be detected by a biopsy) are at much higher risk. There is some data suggesting that the risk of colon cancer in patients with colonic CD is similar to that of UC patients with disease of similar extent. Other cancers, such as lymphoma or carcinoma of the small intestine or anus, may be slightly more common in Crohn's disease but the risk is not high. In the presence of longstanding (> 7-8 years) UC which involves more than the rectum and sigmoid colon or extensive Crohn's colitis then the consensus of informed medical opinion is that the patient should have a regular (yearly or every second year) screening colonoscopy to look for evidence of dysplasia. If that is found then the safest option is for a colectomy to be performed. This strategy does not guarantee that cancer can be avoided but seems to significantly increase the probability that it is not life threatening if and when it is detected. Q: Are there other factors predisposing to the development of colon cancer? Patients who have both UC and sclerosing cholangitis may be at even greater risk of developing colon cancer. Accordingly screening should be done with particular vigilance in these patients. There is also some data suggesting that low folic acid levels may predispose to the development of colon cancer in UC patients. Q: Are there ways to reduce the risk of developing colon cancer? The only certain way is to have a colectomy: in other words to have the colon removed surgically. However, there is circumstantial evidence that taking 5-ASA drugs drugs such as azulfidine [See Section 2.1.1] might reduce the risk of colon cancer also. Also there is some data that eating a diet rich in fruit and vegetables (five servings a day) and low in red meat is associated with a reduced risk of colon cancer in people without colitis. Regular exercise also seems to be associated with a reduced risk of colon cancer. These associations may also be true for UC and CD patients but they have not been studied. 1.3 Q: What are the causes of Crohn's disease and ulcerative colitis? The answer, unfortunately, is that no cause is yet known. 1.4 Q: Could IBD be an inherited condition? Many researchers believe these diseases may be result of an "inherited predisposition" combined with a triggering environmental agent (possibly a bacteria or a virus). There is no simple, predictable pattern of inheritance though there is certainly some evidence to suggest that heredity has some role to play. For example, when two immediate family members both have IBD, the most common combination is mother-child, followed by sibling-sibling, with father-child being least common. About 15 to 20% of people with IBD have immediate family members with IBD. Heredity factors seem to be more important in CD than UC. 1.5 Q: Who gets these diseases? Up to 2,000,000 Americans are estimated to suffer from IBD with males and females affected equally. The diseases can appear at any age, but the age at which patients are usually first diagnosed falls neatly onto a bell curve centered at about 24 years old, falling off quickly in the late teens and early thirties. However, there are also a significant number of patients in whom the diseases first occur in later life. There are significantly more cases in western Europe and North America than in other parts of the world. 1.6 Q: Are there any factors that predispose to the development of UC and/or CD? Smoking appears to enhance the likelihood of developing CD. 1.7 Q: Are there any factors that protect against the development of UC and/or CD? Smoking appears to protect against the development of UC. There is data that surprisingly few UC patients have had their appendix removed (appendectomy). This suggests that removal of the appendix may protect against the subsequent development of UC. There is no apparent relationship between appendectomy and CD. 1.8 Q: How is ulcerative colitis diagnosed? Diagnosis is made based on symptoms and the exclusion of other diseases by observation of typical findings at endoscopy and failure to find evidence of infection. The presence of often bloody diarrhea will prompt your doctor to perform an endoscopic examination; either a sigmoidoscopy and/or colonoscopy (described below). If inflammation is seen by these techniques, the physician will then attempt to rule out an infectious cause with stool cultures and blood tests. Usually it is possible to tell the difference between CD and UC but not always. Particularly, there may be some uncertainty between a diagnosis of UC and CD affecting the colon; this is termed indeterminate colitis. Occasionally a diagnosis of UC will eventually turn out to be CD. 1.8.1 Q: What are flexible sigmoidoscopy and colonoscopy? Flexible sigmoidoscopy and colonoscopy are endoscopic procedures that allow doctors to examine the lining of the large intestine. In both procedures, the physician inserts a flexible tube known generically as an endoscope through the anus. The doctor is able to move this tube through the gut to view the mucosal lining of the intestines. This also enables him to take tiny samples of the lining using a forceps passed through the endoscope. These samples (called biopsies) can then be viewed under a microscope by a pathologist. Examination of these biopsies by a pathologist is particularly helpful in making the distinction between CD and UC and also for detecting the early evidence of cancerous change indicated by dysplasia. Flexible sigmoidoscopy is an endoscopic procedure done without sedation which examines the rectum, sigmoid colon and often a little bit more of the colon reaching as far as the splenic flexure (the bend at which point the descending colon and transverse colon meet). Colonoscopy is a more elaborate procedure that is used to examine the entire length of the colon which is usually done with sedation. >From the patient's perspective, the main difference between the two procedures is that flexible sigmoidoscopy may be performed in the doctors office and does not normally reach farther than the splenic flexure. Biopsies, or tissue samples may be taken during either procedure. 1.9 Q: How is Crohn's disease diagnosed? Diagnosis of Crohn's disease of the colon is similar to diagnosis of ulcerative colitis. The differences between the two are found by studying the nature and location of the specific inflammation. Colonic CD has larger, deeper, thicker ulcers than UC (which instead has an even "micro-carpet" of tiny ulcers on the surface lining of the inner mucosa). In CD, areas of ulceration are often separated by skip areas, a phenomenon not seen in UC. There is a marked contrast between the "cobblestone" appearance often seen with CD and the even "micro-carpet" seen with UC. Sometimes, "granulomas", a microscopic indicator of CD may be seen on biopsy samples. A diagnosis of probable small bowel CD is frequently made by clinical observations of small bowel Crohn's symptoms accompanied by the detection on physical examination of a palpable mass (which may be tender) in the right lower part of the abdomen. To confirm the diagnosis an upper GI barium x-ray with small bowel follow through is generally performed. In small bowel follow through the small bowel is radiographed as barium passes through it producing silhouette images of the lining. The barium can be introduced either by swallowing, or via a "small-bowel enema" (in which the barium is pumped to the small bowel through a tube). The former method, while more comfortable for the patient and much more commonly used, produces inferior results because the barium is diluted by gastric juices. The latter method is generally used in more perplexing cases. A small bowel enema is also know as an "enteroclysis." 2.1 Q: What Drug therapies are used in IBD? Lots. The two most widely used drug families are steroids and 5-aminosalicylic acid (5-ASA) drugs , both of which reduce inflammation of the affected parts of the intestines. Immunosuppressive drugs such as 6-mercaptopurine (Purinethol) are being increasingly used for long-term treatment of IBD. They are particularly useful in the setting of a patient who is dependent on chronic high-dose steroid therapy with its severe and predictable side effects. 2.1.1 Q: What are 5-ASA Drugs? 5-aminosalicylic acid (5-ASA), also called mesalamine, is an anti-inflammatory drug used in treating IBD. 5-ASA has a similar chemical structure to aspirin, but has a 5-amino group in place of aspirin's acetyl group (aspirin is acetylsalicylic acid). Pure unmodified 5-ASA is easily absorbed in the upper GI tract. To enable its delivery to the lower GI tract where it is needed it must be chemically modified or packaged. Different 5-ASA drugs are formulated to allow delivery to different locations. Because of the chemical similarities to aspirin, patients allergic to aspirin should not take 5-ASA drugs. Q: What is Azulfidine? Sulfasalazine (Azulfidine, Azulfidine EN-Tabs in the US; Salazopyrin EN-Tabs, SAS in Canada; salazosulfapyridine, salicylazosulfapyridine): This is the "staple" drug generally first prescribed for IBD patients. It is taken by mouth and is intended to first reduce inflammation of the intestinal lining and then to maintain remission in mild to moderate cases. Sulfasalazine is a combination of sulfapyridine and an aspirin-like compound, 5-aminosalicylic acid (5-ASA). The bond between the two is broken by intestinal bacteria, making the 5-ASA available in the terminal ileum and colon. A significant amount of the sulfapyridine component is absorbed, metabolized by the liver, and excreted in urine. Side effects are experienced by some patients and can include nausea, heartburn, headache, dizziness, anemia, and skin rashes. It is also known to cause a reduced sperm count in men, but only for the duration of treatment. It may also turn urine a bright orange-yellow color. The side effects generally result from the sulfapyridine component. Hence the efforts to develop formulations of 5-ASA which do not contain sulfapyridine or other sulfa drugs. Azulfidine was developed in the 1930's for the treatment of rheumatoid arthritis. During clinical trials in the 1940's, arthritis patients who also suffered from IBD reported improvements in their IBD symptoms while taking it. This led to its current use as the mainstay IBD treatment. For active disease initially, 1 gram every 6-8 hours is taken by mouth. Adverse effects may be lessened by reducing the dosage to 500 mg every 6-12 hours. Maintenance dose is usually 500 mg every 6 hours, adjusted to patient response and tolerance. Total doses of more than 4 g/day may increase the risk of adverse effects and toxicity but some patients may benefit from taking up to 6 g/day. Azulfadine is generally taken with a full glass of water after meals or with food to minimize indigestion. When indigestion is a problem enteric-coated tablets may be used which are frequently better tolerated. Q: What is Dipentum? Olsalazine Sodium (Dipentum) Olsalazine is a drug that uses a different mechanism to deliver 5-ASA to the terminal ileum and colon. Whereas sulfasalazine links a 5-ASA molecule with a sulfapyridine molecule, olsalazine links two 5-ASA molecules. This compound passes through the stomach and upper ileum. It is then broken down by intestinal bacteria in the terminal ileum, making 5-ASA available there and also in the colon. The major side effect is watery diarrhea, seen in many patients. Patients with UC or CD affecting the entire colon seem especially susceptible. Increased cramping and audible bowel sounds are also commonly reported. The usual dose of olsalazine is 500 mg by mouth twice a day. Q: What is Asacol? Mesalamine, USA; Mesalazine, Europe : Asacol is essentially "Azulfidine without the sulfa". The Asacol formulation of 5-ASA places 5-ASA in an acrylic resin coating which dissolves at pH greater than 7. The tablets are then able to pass through the stomach and upper ileum before the coating is dissolved, releasing the drug in the terminal ileum and colon where the pH is typically greater than 7. Asacol is generally well tolerated. The recommended dose is 2.4 g a day though patients frequently seem to tolerate and benefit from taking up to 4.8 g daily. Q: What is Salofalk? Mesalazine, Europe (Salofalk) Similar to Asacol, but dissolves at pH greater than 6. Q: What is Pentasa? Mesalamine, USA; Mesalazine, Europe (Pentasa) : Yet another "Azulfidine without the sulfa" formulation, this drug packages 5-ASA in a time-release capsule. This method of delivery is thought to make the drug available throughout most of the intestines and provide better release in the small intestine than the other 5-ASA drugs. For this reason Pentasa is the 5-ASA preparation of choice for Crohn's disease involving the small intestine. Pentasa is generally well tolerated. The recommended dose is 2g a day though patients frequently seem to tolerate and benefit from taking up to 4g daily. There is data that the higher dose may be more effective. Q: What is Balsalazide? Balsalazide: Another 5-ASA drug that uses a variant on sulfasalazine's delivery mechanism, Balsalazide contains 5-ASA joined to an inert vehicle. This combination passes through the stomach and upper ileum. It is then broken down by intestinal bacteria in the terminal ileum, making 5-ASA available in the terminal ileum and colon. Q: What is Rowasa? Mesalamine (Rowasa) : Rowasa is 5-ASA in enema form and is effective in treating distal UC, which is simply UC affecting the lower part of the colon, near the rectum, and the rectum itself. One enema contains 4 g of 5-ASA. Rowasa also comes in suppository form for treating proctitis (rectal inflammation). Each suppository contains 500 mg of 5-ASA. 2.1.2 Q: What is Metronidazole? Metronidazole (Flagyl) : Metronidazole is an antibiotic that is most frequently used for treating vaginal infections. However, there is some evidence (much of it anecdotal rather than derived from formal studies) that it is useful in treating CD. Some studies have shown that it has an anti-inflammatory action on CD that is at least as effective as sulfasalazine. The mechanism of this action is unknown, and it has not been found in other antibiotics having the same antibiotic spectrum. Metronidazole appears to be particularly effective in the treatment of CD in the colon. The dose is generally 250 mg three times a day. Some patients are unable to tolerate alcohol while taking metronidazole; accordingly it is generally recommended that patients avoid alcohol while taking it. Though it has been shown to cause cancer in laboratory rodents exposed to very high doses (much, much higher than used in humans) there is NO evidence that it has any similar effect in humans. The major side effect of metronidazole is irritation of nerves which can result in permanent nerve damage if the medication is not promptly stopped. The first hint of this problem is usually a sensation of "pins and needles" in the finger tips and toes. If this is noted the medication should be stopped immediately. Current issues of the PDR contain the disclaimer "Crohn's disease is not an approved indication for metronidazole". 2.1.3 Q: What is Ciprofloxacin? Ciprofloxacin ("Cipro") is another antibiotic frequently used in the treatment of CD. Many physicians and patients report positive results from a trial of cipro, although the formal evidence to justify its use is limited. An infrequent side effect of prolonged use is the development of inflammation of tendons (tendonitis) which may result in rupture especially of the achilles tendon. 2.1.4 Q: What is Clarithromycin (Biaxin)? Another antibiotic used in the treatment of CD. As with the others there is currently little formal evidence to justify its use. 2.1.5 Q: What are adrenal corticosteroids (steroids), and when and why are they used? Prednisone, Prednisolone, Hydrocortisone: When 5-ASA drugs fail or when symptoms are more severe, the next therapeutic step usually involves steroids which are very powerful anti-inflammatory drugs. These are available in oral, enema, or suppository forms. The topical forms are useful in treating distal colitis, the oral forms are useful for achieving remission in mild to moderate active UC and CD. They are NOT useful for continued use in order to maintain a remission. The oral forms can, however, be effective in suppressing active CD to the point where it appears to be in remission. Q: What are the side effects from taking steroids? Side effects from steroids vary widely between patients, but are generally pretty severe particularly when used at moderate to high doses (> 15mg prednisone daily). Common side effects include rounding of the face (moon face) and increase in the size of fat pads on the upper back and back of the neck (buffalo hump), acne, increased appetite with consequent weight gain, increased body hair, osteoporosis (especially in women), compression fractures in vertebrae, diabetes, hypertension, cataracts, increased susceptibility to infections, glaucoma, weakness of arm, leg, shoulder, and pelvic muscles, personality changes including depression (suicidal tendencies are not uncommon), irritability, nervousness, and insomnia. Children's growth may also be affected, even by small doses. An important and serious complication of steroid therapy is avascular necrosis of the hip. This results in death of the bone in the hip joint resulting in arthritis and severe pain. Fortunately, it is a rare complication. Side effects are not as severe with the topical forms in the short term, but increase to about the level of the oral drugs with long term use. Some people report inconsistent response to treatment with Prednisone, saying they respond better at some times to a particular treatment course than they do at others. Corticosteroids suppress the activity of the adrenal glands, which must be restored gradually when the drug is discontinued. This requires gradual tapering of the steroid. Most physicians will not taper long term steroid users faster than roughly 1mg per week or 5 mg per month. For short term users, dosage may be lowered at a faster rate, such as 5 to 10 mg per week. Withdrawal symptoms can occur when the dosage is lowered too quickly. These may include fever, malaise, and joint pains. Since these can also be symptoms of IBD, it is often difficult to tell whether they are the result of insufficient steroid levels, or a true relapse of IBD. If IBD symptoms begin to return during tapering, standard procedure is to return to a slightly higher dose, which is maintained until symptoms subside. Tapering may then be resumed at a slower rate. Long term use of steroids (more than a few days) suppresses the adrenal gland's normal production of steroids and can affect its function for a long time (up to a year, or in some cases even two) even after steroid use has stopped. During this period, the body may not be able to produce an adequate supply of steroids during extreme stress, such as surgery or severe infection. If you've been taking steroids for a while you should probably wear a MEDIC-ALERT necklace or bracelet indicating the quantity and duration of steroid use. (Some suggest carrying a note in the wallet, but such a note will likely never be seen because standard operating procedure for emergency medical personnel is to avoid any contact with a patient's valuables for liability reasons). If you require emergency surgery, this information can be of vital importance since you'll need to be administered additional steroids. Your body isn't capable of producing enough steroids on its own to help survive the stress. Because of the potential problems it is very important that steroid therapy is closely supervised by a physician. Q: What is meant by "Alternate Day Therapy"? Increasing the period of time between steroid doses can allow the adrenal glands to recover somewhat. Alternate day therapy is simply taking double the daily dose on every other day. Due to the duration of the effects of steroids such as Prednisone, this can have the same therapeutic results with fewer side effects. Q: What is Budesonide? Budesonide is currently in "beta testing". It is a steroid that is processed by the liver so that there are less severe side effects. Oral and enema forms are available, depending upon the location of the disease to be treated. Its role compared to the more established steroid agents has yet to be defined. The impression of many is that though it may be safer it may also be less effective. Q: What is ACTH? Adreno-cortico-tropic hormone is a drug that stimulates the adrenal gland to release cortisone. It is seldom used any more. Q: What do steroids do to bones? Steroid drugs unfortunately can cause osteoporosis. Osteoporosis is a disease which results in the destruction of bones causing them to become weak and much more likely to fracture. Without protection within the first six months of steroid therapy a person can lose 10 percent to 20 percent of bone mass. As many as one in four of these people may eventually suffer a fracture as a result. Unlike osteoporosis associated with aging, steroid-induced osteoporosis can occur at any age, even in children. For many years it was thought that only high (>20mgs a day) doses of steroids were a problem, more recent studies have shown that chronic use of low oral doses -- as little as 7.5 milligrams a day -- can cause significant though gradual bone loss. Steroids reduce the amount of calcium the body absorbs from food and increase calcium loss through the kidneys. These actions result in a tendency for the level of calcium in the blood to fall. To prevent this happening the body responds by producing increased amounts of parathyroid hormone. Parathyroid hormone is released to remove calcium from storage in the bone and restore a normal level. In addition steroids also cause bone breakdown directly. Q: What should be done to minimize the damage done by steroids to bones when I am being treated for IBD? The best strategy is to avoid the problem entirely by using the lowest effective dose of steroid. Also to use topical steroids if possible instead of systemic steroids by mouth. Recently the American College of Rheumatology recommended that either before or at the very start of steroid therapy, patients should ideally be given a bone density test, especially of the lower spine and the neck of the thigh bone near where it meets the pelvis. This test should be repeated every six to 12 months to monitor the effectiveness of preventive measures and, if necessary, to modify the course of treatment. Everyone who must take corticosteroids should consume at least 1,500 milligrams of calcium and 800 international units of vitamin D a day, either through diet or supplements. Vitamin D is needed to enhance the body's ability to absorb calcium and use it to build bone. Patients on steroids should get regular weight-bearing exercise, preferably for 30 to 60 minutes a day as this can help prevent bone loss. They should should not smoke or drink more than moderate amounts of alcohol as these are associated with increased rates of bone loss. Consideration should be given to hormone replacement therapy in woman who are post menopause. Women who have not yet reached menopause whose periods become irregular or stop while on steroids should take oral contraceptives unless there is a medical reason for not taking them. For men on steroids consideration should be given to measuring their testosterone level and, if found to be low, given testosterone replacement. 2.1.6 Q: What are immunosuppressive drugs and when are they used? Immunosuppressives such as 6-mercaptopurine (6-MP or purinethol) or azathioprine (imuran) are increasingly used in treating more severe IBD that does not respond to 5-ASA therapy and short term steroid therapy. The most frequent use of these drugs is in the context of inability to reduce the steroid dosages in steroid dependent patients without causing a disease flare. Physicians without significant experience in their use can be reluctant to try them because they rarely can have extreme side effects. Generally these side effects occur at higher doses than are used in the treatment of IBD. However, the emphatic opinion of most physician experts in the management of IBD is that they are significantly safer and more effective than long term use of high dose steroids. The side effects that occur in a small minority of the patients who take them can include various blood problems, bone marrow suppression, extensive immune suppression, kidney damage, liver damage and others. There is no convincing evidence that they predispose to the development of cancer at the doses used in treating IBD patients. Usage of these drugs requires frequent monitoring by blood tests; ideally a complete blood count should be obtained every 3 months. Q: What are Azathioprine and 6-MP? Azathioprine (Imuran) 6-Mercaptopurine (6-MP, Purinethol ) : Azathioprine is a drug that was originally used to prevent rejection in organ transplant patients. 6-MP is one of the metabolites of Azathioprine; that means that Azathioprine is converted into 6-MP in the body. Both drugs have shown some degree of efficacy when used in combination with prednisone. Because they facilitate the use of lower steroid doses they are frequently called "steroid sparing" drugs. Most people can tolerate these drugs without difficulty thus helping avoid long term high dose steroids and the predictable associated side effects. At this time it is the consensus of experts in the management of IBD that it is clearly preferable to treat a patient with long term Azathioprine or 6-MP rather than with continued or even intermittent high dose steroids. Despite impressive data from clinical trials supporting the use of 6-MP and azathioprine in both CD and UC many patients are still treated with prednisone for longer periods than are appropriate because of the erroneous perception that Azathioprine and 6-MP are more hazardous. This perception is derived in part from the side effect profile seen when these drugs were originally used in preventing transplant rejection and also in the treatment of leukemia. The important difference is that significantly higher doses were used in these situations than are now used in the treatment of both CD and UC. These drugs were developed in the 1950s and were first used for the treatment of IBD 30 years ago! Obviously a lot has been learned about how to use them to maximum advantage over the intervening years. The minimum time to respond to the drug is about three months and can be as long as 12 months. These drugs are effective in maintaining remission in 60 - 80% of patients. An important side effect that occurs in 3-5% of patients is pancreatitis. This usually occurs within a few weeks of starting treatment and is manifested by upper abdominal pain which may radiate to the back and be associated with nausea and vomiting. If pancreatitis occurs then the patient cannot take either Azathioprine or 6-MP in the future. Because of occasional problems with a reduced white blood cell count it is recommended that patients have complete blood counts on a regular basis; every three months is recommended though they should be more frequent during the first few months of therapy. The issue of how long these drugs can safely be used for has not been definitively resolved. An increasing number of patients have been maintained on these drugs for several years (> 3) without any significant long term side effects noted. Q: What is Methotrexate? Methotrexate (Folex, Mexate in the US) : Like the other immunosuppressants, methotrexate may have some benefit in treating active Crohn's disease. Methotrexate has not been used as extensively as Azathioprine or 6-MP but there is increasing data that it may be useful. Methotrexate may be a useful option in patients who are intolerant of Azathioprine or 6-MP. Because of the occurence of liver disease in patients taking methotrexate over a sustained period careful monitoring of liver function is necessary. Patients should not drink alcohol while taking methotrexate. Methotrexate should not be used in pregnancy. Patients taking methotrexate should not get pregnant. Q: What is Cyclosporine? Cyclosporine is another immunosuppressant drug that was originally and is still used extensively for preventing rejection of organ transplants such as kidney and liver transplants. Though initial hopes were high that it would be a very good drug for severe and complicated CD the results have been somewhat disappointing. In severe CD particularly complicated by fistulas there is data that high dose intravenous cyclosporine may be useful in the short term. Low dose therapy for maintenance of remission does not seem to be effective and has unacceptable side effects. In severe UC, particularly when a patient is on the threshold of requiring urgent surgery there has been some success with cyclosporine in inducing a remission. These patients are generally treated simulataneously with high dose steroids also and are started on 6-MP or azathioprine also. After 3-6 months of therapy, when 6-MP or azathioprine has hopefully become effective, cyclosporine is stopped and simultaneously steroids are reduced and stopped if possible. This approach seems to be effective in the short term with a significant proportion of patients with severe UC. However, a significant proportion of these patients subsequently have surgery because of inability to maintain them in remission. 2.2 Q: Are any other drugs used to treat IBD? There are several different drugs in various stages of development for IBD. 2.2.1 Q Are nicotine patches ever used to treat UC? Many UC patients have reported that their symptoms began after quitting smoking. In fact in the vast majority of studies where it has been checked a significantly lower proportion of UC patients smoke in comparison to controls. This data is clearly consistent with smoking having a preventive effect in UC. The mechanism of this is not understood. In marked contrast a higher proportion of CD patients smoke compared to controls and continued smoking is a predictor of post surgical recurrence of CD. This data suggests that smoking may be a co-factor predisposing to the development of CD. The mechanism of this predisposition is not understood. Due to the health risks of smoking, doctors have been skeptical of this data. Recently more attention has been devoted to understanding the relationship between smoking and IBD. One question that has stimulated considerable work has been whether nicotine is responsible for the apparently protective effect of smoking in UC? Two relevant articles were recently published in The New England Journal of Medicine looking at the potential therapeutic benefit of nicotine patches, normally used to help people stop smoking, to induce remission of active UC and to maintain remission. The patches were helpful in some patients in the induction of remission but were not helpful in the maintenance of remission. Most non smoking patients in the studies suffered some side effects from the nicotine, including nausea, vomiting, lightheadedness, headache and sleeplessness. More work needs to be done to clarify the role of nicotine in therapy of UC. 2.2.2 Q: What about antibodies against TNF (Tumor Necrosis Factor)? It is important to note that IBD has features in common with inflammatory diseases that involve other parts of the body such as rheumatoid arthritis and psoriasis for example. So therapies that are being developed for these diseases may also be useful for treating IBD. There has been considerable publicity recently given to the new data about the treatment of CD with antibodies against Tumor Necrosis Factor (TNF). These antibodies are also being evaluated in the treatment of rheumatoid arthritis. Q: What is Tumor Necrosis Factor or TNF? When the immune system is activated resulting in inflammation many chemical messengers are released. These chemical messengers are produced by the cells of the immune system and are called cytokines. These cytokines interact with other cells encouraging them to become activated and thus make the inflammation worse. TNF is one of the most important cytokines involved in this process. The term Tumor Necrosis Factor refers to one of its actions which led to its discovery. Q: Does TNF serve any useful function? In the setting of an infection TNF frequently plays an important role in helping the immune system respond promptly and effectively. However, it is believed that excessive and inappropriate production of TNF may be an important contributory factor in the development of several diseases characterized by inflammation and activation of the immune system such as multiple sclerosis, rheumatoid arthritis and others. Q: Is TNF important in IBD? just CD? what about UC? Various strategies have been used to evaluate the importance of TNF in both CD and ulcerative colitis (UC). Though some data does support a role it has been difficult to convincingly demonstrate that there is excessive production of TNF in either disease. The available data does seem to suggest that TNF may be of more importance in CD than UC. The fact that the new anti-TNF treatments seem effective in some patients is the best evidence that TNF is important in the disease process of CD. There has been one small study of an anti-TNF antibody in UC and a preliminary report did not show impressive results. Q: What is this new anti-TNF treatment? The treatment consists of an antibody which is a protein that neutralizes the action of TNF. Originally, the antibody was made by a mouse when it was injected with human TNF. The immune system of the mouse recognized the foreign nature of the human TNF and made antibodies against it. One of these mouse antibodies was modified or humanized so that it would be less likely to provoke an adverse reaction when injected into a human. There are two antibodies that have been used to treat CD. The first, named cA2, was developed by the biotechnology company Centecor. The cA2 antibody was initially used in the treatment of severe infection. More recently it has been evaluated for the treatment of rheumatoid arthritis. Because of promising results in the arthritis studies a group of Dutch physicians gave the antibody to a child with severe CD and there was a dramatic response. This encouraged more comprehensive studies of the effectiveness of the cA2 antibody to treat CD in Europe and the United States. The second anti-TNF antibody has been developed by the biotechnology company British Biotechnology and is called CDP571. Q: How does the anti-TNF treatment work? The antibodies blocks the action of TNF. The fact that it is so effective in some patients has raised the question whether it is having some additional effects on the immune system; however this remains to be clarified. The most important aspect of its use is that it implies that TNF does indeed seem to have an important role in the development of inflammation of CD in a significant percentage of patients. Q: Are there problems with the treatment? Like most treatments for IBD it does not seem to work in all patients. In the recently reported studies most patients who received the treatment had a beneficial response about half of whom actually went into remission. In those patients who have a response the effect is temporary, lasting several months at best. The antibody is given by intravenous infusion and cannot be given by mouth. It is not clear whether it can be given safely to the same patient more than once. If indeed it can be given repeatedly it remains to be seen whether it will continue to have a beneficial effect or whether resistance will emerge. The treatment will only be available as part of formal clinical studies for the next few years. If it continues to have positive results and becomes available as a standard therapy in the next few years it is likely to be expensive. Q: What sort of patients are suitable candidates for treatment with anti-TNF antibody? CD patients with active disease despite therapy with steroids; this is a prerequisite for enrollment in the studies. Those patients who may particularly be suitable for the anti-TNF therapy are those who cannot tolerate 6-mercaptopurine or in whom 6-mercaptopurine has not worked or have just been started on 6-mercaptopurine and a therapeutic effect is not expected for several months. IMPORTANT: the anti-TNF antibodies are only available as part of formal studies at present. Q: What are the alternatives available at present? The best tested and most effective medications at present are 6-MP and methotrexate. Other medications are also being developed which block the action of TNF which may be useful in the treatment of IBD in the future. 2.2.3 Q: What about Interleukin-10 (IL-10) therapy for CD? IL-10 is another cytokine like TNF. Cytokines are chemical messengers produced by the cells of the immune system that regulate its activity. Unlike TNF, IL-10 suppresses the immune system and is presently being studied in the treatment of CD. The results of this study are eagerly awaited. 2.2.4 Q: What about fish oil for therapy? There is some evidence that fish oil (attributed to the eicosapentaenoic acid) has anti-inflammatory properties which may be useful in the treatment of IBD and rheumatoid arthritis. In addition it may also be helpful in preventing atherosclerotic cardiovascular disease. Patient acceptance of fish oil therapy has been poor because of the indigestion and bad breath associated with therapy. An Italian study last year using coated capsules containing fish oil showed evidence of benefit in preventing recurrences of CD with miminal side-effects. However, these capsules are not widely available at present. In the interim various fish oil preparations containing eicosapentaenoic acid are available from pharmacies and health food stores which may be of therapeutic benefit despite the possible side-effect of increased susceptibility to bleeding. Alternatively it may be helpful to simply eat more fish in one's diet! 2.3 Q: Can different drugs be used together to treat IBD? Many patients require treatment with more than one medication to adequately control their symptoms. Frequently, several different combinations are tried before the best one is found. Once symptoms are brought under control then attempts are made to reduce the medications to a minimum. 2.4 Q: Will I need to keep taking medications permanently? At this point in time because there is no cure for IBD (except removal of the colon for patients with UC) it is advisable for many patients to continue taking medications to keep them in remission. The reason for this, which is supported by some studies, is that it is much easier to keep a patient in remission rather than treat a flare of the disease. Similarly, it is much easier to use sun screen to prevent sunburn rather than try to treat sunburn after it has happened. 3.1 Q: Drugs aren't working, what can surgery do for my UC? Drug treatments are ineffective in about 20% of UC patients. These patients must have their colons removed due to debilitating symptoms. The colon may also removed because of the threat of cancer. Removal of the colon permanently cures the UC and usually all related symptoms. Patients having these surgeries are generally hospitalized for about a week and return to work in three to six weeks. There is NO role for resections of only part of the colon in UC even when the disease is limited in extent as it inevitably recurs in the colonic remnant. Once the colon is removed there are several options which may avoid the need to wear a bag appliance to collect waste. 3.1.1 Q: What's an ileostomy? The entire colon and rectum are removed and a small opening, about the size of a quarter, called an ileostomy is made in the lower right corner of the abdominal wall. The small intestine is then connected to this opening and a colostomy bag is worn over the opening to collect waste. The patient then empties the bag about four times a day. 3.1.2 Q: What's a Continent Ileostomy? Another operation that gained popularity over an ileostomy avoids the use of a colostomy bag by forming a pouch from the last 15-40 cm of ileum inside the wall of the lower abdomen. A nipple valve in the abdominal wall allows the patient to empty the pouch by inserting a catheter through the ileostomy. Initially, the pouch must be emptied frequently, eight to ten times daily. The pouch stretches and, after several months it will only have to be emptied four to five times a day. This operation used to be performed in two separate steps and the patient would have to wear a colostomy bag for several months before the pouch could be attached. The operation is now generally performed in one step, though it may be performed as two steps if the patient is severely ill at the time of surgery. This procedure is generally not performed because it has many of the possible complications and none of the benefits of the Ileoanal Anastomosis, described below. 3.1.3 Q: What's an Ileoanal Anastomosis, or Ileoanal Pull-Through? Since UC inflames only the innermost layer of the colon, the rectum can be stripped of this layer and attached to the ileum after the colon is removed. Early attempts to perform this surgery were frustrating as patients predictably suffered from incapacitating diarrhea. The operation was modified in 1980, adding an S or J shaped pouch just above the rectum and patients achieved continence. The patient can then pass stools normally, though bowel movements are more frequent and watery than in an otherwise healthy individual without IBD. Like the Kock pouch, eight to ten bowel movements a day are typical immediately after the surgery. The pouch continues to stretch for several years and eventually it's only necessary to have four or five bowel movements a day. In rare cases (around 5% when the surgery is performed by an appropriately trained surgeon) when other complications, such as infection occur, the pouch may need to be converted to an ileostomy. 3.1.4 Q: What can go wrong with these surgeries? The most common complication of these operations is inflammation of the pouch, called pouchitis. Symptoms include pain, bloating, and diarrhea. Most patients can control this by irrigating the pouch with saline solution and taking antibiotics. In a few cases, a diagnosis of CD is confirmed in patients thought originally to be suffering from UC. Problems with the nipple valve in a continent ileostomy can cause leakage of stool and an inability to insert the catheter. About 10% of patients require a second operation to repair the nipple valve. Remember that these have the same risks as any surgery, but that's outside the scope of this FAQ. 3.2 Q: Are there surgical treatments for Crohn's? Unlike in UC, there is no surgical cure for CD. Physicians use the phrases "minimalist surgery" and "surgery avoidance" when discussing surgical options for CD. This is because new Crohn's lesions can appear after previously diseased areas have been removed and even diseased tissue may be functionally useful. Many surgeons also feel that "surgery in Crohn's patients just leads to more surgery". Surgery for CD is usually a resection of the small intestines. 3.2.1 Q: What's a resection? Severely affected portions of the intestine are removed and the healthy ends are sewn together. This in no way prevents inflammation from recurring later and is generally performed only when the inflammation is unable to be controlled by medical therapy. 3.2.2 Q: After surgery for CD can anything be done to prevent it recurring again? Smoking is associated with recurrent disease following surgery in CD patients. Clearly, CD patients must be strongly encouraged to stop smoking. There is some evidence that 5-ASA drugs (especially Pentasa for small bowel disease) may be useful in preventing disease recurrence after surgery. Some experts use 6-MP following surgery in patients with a high risk of recurrence and there is a trial in progress to see if it works in this setting. There is also some limited evidence that metronidazole may be helpful in preventing disease recurrence following surgery. Fish oil may also be a relatively safe option though it is not of proven benefit. 4.1 Q: What role does diet play in IBD? Most patients find that certain foods are tolerated less well than others when symptoms are active, but there is no evidence that these foods directly affect the inflammation. The most common offenders are milk products (see the section on lactose intolerance below), spicy foods, fats, and sugars. In general, a bland low fiber diet avoiding fruits, vegetables, nuts, and whole grains is preferable when the disease is active. A high fiber diet is to be recommended when symptoms aren't present. Due to reduced appetite, malabsorption of nutrients, and increased nutritional needs, it's important to make sure you follow a proper diet. Since the small intestine is where the body absorbs nutrients from food, CD patients may have problems absorbing these nutrients. If more than two or three feet are either diseased or surgically removed,malabsorption, especially of fats, the minerals calcium and magnesium, and the fat soluble vitamins A,E, and D, can be a problem. Resection of at least two feet may also increase absorption of oxalate, which reacts with calcium to form kidney stones. A low oxalate and low fat diet will help prevent kidney stones. Spinach, cocoa beans, rhubarb, beets, instant coffee, diet sodas and tea are all high in oxalate. If only the terminal ileum, the last two to three feet of the small intestine, is diseased or resected, absorption will be normal except for vitamin B-12 which can be supplemented by monthly injections. Iron supplements are helpful in treating the anemia and patients should drink plenty of fluids to replace those lost from diarrhea. 4.1.1 Q: What is an elemental or astronaut diet? Astronaut diets (for example Ensure, Sustacal and Peptamen) are liquids meeting all nutritional needs and are almost completely absorbed in the upper intestinal tract. Because they don't require much digestive effort by diseased bowel they often seem to be better tolerated than regular food by patients with active and/or severe disease. Elemental diets (for example Vivonex) consist mainly of pure amino acids (the building blocks that make up proteins) and are even easier to digest. There is some evidence that elemental diets may be helpful therapeutically in CD. However, these diets are expensive and patients find it difficult to comply with them on a long term basis so they have not evolved into a practical treatment. In contrast there is no evidence that elemental diets are of benefit in UC. 4.1.2 Q: What is total parenteral nutrition? Total parenteral nutrition (TPN), or hyperalimention, delivers a concentrated solution of nutrients intravenously. This is used in very active disease either giving it time to subside, or to nourish the patient before surgery. People with Crohn's Disease generally benefit more than those with UC because CD usually affects the small intestine, which is where nutrients are absorbed. TPN may, however, occasionally be warranted in critically ill people with UC. 4.1.3 Q: What is lactose intolerance? It's commonly estimated that about 30% of the world's adult population suffers from lactose intolerance, though this may be even higher in patients with IBD. A much higher than normal fraction of Asians suffer from lactose intolerance. Lactose is a sugar found in milk, milk products, and foods made with milk. The enzyme lactase, normally produced in our intestines, breaks down lactose during digestion. Lactose intolerant people don't produce enough lactase and therefore cannot digest lactose. Symptoms of lactose intolerance include a bloated feeling, abdominal pain, flatulence, and diarrhea shortly after consuming milk or milk products. Sound familiar? It's not something that you want to subject yourself to in addition to the symptoms of Crohn's or UC. A simple laboratory test can determine whether one is lactose intolerant or not. The severity of symptoms is highly individual and most people do not need to eliminate lactose from their diet entirely. Q: So what can I do about lactose intolerance? 1. Reduce or Remove milk and milk containing foods from your diet. These include milk chocolate, butter, cheeses, ice cream and lactose--it's an ingredient by itself in some foods. Check the label! 2. Eat foods containing lactose with meals containing protein and fat, not alone. 3. Use a lactose reducing product available over the counter at most pharmacies (Dairy Ease or Lactaid). These contain lactase and are either consumed with lactose rich food or added to it before eating. Some dairy products have reduced lactose content. These include yogurt and Lactaid Milk. 4. Fermented milk products, such as aged cheeses, contain less lactose and are usually better tolerated. Cottage and ricotta cheese are OK, cheddar has about the least. Buttermilk contains as much lactose as milk. 5. A calcium supplement may be needed if dairy products are reduced or eliminated from your diet. 5.1 Q: What part does stress play in IBD? Emotional stress plays a large part in the health of some patients and is often cited as the trigger of a relapse, though there is no clear cause and effect relationship proven. It may be more likely be that stress is one result of a flare-up rather than being a factor contributing to one. Treatment of IBD sometimes may usefully include the teaching of stress reduction techniques such as meditation. This is a controversial subject with somewhat "political" overtones. Many patients resent the assumption of family and friends and even some doctors that stress is a cause of their illness, when in fact it is just an exacerbating factor (as is the case with other illnesses, as well). Many people need reassurance that all this is not their fault or "all in their head". It's been proven that stress does NOT cause IBD, although with IBD as with any illness stress can exacerbate symptoms. Because of the nature of these illnesses and the unpleasant symptoms that result patients frequently feel very uncomfortable about discussing them even with close friends and family. Denial may be a factor that inhibits patients from getting appropriate evaluation and therapy. Many patients find patient support groups to be extremely helpful in addressing these issues and enabling patients to constructively and positively learn how to live with these chronic illnesses. Many patients not comfortable with group discussions have found it particularly helpful to consult with a psychologist experienced in the evaluation of patients with IBD. 5.2 Q: Can anything else cause a flare up? Significant anecdotal evidence suggests that flares of IBD often occur after increased use of non-steroidal anti-inflammatory drugs (NSAID's), such as aspirin and ibuprofen. Accordingly, patients should be very careful about taking these medications and be aware that they may cause a flare of their disease. In fact, some physicians who are very experienced in managing IBD feel these drugs should rarely if ever be used by IBD patients. 6.1 Q: How can I make the most of my consultations with my physician? For your physician to treat you most effectively it is vital that you adequately describe your symptoms. Many patients are reticent about describing urgency and episodes of incontinence for example which may be readily treated with local topical therapy. If despite the best efforts of your physician you are not doing well either having continued symptoms or requiring continued high dose steroids then it may be appropriate to consider asking for a second opinion. This is best done in conjunction with your regular physician. ====================================================================== COPYRIGHT NOTICE Copyright 1997 by Kevin Horgan, M.D., Christopher Holmes and Michael Bloom. All rights reserved. This document, or any derivative works thereof, may not be sold or redistributed for profit in any way without express (not email) written permission of the authors. This includes, but is not limited to, translations into foreign languages, mass archival as on a CD_ROM and inclusion in commercially published compilations (books). You are free to copy this list for personal use, or to make it available for redistribution in its electronic format, provided that: (1) it remains wholly unedited and unmodified, (2) no fee or compensation is charged for copies of or access to this list, and (3) this copyright notice and the following disclaimer remain attached. DISCLAIMER: ========== This FAQ is provided by the authors "as is", and any express or implied warranties, including, but not limited to, the implied warranties of merchantability and fitness for a particular purpose are disclaimed. In absolutely no event shall the authors be liable for any direct, indirect, incidental, special, exemplary, or consequential damages (including, but not limited to, procurement of substitute goods or services; loss of use, data, or profits; or business interruption) however caused and on any theory of liability, whether in contract, strict liability, or tort (including negligence or otherwise) arising in any way out of the use of the information herein contained, even if advised of the possibility of such damage. In other words, this document is in no way intended to be a substitute for medical care; the information contained herein is presented by the authors purely for informational purposes only. In no way are any of the materials presented here meant to be a substitute for professional medical care or attention by a qualified practitioner, nor should they be inferred as such. ALWAYS check with your doctor if you have any questions or concerns about your condition, or before starting a new course of treatment or otherwise making any decisions about treatment. ______________________________________________________________________________ Kevin Horgan, MD khorgan@ucla.edu 310-206-3580 phone 310-206-9049 fax -- November 15 Today I made a Black Forest cake out of five pounds of cherries and a live beaver, challenging the very definition of the word cake. I was very pleased. Malraux said he admired it greatly, but could not stay for dessert. Still, I feel that this may be my most profound achievement yet, and have resolved to enter it in the Betty Crocker Bake-Off.