Crohn's disease, also known as regional enteritis, is an inflammatory disease of the intestines that may affect any part of the gastrointestinal tract from mouth to anus, causing a wide variety of symptoms. It primarily causes abdominal pain, diarrhea (which may be bloody if inflammation is at its worst), vomiting, or weight loss, but may also cause complications outside the gastrointestinal tract such as skin rashes, arthritis, inflammation of the eye, tiredness, and lack of concentration.
Crohn's disease is thought to be an autoimmune disease, in which the body's immune system attacks the gastrointestinal tract, causing inflammation; it is classified as a type of inflammatory bowel disease. There is evidence of a genetic link to Crohn's disease, putting individuals with siblings afflicted with the disease at higher risk. Males and females are equally affected. Smokers are two times more likely to develop Crohn's disease than nonsmokers. Crohn's disease affects between ( 400,000 and 600,000) people in North America. Crohn's disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age. There is no known pharmaceutical or surgical cure for Crohn's disease. Treatment options are restricted to controlling symptoms, maintaining remission, and preventing relapse.
The disease was named after American gastroenterologist Burrill Bernard Crohn, who, in 1932, together with two colleagues, described a series of patients with inflammation of the terminal ileum, the area most commonly affected by the illness. For this reason, the disease has also been called regional ileitis or regional enteritis. The condition, however, had previously been independently described in medical literature by others. The most notable case was in 1904 by Polish surgeon Antoni Lesniowski for whom the condition is alternatively named Lesniowski-Crohn's disease in Polish literature.
Crohn's disease is a chronic condition for which there is currently no cure. It is characterised by periods of improvement followed by episodes when symptoms flare up. With treatment, most people achieve a healthy weight, and the mortality rate for the disease is relatively low. However, Crohn's disease is associated with an increased risk of small bowel and colorectal carcinoma, including bowel cancer.
While the exact cause of Crohn's disease is unknown, the condition is linked to a problem with the body's immune system response.
Normally, the immune system helps protect the body, but with Crohn's disease the immune system can't tell the difference between normal body tissue and foreign substances. The result is an overactive immune response that leads to chronic inflammation. This is called an autoimmune disorder.
People with Crohn's disease have ongoing (chronic) inflammation of the gastrointestinal tract. Crohn's disease may occur in any area of the digestive tract. There can be healthy patches of tissue between diseased areas. The inflammation causes the intestinal wall to become thick.
There are different types of Crohn's disease, depending on the part of the gastrointestinal tract that is affected. Crohn's disease may involve the small intestine, the large intestine, the rectum, or the mouth.
A person's genes and environmental factors seem to play a role in the development of Crohn's disease. The body may be overreacting to normal bacteria in the intestines. he disease may occur at any age, but it usually occurs in people between ages 15 - 35. Risk factors include:
Symptoms depend on what part of the gastrointestinal tract is affected. Symptoms range from mild to severe, and can come and go with periods of flare-ups.
The main symptoms of Crohn's disease are:
DIET AND NUTRITION
• No specific diet has been shown to improve or worsen symptoms in Crohn's disease. Specific food problems may vary from person to person.
• You should eat a well-balanced, healthy diet. It is important for you to get enough calories, protein, and essential nutrients from a variety of food groups.
• Certain types of foods may worsen diarrhea and gas symptoms. The problem is more likely during periods when symptoms are present. Possible changes you can make to your diet include:
• Eat small amounts of food throughout the day.
• Drink lots of water (drink small amounts often throughout the day).
• Avoid high-fiber foods (bran, beans, nuts, seeds, and popcorn).
• Avoid fatty, greasy or fried foods and sauces (butter, margarine, and heavy cream).
• If your body does not digest dairy foods well, limit dairy products. Try low-lactose cheeses, such as Swiss and cheddar, and an enzyme product, such as Lactaid, to help break down lactose.
• Avoid foods that you know cause you gas, such as beans, spicy food, cabbage, broccoli, cauliflower, raw fruit juices and fruits -- especially citrus fruits.
• People who have a blockage of the intestines may need to avoid raw fruits and vegetables and other high-fiber foods.
• Ask your doctor about extra vitamins and minerals you may need:
• Iron supplements (if you are anemic)
• Calcium and vitamin D supplements to help keep your bones strong
• Vitamin B12 to prevent anemia
• You may feel worried, embarrassed, or even sad and depressed about having a bowel accident. Other stressful events in your life, such as moving, a job loss, or the loss of a loved one can cause digestive problems.
• Ask your doctor or nurse for tips on how to manage your stress.
• You can take medication to treat very bad diarrhea. Loperamide (Imodium) can be bought without a prescription. Always talk to your doctor or nurse before using these drugs.
• Other medicines to help with symptoms include:
• Fiber supplements may help your symptoms. You can buy psyllium powder (Metamucil) or methylcellulose (Citrucel) without a prescription. Ask your doctor about these products.
• Always talk to your doctor before using any laxative medicines.
• You may use acetaminophen (Tylenol) for mild pain.
• Drugs such as aspirin, ibuprofen (Advil, Motrin), or naproxen (Aleve, Naprosyn) may make your symptoms worse.
• Your doctor may also give you a prescription for stronger pain medicines.
Medicines that may be prescribed include:
• Aminosalicylates (5-ASAs) are medicines that help control mild to moderate symptoms. Some forms of the drug are taken by mouth; others must be given rectally.
• Corticosteroids (prednisone and methylprednisolone) are used to treat moderate to severe Crohn's disease. They may be taken by mouth or inserted into the rectum.
• Medicines such as azathioprine or 6-mercaptopurine quiet the immune system's reaction.
• Antibiotics may be prescribed for abscesses or fistulas.
• Biologic therapy is used to treat patients with severe Crohn's disease that does not respond to any other types of medication. Medicines in this group include Infliximab (Remicade) and adalimumab (Humira), certolizumab (Cimzia), and natalizumab (Tysabri).
• If medicines do not work, a type of surgery called bowel resection may be needed to remove a damaged or diseased part of the intestine or to drain an abscess. However, removing the diseased portion of the intestine does not cure the condition.
• Patients who have Crohn's disease that does not respond to medications may need surgery, especially when there are complications such as:
• Bleeding (hemorrhage)
• Failure to grow (in children)
• Fistulas (abnormal connections between the intestines and another area of the body)
• Infections (abscesses)
• Narrowing (strictures) of the intestine
There is no cure for Crohn's disease. The condition is marked by periods of improvement followed by flare-ups of symptoms. It is very important to stay on medications long-term to try to keep the disease symptoms from returning. If you stop or change your medications for any reason, let your doctor know right away. You have a higher risk for small bowel and colon cancer if you have Crohn's disease.
o Bowel obstructions
o Complications of corticosteroid therapy, such as thinning of the bones
o Erythema nodosum
o Fistulas in the following areas:
o Impaired growth and sexual development in children
o Inflammation of the joints
o Lesions in the eye
o Nutritional deficiency (particularly vitamin B12 deficiency)
o Pyoderma gangrenosum
Crohn's disease is more common in northern countries, and shows a higher preponderance in northern areas of the same country. The incidence of Crohn's disease is thought to be similar in Europe but lower in Asia and Africa. It also has a higher incidence in Ashkenazi Jews and smokers.
Crohn's disease has a bimodal distribution in incidence as a function of age: the disease tends to strike people in their teens and twenties, people in their fifties through their seventies, and ages in between due to not being diagnosed with Crohn's and being diagnosed instead with irritable bowel syndrome (IBS). It is rarely diagnosed in early childhood. It usually strikes females who are pediatric patients more severely than males. However, only slightly more women than men have Crohn's disease. Parents, siblings or children of people with Crohn's disease are three to twenty times more likely to develop the disease. Twin studies show a concordance of greater than fifty five percent for Crohn's disease.
At the present time, there is no cure for Crohn's disease and remission may not be possible or prolonged if achieved. In cases where remission is possible, relapse can be prevented and symptoms controlled with medication, lifestyle changes, and, in some cases, surgery. Adequately controlled, Crohn's disease may not significantly restrict daily living. Treatment for Crohn's disease is only when symptoms are active and involve first treating the acute problem, then maintaining remission.
Certain lifestyle changes can reduce symptoms, including dietary adjustments Elemental diet, proper hydration, and smoking cessation. Smoking may increase Crohn's disease; stopping is recommended. Eating small meals frequently instead of big meals may also help with a low appetite. To manage symptoms have a balanced diet with proper portion control. Fatigue can be helped with regular exercise, a healthy diet, and enough sleep. A food diary may help with identifying foods that trigger symptoms. Some patients should follow a low dietary fiber diet to control symptoms especially if fibrous foods cause symptoms. Patients should avoid milk or dairy products as they have been shown in recent research (2007) to contribute to or even cause Crohn's disease.
Crohn's cannot be cured by surgery, though it is used when partial or a full blockage of the intestine occurs. Surgery may also be required for complications such as obstructions, fistulas and/or abscesses, or if the disease does not respond to drugs. After the first surgery, Crohn's usually shows up at the site of the resection, however it can appear in other locations. After a resection, scar tissue builds up, which can cause strictures, which form when the intestines become too small to allow excrement to pass through easily, which can lead to a blockage. After the first resection, another resection may be necessary within five years..
For patients with an obstruction due t. o a stricture, two options for treatment are strictureplasty and resection of that portion of bowel.
Another complication following surgery for Crohn's disease in which the terminal ileum has been removed is the development of excessive watery diarrhea. This is due to an inability of the ileum to reabsorb bile acids after resection of the terminal ileum.
More than half of people with Crohn's disease have tried complementary or alternative therapy. These include diets, probiotics, fish oil and other herbal and nutritional supplements. The benefit of these medications is uncertain.
Acupuncture is used to treat inflammatory bowel disease in China, and is being used more frequently in Western society. However, there is little evidence that acupuncture has benefits beyond the placebo effect.
Homeopathy is frequently used in Germany as a treatment for Crohn's disease, though no clinical trials exist that demonstrate effectiveness.
Crohn's disease is one type of inflammatory bowel disease (IBD). It typically manifests in the gastrointestinal tract and can be categorized by the specific tract region affected. A disease of both the ileum (the last part of the small intestine, which connects to the large intestine), and the large intestine, Ileocolic Crohn's accounts for fifty percent of cases. Crohn's ileitis, manifest in the ileum only, accounts for thirty percent of cases, while Crohn's colitis, of the large intestine, accounts for the remaining twenty percent of cases and may be particularly difficult to distinguish from ulcerative colitis. Gastroduodenal Crohn's disease causes inflammation in the stomach and first part of the small intestine, called the duodenum. Jejunoileitis causes spotty patches of inflammation in the top half of the small intestine, called the jejunum . The disease can attack any part of the digestive tract, from mouth to anus. However, individuals affected by the disease rarely fall outside these three classifications, with presentations in other areas.
Crohn's disease may also be categorized by the behavior of disease as it progresses. These categorizations formalized in the Vienna classification of the disease. There are three categories of disease presentation in Crohn's disease: stricturing, penetrating, and inflammatory. Stricturing disease causes narrowing of the bowel that may lead to bowel obstruction or changes in the caliber of the feces. Penetrating disease creates abnormal passageways (fistulae) between the bowel and other structures, such as the skin. Inflammatory disease (or nonstricturing, nonpenetrating disease) causes inflammation without causing strictures or fistulae.
Endoscopy image of colon showing serpiginous ulcer, a classic finding in Crohn's disease
Many people with Crohn's disease have symptoms for years prior to the diagnosis. The usual onset is between fifteen and thirty ears of age, but can occur at any age. Because of the 'patchy' nature of the gastrointestinal disease and the depth of tissue involvement, initial symptoms can be more subtle than those of ulcerative colitis. People with Crohn's disease experience chronic recurring periods of flare-ups and remission.
Abdominal pain may be the initial symptom of Crohn's disease. It is often accompanied by diarrhea, especially in those who have had surgery. The diarrhea may or may not be bloody. People who have had surgery or multiple surgeries often end up with short bowel syndrome of the gastrointestinal tract. The nature of the diarrhea in Crohn's disease depends on the part of the small intestine or colon involved. Ileitis typically results in large-volume, watery feces. Colitis may result in a smaller volume of feces of higher frequency. Fecal consistency may range from solid to watery. In severe cases, an individual may have more than twenty bowel movements per day and may need to awaken at night to defecate. Visible bleeding in the feces is less common in Crohn's disease than in ulcerative colitis, but may be seen in the setting of Crohn's colitis. Bloody bowel movements are typically intermittent, and may be bright or dark red in color. In the setting of severe Crohn's colitis, bleeding may be copious. Flatulence and bloating may also add to the intestinal discomfort.
Symptoms caused by intestinal stenosis are also common in Crohn's disease. Abdominal pain is often most severe in areas of the bowel with stenoses. In the setting of severe stenosis, vomiting and nausea may indicate the beginnings of small bowel obstruction. Although the association is greater in the context of ulcerative colitis, Crohn's disease may also be associated with primary sclerosing cholangitis, a type of inflammation of the bile ducts.
Perianal discomfort may also be prominent in Crohn's disease. Itchiness or pain around the anus may be suggestive of inflammation, fistulization or abscess around the anal area or anal fissure. Perianal skin tags are also common in Crohn's disease. Fecal incontinence may accompany perianal Crohn's disease. At the opposite end of the gastrointestinal tract, the mouth may be affected by non-healing sores (aphthous ulcers). Rarely, the esophagus, and stomach may be involved in Crohn's disease. These can cause symptoms including difficulty swallowing (dysphagia), upper abdominal pain, and vomiting.
Crohn's disease, like many other chronic, inflammatory diseases, can cause a variety of systemic symptoms. Among children, growth failure is common. Many children are first diagnosed with Crohn's disease based on inability to maintain growth. As it may manifest at the time of the growth spurt in puberty, up to thirty percent of children with Crohn's disease may have retardation of growth. Fever may also be present, though fevers greater than (101.3 °F) are uncommon unless there is a complication such as an abscess. Among older individuals, Crohn's disease may manifest as weight loss, usually related to decreased food intake, since individuals with intestinal symptoms from Crohn's disease often feel better when they do not eat and might lose their appetite. People with extensive small intestine disease may also have malabsorption of carbohydrates or lipids, which can further exacerbate weight loss.
A colonoscopy is the best test for making the diagnosis of Crohn's disease, as it allows direct visualization of the colon and the terminal ileum, identifying the pattern of disease involvement. On occasion, the colonoscope can travel past the terminal ileum, but it varies from patient to patient. During the procedure, the gastroenterologist can also perform a biopsy, taking small samples of tissue for laboratory analysis, which may help confirm a diagnosis. As thirty percent of Crohn's disease involves only the ileum, cannulation of the terminal ileum is required in making the diagnosis. Finding a patchy distribution of disease, with involvement of the colon or ileum, but not the rectum, is suggestive of Crohn's disease, as are other endoscopic stigmata. The utility of capsule endoscopy for this, however, is still uncertain. A "cobblestone"-like appearance is seen in approximately forty percent of cases of Crohn's disease upon colonoscopy, representing areas of ulceration separated by narrow areas of healthy tissue.
A small bowel follow-through may suggest the diagnosis of Crohn's disease and is useful when the disease involves only the small intestine. Because colonoscopy and gastroscopy allow direct visualization of only the terminal ileum and beginning of the duodenum, they cannot be used to evaluate the remainder of the small intestine. CT and MRI scans are useful for evaluating the small bowel. . They are also useful for looking for intra-abdominal complications of Crohn's disease, such as abscesses, small bowel obstructions, or fistulae. Magnetic resonance imaging (MRI) is another option for imaging the small bowel as well as looking for complications, though it is more expensive and less readily available.
Multiphase white blood cell scans have been shown to be effective in detecting the locations of active Crohn's disease, particularly in hard to diagnose patients suffering with the early stages or a mild form of the disease with negative endoscopic and radiologic findings. The procedure, a type of nuclear medicine, uses white blood cells removed from the patient; they are tagged with a radioisotope, and then injected intravenously into the patient, and later scanned at several intervals to detect any abnormal white blood cell accumulation, such as pooling in the intestinal tract.
A complete blood count may reveal anemia, which may be caused by blood loss, by vitamin B12 deficiency or, possibly, autoimmune hemolysis. The latter may be seen with ileitis because vitamin B12 is absorbed in the ileumi.
Comparison with ulcerative colitis
The most common disease that mimics the symptoms of Crohn's disease is ulcerative colitis, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases, since the course of the diseases and treatments may be different. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis.
Historically, marijuana has been used to treat diarrhea and has been advocated for the treatment of a variety of other gastrointestinal problems, including Crohn's disease. More recent pharmacological studies have clearly established that cannabinoids inhibit gastrointestinal motility and secretion by acting on CB1 receptors located on the terminals of both intrinsic and extrinsic submucosal neurons. When administered to mice with chemically induced enteritis,cannabinoids also reduce inflammation and fluid accumulationin in the gut. In these latter studies, high levels of anandamide and 2-arachidonoylglycerol as well as increased expression of CB1 receptors have been detected in the inflamed intestines.
The novelty in the findings of Massa et al is the active protective role of the endocannabinoid system, as indicated by the altered inflammatory response of mice lacking CB1 receptors or FAAH. Furthermore, CB1 activation reversed the electrophysiological signs of smooth muscle irritability and, at the same time, blunted the increase in tissue myeloperoxidase activity, a measure of leukocyte infiltration. These observations suggest that endocannabinoids protect the gut not only by decreasing bowel motility but also by inhibiting the inflammatory process itself.
In 2008, a team of researchers in Switzerland isolated a little-known compound in cannabis called beta-caryophyllene from oily resin in Cannabis sativa L. buds. The scientists induced an immune attack in laboratory mice, then fed the cannabis compound to the rodents. After the mice ate the extract, their inflammation went down. The team then demonstrated that beta-caryophyllene works by turning on CB2 cannabinoid receptors, known to reduce swelling, pain and inflammation. The compound is structurally different from anti-inflammatory medications now on the market, and it provides a novel approach for those who suffer from Crohn’s and other immune diseases. Unlike THC, a cannabis compound with similar anti-inflammatory properties, beta-caryophyllene does not affect CB1 receptors in the brain, and thus has no psychoactive effect whatsoever.
“Crohn’s disease, characterized by intestinal inflammation, is another example of a Th1-mediated disease. Anecdotal reports of beneficial marijuana use for this disease gain support by examining modern pharmaceutical approaches. Down-regulation of Th1 effectors has produced dramatic results in the treatment of this disease. New immuno-therapeutic strategies that treat Crohn’s disease with antitumor necrosis factor (TNF-alpha) antibodies, have induced complete remissions and few side effects. THC has been shown to inhibit THF-alpha. Thus, the same therapeutic targets of the newest pharmaceuticals are acted upon by one of nature’s oldest medicines.”
“Curative leaf - Compound in marijuana reduces inflammation without the psychological effects” Amy Maxmen, Science News, June 23rd, 2008
The endogenous cannabinoid system in the gut of patients with inflammatory bowel disease
A Di Sabatino, N Battista, P Biancheri, C Rapino, L Rovedatti, G Astarita, A Vanoli, E Dainese, M Guerci, D Piomelli, S L F Pender, T T MacDonald, M Maccarrone and G R Corazza
Activation of cannabinoid receptors (CBs) by endocannabinoids impacts on a number of gastrointestinal functions. Recent data indicate that CB1 agonists improve 2,4-dinitrobenzene sulfonic acid-induced colitis in mice, thus suggesting a role for the endocannabinoid agonist anandamide (AEA) in protecting the gut against inflammation. We here examined the gut endocannabinoid system in inflammatory bowel disease (IBD) patients, and investigated the ex vivo and in vitro effects of the non-hydrolysable AEA analog methanandamide (MAEA) on the mucosal proinflammatory response. The content of AEA, but not of 2-arachidonoyl-glycerol and N-palmitoylethanolamine, was significantly lower in inflamed than uninflamed IBD mucosa, and this was paralleled by lower activity of the AEA-synthesizing enzyme N-acyl-phosphatidylethanolamine-specific phospholipase D and higher activity of the AEA-degrading enzyme fatty acid amide hydrolase. MAEA significantly downregulated interferon-γ and tumor necrosis factor-α secretion by both organ culture biopsies and lamina propria mononuclear cells. Although these results are promising, further studies are needed to determine the role of cannabinoid pathways in gut inflammation.
In 2005 New Scientist published a joint study by Bristol University and the University of Bath on the apparent healing power of cannabis on IBD. Reports that cannabis eased IBD symptoms indicated the possible existence of cannabinoid receptors in the intestinal lining, which respond to molecules in the plant-derived chemicals. CB1 cannabinoid receptors – which are known to be present in the brain – exist in the endothelial cells which line the gut, it is thought that they are involved in repairing the lining of the gut when damaged. The team deliberately damaged the cells to cause inflammation of the gut lining and then added synthetically produced cannabinoids; the result was that gut started to heal: the broken cells were repaired and brought back closer together to mend the tears. It is believed that in a healthy gut, natural endogenous cannabinoids are released from endothelial cells when they are injured, which then bind to the CB1 receptors. The process appears to set off a wound-healing reaction, and when people use cannabis, the cannabinoids bind to these receptors in the same way. Previous studies have shown that CB1 receptors located on the nerve cells in the gut respond to cannabinoids by slowing gut motility, therefore reducing the painful muscle contractions associated with diarrhea. The team also discovered another cannabinoid receptor, CB2, in the guts of IBD sufferers, which was not present in healthy guts. These receptors, which also respond to chemicals in cannabis, appear to be associated with apoptosis – programmed cell death – and may have a role in suppressing the overactive immune system and reducing inflammation by mopping up excess cells.
Cannabis and GI Disorders / Crohn’s Disease
Research suggests that cannabis is effective in treating the symptoms of these GI disorders in part because it interacts with the endogenous cannabinoid receptors in the digestive tract, which can result in calming spasms, assuaging pain, and improving motility. Cannabis has also been shown to have anti-inflammatory properties and recent research has noids playing crucial neuromodulatory roles in controlling the operation of the gastrointestinal system, with synthetic and natural cannabinoids acting powerfully to control gastrointestinal motility and inflammation.
Recommendation: Indica hybrid. Use whole plant extracts. Tinctures, teas, suppositories, vaporizer, cannabutter, edibles (maybe).
Best Strains for Crohn's disease: Blueberry, Auntie Em, Blackberry, God Bud, Williams Wonder, Afghani Bullrider, OG, AK47, Northern Lights, Kandy Kush, Bubba Kush, Black Domina, Blue Fruit, Chemo, Cripple Creek, Dynamite, G13, Super Silver Haze, Ultimate Indica, Purple Kush, Santa Maria, Platinum Bubba.
1. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of American College of Gastroenterology. Management of Crohn's disease in adults. Am J Gastroenterol. 2009;104(2):465-483. [PubMed]
2. Fry RD, Mahmoud N, Maron DJ, Ross HM, Rombeau J. Colon and rectum. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 50.
3. Sands BE, Siegel CA. Crohn's disease. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 9th ed. Philadelphia, Pa: Saunders Elsevier;2010:chap 111.
^ a b c d e f g h i j k l m n o Baumgart DC, Sandborn WJ (12 May 2007). "Inflammatory bowel disease: clinical aspects and established and evolving therapies.". The Lancet 369 (9573): 1641–57. doi:10.1016/S0140-6736(07)60751-X. PMID 17499606.
^ Mayo Clinic: Crohn's Disease
^ National Digestive Diseases Information Clearinghouse
1. ^ Barrett, JC et al.; Hansoul, S; Nicolae, DL; Cho, JH; Duerr, RH; Rioux, JD; Brant, SR; Silverberg, MS et al. (August 2008). "Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease". Nature Genetics 40 (8): 955–962. doi:10.1038/ng.175. PMC 2574810. PMID 18587394.
2. ^ a b Cosnes J (June 2004). "Tobacco and IBD: relevance in the understanding of disease mechanisms and clinical practice". Best Pract Res Clin Gastroenterol 18 (3): 481–96. doi:10.1016/j.bpg.2003.12.003. PMID 15157822.
3. ^ Loftus, E.V.; P. Schoenfeld, W. J. Sandborn (January 2002). "The epidemiology and natural history of Crohn's disease in population-based patient cohorts from North America: a systematic review". Alimentary Pharmacology & Therapeutics 16 (1): 51–60. doi:10.1046/j.1365-2036.2002.01140.x. PMID 11856078.
4. ^ a b Bernstein, Charles N.; Wajda, A; Svenson, LW; Mackenzie, A; Koehoorn, M; Jackson, M; Fedorak, R; Israel, D et al. (July 2006). "The epidemiology of inflammatory bowel disease in Canada: a population-based study". The American Journal of Gastroenterology 101 (7): 1559–68. doi:10.1111/j.1572-0241.2006.00603.x. PMID 16863561.
5. ^ a b c d e f g h i Wu, George Y; Marcy L Coash, Senthil Nachimuthu (March 17, 2010). "Crohn Disease". eMedicine. http://emedicine.medscape.com/article/172940-overview. Retrieved 2010-04-15.
6. ^ Le, Tri H (March 17, 2010). "Ulcerative colitis". eMedicine. http://emedicine.medscape.com/article/183084-overview. Retrieved 2010-04-15.
7. ^ a b c Crohn BB, Ginzburg L, Oppenheimer GD (2000). "Regional ileitis: a pathologic and clinical entity. 1932". Mt. Sinai J. Med. 67 (3): 263–8. PMID 10828911.
8. ^ a b Gasche C, Scholmerich J, Brynskov J, D'Haens G, Hanauer S, Irvine E, Jewell D, Rachmilewitz D, Sachar D, Sandborn W, Sutherland L (2000). "A simple classification of Crohn's disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998". Inflamm Bowel Dis 6 (1): 8–15. doi:10.1002/ibd.3780060103. PMID 10701144.
9. ^ Dubinsky MC, Fleshner PP. (2003). "Treatment of Crohn's Disease of Inflammatory, Stenotic, and Fistulizing Phenotypes". Curr Treat Options Gastroenterol 6 (3): 183–200. doi:10.1007/s11938-003-0001-1. PMID 12744819.
10. ^ a b c d e f internetmedicin.se > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
11. ^ a b c d e Hanauer, Stephen B.; William Sandborn (2001-03-01). "Management of Crohn's disease in adults" (PDF). American Journal of Gastroenterology 96 (3): 635–43. doi:10.1111/j.1572-0241.2001.03671.x. PMID 11280528. http://www.acg.gi.org/physicians/guidelines/CrohnsDiseaseinAdults.pdf. Retrieved 2009-11-07.
12. ^ a b Pimentel, Mark; Michael Chang, Evelyn J. Chow, Siamak Tabibzadeh, Viorelia Kirit-Kiriak, Stephan R. Targan, Henry C. Lin (2000). "Identification of a prodromal period in Crohn's disease but not ulcerative colitis". American Journal of Gastroenterology 95 (12): 3458–62. doi:10.1111/j.1572-0241.2000.03361.x. PMID 11151877.
13. ^ Crohn's Disease Overview
14. ^ a b Zieve, David; George F Longstreth (October 18, 2009). "Crohn's Disease". ADAM Health Illustrated Encyclopedia. http://www.healthline.com/adamcontent/crohns-disease. Retrieved 2010-08-16.
15. ^ a b c d Podolsky, Daniel K. (2002). "Inflammatory bowel disease". New England Journal of Medicine 346 (6): 417–29. doi:10.1056/NEJMra020831. PMID 12167685. http://content.nejm.org/cgi/content/extract/347/6/417. Retrieved 2006-07-02.
16. ^ Mueller, M. H.; M. E. Kreis, M. L. Gross, H. D. Becker, T. T. Zittel & E. C. Jehle (2002). "Anorectal functional disorders in the absence of anorectal inflammation in patients with Crohn's disease". British Journal of Surgery 89 (8): 1027–31. doi:10.1046/j.1365-2168.2002.02173.x. PMID 12153630.
17. ^ Kumar, Vinay; Abul K. Abbas, Nelson Fausto (July 30, 2004). "Ch 17: The Gastrointestinal Tract". Robbins and Cotran: Pathologic Basis of Disease (7th ed.). Philadelphia, Pennsylvania: Elsevier Saunders. pp. 847. ISBN 0-7216-0187-1.
18. ^ Taylor B, Williams G, Hughes L, Rhodes J (1989). "The histology of anal skin tags in Crohn's disease: an aid to confirmation of the diagnosis". Int J Colorectal Dis 4 (3): 197–9. doi:10.1007/BF01649703. PMID 2769004.
19. ^ Fix, Oren K.; Jorge A. Soto, Charles W. Andrews and Francis A. Farraye (2004). "Gastroduodenal Crohn's disease". Gastrointestinel Endoscopy 60 (6): 985. doi:10.1016/S0016-5107(04)02200-X. PMID 15605018.
20. ^ a b Beattie, R.M.; N. M. Croft, J. M. Fell, N. A. Afzal and R. B. Heuschkel (2006). "Inflammatory bowel disease". Archives of Disease in Childhood 91 (5): 426–32. doi:10.1136/adc.2005.080481. PMC 2082730. PMID 16632672.
21. ^ Büller, H.A. (1997). "Problems in diagnosis of IBD in children". The Netherlands Journal of Medicine 50 (2): S8–S11. doi:10.1016/S0300-2977(96)00064-2. PMID 9050326.
22. ^ O'Keefe, S. J. (1996). "Nutrition and gastrointestinal disease". Scandinavian Journal of Gastroenterology Supplement 31 (220): 52–9. doi:10.3109/00365529609094750. PMID 8898436.
23. ^ Danese, Silvio; Stefano Semeraro, Alfredo Papa, Italia Roberto, Franco Scaldaferri, Giuseppe Fedeli, Giovanni Gasbarrini, Antonio Gasbarrini (2005). "Extraintestinal manifestations in inflammatory bowel disease". World Journal of Gastroenterology 11 (46): 7227–36. PMID 16437620. http://www.wjgnet.com/1007-9327/11/7227.asp. Retrieved 2009-11-07.
24. ^ a b Crohn's disease. professionals.epilepsy.com. Retrieved on July 13, 2007.
25. ^ MedlinePlus Encyclopedia Small bowel bacterial overgrowth
26. ^ Zadik Y, Drucker S, Pallmon S (Aug 2011). "Migratory stomatitis (ectopic geographic tongue) on the floor of the mouth". J Am Acad Dermatol 65 (2): 459-60. PMID 21763590. http://www.sciencedirect.com/science/article/pii/S0190962210004883.
27. ^ Prevalence defined as at least 5 health care contacts in a 10 year period for the condition, according to: Greenstein, AJ; Janowitz, HD; Sachar, DB (1976). "The extra-intestinal complications of Crohn's disease and ulcerative colitis: a study of 700 patients". Medicine 55 (5): 401–12. PMID 957999.edit
28. ^ http://emedicine.medscape.com/article/442000-overview
29. ^ Ekbom A, Helmick C, Zack M, Adami H (1990). "Increased risk of large-bowel cancer in Crohn's disease with colonic involvement". Lancet 336 (8711): 357–9. doi:10.1016/0140-6736(90)91889-I. PMID 1975343.
30. ^ Collins P, Mpofu C, Watson A, Rhodes J (2006). Watson, Alastair J. ed. "Strategies for detecting colon cancer and/or dysplasia in patients with inflammatory bowel disease". Cochrane Database Syst Rev (2): CD000279. doi:10.1002/14651858.CD000279.pub3. PMID 16625534.
31. ^ Lynne V McFarland (2008). "Colorectal cancer and dysplasia in inflammatory bowel disease". World Journal of Gastroenterology: 2665.
32. ^ Evans J, Steinhart A, Cohen Z, McLeod R (2003). "Home total parenteral nutrition: an alternative to early surgery for complicated inflammatory bowel disease". J Gastrointest Surg 7 (4): 562–6. doi:10.1016/S1091-255X(02)00132-4. PMID 12763417.
33. ^ "Complications of Crohn's Disease". Centocor Ortho Biotech. https://www.livingwithcrohnsdisease.com/livingwithcrohnsdisease/crohns_disease/complications_of_crohns.html. Retrieved 2009-11-07.
34. ^ Kaplan, C (2005-10-21). "IBD and Pregnancy: What You Need to Know". Crohn's and Colitis Foundation of America. http://www.ccfa.org/about/news/pregnancy. Retrieved 2009-11-07.
35. ^ a b c d Kornbluth, Asher; David B. Sachar (July 2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee" (PDF). American Journal of Gastroenterology 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x. PMID 15233681. Archived from the original on April 6, 2008. http://web.archive.org/web/20080406030552/http://www.acg.gi.org/physicians/guidelines/UlcerativeColitisUpdate.pdf. Retrieved 2009-11-07.
36. ^ Crohn's Disease Overview
37. ^ Braat H, Peppelenbosch MP, Hommes DW (August 2006). "Immunology of Crohn's disease". Ann. N. Y. Acad. Sci. 1072: 135–54. doi:10.1196/annals.1326.039. PMID 17057196.
38. ^ Henckaerts L, Figueroa C, Vermeire S, Sans M (May 2008). "The role of genetics in inflammatory bowel disease". Curr Drug Targets 9 (5): 361–8. doi:10.2174/138945008784221161. PMID 18473763.
39. ^ a b c Marks DJ, Harbord MW, MacAllister R, Rahman FZ, Young J, Al-Lazikani B, Lees W, Novelli M, Bloom S, Segal AW (2006). "Defective acute inflammation in Crohn's disease: a clinical investigation". Lancet 367 (9511): 668–78. doi:10.1016/S0140-6736(06)68265-2. PMC 2092405. PMID 16503465.
40. ^ Comalada M, Peppelenbosch MP (September 2006). "Impaired innate immunity in Crohn's disease". Trends Mol Med 12 (9): 397–9. doi:10.1016/j.molmed.2006.07.005. PMID 16890491.
41. ^ "Crohn's disease has strong genetic link: study". Crohn's and Colitis Foundation of America. 2007-04-16. http://www.ccfa.org/reuters/geneticlink. Retrieved 2009-11-07.
42. ^ Ogura Y, Bonen DK, Inohara N, et al. (2001). "A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease". Nature 411 (6837): 603–6. doi:10.1038/35079114. PMID 11385577.
43. ^ Cuthbert A, Fisher S, Mirza M, et al. (2002). "The contribution of NOD2 gene mutations to the risk and site of disease in inflammatory bowel disease". Gastroenterology 122 (4): 867–74. doi:10.1053/gast.2002.32415. PMID 11910337.
44. ^ Kaser, A; Lee, AH; Franke, A; Glickman, JN; Zeissig, S; Tilg, H; Nieuwenhuis, EE; Higgins, DE et al. (5 September 2008). "XBP1 Links ER Stress to Intestinal Inflammation and Confers Genetic Risk for Human Inflammatory Bowel Disease". Cell (Cell Press) 134 (5): 743–756. doi:10.1016/j.cell.2008.07.021. PMC 2586148. PMID 18775308.
45. ^ Clevers, H (2009). "Inflammatory Bowel Disease, Stress, and the Endoplasmic Reticulum". N Engl J Med 360 (7): 726–727. doi:10.1056/NEJMcibr0809591. PMID 19213688.
46. ^ a b R Shoda, K Matsueda, S Yamato and N Umeda (1996). "Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan". American Journal of Clinical Nutrition (The American Society for Clinical Nutrition) 64 (5): 741–745. PMID 8615358.
47. ^ Lesko S, Kaufman D, Rosenberg L, et al. (1985). "Evidence for an increased risk of Crohn's disease in oral contraceptive users". Gastroenterology 89 (5): 1046–9. PMID 4043662.
48. ^ Reddy D, Siegel CA, Sands BE, Kane S (July 2006). "Possible association between isotretinoin and inflammatory bowel disease". The American journal of gastroenterology 101 (7): 1569–73. doi:10.1111/j.1572-0241.2006.00632.x. PMID 16863562.
49. ^ Borobio E, Arín A, Valcayo A, Iñarrairaegui M, Nantes O, Prieto C (2004). "[Isotretinoin and ulcerous colitis]" (in Spanish; Castilian). An Sist Sanit Navar 27 (2): 241–3. PMID 15381956.
50. ^ Reniers DE, Howard JM (October 2001). "Isotretinoin-induced inflammatory bowel disease in an adolescent". Ann Pharmacother 35 (10): 1214–6. doi:10.1345/aph.10368. PMID 11675849. http://www.theannals.com/cgi/pmidlookup?view=long&pmid=11675849.
51. ^ Cobrin GM, Abreu MT (2005). "Defects in mucosal immunity leading to Crohn's disease". Immunol. Rev. 206: 277–95. doi:10.1111/j.0105-2896.2005.00293.x. PMID 16048555.
52. ^ a b Elson, CO; Cong, Y; Weaver, CT; Schoeb, TR; Mcclanahan, TK; Fick, RB; Kastelein, RA (2007). "Monoclonal Anti–Interleukin 23 Reverses Active Colitis in a T Cell–Mediated Model in Mice". Gastroenterology 132 (7): 2359–70. doi:10.1053/j.gastro.2007.03.104. PMID 17570211.
53. ^ Prescott NJ, Fisher SA, Franke A, et al. (2007). "A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn's disease and is independent of CARD15 and IBD5". Gastroenterology 132 (5): 1665–71. doi:10.1053/j.gastro.2007.03.034. PMID 17484864.
54. ^ Marks DJ, Segal AW. (January 2008). "Innate immunity in inflammatory bowel disease: a disease hypothesis". J Pathol. 214 (2): 260–6. doi:10.1002/path.2291. PMC 2635948. PMID 18161747.
55. ^ Dessein R, Chamaillard M, Danese S (September 2008). "Innate immunity in Crohn's disease: the reverse side of the medal". J Clin Gastroenterol 42 (Suppl 3 Pt 1): S144–7. doi:10.1097/MCG.0b013e3181662c90. PMID 18806708.
56. ^ "OVERVIEW: MAP and Crohn's Disease Research". Paratuberculosis Awareness & Research Association. http://www.crohns.org/research/index.htm. Retrieved 2009-11-07.
57. ^ Sartor, R. (July 2006). "Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis". Nature Clinical Practice Gastroenterology & Hepatology 3 (7): 390–407. doi:10.1038/ncpgasthep0528. PMID 16819502. http://www.nature.com/nrgastro/journal/v3/n7/full/ncpgasthep0528.html.
58. ^ Naser SA, Collins MT (2005). "Debate on the lack of evidence of Mycobacterium avium subsp. paratuberculosis in Crohn's disease". Inflamm. Bowel Dis. 11 (12): 1123. doi:10.1097/01.MIB.0000191609.20713.ea. PMID 16306778.
59. ^ Giaffer MH, Clark A, Holdsworth CD (1992). "Antibodies to Saccharomyces cerevisiae in patients with Crohn's disease and their possible pathogenic importance". Gut 33 (8): 1071–5. doi:10.1136/gut.33.8.1071. PMC 1379444. PMID 1398231.
60. ^ Baumgart M et al. (2007). "Culture independent analysis of ileal mucosa reveals a selective increase in invasive Escherichia coli of novel phylogeny relative to depletion of Clostridiales in Crohn's disease involving the ileum". The ISME Journal 1 (5): 403–18. doi:10.1038/ismej.2007.52. PMID 18043660. http://www.nature.com/ismej/journal/v1/n5/full/ismej200752a.html.
61. ^ "Possible links between Crohn’s disease and Paratuberculosis" (PDF). EUROPEAN COMMISSION DIRECTORATE-GENERAL HEALTH & CONSUMER PROTECTION. http://ec.europa.eu/food/fs/sc/scah/out38_en.pdf. Retrieved 2009-11-07.
62. ^ Gui GP, Thomas PR, Tizard ML, Lake J, Sanderson JD, Hermon-Taylor J (March 1997). "Two-year-outcomes analysis of Crohn's disease treated with rifabutin and macrolide antibiotics" (PDF). J. Antimicrob. Chemother. 39 (3): 393–400. doi:10.1093/jac/39.3.393. PMID 9096189. http://jac.oxfordjournals.org/cgi/reprint/39/3/393.
63. ^ Cenac N, Andrews CN, Holzhausen M, et al. (March 2007). "Role for protease activity in visceral pain in irritable bowel syndrome". J. Clin. Invest. 117 (3): 636–47. doi:10.1172/JCI29255. PMC 1794118. PMID 17304351.
64. ^ Cenac N, Coelho AM, Nguyen C, et al. (November 2002). "Induction of intestinal inflammation in mouse by activation of proteinase-activated receptor-2". Am. J. Pathol. 161 (5): 1903–15. doi:10.1016/S0002-9440(10)64466-5. PMC 1850779. PMID 12414536. http://ajp.amjpathol.org/cgi/pmidlookup?view=long&pmid=12414536.
65. ^ Boorom KF, Smith H, Nimri L, et al. (October 2008). "Oh my aching gut: irritable bowel syndrome, Blastocystis, and asymptomatic infection". Parasit Vectors 1 (1): 40. doi:10.1186/1756-3305-1-40. PMC 2627840. PMID 18937874.
66. ^ Hugot, Jean-Pierre; Alberti, Corinne; Berrebi, Dominique; Bingen, Edouard; Cezard, Jean-Pierre (2003-12-13). "Crohn's disease: the cold chain hypothesis". The Lancet 362 (9400): 2012–2015. doi:10.1016/S0140-6736(03)15024-6. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(03)15024-6.
67. ^ "Fridges blamed for Crohn's disease rise". Medical News TODAY. 2003-12-12. http://www.medicalnewstoday.com/articles/4849.php.
68. ^ Forbes, Alastair; Kalantzis, Tommy (July 2006). "Crohn's disease : the cold chain hypothesis". International Journal of Colorectal Disease (Springer Berlin / Heidelberg) 21 (5): 399–401. doi:10.1007/s00384-005-0003-7. ISSN 0179-1958. PMID 16059694. http://www.springerlink.com/content/p6q21tp76x013u51/. Retrieved 2009-11-04.
69. ^ Subramanian, Sreedhar; Carol, L. Roberts; Hart, C. Anthony; Martin, Helen M.; Edwards, Steve W.; Rhodes, Jonathan M.; Campbell, Barry J. (2008). "Replication of Colonic Crohn's Disease Mucosal Escherichia coli Isolates within Macrophages and Their Susceptibility to Antibiotics". Antimicrobial Agents and Chemotherapy 52 (2): 427–434. doi:10.1128/AAC.00375-07. PMC 2224732. PMID 18070962. http://aac.asm.org/cgi/content/abstract/52/2/427.
70. ^ Mpofu, Chiedzo M.; Cambell, Barry J.; Subramanin, Sreedhar; Marshall-Clarke, Stuart; Hart, Anthony C.; Cross, Andy; Roberts, Carol L.; McGoldrick, Adrian et al. (2007). "Microbial Mannan Inhibits Bacterial Killing by Macrophages: A Possible Pathogenic Mechanism for Crohn’s Disease". Gastroenterology, the official journal of the AGA Institute 133 (5): 1487–1498. doi:10.1053/j.gastro.2007.08.004. PMID 17919633. http://www.gastrojournal.org/article/S0016-5085(07)01450-3/abstract.
71. ^ "New insights into Crohn's Disease". http://www.liv.ac.uk/researchintelligence/issue33/crohns.htm.
72. ^ Crawford JM. "The Gastrointestinal tract, Chapter 17". In Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease: 5th Edition. W.B. Saunders and Company, Philadelphia, 1994.
73. ^ HCP: Pill Cam, Capsule Endoscopy, Esophageal Endoscopy
74. ^ Scheinfeld NS, Teplitz E, McClain SA (November 2001). "Crohn's disease and lichen nitidus: a case report and comparison of common histopathologic features". Inflammatory bowel diseases 7 (4): 314–8. doi:10.1097/00054725-200111000-00006. PMID 11720321.
75. ^ a b Hara, Amy K.; Jonathan A. Leighton, Russell I. Heigh, Virender K. Sharma, Alvin C. Silva, Giovanni De Petris, Joseph G. Hentz and David E. Fleischer (January 2006). "Crohn disease of the small bowel: preliminary comparison among CT enterography, capsule endoscopy, small-bowel follow-through, and ileoscopy". Radiology 238 (1): 128–34. doi:10.1148/radiol.2381050296. PMID 16373764.
76. ^ Triester, Stuart L.; Jonathan A. Leighton, Grigoris I. Leontiadis, Suryakanth R. Gurudu, David E. Fleischer, Amy K. Hara, Russell I. Heigh, Arthur D. Shiff, and Virender K. Sharma (2006). "A meta-analysis of the yield of capsule endoscopy compared to other diagnostic modalities in patients with non-stricturing small bowel Crohn's disease". The American Journal of Gastroenterology 101 (5): 954–64. doi:10.1111/j.1572-0241.2006.00506.x. PMID 16696781.
77. ^ Dixon, P.M.; M.E. Roulston and D.J. Nolan (1993). "The small bowel enema: a ten year review". Clinical Radiology 47 (1): 46–8. doi:10.1016/S0009-9260(05)81213-9. PMID 8428417.
78. ^ Carucci, L. R.; M. S. Levine (2002). "Radiographic imaging of inflammatory bowel disease". Gastroenterology Clinics of North America 31 (1): 93–117. doi:10.1016/S0889-8553(01)00007-3. PMID 12122746.
79. ^ Rajesh, A.; D.D.T. Maglinte (2006). "Multislice CT enteroclysis: technique and clinical applications". Clinical Radiology 61 (1): 31–9. doi:10.1016/j.crad.2005.08.006. PMID 16356814.
80. ^ Zissin, Rivka; Marjorie Hertz, Alexandra Osadchy, Ben Novis and Gabriela Gayer (2005). "Computed Tomographic Findings of Abdominal Complications of Crohn's Disease—Pictorial Essay" (PDF). Canadian Association of Radiologists Journal 56 (1): 25–35. PMID 15835588. Archived from the original on April 6, 2008. http://web.archive.org/web/20080406030552/http://www.carj.ca/issues/2005-Feb/25/pg25.pdf. Retrieved 2009-11-07.
81. ^ MacKalski, B. A.; C. N. Bernstein (2005). "New diagnostic imaging tools for inflammatory bowel disease". Gut 55 (5): 733–41. doi:10.1136/gut.2005.076612. PMC 1856109. PMID 16609136.
82. ^ Goh, Jason; C. A. O'Morain (2003). "Review article: nutrition and adult inflammatory bowel disease". Alimentary Pharmacology & Therapeutics 17 (3): 307–20. doi:10.1046/j.1365-2036.2003.01482.x. PMID 12562443.
83. ^ Chamouard, Patrick; Zoe Richert, Nicolas Meyer, Gabriel Rahmi, René Baumann (2006). "Diagnostic Value of C-Reactive Protein for Predicting Activity Level of Crohn's Disease". Clinical Gastroenterology and Hepatology 4 (7): 882–7. doi:10.1016/j.cgh.2006.02.003. PMID 16630759.Epub ahead of print
84. ^ Kaila, B; K Orr and C N Bernstein (2005). "The anti-Saccharomyces cerevisiae antibody assay in a province-wide practice: accurate in identifying cases of Crohn's disease and predicting inflammatory disease". The Canadian Journal of Gastroenterology 19 (12): 717–21. PMID 16341311. http://www.pulsus.com/journals/abstract.jsp?sCurrPg=journal&jnlKy=2&atlKy=743&isuKy=263&isArt=t. Retrieved 2006-07-02.
85. ^ Israeli, E.; I. Grotto, B. Gilburd, R. D. Balicer, E. Goldin, A. Wiik and Y. Shoenfeld (2005). "Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease". Gut 54 (9): 1232–6. doi:10.1136/gut.2004.060228. PMC 1774672. PMID 16099791.
86. ^ Ferrante, M.; L. Henckaerts, M. Joossens, M. Pierik, S. Joossens, N. Dotan, G.L. Norman , R.T. Altstock , K. Van Steen , P. Rutgeerts , G. Van Assche and S.Vermeire (2007). "New serological markers in inflammatory bowel disease are associated with complicated disease behaviour". Gut 56 (10): 1394–403. doi:10.1136/gut.2006.108043. PMC 2000264. PMID 17456509.
87. ^ Papp, M.; I. Altorjay, N. Dotan, K. Palatka, I. Foldi, J. Tumpek, S. Sipka, M. Udvardy, T. Dinya, L. Lakatos, A. Kovacs, T. Molnar, Z. Tulassay, P. Mihelle, G.L. Norman, T. Szamosi , J. Papp; Hungarian IBD Study Group and P.L. Lakatos (2008). "New serological markers for inflammatory bowel disease are associated with earlier age at onset, complicated disease behavior, risk for surgery, and NOD2/CARD15 genotype in a Hungarian IBD cohort". Am J Gastroenterol 104 (6): 1426–34. doi:10.1111/j.1572-0241.2007.01652.x. PMID 18047543.
88. ^ Seow, C.H.; J.M. Stempak, W. Xu, H. Lan, A.M. Griffiths, G.R. Greenberg, A.H. Steinhart, N. Dotan and M.S. Silverberg (2009). "Novel anti-glycan antibodies related to inflammatory bowel disease diagnosis and phenotype". Am J Gastroenterol 104 (6): 1426–34. doi:10.1038/ajg.2009.79. PMID 19491856.
89. ^ Dotan, I. (2007). "Serologic markers in inflammatory bowel disease: tools for better diagnosis and disease stratification". Expert Rev Gastroenterol Hepatol 1 (2): 265–74. doi:10.1586/17474126.96.36.1995. PMID 19072419.
90. ^ Broomé, Ulrika; Annika Bergquist (February 2006). "Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer". Seminars in Liver Disease 26 (1): 31–41. doi:10.1055/s-2006-933561. PMID 16496231.
91. ^ Shepherd, NA. (August 2002). "Granulomas in the diagnosis of intestinal Crohn's disease: a myth exploded?". Histopathology 41 (2): 166–8. doi:10.1046/j.1365-2559.2002.01441.x. PMID 12147095.
92. ^ Mahadeva, U.; Martin, JP.; Patel, NK.; Price, AB. (July 2002). "Granulomatous ulcerative colitis: a re-appraisal of the mucosal granuloma in the distinction of Crohn's disease from ulcerative colitis.". Histopathology 41 (1): 50–5. doi:10.1046/j.1365-2559.2002.01416.x. PMID 12121237.
93. ^ a b Pages 152-156 (Section: Inflammatory bowel disease(IBD)) in:Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6.
94. ^ Feller, M.; Huwiler, K.; Schoepfer, A.; Shang, A.; Furrer, H.; Egger, M. (2010). "Long-term antibiotic treatment for Crohn's disease: systematic review and meta-analysis of placebo-controlled trials". Clinical Infectious Diseases 50 (4): 473–480. doi:10.1086/649923. PMID 20067425.edit
95. ^  Section "Antibiotics and Ulcerative Colitis" in: Prantera, C.; Scribano, M. (2009). "Antibiotics and probiotics in inflammatory bowel disease: why, when, and how". Current opinion in gastroenterology 25 (4): 329–333. doi:10.1097/MOG.0b013e32832b20bf. PMID 19444096.edit
96. ^ "Clinical Research Alliance Update" (PDF). Crohn's and Colitis Foundation of America. 2007-05-01. http://www.ccfa.org/ccfaprof/research-grant-opps/documents/May-2007-Newsletter.pdf. Retrieved 2008-02-14.
97. ^ a b Fries, WS; Nazario, B (2007-05-16). "Crohn's Disease: 54 Tips to Help You Manage". WebMD. http://www.webmd.com/digestive-disorders/features/crohns-disease-54-tips-to-help-you-manage. Retrieved 2008-02-14.
98. ^ Shanahan, Fergus (2002). "Crohn's disease". The Lancet (Elsevier Science) 359 (9300): 67.
99. ^ Food and Drug Administration (April 22, 2008). "FDA Approves Cimzia to Treat Crohn's Disease". Press release. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2008/ucm116882.htm. Retrieved 2009-11-04.
100. ^ Sandborn, W.J.; Colombel, J.F.; Enns, R.; Feagan, B.G.; Hanauer, S.B.; Lawrance, I.C.; Panaccione, R.; Sanders, M.; Schreiber, S.; Targan, S.; Others, (2005). "Natalizumab Induction and Maintenance Therapy for Crohn's Disease". New England Journal of Medicine 353 (18): 1912–25. doi:10.1056/NEJMoa043335. PMID 16267322.
101. ^ Macdonald, JK; Mcdonald, JW; McDonald, J.W.D. (2006). MacDonald, John. ed. "Natalizumab for induction of remission in Crohn's disease (Cochrane Review)". The Cochrane Database of Systematic Reviews 3: 1465–858. doi:10.1002/14651858.CD006097. PMID 16856112. http://dellboy.update-software.com/abstracts/AB006097.htm. Retrieved 2008-02-15.[dead link]
102. ^ Longmore, Murray; Ian Wilkinson, Tom Turmezei, Chee Kay Cheung (2007). Oxford Handbook of Clinicial Medicine, 7th edition. Oxford University Press. pp. 266–7. ISBN 0-19-856837-1.
103. ^ Tresca, AJ (2007-01-12). "Resection Surgery for Crohn's Disease". About.com. http://ibdcrohns.about.com/od/surgeryprocedures/a/resectioncrohns.htm. Retrieved 2008-02-14.
104. ^ Ozuner G, Fazio VW, Lavery IC, Milsom JW, Strong SA (1996). "Reoperative rates for Crohn's disease following strictureplasty. Long-term analysis". Dis. Colon Rectum 39 (11): 1199–203. doi:10.1007/BF02055108. PMID 8918424.
105. ^ Short Bowel Syndrome as defined by the National Institute of Diabetes and Digestive and Kidney Diseases
106. ^ Rhodes, M (2006-10-24). "Intestinal transplant for Crohn's disease". Everyday Health. http://www.revolutionhealth.com/conditions/digestive/crohns-disease/surgery/intestinal-transplant. Retrieved 2009-03-22.
107. ^ Caprilli R, Gassull M, Escher J et al. (2006). "European evidence based consensus on the diagnosis and management of Crohn's disease: special situations". Gut 55 Suppl 1: i36–58. doi:10.1136/gut.2005.081950c. PMC 1859996. PMID 16481630.
108. ^ a b Smart, H.L.; J.F. Mayberry, M. Atkinson (1986). "Alternative medicine consultations and remedies in patients with the irritable bowel syndrome". Gut - an international journal of Gastroenterology and Hepatology 27 (7): 826–828. doi:10.1136/gut.27.7.826. http://gut.bmj.com/content/27/7/826.abstract. Retrieved 21 September 2010. "This study has shown that the use of alternative medicine is common in patients with irritable bowel syndrome and this does not appear to be explicable in terms of the nature, chronicity or refractoriness to treatment of symptoms.".
109. ^ "Use of complementary and alternative medicine in Germany – a survey of patients with inflammatory bowel disease". BioMed Central. http://www.biomedcentral.com/1472-6882/6/19. Retrieved 21 September 2010. "At the same time, further clinical studies assessing the most commonly used CAM therapies are urgently needed. Research in CAM offers the chance to discover new treatment options in the management of IBD but may also protect patients from ineffective and expensive 'pseudo'-therapies."
110. ^ a b Joos S, Brinkhaus B, Maluche C, et al. (2004). "Acupuncture and moxibustion in the treatment of active Crohn's disease: a randomized controlled study". Digestion 69 (3): 131–9. doi:10.1159/000078151. PMID 15114043.
111. ^ "The second European evidence-based Consensus on the diagnosis and management of Crohn's disease: Special situations". ScienceDirect. Journal of Crohn's and Colitis (2010) 4, 63-101. https://www.ecco-ibd.eu/documents/CD_guidelines_2010_special_situations.pdf. Retrieved 21 September 2010. "the colitis activity index fell significantly in the treatment group compared to the sham acupuncture group. However, recruitment did not reach its target and the number of patients was small."
112. ^ Canavan, C; Abrams, KR; Mayberry, J; K. R. Abrams, J. Mayberry (2006). "Meta-analysis : colorectal and small bowel cancer risk in patients with Crohn's disease". Alimentary pharmacology & therapeutics 23 (8): 1097–104. doi:10.1111/j.1365-2036.2006.02854.x. ISSN 0269-2813. PMID 16611269. http://cat.inist.fr/?aModele=afficheN&cpsidt=17660183. Retrieved 2007-05-23.
113. ^ a b Hiatt, Robert A.; Leon Kaufman (1988). "Epidemiology of inflammatory bowel disea