Fight back against inflammatory bowel disease Michael W.

Day RN, CCRN, MSN Nursing2008 November 2008 Volume 38 Number 11 Pages 34 - 40 Abstract It takes guts to live with Crohn's disease or ulcerative colitis, both of which can take a heavy toll on their victims. Find out how to help your patient tame the attacks.

WHEN A PATIENT is admitted to your unit with a diagnosis of inflammatory bowel disease (IBD), she has one of two disorders: Crohn's disease or ulcerative colitis. Both cause chronic diarrhea, abdominal pain, fever, arthritis of the spine and large joints of the arms and legs, and anorexia, and both can be extremely debilitating, even life-threatening. But they're not the same disease, and you must understand the difference to intervene appropriately. In this article, I'll discuss the similarities and differences, including diagnostic tests and treatments for each and what nursing care and teaching you must be prepared to provide for your patient after the diagnosis. Similar but not the same Crohn's disease and ulcerative colitis are classified as IBD because they're characterized by chronic inflammation at various sites in the gastrointestinal (GI) tract. The inflammation usually causes diarrhea and abdominal pain. Both types of IBD are chronic, wax and wane in severity, and can cause signs and symptoms in other parts of the body. However, ulcerative colitis, which is confined to the colon, can be cured by removing the colon. Because Crohn's disease can affect the entire GI tract, it's considered manageable but incurable. Both types of IBD can strike at any age but most patients first experience problems between ages 10 and 30, with a smaller peak incidence between ages 50 and 60. The risk is higher among white patients compared with nonwhites and among Jewish patients compared with those with a non-Jewish background. Both diseases have a familial tendency: 10% to 20% of patients with IBD have at least one relative who also has IBD.1 Research indicates that both diseases stem from dysfunction of the epithelial cells in the GI tract and that a distinct immunologic process is responsible.2 Although no single feature absolutely distinguishes Crohn's disease from ulcerative colitis, the disorders generally differ in several ways. For example, ulcerative colitis is usually confined to the rectum and lower colon, with inflammation limited to the intestinal wall's inner lining. In contrast, Crohn's disease typically affects the lower part of the small bowel (ileum) but may extend throughout the GI tract. In addition, inflammation can affect all layers of the intestinal wall.1 (See How Crohn's disease and ulcerative colitis compare for more distinguishing features.) In the few patients in whom the disease can't be differentiated, the diagnosis is indeterminate colitis. Figure. No caption available. Precise causes of IBD aren't well understood, although an induced immune reaction in people with a genetic predisposition is probably involved.2 Possible triggers for the immune reaction include diet, environment, and infection. For unknown reasons, smoking increases the risk of Crohn's disease but

decreases the risk of ulcerative colitis.1,3 For more about IBD risk factors, see What increases the risk of IBD? Beyond the GI tract The underlying inflammation of IBD can lead to disorders elsewhere in the body. For example: * erythema nodosum causes tender, erythematous nodules, most often on the ankles or shins * pyoderma gangrenosum, a painful and progressive destructive skin disorder, is characterized by deep skin ulceration * peripheral arthritis in large joints may or may not involve joint swelling and redness * stomatitis. These disorders tend to flare and resolve along with IBD attacks. Other syndromes that may be related to IBD but don't coincide with exacerbations include uveitis, ankylosing spondylitis, and primary sclerosing cholangitis (PSC), a chronic liver disease involving inflammation and scarring of the bile ducts. In fact, PSC may precede the diagnosis of IBD by years and always merits an investigation for IBD. Patients with IBD also have a greater incidence of thromboembolic events and may develop abnormal liver function tests, indicating liver disease.4 Nutritional deficiencies are a particular problem in IBD, especially in Crohn's disease. Loss of appetite, malabsorption of nutrients, increased calorie requirements, loss of electrolytes and protein, and the effects of therapy contribute to nutritional deficiencies. Now let's take a closer look at each disorder, starting with Crohn's disease. Crohn's disease: "Skip" the lesions Although Crohn's disease can involve the entire GI tract, only rarely does it affect the esophagus, stomach, or duodenum. However, mouth ulcers are common. The most common complication is intestinal obstruction.3 Crohn's disease is characterized by well-demarcated lesions, called "skip" lesions, surrounded by tissue that appears normal. The lesions penetrate the bowel's submucosal layer but don't usually extend to bowel muscle. Table. How Crohn's disease and ulcerative colitis compare As Crohn's disease progresses, the affected portion of the bowel becomes semirigid and thickened. Chronic inflammation causes hypertrophy of bowel muscle, leading to fibrosis and strictures. All these changes can lead to abscesses, fistulas, and bowel obstruction. About 30% of patients with Crohn's disease develop fistulas, usually in high-pressure areas just proximal to strictures. These may penetrate nearby structures, including the bladder, other bowel loops, or muscle, and become infected. An enterocutaneous fistula may extend out of the abdominal cavity, causing bowel contents to leak through a skin opening. Most fistulas occur in the perianal area.5 Signs and symptoms of Crohn's disease vary, depending on how long the patient has had the disease. Initial

symptoms may be mistaken for appendicitis or bowel obstruction. The patient may initially report fever, persistent diarrhea, and cramping abdominal pain. When disease is confined to the small bowel, the patient will pass larger volume stools without urgency or tenesmus (ineffectual straining to pass stool). Rectal bleeding, although less common, can occur if he has lesions in the colon. Pain related to abscesses, obstruction, or adhesions from previous surgeries is common as the disease progresses; draining fistulas are less common. Other common signs and symptoms include fever, weight loss, and various non-GI syndromes. Malnutrition results from the disease itself, which destroys healthy bowel tissue, and the surgery that some patients require. Removing a significant portion of the small bowel leads to malabsorption, typically causing deficiencies in electrolytes, minerals, fat-soluble vitamins, and vitamin B12. These deficiencies can lead to clotting disorders, bone demineralization, and delayed growth and development in children. The degree of malabsorption is usually related to the extent of small-bowel involvement. Pinning down the diagnosis Crohn's disease mimics many other disorders, and no single test is diagnostic. The healthcare provider will rely on the patient's history and results of various tests to rule out other disorders, such as diverticulitis or appendicitis, and make the diagnosis. * Lab studies include a complete blood cell count, which may reveal anemia and leukocytosis; liver function tests; and a basic metabolic panel. Inflammatory markers, such as erythrocyte sedimentation rate and C-reactive protein, and nutritional markers, such as albumin, prealbumin, and transferrin, help the healthcare provider monitor disease progress. * Imaging studies commonly include plain abdominal X-rays and computed tomography or magnetic resonance imaging of the abdomen. In women, ultrasound of the abdomen and pelvis may be indicated to rule out gynecologic problems. * Endoscopy allows the clinician to visualize lesions in the colon up to the terminal ileum and remove specimens for biopsy. * Capsule endoscopy, a newer procedure, may provide better images of the small intestine. The patient swallows a capsule containing a tiny camera, which radios data to a sensor as it passes through the GI tract.6 * Barium contrast studies, such as an upper GI series, can help define the distribution and severity of disease. A barium enema may be indicated when diarrhea is the primary symptom, indicating greater colon involvement. Managing Crohn's disease with medication Although Crohn's disease isn't curable, various interventions can help the patient cope with debilitating signs and symptoms. For example, cautious use of the antidiarrheal loperamide, taken just before meals, can help him manage cramping and diarrhea. Bulking laxatives (psyllium [Metamucil]) increase stool firmness and may help prevent anal irritation from diarrhea.4 However, these drugs mustn't be used when Crohn's disease affects the colon because they could trigger toxic megacolon, a potentially life-threatening condition (see Toxic megacolon takes a toll for details).

For more about drugs commonly prescribed to manage Crohn's disease, see Managing IBD medically. Surgical options Up to 75% of patients with Crohn's disease undergo some type of surgery, usually to remove lesions. However, surgery is never the first choice because it doesn't cure the disease. About 50% of patients experience a recurrence of symptoms within 5 years, and about half of these need more surgery. But longterm drug therapy following surgery may help maintain remission.7 If the patient develops a bowel obstruction, he'll be treated initially with gastric suctioning, I.V. fluids, and possibly parenteral nutrition (PN). Obstructions associated with Crohn's disease generally resolve within days, but if they don't, surgery is usually indicated. If the patient develops significant fever and vomiting, rebound tenderness, or a palpable abdominal mass, he also needs hospital admission for treatment with I.V. fluids and antibiotics and drainage of abscesses, if present. Once infection is ruled out or controlled, he may begin corticosteroid therapy. If he doesn't respond within a week, surgery is usually indicated. A patient who develops perianal fistulas may need a temporary diverting colostomy, but fistulas almost always recur when the colostomy is reversed. For this reason, a diverting colostomy is used as a temporary measure until definitive surgery can be done to resect the colon. Ulcerative colitis: Confined to the colon Although a few patients recover completely after one episode, ulcerative colitis is usually chronic and characterized by remissions and exacerbations. The course and severity vary widely, from relatively benign to severely debilitating. The risk of colon cancer increases with the length of time a patient has ulcerative colitis and the amount of bowel involved. Unlike Crohn's disease, ulcerative colitis is confined to the large bowel, with lesions usually developing initially in the rectum. And unlike the skip lesions of Crohn's disease, the lesions of ulcerative colitis are continuous. Typically they affect only the mucosa (inner lining of the intestinal wall), but they may extend into the submucosal muscle layer in severe disease.2 In the early stages of ulcerative colitis, mucosa is edematous and friable with areas of bleeding. As the disease progresses, the lesions produce large amounts of purulent drainage. If lesions extend into the muscle layer, the bowel loses tone and begins to dilate, raising the risk of toxic megacolon. Classic signs of ulcerative colitis Intermittent bouts of bloody diarrhea between periods of normal bowel movements is a classic sign of ulcerative colitis. Tenesmus is common. The frequency of signs and symptoms varies with disease severity. * With mild disease, the patient may have normal stools yet leak blood, mucus, and pus with or between bowel movements. He may also have mild cramping, urgency, and diarrhea. * A patient with severe disease may have 30 to 40 bowel movements a day, primarily watery stool with significant amounts of blood, mucus, and pus. Diarrhea attacks are commonly accompanied by fever, abdominal pain, and cramping. Some patients lose so much blood that they become anemic. Nighttime diarrhea may interrupt sleep and further debilitate the patient. Diarrhea also causes significant electrolyte

imbalances, particularly hypokalemia. * Fulminant colitis, in which ulcerative colitis lesions penetrate the bowel muscle, is characterized by sudden, violent diarrhea with rebound tenderness, abdominal pain, and toxemia. Some patients have these signs and symptoms during the initial episode of the disease. Fulminant colitis may also cause toxic megacolon or bowel perforation. Along with acute signs and symptoms, ulcerative colitis may cause weight loss, malaise, fever, anemia, and anorexia. Other parts of the body are also affected by flares (disease exacerbations), so the patient may develop arthritis or a skin condition such as erythema nodosum. Testing for ulcerative colitis For a definitive diagnosis of ulcerative colitis, many other conditions must be ruled out. Diagnostic testing is similar to that for Crohn's disease. * Lab studies. A complete blood cell count and albumin and basic metabolic panel are useful to evaluate the patient's overall health. Anemia may point to intestinal bleeding. Stool samples for culture and sensitivity and tests for ova and parasites and Clostridium difficile toxin help rule out other causes of diarrhea. * Endoscopy and biopsy. Because ulcerative colitis usually develops first in the rectum, the healthcare provider may start with a sigmoidoscopic examination. If lesions extend beyond the left colon, he may perform a colonoscopy. Collecting tissue samples for biopsy may help identify the cause of lesions. * Imaging studies. Endoscopy and biopsies typically eliminate the need for plain abdominal X-rays, although X-rays may help the healthcare provider identify large accumulations of gas or toxic megacolon. He may also order a barium enema study to outline lesions. A word of warning: Endoscopy and barium enemas are contraindicated in patients with toxic megacolon because these procedures could cause perforation. Treatment options for ulcerative colitis As with Crohn's disease, medical management of ulcerative colitis aims to establish and maintain disease remission. See Managing IBD medically for details on drug therapy to manage flares and maintain remission. From 25% to 35% of patients with ulcerative colitis may require some type of surgery.8 The reasons include cancerous lesions, strictures, complications such as toxic megacolon, or recurrent and severe signs and symptoms that cause significant hardship for the patient. Unlike surgery for Crohn's disease, proctocolectomy (removal of the rectum and colon) cures ulcerative colitis. Here's a quick look at two widely used surgical options.9 Proctocolectomy with ileostomy. After removing the colon, rectum, and anus, the surgeon creates a stoma in the abdominal wall. Intestinal waste drains from the end of the ileum through the stoma into an ostomy pouch. Restorative proctocolectomy. If the patient isn't critically ill and his anal sphincter is free from lesions, the surgeon may remove the colon and rectum but leave the anus intact. He then forms an internal pouch from the distal ileum and connects it to the anal sphincter, allowing the patient to have continent bowel

movements. (This option usually requires two surgical procedures.) After healing in about 12 months, the typical patient will have five or six bowel movements a day but remain continent. Up to 30% of patients who have this procedure develop pouchitis (inflammation of the ileal pouch), which is treated with an antibiotic such as ciprofloxacin or an antiprotozoal such as metronidazole. If inflammation persists, the ileal pouch may be converted to another type of ileal diversion, such as a Kock pouch or ileostomy. Small-bowel obstruction, a less common complication, usually responds to bowel rest and conservative treatment, but some patients require surgery to remove the blockage.8 If necessary to treat massive hemorrhage or perforation, the surgeon may perform a subtotal colectomy with an ileostomy and a mucous fistula. (The remaining colon is attached to the anus.) This is a relatively quick intervention to treat an acute, life-threatening complication. Later, the surgeon will perform definitive surgery, removing the rectal stump to prevent recurrence of ulcerative colitis or cancer.4 When your patient has an ileostomy, he continues to lose fluid and electrolytes. Without the colon, his body can't reabsorb GI fluids, and the ileostomy effluence is very watery with a high concentration of electrolytes. Over time, however, the GI tract becomes more efficient at absorbing water and electrolytes. Nursing considerations for IBD When you care for a patient with Crohn's disease or ulcerative colitis, use the following measures to help manage his signs and symptoms, monitor for complications, and promote healing and well-being. Manage the effects of diarrhea. For most patients, diarrhea is the worst symptom of IBD. Perform these measures and teach your patient how to do them at home: Thoroughly clean the rectal area after each bowel movement to decrease pain and skin irritation, using nonirritating cleansers and wipes. Apply a barrier cream after cleaning to help protect sensitive skin. If the perianal skin is damaged, apply a rectal pouch to protect it from contact with stool. Limit activity. Encourage the patient to take intermittent rest breaks during the day to conserve energy. During acute attacks, curtailing activity will decrease gut motility. Monitor stool. Monitor the amount, consistency, and color and assess it for blood. Tell the patient to report changes to his healthcare provider. Monitor fluid and electrolyte levels. Diarrhea can cause large losses of fluids and electrolytes, so routinely monitor the patient's fluid status and evaluate lab results. Manage your patient's pain. Assess pain using a valid and reliable pain intensity rating scale. Changes in the nature or intensity of pain may indicate a worsening condition, so report them immediately; your patient's treatment plan may need to change dramatically. Administer pain medications as scheduled, assessing the nature and intensity of pain beforehand and afterward. Opioid medications are usually used sparingly because they increase the risk of toxic megacolon. Provide postoperative care. If your patient's colon has been removed but the rectal stump remains, he'll have an ileostomy and a mucous fistula. If the rectum and anus are also removed, he'll have an ileostomy alone. In both cases, frequently monitor the stoma, which should be red and moist but not painful. A dusky appearance, cyanosis, or pallor indicates compromised blood supply. Monitor the stoma output for color, consistency, and amount. Assess the patient for abdominal pain or distension, indicating possible ileus. Finally, when his nasogastric tube is removed, slowly advance his diet as ordered.

Provide nutritional support. The patient needs nutritional support to help reverse wasting from IBD. If he has mild disease, he may get adequate nutrition from a low-fat diet supplemented with vitamins and minerals while he undergoes medical treatment. A patient who's undergone surgery or who has severe disease may require PN. While on PN, he may also receive enteral feedings at 5 to 10 mL/hour to continue nutrition to his small bowel. As he's slowly weaned from PN, gradually increase his enteral feedings. Consult with a dietitian as indicated. Help the patient adapt. Because of body image changes, chronic diarrhea, and other persistent problems, most patients with IBD have significant psychosocial issues. Many patients say that fecal incontinence (or fear of it) is the most limiting aspect of the disease. Altered body image is a significant issue with anyone who has an ostomy. As soon as possible, show the patient his stoma and the associated equipment so he can begin to integrate it into his body image. Use proper terms to describe anatomy and the stoma equipment and encourage him to help with stoma care. Provide care in an open, accepting manner and encourage the patient and his family to express their feelings about the stoma. Provide your patient and his family with resources so they realize they aren't alone in dealing with IBD. They can find resources at the Crohn's and Colitis Foundation (http://www.ccfa.org in the United States and http://www.ccfc.ca in Canada). Living with IBD By understanding IBD and the measures needed to manage its various manifestations, you're better prepared to help him through disease exacerbations and live more comfortably with his disease. Toxic megacolon takes a toll When the colon dilates to a diameter greater than 6 cm in a short time (usually 1 to 2 days), the patient has toxic megacolon, a life-threatening complication of IBD. Use of antidiarrheal drugs to significantly decrease GI motility sometimes precipitates this complication. Signs and symptoms include abdominal pain, tenderness, and distension; dehydration; fever; and tachycardia. Potentially fatal consequences of toxic megacolon include perforation, sepsis, shock, and systemic inflammatory response syndrome. Treatment for toxic megacolon associated with IBD includes I.V. corticosteroids, placement of a long intestinal tube, fluid and electrolyte replacement, and antibiotics. The healthcare provider may consider placing a soft rectal tube to decompress the colon, but he must use extreme caution to avoid perforating friable tissue. If the patient doesn't respond to conservative treatment in 24 to 48 hours, he'll need a colectomy to save his life. What increases the risk of IBD? Inflammatory bowel disease is considered primarily an immune system disorder with a strong genetic component. Having a relative with IBD increases the risk by about 10 times; the risk is 30 times greater if the relative is a brother or sister.6 Psychological factors, although probably not a direct cause, can contribute to the onset and severity of IBD. These factors may also influence disease development: * Smoking increases the risk of Crohn's disease but decreases the risk of ulcerative colitis. 1,3

* Breast-feeding decreases the child's future risk of both Crohn's disease and ulcerative colitis.10 Managing IBD medically The goal of treatment for IBD is to establish and maintain remission. A low-fiber diet may help the patient prevent or manage diarrhea. If his IBD affects the colon, warn him not to use antidiarrheal medications because of the risk of triggering toxic megacolon. Drugs in the following categories are mainstays of treatment for IBD. * Aminosalycilates, which contain the compound 5-aminosalicyclic acid (5-ASA), reduce inflammation in the GI tract. Examples include sulfasalazine and mesalamine, which are available in oral formulations; mesalamine is also available in enema and suppository form for treating inflammation in the rectum and lower colon. Numerous but infrequent adverse reactions, including nausea, fatigue, and headache, limit the usefulness of this treatment for some patients. But if the patient responds to therapy and tolerates it well, he may continue on maintenance therapy to prolong remission. * Antibiotics may be prescribed initially, depending on signs and symptoms, or later if the patient fails to respond to several weeks of treatment with 5-ASA. If he has recurrent fistulas or abscesses, he may continue to take an antibiotic such as ciprofloxacin as long-term therapy. * Corticosteroids such as prednisone and methylprednisolone are another option if the patient doesn't respond to 5-ASA or has significant pain, fever, or vomiting. These drugs, which help reduce inflammation, are usually given orally but are also available as enemas and suppositories. Generally they're used to manage disease flares, not as maintenance therapy. But budesonide (Entocort EC), a newer corticosteroid approved to treat mild to moderate Crohn's disease, may be continued for up to 3 months to maintain remission. * Immunomodulators such as azathioprine, 6-mercaptopurine, or methotrexate help reduce immune system activity. Associated with fewer adverse reactions than corticosteroids, they may be used to maintain remission. * Biologic response modifiers such as infliximab (Remicade), adalimumab (Humira), and certolizumab (Cimzia) block tumor necrosis factor, a component of the inflammatory response. Given by I.V. infusion, these drugs help control inflammation, trigger remission, and allow fistulas to close. Although generally well tolerated, they may cause infusion reactions, malignancies, and potentially serious infections (see 'TNF blockers: Stronger labeling warns of fungal infections' in Drug News on page 14 of this issue). Because of these risks, they're generally reserved for patients who haven't responded well to other therapies. References 1. Achkar JP. Inflammatory bowel disease. The Cleveland Clinic Foundation. http://www.acg.gi.org . [Context Link] 2. Alterations in gastrointestinal function. In Porth CM, Essentials of Pathophysiology: Concepts of Altered Health States, 2nd edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. [Context Link] 3. Mahid SS, et al. Smoking and inflammatory bowel disease: A meta-analysis. Mayo Clin Proc. 2006;81(11):1462-1471. [Context Link] 4. Inflammatory bowel disease. The Merck Manual of Diagnosis and Therapy, 18th edition. Whitehouse

Station, NJ: Merck & Co., Inc.; 2006. [Context Link] 5. About Crohn's disease. Crohn's and Colitis Foundation of America, 2008. http://www.ccfa.org/info/about/crohns . [Context Link] 6. Li CZ. Viewing the small intestine via capsuleendoscopy. Nursing. 2004;34(4):70-71. [Context Link] 7. Surgery for Crohn's disease. Crohn's and Colitis Foundation of America, 2008. http://www.ccfa.org/info/surgery/surgerycd . [Context Link] 8. About ulcerative colitis and proctitis. Crohn's and Colitis Foundation of America, 2008. http://www.ccfa.org/info/about/ucp . [Context Link] 9. Surgery for ulcerative colitis. Crohn's and Colitis Foundation of America, 2008. http://www.ccfa.org/info/surgery/surgeryuc . [Context Link] 10. Klement E, et al. Breastfeeding and risk of inflammatory bowel disease: A systematic review with meta-analysis. Am J Clin Nutr. 2004; 80(5):1342-1352. [Context Link] Bamias G, et al. New concepts in the pathophysiology of inflammatory bowel disease. Ann Intern Med. 2005;143(12):895-904. Cima RR, Pemberton JH. Medical and surgical management of chronic ulcerative colitis. Arc SurgChicago. 2005;140(3):300-310. Collins P, Rhodes J. Ulcerative colitis: Diagnosis and management. Brit Med J. 2006;333(7563):340-343. Colombel JF, et al. Adalimumab for maintenance of clinical response and remission in patients with Crohn's disease: The CHARM trial. Gastroenterology. 2007;132(1):52-65. Lichtenstein GR, et al. American Gastroenterological Association Institute technical review of corticosteroids, immunomodulators, and infliximab in inflammatory bowel disease. Gastroenterology. 2006;130(3):940-987. Copyright 1996-2004 Lippincott Williams & Wilkins, Inc., A Wolters Kluwer Company. All rights reserved.

Probiotics and Prebiotics as Functional Ingredients in Inflammatory Bowel Disease Mirjam A.C. Looijer-van Langen MD Nutrition Today Vimal Prajapati November/December 2008 Levinus A. Dieleman MD, PhD Volume 43 Number 6 Pages 235 - 242 Abstract Probiotics and prebiotics are promising nutraceuticals that may exert a beneficial effect in many medical conditions including inflammatory bowel disease. With the increasing occurrence of antibiotic resistance, the search for medication with little side effects, and the need for options for patients with inflammatory bowel disease who are unresponsive to current therapies, research into alternative therapeutic options is justified. Preclinical studies have provided insights into the effects of probiotics and prebiotics on the immune system and gut microbiota. This new information, along with the older evidence, shows that probiotics and prebiotics may ameliorate chronic intestinal inflammation. This article gives a short overview on current knowledge of probiotics and prebiotics.

Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders that include Crohn disease (CD), ulcerative colitis (UC), and chronic pouchitis. Crohn disease can affect the entire gastrointestinal tract anywhere from mouth to anus. The chronic inflammation is not limited to the lining of the bowel but affects the entire bowel wall, sometimes resulting in intra-abdominal abscesses and fistula (abnormal connections between the lumen of the bowel, other organs, or the surface of the skin) and intestinal obstruction. Patients typically experience symptoms of mild diarrhea, right lower quadrant pain, and low-grade fever. Ulcerative colitis is limited to the colon, and patients experience rectal bleeding, abdominal pain, and diarrhea. The inflammation in UC is confined to the upper layer of the colonic wall and the mucosa. Patients with CD and those with UC both experience periods of remission and relapses. Chronic pouchitis is a chronic inflammation of the ileoanal pouch. An ileoanal pouch is an internal reservoir, constructed for patients with UC who have had their large intestine surgically removed mostly because of severe inflammation refractory to medical treatment. Patients with pouchitis typically present with bloody diarrhea, urgency in passing stools, or discomfort while passing stools. Rarely, pain occurs with pouchitis. Inflammatory bowel disease is caused by multiple factors that disturb intestinal homeostasis. An abnormal immune response to commensal bacteria or dietary factors in genetically susceptible hosts plays a major role in the pathogenesis. Environmental factors including psychological stress, use of nonsteroidal antiinflammatory drugs, and cigarette smoking can also contribute to IBD. The current treatment of IBD mainly consists of drugs directed against the overactive adaptive immune response, such as 5aminosalicylic acid compounds, steroids, azathioprine/6-mercaptopurine, methotrexate, cyclosporine, and biologics such as infliximab. Most patients respond well to these medications, but for some, it is inadequate or induces intolerable adverse effects. Therefore, interest has been raised in nutraceutical therapies such as probiotics, prebiotics, or a combination of these, called synbiotics, as a good therapeutic option for nonresponding patients with IBD. The concept that ingestion of certain bacteria may promote health is not new. Fermented milk products have been consumed by human beings for thousands of years with the belief that they provide health benefits.1 For example, according to Persian tradition, Abraham of the Old Testament owed his longevity to sour milk.2 In the early 20th century, the Russian immunologist, Elie Metchnikoff, proposed that ingestion of

lactic acid bacteria promoted health and longevity of life.3 He based his theory on the observation that Bulgarians who consumed large quantities of fermented milk lived longer than those who did not. Around the same time, the first attempt to treat disease with bacteria was made by Dr Henry Tissier, a French pediatrician, who discovered Y-shaped or "bifid" bacteria (now known as Bifidobacterium) and recommended administration of isolated bifid cultures to infants with diarrhea to help restore a healthy gut flora.4 Metchnikoff and Tissier are largely credited for being the first individuals to make scientific suggestions about probiotic bacteria, although the term probiotic was not coined until 1965. The term probiotic, which literally means "for life," was first introduced by Lilly and Stillwell5 in 1965 to describe "substances produced by one microorganism which stimulate the growth of another." Since that time, the definition has undergone many revisions. In an attempt to provide an agreed upon definition, a joint Food and Agricultural Organization/World Health Organization Expert Consultation redefined probiotics as "live microorganisms which when administered in adequate amounts confer a health benefit on the host."4 Currently, this is the most widely accepted definition. Probiotics can be bacteria or yeast, although the vast majority is bacteria. The most common bacteria used as probiotics are lactic acid bacteria from the genera Lactobacillus and Bifidobacterium. Certain species from other genera such as Streptococcus, Enterococcus, and Escherichia have also been used but to a lesser extent. The only yeast that is considered a probiotic is Saccharomyces boulardii (Table 1). Probiotics are available in a variety of food products, especially dairy products such as yogurt, milk, cottage cheese, and dietary supplement products. Dietary supplements containing freeze-dried probiotics in capsule, powder, or tablet form are becoming a popular choice. Table 1. Common Probiotic Organisms Multiple mechanisms of action have been postulated to account for the beneficial effects of probiotics in IBD. In broad terms, probiotics are thought to improve the epithelial barrier function of the intestine, alter the composition of the intestinal microflora, and modulate the immune response of the intestinal mucosa. However, the exact mechanism is likely to vary from one probiotic organism to another (Table 2). Table 2. Proposed Benefits of Probiotics to the Well-being and Health of the Animal Host Normal epithelial barrier function of the intestine requires an intact layer of epithelial cells and an adequate production of overlying mucus to prevent uptake of potentially harmful organisms and substances into the body. A disrupted and leaky intestinal epithelial barrier may be one of the initiating events in the pathogenesis of IBD.6 In addition, increased apoptosis (programmed cell death) of intestinal epithelial cells and decreased mucus production have been documented in patients with IBD and are thought to contribute to the pathogenesis. Several probiotics have demonstrated the ability to enhance the epithelial barrier function of the intestine. For example, Lactobacillus rhamnosus GG improves barrier function by inhibiting apoptosis of intestinal epithelial cells.7Streptococcus salivarius subsp thermophilus and Lactobacillus acidophilus have been shown to enhance the tight junctions between epithelial cells, thereby preventing infection from the invasion of pathogenic bacteria such as enteroinvasive Escherichia coli.8 Also, several Lactobacillus strains have been found to increase mucus production.9 Madsen10 showed that a synthetic probiotic mixture, VSL#3 (containing 4 Lactobacillus spp, 3 Bifidobacterium spp, and S salivarius subsp thermophilus), also restored the epithelial barrier function in a chronic colitis mouse model. The improvement of the

barrier function is probably the result of a direct effect of probiotic bacteria or their secreted bacterial products. Normally, there is a balance between the beneficial bacterial species and the detrimental bacterial species that make up the intestinal microflora. In IBD, a number of genetic and environmental factors are thought to upset this balance such that there is a relative predominance of detrimental disease-inducing bacteria that contribute to the chronic inflammatory process in IBD.11 Probiotics can help restore a healthy intestinal microflora by directly increasing the population of beneficial bacteria and by suppressing the growth and function of detrimental bacteria. For example, Bifidobacterium infantis has been shown to suppress the growth of Bacteroides vulgatus, a pathogenic microbe possibly responsible for the induction and perpetuation of IBD.12 Probiotic organisms can inhibit pathogenic bacteria in several ways. First of all, they competitively exclude pathogens by occupying the limited physical space available for colonization in the gut. In addition, probiotic organisms can either directly secrete antimicrobial substances (eg, organic acids, hydrogen peroxide, and bacteriocins) and/or stimulate host intestinal cells to secrete antimicrobial substances (ie, defensin molecules), which destroy pathogens before they can colonize the gut.13 Several probiotics have demonstrated the ability to prevent epithelial adhesion and invasion of pathogenic bacteria. For example, E coli Nissle 1917 inhibits epithelial adhesion and invasion of a pathogenic E coli strain isolated from patients with CD.14 Inflammatory bowel disease is thought to be caused by an overly aggressive immune response to the endogenous gut microflora in genetically susceptible individuals. This results in an increased production of chemical signals that promote inflammation. These proinflammatory cytokines include, for example, tumor necrosis factor [alpha] and interferon [gamma]. Anti-inflammatory cytokines are interleukin 10 and transforming growth factor [beta]. Probiotic organisms are generally thought to modify the immune system of the intestinal mucosa by reducing the production of proinflammatory cytokines and increasing the production of anti-inflammatory mediators. Studies have shown that Lactobacillus plantarum, L rhamnosus GG, and VSL#3 can increase the production of interleukin 10 and that specific lactobacilli and bifidobacteria species can reduce the production of tumor necrosis factor [alpha] and interferon [gamma].15,16 The mechanisms by which probiotics exert their immunomodulatory effects are complex and beyond the scope of this review. Probiotics are generally well tolerated and have an excellent overall safety record. This is not surprising because many of the organisms used as probiotics are commensal, nonpathogenic inhabitants of the human gut and have been used safely in the production of fermented foods for centuries. The most common adverse effects of probiotics include bloating, flatulence, and constipation. There have been some reports of probiotics inducing serious infections such as bacterial and fungal sepsis. However, these cases occurred in immunocompromised patients. There are no reports of such cases in healthy people.1 Animal models have been used extensively to study the efficacy of probiotics in treating chronic intestinal inflammation and to elucidate the mechanisms by which probiotics work. Successful reduction of intestinal inflammation in many of these experimental models has provided the support for human clinical trials16,17 (Table 3). Escherichia coli Nissle 1917, VSL#3, and bifidobacteriafermented milk have been shown to have some success at inducing and maintaining remission of UC and reducing disease activity.22,25 Table 3. Clinical Studies Testing Probiotics in the Treatment of Human Inflammatory Bowel Disease

VSL#3 proved to be effective in maintaining remission of chronic relapsing pouchitis, preventing the development of pouchitis compared with placebo treatment; in addition, it also significantly improved patient quality of life.20 One study with L rhamnosus GG, however, was ineffective in reducing pouchitis disease activity.30 The efficacy of probiotics in CD is still controversial. For example, Lactobacillus salivarius, VSL#3, and S boulardii in combination with conventional therapy (mesalamine) have had some success.29 On the other hand, there are numerous studies reporting the ineffectiveness of various probiotics in CD.31-35 Because the viability of probiotics in some food products and during transit through the gastrointestinal tract is variable, the prebiotic concept has been developed. Prebiotics are nondigestible short-chain carbohydrates, originally defined as selectively fermented ingredients that allow specific changes, both in the composition and/or activity in the gastrointestinal microflora that confer benefits upon host's well-being and health.36 Substances are considered prebiotics according to the following conditions: (1) when they are not broken down nor absorbed by enzymes in the upper part of the mammalian gastrointestinal tract, (2) when they are selectively fermented by one or a limited number of potentially beneficial bacteria in the intestine, and (3) when they are able to alter the colonic microflora toward a healthier composition.36,37 Prebiotics have become very popular food ingredients. The most commonly used prebiotics, inulin and oligofructose, are natural food ingredients or dietary fibers present in plants as storage carbohydrates. Wheat, chicory, bananas, onions, leeks, Jerusalem artichokes, asparagus, and garlic contain prebiotics. Most commercially used prebiotics are synthesized from sucrose or extracted from chicory roots. They are used in, for example, confectioneries, bakery products, fruit juices, desserts, spreads, taste improver, sweetener, and fat replacers and sometimes used as viscosityincreasing agents.38 Inulin and oligofructose, also called [beta]-fructans, are composed of fructose units joined by [beta]glycosidic links. Because of their different fructose chain lengths, inulin and oligofructose are used for different purposes. Inulin has a longer chain length and is therefore less soluble and suitable as a fat replacer. Oligofructose is composed of a shorter chain length of fructose molecules and is, for example, used to replace sugar.39 Depending on the diet, the daily intake of prebiotics in Western societies varies from 3 to 13 g per day.40 Many substances are claimed to have prebiotics effects but only fructo-oligosaccharides, galactooligosaccharides, lactulose, and inulin have been shown to meet all 3 before mentioned criteria.41 Other potential prebiotic candidates42 are mentioned in Table 4. Table 4. Potential Candidate Prebiotic Substrates Different medical conditions have been speculated to ameliorate upon treatment with prebiotics,

including improvement of mineral absorption, reduced risk for colon cancer, improvement of food allergies, alleviation of constipation, regulation of lipid metabolism, and reduction of antibioticinduced diarrhea.38,43 The working mechanisms of prebiotics are not fully understood yet, but many theories have been formed (Table 5).44,45 In broad terms, the beneficial effects are believed to be due to the stimulation of protective intestinal organisms and the production of short-chain fatty acids (SCFAs) as fermentation products of prebiotics. Table 5. Proposed Benefits of Prebiotics to the Well-being and Health of the Animal Host The intestinal barrier functions to protect the individual from potential bacterial threats. The mucus layer in the gastrointestinal tract plays a major role by preventing the attachment and translocation of bacteria across the epithelial wall. A decrease in mucus production is seen in IBD. Prebiotics have been shown to increase the mucus layer in a rat model of colitis.46 As mentioned before, intestinal bacteria play an important role in the pathogenesis and attenuation of IBD. Prebiotics change the intestinal microflora in animal models and human studies by increasing the numbers of intestinal protective bacteria, for example, lactobacilli and bifidobacteria, and decreasing the proportion of pathogenic bacteria.47 Several studies performed in infants confirmed this, showing that the intestinal microbiota of breast-fed infants (containing milk oligosaccharides) is generally dominated by bifidobacteria and lactic acid bacteria. In contrast, formula-fed infants' intestinal microflora contains lower numbers of bifidobacteria and lactic acid bacteria and contains more bacteroides, clostridia, and enterobacteriaceae.48 However, after the prebiotic diet is stopped, these microflora changes gradually return to baseline levels.49 Short-chain fatty acids include butyrate, acetate, and propionate. Butyrate is the major energy source for colonic epithelial cells and plays an essential role in the maturation of colonic epithelium, regeneration of mucosa, induction of epithelial cell differentiation, and stimulation of their apoptosis.40 A reduced level of luminal SCFAs may play a role in the onset of IBD. The amount of SCFAs produced in the colon depends on the composition of intestinal microflora, their substrates, and the gut transit time. Fermentation of prebiotics by colon bacteria results in higher luminal SCFA production, which results in acidification of the colonic content. Intraluminal acidification may inhibit the growth of harmful or disease-inducing bacteria.50 Several studies show that the prebiotic effects are different for each prebiotic substance and that these depend on intestinal pH, prebiotic dosages, intraluminal concentrations of prebiotics, duration of intake, locations in the gut where fermentation occurs, and composition of endogenous intestinal microflora.40 Prebiotics have been part of human diets for centuries and are generally recognized as safe to consume. However, they can cause symptoms of abdominal pain, eructation, flatulence, bloating, abdominal cramps, and diarrhea.38 There are some reports of increased bacterial translocation of pathogenic bacteria during prebiotic treatment, such as Salmonella, and in sepsis models, but these results are controversial and are not seen in patients.51 More research in this area is needed. The effects of prebiotics are most extensively studied in different rodent models of IBD. Various efficacy of prebiotics and synbiotics (combination of probiotics and prebiotics) in different IBD models was found, but in most studies, prebiotics seem to ameliorate intestinal inflammation. Inulin,52 starch,53 lactulose,54 combination of oligofructose and inulin,55 and goat milk oligosaccharides56 reduced colitis. Some fructo-oligosaccharides showed mixed results, whereas

galacto-oligosaccharides57 failed to reduce intestinal inflammation. Currently, only a few studies with prebiotics in patients with IBD have been published. Emerging small short-term studies using prebiotics or synbiotics showed reduction of inflammation in patients with pouchitis, UC, and CD (Table 6). A small open-label study in patients with active ileocolonic CD treated with a combination of oligofructose and inulin showed a significant reduction in disease activity.60 A recent pilot study investigated the adjunct effect of oligofructose-enriched inulin in patients with mild to moderate UC with concomitant 5-aminosalicylic acid treatment (n = 19). This placebo-controlled study reported a significant reduction of fecal calprotectin (marker of intestinal inflammation) in the prebiotic-treated patients compared with the placebo group, suggesting that these prebiotics reduced chronic intestinal inflammation.62 Table 6. Clinical Studies Testing Prebiotics or Synbiotics in the Treatment of Human Inflammatory Bowel Disease A randomized double-blind crossover study in pouchitis patients after colectomy for UC treated with inulin resulted in the reduction of mucosal inflammation58 However, Chermesh et al61 could not show prevention of relapse of CD after surgical resection with synbiotic treatment, although this study may be underpowered. Conclusion and Future Perspectives Probiotics and prebiotics are emerging as promising therapeutic options for the treatment and prevention of flare-ups of IBD. A significant number of studies in both animal models and human IBD have documented the efficacy of these therapies in ameliorating chronic intestinal inflammation. In addition, these studies have led to a greater understanding of the mechanisms by which probiotics and prebiotics exert their beneficial effects. However, it is important to remember that the mechanisms elucidated cannot be generalized, as not all probiotics and prebiotic have similar therapeutic effects. Probiotics and prebiotics are widely available, are easy to consume, and are recognized as safe to consume. Side effects are rare, but some adverse effects such as bloating and flatulence tend to limit subsequent intake. The results obtained thus far warrant further rigorous well-designed and larger clinical trials to firmly establish the safety and efficacy of probiotics and prebiotics in IBD. REFERENCES 1. Boyle RJ, Robins-Browne RM, Tang MLK. Probiotic use in clinical practice: what are the risks? Am J Clin Nutr. 2006;83:1256-1264. [Context Link] 2. Schrezenmeir J, de Vrese M. Probiotics, prebiotics, and synbiotics-approaching a definition. Am J Clin Nutr. 2001;73(suppl):361S-364S. [Context Link] 3. Metchnikoff E. The prolongation of life: optimistic studies. London, England: ButterworthHeinemann; 1907. [Context Link] 4. FAO/WHO. Health and nutritional properties in food including powder milk with live lactic acid bacteria. 2001. http://www.fao.org/ag/agn/agns/micro_probiotics_en.asp . Accessed June 9, 2007. [Context Link] 5. Lilly DM, Stillwell RH. Probiotics: growth promoting factors produced by microorganisms.

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52. Videla S, Vilaseca J, Antol[latin dotless i]n M, et al. Dietary inulin improves distal colitis induced by dextran sodium sulfate in the rat. Am J Gastroenterol. 2001;96:5. [Context Link] 53. Moreau NM, Martin LJ, Toquet CS, et al. Restoration of the integrity of rat caeco-colonic mucosa by resistant starch, but not by fructo-oligosaccharides, in dextran sulfate sodium-induced experimental colitis. Br J Nutr. 2003;90:75-85. [Context Link] 54. Rumi G, Tsubouchi R, Okayama M, et al. Protective effect of lactulose on dextran sulfate sodiuminduced colonic inflammation in rats. Dig Dis Sci. 2004;49:1466-1472. [Context Link] 55. Hoentjen F, Welling GW, Harmsen HJM, et al. Reduction of colitis by prebiotics in HLA-B27 transgenic rats is associated with microflora changes and immunomodulation. Inflamm Bowel Dis. 2005;11:11. [Context Link] 56. Daddaoua A, Puerta V, Requena P, et al. Goat milk oligosaccharides are anti-inflammatory in rats with hapten-induced colitis. J Nutr. 2006;136:672. [Context Link] 57. Holma R, Juvonen P, Asmawi MZ, et al. Galacto-oligosaccharides stimulate the growth of bifidobacteria but fail to attenuate inflammation in experimental colitis in rats. Scand J Gastroenterol. 2002;37:1042-1047. [Context Link] 58. Welters CFM, Heineman E, Thunissen FBJM, et al. Effect of dietary inulin supplementation on inflammation of pouch mucosa in patients with an ileal pouch-anal anastomosis. Dis Colon Rectum. 2002;45:621-627. [Context Link] 59. Furrie E, Macfarlane S, Kennedy A, et al. Synbiotic therapy (Bifidobacterium longum/synergy 1) initiates resolution of inflammation in patients with active ulcerative colitis: a randomised controlled pilot trial. Gut. 2005;54:242-249. 60. Lindsay JO, Whelan K, Stagg AJ, et al. Clinical, microbiological, and immunological effects of fructo-oligosaccharide in patients with Crohn's disease. Gut. 2006;55:348-355. [Context Link] 61. Chermesh I, Tamir A, Reshef R, et al. Failure of synbiotic 2000 to prevent postoperative recurrence of Crohn's disease. Dig Dis Sci. 2007;52:385-389. [Context Link] 62. Casellas F, Norruel N, Torrjeo A, et al. Oral oligofructose-enriched inulin supplementation in acute ulcerative colitis is well tolerated and associated with lowered faecal calprotectin. Aliment Pharmacol Ther. 2007;25:1061-1067. [Context Link] Copyright 1996-2004 Lippincott Williams & Wilkins, Inc., A Wolters Kluwer Company. All rights reserved.

Risk of Infertility in Women Triples After Common Inflammatory Bowel Disease Surgery (press release)
by NaturalNews, citizen journalist The risk of infertility in women triples after the most major surgery for the inflammatory bowel disease ulcerative colitis, suggests research published ahead of print in the journal Gut. The authors base their finding on an extensive trawl of print and online research archives, and a detailed analysis of eight published studies. Infertility was defined as a failure to conceive after 12 months of trying. Ulcerative colitis is a condition in which sores and inflammation develop along the lining of the large intestine, producing severe diarrhoea and rectal bleeding. It affects around 1 to 2% of the population. Surgical removal of the colon is sometimes needed to alleviate persistent and painful symptoms. Ileal pouch anal anastomosis is a standard procedure in which the lower section of the large intestine is removed and a surgical pouch artificially created from the small intestine. This is then joined to a short remaining cuff of the rectum to ensure as normal bowel function as possible. The evidence from the published studies showed that the risk of infertility after drug treatment was around 1 in 7 or 15%. But this risk tripled to 48% after ileal pouch anal anastomosis. All patients seemed to be at risk of infertility, so there were no obvious factors among the patients or the procedure itself to account for the increased risk. Based on previous X-ray studies of the fallopian tubes, which transport ripened eggs from the ovary to the womb, the authors suggest that such extensive surgery may scar or block these tubes.

Inflammatory Bowel Disease in Children An Overview for Pediatric Healthcare Providers Angel Merchant MSN, RN, FNP Gastroenterology Nursing July/August 2007 Volume 30 Number 4 Pages 278 - 282

Abstract This article provides an overview of the clinical findings of pediatric inflammatory bowel disease (IBD) and the more common medication and treatment options that are available for children and adolescents with Crohn disease and colitis. Increasing awareness and education about Crohn disease and colitis among nurses and healthcare providers is vital. When healthcare providers are able to recognize the signs and symptoms of IBD, earlier referrals can be made and effective treatments can be initiated. As the mother of a child with colitis, the sister of a patient with Crohn disease, and a sufferer of Crohn disease myself, I write this article from both personal experience and clinical practice as a registered nurse, hoping it will be helpful to you.

Inflammatory bowel disease (IBD) is the collective term used to refer to the gastrointestinal (GI) diseases of ulcerative colitis and Crohn disease (Kugathasan et al., 2003; UpToDate, 2006). It is estimated that over 2,000,000 Americans suffer from some form of IBD. At least 300,000 of these are children and adolescents (UpToDate, 2006). Inflammatory bowel disease occurs regardless of gender, race, ethnicity, or income level and is equally prevalent in rural and urban areas (Kugathasan et al., 2003; National Institute of Health and National Institute of Diabetes and Digestive and Kidney Disease [NIDDK], 2006). Although there appears to be a genetic link and a familial predisposition, the cause of IBD is not known (Mayo Foundation for Medical Education and Research [Mayo], 2005; NIDDK, 2006). Clinical Signs and Symptoms Both Crohn disease and ulcerative colitis are characterized by ulcers and inflammation in the lining of the GI tract (Mayo, 2005; NIDDK, 2006; UpToDate, 2006). In colitis, the ulcerations are found only in the large intestine and penetrate only the first few layers of the mucosal lining (Mayo, 2006; UpToDate, 2006). In Crohn disease, however, the ulcerations can be found anywhere throughout the GI tract, including the esophagus and mouth (Mayo, 2005; NIDDK, 2006). These ulcers are often deeper and can affect all layers of the intestinal mucosa, causing fissures or fistulas (NIDDK, 2006). In both Crohn disease and colitis, the patient can have periods of remission and exacerbations throughout his or her life, which may last months or years (UpToDate, 2006). Because irritable bowel syndrome, lactose intolerance, diverticulitis, colon cancer, allergic colitis, gastroesophageal reflux disease, peptic ulcer disease, and gastroenteritis can all mimic IBD, a detailed history from the parent and, if possible, the child is invaluable to the diagnosis of IBD. The timing and onset of symptoms in relation to eating and activity should be noted carefully as pain is often worse after eating and increases in times of stress (UpToDate, 2006). Historical assessment should include questions regarding poor appetite, indigestion, and frequent nausea. Failure to thrive or initially good growth followed by a gradual or sudden decline should be noted. In prepubescent children, growth retardation is a primary finding of IBD (Mayo, 2006; NIDDK, 2006; Saha, Ruuska, Laippala, & Lento, 1998). A history of multiple food allergies or intolerances should be noted. A dietary record should be kept to look at caloric intake and variety of foods. For example, lactose intolerance can often cause GI upset and symptoms of IBD (Mayo, 2005). The nurse or healthcare provider should ask about any recent travel or exposure to illness indicative of possible viral or

bacterial infections. A family history of Crohn disease, colitis, or irritable bowel syndrome is often a "red flag" in the pediatric patient with symptoms. The most common presentations of IBD are a general feeling of malaise, abdominal pain, fatigue, bloating, diarrhea, nausea, and weight loss (Kugathasan et al., 2004). The patient may also present with fever, bloody stools, and poor appetite (Kugathasan et al., 2004; Saha et al., 1998; UpToDate, 2006). In some children, particularly in those with Crohn disease, aphthous ulcers, myalgias, arthralgias, skin problems, and anemia may also occur. Phrases such as "I'm sick," "I don't feel good," and "my stomach hurts" are common in IBD. Because the signs and symptoms are similar, differentiating between Crohn disease and colitis can be very difficult (Mayo, 2005; NIDDK, 2006; UpToDate, 2006). Table 1 provides a brief comparison of the more common signs and symptoms found in Crohn disease and colitis. TABLE 1 Characteristics of Ulcerative Colitis Versus Crohn Disease Diagnostic and Laboratory Tests If Crohn disease or colitis is suspected in a child, some initial laboratory tests should be obtained. These should include a complete blood count (CBC) to check for anemia and infection and a comprehensive metabolic profile (CMP) to check renal and liver function, along with electrolytes and nutritional status. An erythrocytic sedimentation rate (ESR), which is a marker of inflammation, should also be drawn as it is commonly elevated with IBD. Stool samples should be obtained to rule out the presence of a bacterial or viral infection, parasites, or amoebae such as Clostridium difficile, Helicobacter pylori, or Escherichia coli (Mayo, 2005). Although several options are available, the radiological evaluation of IBD in the pediatric population is challenging (Crohn's and Colitis Foundation of America [CCFA], 2006). Thorough explanations and much emotional support are needed for both the patient and the family prior to any invasive or radiological procedures. An upper GI series with contrast can show masses, areas of inflammation, or structural abnormalities in the stomach and small intestines; however, this series is usually not well tolerated in the pediatric population because of the unsavory taste of the contrast (Mayo, 2006). A barium enema can also be used to show abnormalities in the colon. This exam, for obvious reasons, would not be a good choice for most children without counseling, but may be a possibility for adolescents when appropriate (Mayo, 2006). An abdominal computed tomography (CT) scan or magnetic resonance imaging (MRI) could also show abnormalities, inflammation, and areas of ulceration, but both require the patient to remain perfectly still, which is difficult to do for most children without sedation. If the child is claustrophobic or afraid of machinery or loud noises, this experience could be very traumatic for him or her. To definitively diagnose either Crohn disease or colitis, the gold standard is endoscopy (Mayo, 2006). In this situation, the child is sedated and monitored, allowing a thorough exam to be performed. In a colonoscopy, a small scope is passed through the large intestine via the rectum. In an esophagogastroduodenoscopy (EGD), a small scope is passed through the stomach and small intestine via the esophagus. With endoscopy, any areas of inflammation or ulceration can be seen and biopsies can be obtained from the affected area. These biopsies are then sent to pathology for diagnosis or to rule out Crohn disease or colitis. Medication and Treatment Options The treatment and management of IBD in the pediatric population is, at best, difficult. Ideally and preferably, when IBD is suspected, the child is referred to a specialist trained in the diagnosis, management, and treatment of IBD; however, particularly in rural settings, the availability of specialists, transportation issues, and financial concerns can prevent this from happening. In these cases, it may be up to the child's primary care provider to treat them.

The CCFA (2006) has a wonderful Web site with up to date information and many resources for both providers and patients alike and is a good place to start when looking for information on IBD. Medical databases such as UpToDate, Epocrates, and WebMD are also helpful for healthcare providers and contain vast sources of information on almost any medical condition. The CCFA (http://www.ccfa.org ) has developed a great online resource for children and teens with stories, chat rooms, and medical terms in a language they can understand. They also sponsor a summer camp for children with IBD. The treatment of IBD is generally twofold and consists of both symptom relief and the suppression of disease progression (CCFA, 2006; Mayo, 2005; NIDDK, 2006; UpToDate, 2006). Medication management occurs at three basic levels or stages and is categorized as mild, moderate, or severe on the basis of the severity of symptoms and the amount of intestinal involvement (CCFA, 2006; Mayo, 2005; NIDDK, 2006; UpToDate, 2006). There are several categories of medications that are used to treat pediatric IBD. Most of the medications used in the treatment of adults with Crohn disease and colitis are also used in children and are based on the patient's weight (CCFA, 2006). Because the use of some of these drugs in the pediatric population is associated with higher risks, many of these drugs are used only by pediatric GI specialists. The age of the child, severity of the disease, and availability of specialists should all be considered. The first line or tier of medications used are generally the aminosalicylates (5-ASA preparations) such as mesalamine (Pentasa, Asacol) and sulfasalazine (Azulfidine). These medications decrease the inflammation in the intestines and begin to heal the ulcers. They are often very useful in mild-tomoderate ulcerative colitis and Crohn disease (Anonymous, 2005; CCFA, 2006; Mayo, 2006; NCCAM, 2006). The aminosalicylates are dosed in mg/kg/day in divided doses and are available in pills, suppositories, and enemas, depending on the areas of involvement. The oral form is often better tolerated in the younger population, for obvious reasons, and may be opened or crushed and placed in applesauce, yogurt, or pudding. Sulfasalazine is also just as effective as mesalamine, but it tends to have more side effects, such as headache, light sensitivity, and rash. An addition to this first tier also may be low-dose antimicrobials, such as metronidazole (Flagyl) or ciprofloxacin (Cipro) daily to suppress the bacteria and aid in healing. It is important to stress to adolescents the importance of not drinking alcohol while taking Flagyl, as severe vomiting and diarrhea may occur. Children need to be monitored carefully for side effects of antibiotic use (e.g., increased diarrhea or superimposed infections, such as yeast) while on these medications. For diarrhea, loperamide HCl (Imodium) is often helpful. Lomotil is not recommended in the pediatric population because of the anticholinergic effects (CCFA, 2006; Mayo, 2005). Simethicone can be used to decrease gas and bloating, which may help to relieve some of the abdominal pain. The second tier of treatment in more resistant, moderate disease cases is the addition of corticosteroids, such as methylprednisolone or prednisone, to the above regime (Anonymous, 2005; CCFA, 2006; NCCAM, 2006). Although these steroids are 60% to 80% effective in reducing inflammation and inducing remission, they are very immunosuppressive and carry a great risk of dependency; once started, it is often hard to wean IBD patients from these drugs. The short-term effects of steroid use, such as weight gain, moon face, nervousness, tremors, hyperglycemia, and immunosuppression, generally subside after treatment is stopped. In contrast, the long-term effects, such as failure to thrive, decreased bone density, poor vasculature, mood swings, and acne, can remain indefinitely (CCFA, 2006; Kugathasan et al., 2004; Saha et al., 1998). The moon face, weight gain, and acne can be very difficult to deal with, particularly for adolescents, and much counseling and emotional support may be needed.

Within the last several years, a newer nonsystemic steroid, budesonide (Entocort), has become available. This steroid is specific to the intestines and has shown to be very effective in adults with IBD, with few systemic side effects. It has not yet been FDA approved for the pediatric population, but it is likely that it will be coming soon. The third tier of treatment is used in moderate to severe refractory cases of Crohn disease and colitis and involves the addition of immunomodulators and immunosuppressives (Anonymous, 2005; CCFA, 2006; Mayo, 2005; NCCAM, 2006). These medications, though often effective, are potentially dangerous and have numerous side effects. The immunomodulators include drugs such as azathioprine (Imuran) or 6MP (Purinethol). These medications enhance and support the activity of the immune system, thereby inducing remission and reducing the need for steroids. These drugs can often take 3 to 6 months before effectiveness is noted, however. Cyclosporine (Sandimmune), an immunosuppressant used in organ transplant patients, has shown to also be very effective in controlling severe, nonresponsive disease (Anonymous, 2005; CCFA, 2006; Mayo, 2005; NCCAM, 2006). This drug is often used temporarily while waiting for the immunomodulators to begin working. While on these immunomodulators and immunosuppressives, patients must be monitored carefully for infections or illnesses, such as pneumonias, flu, strep, and decreased white blood cell count. Routine monitoring of the patient's CBC and CMP levels are recommended (Mayo, 2005). One of the newest and most helpful medications so far has been infliximab (Remicade). This drug is classified as a biologic and is synthesized from both mouse and human proteins. It has been found to actually block the tumor necrosis factor in the body, which is a key factor present around any areas of ulceration or inflammation. This medication has been shown to heal the ulcers in both inflammatory and fistulizing Crohn disease in children and induces remission in about two thirds of these patients (Mayo, 2005; NIDDK, 2006). It is administered as a series of intravenous infusions over a several month period. Although this medication works well in most cases, there is a significant risk for allergic reaction due to the mouse proteins used, and patients must be carefully monitored during infusion. As with any medication, the patient's insurance plan or method of payment must also be considered because the cost for Remicade is about $16,000 per year (Anonymous, 2005). Many insurance companies will not cover Remicade unless given under the guidance of a specialist using strict criteria. As an alternative to the traditional "allopathic" medicines that are often prescribed, there are several herbal and "naturopathic" remedies that are available and provide relief for many (Mayo, 2005; NCCAM, 2006). Acupuncture and acupressure have been used in Japan and China for centuries and use needles or pressure points to improve the functioning of glands and organs. Massage therapy is extremely relaxing and promotes blood flow, relaxes muscles, and relieves tension (Mayo, 2005; NCCAM, 2006). A variation of this, called colonic massage, is focused on the abdomen and has been very effective in children when done by an experienced practitioner (Thompson, 2000). Craniosacral therapies such as therapeutic touch, yoga, Reiki, and support from spiritual or energy healers can also provide symptom relief and promote healing. In addition to these therapies, there are numerous herbal remedies that are used by patients. Aloe vera juice, Kombucha tea, omega-3 fatty acids, N-acetyl glutamine, and coenzyme Q10 are used for ulceration and inflammation (Mayo, 2005; NCCAM, 2006; Thompson, 2000). Deglycyrrhizinated licorice extract and grape seed extract are soothing for aphthous ulcers. Many herbal teas, such as ginger and raspberry, are soothing to the intestines. Dry curd, L-glutamine, and fiber are helpful for diarrhea (Mayo, 2005; Thompson, 2000). Multiple vitamin, iron, and mineral supplements exist and are definitely recommended to replace and prevent nutrients lost from diarrhea, vomiting, and malnutrition, (CCFA, 2006; NCCAM, 2006; UpToDate, 2006). The list is endless. Although many of these therapies have been used for centuries, it is recommended that patients and providers consult with a naturopathic healer or physician trained in herbal remedies prior to starting a

child on herbal supplements (NCCAM, 2006; Thompson, 2000). It is also very important to ask the patient and the family if they are taking or using any naturopathic remedies or herbal supplements, as they may interfere with medical therapies. The National Institute of Health has established the National Center for Complimentary and Alternative Medicine and has a vast Web site on many different therapies and alternative remedies used in IBD and other conditions. When and if medicinal and naturopathic remedies fail, surgery is often the last resort. Estimates suggest that approximately 50% to 70% of children with Crohn disease and 25% to 50% of those with colitis will require surgery within 10 to 15 years of diagnosis (Mayo, 2005; NIDDK, 2006; UpToDate, 2006). This is a huge and frightening step for many children and their families and must be handled with great care. If possible, counseling and therapy are recommended prior to and after surgery to help children and their families cope with this endeavor. For adolescent females, in particular, the thought of having an abdominal scar after surgery is very traumatic. Although more advances are being made every day, there is only one surgical option at this time for children who have Crohn disease that is resistant to medical management. This treatment is that of a bowel resection in which the diseased portion of the intestine is removed and the healthy portion is resected. This surgery is often quite effective and patients may experience months to years without symptoms. The chance of recurrent disease, however, is significant, and surgical intervention is not an option for esophageal or gastric involvement. Although a drastic measure, a total colectomy (removing the entire colon) is the only definitive cure for ulcerative colitis (Mayo, 2005). Because it is curative, patients remain disease-free thereafter. These patients will always have diarrhea and watery stools. Consequently, these patients will need to be monitored closely for nutrition, hydration, and weight loss, as they no longer have the colon to absorb fluid and nutrients (UpToDate, 2006). These patients will require a colostomy for elimination because the rectum is permanently closed. For this reason, many patients and parents are resistant to this type of surgery. Another more acceptable alternative for the ulcerative colitis patient is a relatively new procedure called ileoanal anastomosis (Mayo, 2005). In this procedure, the entire colon is removed and a pouch (called the j-pouch) is specially made from the small intestine. This new pouch serves as the patient's colon, thereby avoiding the need for a permanent colostomy. Most patients are very pleased with this alternative. The only limitation to this surgery is that there is still a small portion of the colon left where it attaches to the rectum, and this area can still become diseased or ulcerated. The j-pouch can also become inflamed after surgery, referred to as pouchitis (Mayo, 2005; UpToDate, 2006). This inflammation is often well managed by local aminosalicylate enemas, suppositories, or corticosteroids. A newer, controversial treatment option that is now being used in select, severe cases of IBD, namely Crohn disease, is that of a stem cell transplant (Kugathasan et al., 2004; Peck, 2001). In this procedure, the patient's own stem cells are harvested from his or her bone marrow. These stem cells are then multiplied and given back to the patient at a specific point in the treatment, once the patient's own immune system has purposefully been depleted by chemotherapy agents. Originally used for the treatment of cancer, stem cell transplant has shown amazing promise in Crohn patients (Peck, 2001). Some patients have had complete remission, and others have been without evidence of disease for longer than 6 months. Because of the complexity and significant risks of the procedure (severe immunosuppression, 5% mortality rate), there is a lengthy screening process to go through, and only the most severe cases qualify for this option. Because of the above mentioned reasons and risks, this procedure is not yet available for those under 16 years of age. After a 10-year battle with Crohn disease that would not effectively respond to medicines or surgery, my sister was the first person in the world to receive a stem cell transplant for Crohn disease. Within 10

months, she was healthy and enjoying life again. For more information on this procedure, providers may contact the Division of Immunotherapy for Autoimmune Diseases at Northwestern Memorial Hospital in Chicago, Illinois (Peck, 2001). Additional information can also be found at http://www.nmh.org or by calling the referral center at (312) 926-8400. Conclusion From personal experience, I can tell you that the treatment of the child or adolescent with IBD is, at best, difficult and challenging. Each child, family, and case is unique. Each family comes from a different walk of life and socioeconomic background, all with varied levels of understanding, coping mechanisms, and resources. When my son was diagnosed with colitis, I realized I was not thinking like a nurse anymore. When I heard the words "I think your son has Crohn disease," I became a scared, concerned mother with one million questions and just wanted someone to listen. As a nurse, a Crohn patient, and a mom, it is unnerving and frustrating being on the other side of the bed, letting someone take care of you and your family while you imagine all that could go wrong. At the same time, however, it is very comforting to know that someone cares and is willing to listen, even thought they do not necessarily have all of the answers. Nurses can sit with patients and families and talk to them at their level of understanding and need. We can laugh and cry with them, comfort them, and explain medical terms to them in ways that they can understand. As medical liaisons, we can coordinate with other healthcare providers and services to assist the patient with transportation, scheduling, insurance, or counseling if needed. As healthcare providers, we should also encourage our patients and families to be advocates for themselves, finding out as much as possible about Crohn disease and colitis. Encourage them to attend support groups and to speak with others who have been where they are now. No matter what our particular role or specialty, nurses are in a unique position to support our patients and their families, and I am honored to be part of the nursing profession. References Anonymous. (2005). Remicade's approval for ulcerative colitis raises questions about new high-tech versus older approaches. Prescriber's Letter, 12, 65-66. [Context Link] Crohn's and Colitis Foundation of America. (2006). Treating children and adolescents. Retrieved March 1, 2006, from http://www.ccfa.org/info/treatment/kidsmeds [Context Link] Kugathasan, K., Judd, R. H., Hoffmann, R. G., Heikenen, J., Telega, G., Khan, F., et. al. (2003). Epidemiologic and clinical characteristics of children with newly diagnosed inflammatory bowel disease in Wisconsin: A statewide population-based study. Journal of Pediatrics, 143, 525-531. [Context Link] Mayo Foundation for Medical Education and Research. (2005). Ulcerative colitis. Retrieved February 4, 2005, from http://www.mayoclinic.com/health/ulcerative-colitis/DS00598 [Context Link] Mayo Foundation for Medical Education and Research. (2006). Crohn's disease. Retrieved February 23, 2006, from http://www.mayoclinic.org/ [Context Link] National Center for Complimentary and Alternative Medicine. (2006). Alternative therapies in Crohn's disease and colitis. Retrieved January 31, 2006, from http://nccam.nih.gov/ [Context Link] National Institute of Health and National Institute of Diabetes and Digestive and Kidney Disease. (2006). Crohn's disease. Retrieved March 1, 2006, from http://digestive.niddk.nih.gov/ddiseases/pubs/crohns/index.htm [Context Link]

Peck, P. (2001). The story of the first stem cell transplant for Crohn's. Retrieved February 24, 2006, from http://www.webmd.com/news/20010810/first-patient-to-get-stem-cell-treatment-for-crohns-in-remission [Context Link] Saha, M., Ruuska, T., Laippala, P., & Lento, H. L. (1998). Growth of prepubertal children with inflammatory bowel disease. Journal of Pediatric Gastroenterology & Nutrition, 26, 310-314. [Context Link] Thompson, J. (2000). Listen to your gut. Vancouver, British Columbia, Canada: Caramal Publishing. [Context Link] UpToDate. (2006). Overview of the management of Crohn's disease in children and adolescents. Retrieved February 24, 2006, from http://www.uptodate.com [Context Link]

Symptom Correlates in Inflammatory Bowel Disease Sharon Dudley-Brown PhD, APRN, BC, FNP Gastroenterology Nursing Kathy B. Bean PhD, RN, CGRN, APRN, BC March/April 2005 Volume 28 Number 2 Pages 165 - 165 PDF Version Available!

Inflammatory bowel disease, specifically Crohn's disease and ulcerative colitis, is a chronic, destructive inflammatory disease of the gastrointestinal tract with a complex genetic basis. With no affirmed treatment, current management focuses on reducing inflammation and management of symptoms. Typically symptoms in inflammatory bowel disease have been described in terms of exacerbations and remission, although there exists preliminary data to support the notion of symptoms to some degree at all times. Characterizing the multiplicity of symptoms is important in inflammatory bowel disease. This presentation will describe preliminary results of a pilot study funded in part by the Society of Gastroenterology Nurses and Associates. Using a descriptive correlational design, the purpose of the study is to explore the relationships among influencing factors of physiological, psychological, and situational variables and symptoms. The theory of unpleasant symptoms will be used as the theoretical framework to explore the biobehavioral aspects of symptoms in inflammatory bowel disease because this theory considers relevant physiological, psychological and situational factors. Specific aims of this important pilot study will be highlighted in this session along with preliminary findings regarding symptoms experienced with inflammatory bowel disease. Section Description We are pleased to present the Abstracts from the SGNA's 32nd Annual Course: Passion for GI Nursing: Pass It On!! The diversity of these topics certainly reflects the richness and breadth of our specialty. In keeping with the tradition of the Annual Course, we hope the following abstracts will encourage discussions for improving nursing practice and patient care outcomes. Copyright 1996-2004 Lippincott Williams & Wilkins, Inc., A Wolters Kluwer Company. All rights reserved.