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X-Last-Updated: 1999/10/12
From: "Christopher Holmes" <ibdfaq@sdf.lonestar.org> Newsgroups: alt.support.crohns-colitis,alt.answers,news.answers Subject: Inflammatory Bowel Disease FAQ V3.1 Sender: ibdfaq@sdf.lonestar.org Followup-To: alt.support.crohns-colitis Distribution: world Organization: none Reply-to: ibdfaq@sdf.lonestar.org Approved: news-answers-request@MIT.Edu See reader questions & answers on this topic! - Help others by sharing your knowledge Archive-name: medicine/crohns-colitis-faq/part1 Posting-frequency: every two weeks Last-modified: 1999/10/12 Version: 3.1 URL: http://ibdfaq.freeshell.org Inflammatory Bowel Disease Frequently Asked Questions Version 3.1 This document was last modified on 10/12/1999 Part 1 of 2 Introduction: ============ What is Alt.support.crohns-colitis? 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 online 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. Discussions of all types of medicine- conventional and alternative, Western and Eastern, your Aunt Harriet's home remedies, whatever- are welcome here; however, any person discussing a potential remedy which he or she also sells must explicitly begin the "Subject" header of their post with the word "AD" or "ADVERTISEMENT" in all caps, regardless of whether or not they profit from such sales. Spamming is expressly forbidden as violating the rules of netiquette as well as those of this newsgroup. Finally, please keep in mind that no one knows 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 ibdfaq@sdf.lonestar.org. Please do not send me email asking for medical advice, 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 1995-1999 by Christopher Holmes, Kevin Horgan M.D., 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. Web: http://ibdfaq.freeshell.org ftp: rtfm.mit.edu and its mirrors 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. 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? 1.2.6.1 Q: Are there other factors predisposing to the development of colon cancer? 1.2.6.2 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? 2.1.1.1 Q: What is Azulfidine? 2.1.1.2 Q: What is Dipentum? 2.1.1.3 Q: What is Asacol? 2.1.1.4 Q: What is Salofalk? 2.1.1.5 Q: What is Pentasa? 2.1.1.6 Q: What is Balsalazide? 2.1.1.7 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? 2.1.5.1 Q: What are the side effects from taking steroids? 2.1.5.2 Q: What is meant by "Alternate Day Therapy"? 2.1.5.3 What is Budesonide? 2.1.5.4 What is ACTH? 2.1.5.5 Q: What do steroids do to bones? 2.1.5.6 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? 2.1.6.1 Q: What are Azathioprine and 6-MP? 2.1.6.2 Q: What is Methotrexate? 2.1.6.3 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)? 2.2.2.1 Q: What is Tumor Necrosis Factor or TNF? 2.2.2.2 Q: Does TNF serve any useful function? 2.2.2.3 Q: Is TNF important in IBD? just CD? what about UC? 2.2.2.4 Q: What is this new anti-TNF treatment? 2.2.2.5 Q: How does the anti-TNF treatment work? 2.2.2.6 Q: Are there problems with the treatment? 2.2.2.7 Q: What sort of patients are suitable candidates for treatment with anti-TNF antibody? 2.2.2.8 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? 4.2.3.1Q: So what can I do about lactose intolerance? 4.1.3.1 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. 1.2.6.1 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. 1.2.6.2 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. 2.1.1.1 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. 2.1.1.2 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. 2.1.1.3 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. 2.1.1.4 Q: What is Salofalk? Mesalazine, Europe (Salofalk) Similar to Asacol, but dissolves at pH greater than 6. 2.1.1.5 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. 2.1.1.6 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. 2.1.1.7 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. --End of part 1 of 2-- User Contributions:Part1 - Part2 [ Usenet FAQs | Web FAQs | Documents | RFC Index ] Send corrections/additions to the FAQ Maintainer: ibdfaq@sdf.lonestar.org
Last Update March 27 2014 @ 02:11 PM
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