Crohn’s disease

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“Crohn” redirects here. It is not to be confused with Croan, Krone, or Crone.

Crohn’s disease is a type of inflammatory bowel disease (IBD) that may affect any part of the gastrointestinal tract from mouth to anus.[2] Signs and symptoms often include abdominal pain, diarrhea (which may be bloody if inflammation is severe), fever, and weight loss.[1][2] Other complications may occur outside the gastrointestinal tract and include anemia, skin rashes, arthritis, inflammation of the eye, and tiredness.[1] The skin rashes may be due to infections as well as pyoderma gangrenosum or erythema nodosum.[1] Bowel obstruction may occur as a complication of chronic inflammation, and those with the disease are at greater risk of bowel cancer.[1]

While the cause of Crohn’s disease is unknown, it is believed to be due to a combination of environmental, immune, and bacterial factors in genetically susceptible individuals.[6][7][8] It results in a chronic inflammatory disorder, in which the body’s immune system attacks the gastrointestinal tract possibly directed at microbial antigens.[7][9] While Crohn’s is an immune-related disease, it does not appear to be an autoimmune disease (in that the immune system is not being triggered by the body itself).[10] The exact underlying immune problem is not clear; however, it may be an immunodeficiency state.[9][11][12] About half of the overall risk is related to genetics with more than 70 genes found to be involved.[1][13] Tobacco smokers are twice as likely to develop Crohn’s disease as nonsmokers.[3] It also often begins after gastroenteritis.[1] Diagnosis is based on a number of findings including biopsy and appearance of the bowel wall, medical imaging and description of the disease.[1] Other conditions that can present similarly include irritable bowel syndrome and Behçet’s disease.[1]

There are no medications or surgical procedures that can cure Crohn’s disease.[1] Treatment options are intended to help with symptoms, maintain remission, and prevent relapse.[1] In those newly diagnosed, a corticosteroid may be used for a brief period of time to rapidly improve symptoms alongside another medication such as either methotrexate or a thiopurine used to prevent recurrence.[1] Stopping smoking is recommended in people with Crohn’s disease.[1] One in five people with the disease is admitted to hospital each year, and half of those with the disease will require surgery for the disease at some point over a ten-year period.[1] While surgery should be used as little as possible, it is necessary to address some abscesses, certain bowel obstructions, and cancers.[1] Checking for bowel cancer via colonoscopy is recommended every few years, starting eight years after the disease has begun.[1]

Crohn’s disease affects about 3.2 per 1,000 people in Europe and North America.[5] It is less common in Asia and Africa.[14][15] It has historically been more common in the developed world.[16] Rates have, however, been increasing, particularly in the developing world, since the 1970s.[15][16] Inflammatory bowel disease resulted in 47,400 deaths in 2015[17] and those with Crohn’s disease have a slightly reduced life expectancy.[1] It tends to start in the teens and twenties, although it can occur at any age.[1][2] Males and females are equally affected.[2] The disease was named after gastroenterologist Burrill Bernard Crohn, who, in 1932, together with two other colleagues at Mount Sinai Hospital in New York, described a series of patients with inflammation of the terminal ileum of the small intestine, the area most commonly affected by the illness.[18]


  • 1 Signs and symptoms
    • 1.1 Gastrointestinal
    • 1.2 Systemic
    • 1.3 Extraintestinal
  • 2 Cause
    • 2.1 Genetics
    • 2.2 Immune system
    • 2.3 Microbes
    • 2.4 Environmental factors
  • 3 Pathophysiology
  • 4 Diagnosis
    • 4.1 Classification
    • 4.2 Endoscopy
    • 4.3 Radiologic tests
    • 4.4 Blood tests
    • 4.5 Comparison with ulcerative colitis
    • 4.6 Differential diagnosis
  • 5 Management
    • 5.1 Lifestyle changes
    • 5.2 Medication
    • 5.3 Surgery
    • 5.4 Mental health
    • 5.5 Alternative medicine
  • 6 Prognosis
    • 6.1 Complications
  • 7 Epidemiology
  • 8 History
  • 9 Research
  • 10 References
  • 11 External links

Signs and symptoms[edit]


People with Crohn’s can have aphthous ulcers involving the mouth.

Many people with Crohn’s disease have symptoms for years before the diagnosis.[21] The usual onset is between 15 and 30 years of age, but can occur at any age.[22] 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.[23]

Abdominal pain may be the initial symptom of Crohn’s disease usually in the lower right area.[24] It is often accompanied by diarrhea, especially in those who have had surgery. The diarrhea may or may not be bloody. 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 20 bowel movements per day and may need to awaken at night to defecate.[1][25][26][27] 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.[1] Bloody bowel movements typically come and go, and may be bright or dark red in color. In the setting of severe Crohn’s colitis, bleeding may be copious.[25] Flatulence and bloating may also add to the intestinal discomfort.[25]

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. Persistent vomiting and nausea may indicate stenosis from small bowel obstruction or disease involving the stomach, pylorus, or duodenum.[25] 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.[28]

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[1] or anal fissure. Perianal skin tags are also common in Crohn’s disease and may appear with or without the presence of colorectal polyps.[29] Fecal incontinence may accompany perianal Crohn’s disease. At the opposite end of the gastrointestinal tract, the mouth may be affected by recurrent 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.[30]


Crohn’s disease, like many other chronic, inflammatory diseases, can cause a variety of systemic symptoms.[1] Among children, growth failure is common. Many children are first diagnosed with Crohn’s disease based on inability to maintain growth.[31] As it may manifest at the time of the growth spurt in puberty, up to 30% of children with Crohn’s disease may have retardation of growth.[32] Fever may also be present, though fevers greater than 38.5 °C (101.3 °F) are uncommon unless there is a complication such as an abscess.[1] 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.[31] People with extensive small intestine disease may also have malabsorption of carbohydrates or lipids, which can further exacerbate weight loss.[33]


Pyoderma gangrenosum on the leg of a person with Crohn’s disease

In addition to systemic and gastrointestinal involvement, Crohn’s disease can affect many other organ systems.[34] Inflammation of the interior portion of the eye, known as uveitis, can cause blurred vision and eye pain, especially when exposed to light (photophobia).[35] Inflammation may also involve the white part of the eye (sclera), a condition called episcleritis.[35] Both episcleritis and uveitis can lead to loss of vision if untreated.

Crohn’s disease that affects the ileum may result in an increased risk for gallstones. This is due to a decrease in bile acid resorption in the ileum and the bile gets excreted in the stool. As a result, the cholesterol/bile ratio increases in the gallbladder, resulting in an increased risk for gallstones.[35]

Crohn’s disease is associated with a type of rheumatologic disease known as seronegative spondyloarthropathy.[35] This group of diseases is characterized by inflammation of one or more joints (arthritis) or muscle insertions (enthesitis).[35] The arthritis in Crohn’s disease can be divided into two types. The first type affects larger weight-bearing joints such as the knee (most common), hips, shoulders, wrists, or elbows.[35] The second type symmetrically involves five or more of the small joints of the hands and feet.[35] The arthritis may also involve the spine, leading to ankylosing spondylitis if the entire spine is involved or simply sacroiliitis if only the sacroiliac joint is involved.[35] The symptoms of arthritis include painful, warm, swollen, stiff joints, and loss of joint mobility or function.[36]

Crohn’s disease may also involve the skin, blood, and endocrine system. The most common type of skin manifestation, erythema nodosum, presents as raised, tender red nodules usually appearing on the shins.[35][37] Erythema nodosum is due to inflammation of the underlying subcutaneous tissue, and is characterized by septal panniculitis.[37] Another skin lesion, pyoderma gangrenosum, is typically a painful ulcerating nodule. Crohn’s disease also increases the risk of blood clots;[35] painful swelling of the lower legs can be a sign of deep venous thrombosis, while difficulty breathing may be a result of pulmonary embolism. Autoimmune hemolytic anemia, a condition in which the immune system attacks the red blood cells, is also more common in Crohn’s disease and may cause fatigue, a pale appearance, and other symptoms common in anemia. Clubbing, a deformity of the ends of the fingers, may also be a result of Crohn’s disease. Finally, Crohn’s disease increases the risk of osteoporosis, or thinning of the bones.[35] Individuals with osteoporosis are at increased risk of bone fractures.[38]

People with Crohn’s disease may develop anemia due to vitamin B12, folate, iron deficiency, or due to anemia of chronic disease.[39][40] The most common is iron deficiency anemia[39] from chronic blood loss, reduced dietary intake, and persistent inflammation leading to increased hepcidin levels, restricting iron absorption in the duodenum.[40] As Crohn’s disease most commonly affects the terminal ileum where the vitamin B12/intrinsic factor complex is absorbed, B12 deficiency may be seen.[40] This is particularly common after surgery to remove the ileum.[39] Involvement of the duodenum and jejunum can impair the absorption of many other nutrients including folate. If Crohn’s disease affects the stomach, production of intrinsic factor can be reduced.

Crohn’s disease can also cause neurological complications (reportedly in up to 15%).[41] The most common of these are seizures, stroke, myopathy, peripheral neuropathy, headache and depression.[41]

People with Crohn’s often also have issues with small bowel bacterial overgrowth syndrome, which has similar symptoms.[42]

In the oral cavity people with Crohn’s may develop cheilitis granulomatosa and other forms of orofacial granulomatosis, pyostomatitis vegetans, recurrent aphthous stomatitis, geographic tongue, and migratory stomatitis in higher prevalence than the general population.[43]


While the exact cause is unknown, Crohn’s disease seems to be due to a combination of environmental factors and genetic predisposition.[46] Crohn’s is the first genetically complex disease in which the relationship between genetic risk factors and the immune system is understood in considerable detail.[47] Each individual risk mutation makes a small contribution to the overall risk of Crohn’s (approximately 1:200). The genetic data, and direct assessment of immunity, indicates a malfunction in the innate immune system.[48] In this view, the chronic inflammation of Crohn’s is caused when the adaptive immune system tries to compensate for a deficient innate immune system.[49]


NOD2 protein model with schematic diagram. Two N-terminal CARD domains (red) connected via helical linker (blue) with central NBD domain (green). At C-terminus LRR domain (cyan) is located. Additionally, some mutations which are associated with certain disease patterns in Crohn’s disease are marked in red wire representation.[50]

Crohn’s has a genetic component.[51] Because of this, siblings of known people with Crohn’s are 30 times more likely to develop Crohn’s than the general population.

The first mutation found to be associated with Crohn’s was a frameshift in the NOD2 gene (also known as the CARD15 gene),[52] followed by the discovery of point mutations.[53] Over thirty genes have been associated with Crohn’s; a biological function is known for most of them. For example, one association is with mutations in the XBP1 gene, which is involved in the unfolded protein response pathway of the endoplasmic reticulum.[54][55] The gene variants of NOD2/CARD15 seem to be related with small-bowel involvement.[56] Other well documented genes which increase the risk of developing Crohn disease are ATG16L1,[57] IL23R,[58] IRGM,[59] and SLC11A1.[60] There is considerable overlap between susceptibility loci for IBD and mycobacterial infections.[61] Recent genome-wide association studies have shown that Crohn’s disease is genetically linked to coeliac disease.[62]

Crohn’s has been linked to the gene LRRK2 with one variant potentially increasing the risk of developing the disease by 70%, while another lowers it by 25%. The gene is responsible for making a protein, which collects and eliminates waste product in cells, and is also associated with Parkinson’s disease.[63]

Immune system[edit]

There was a prevailing view that Crohn’s disease is a primary T cell autoimmune disorder, however, a newer theory hypothesizes that Crohn’s results from an impaired innate immunity.[64] The later hypothesis describes impaired cytokine secretion by macrophages, which contributes to impaired innate immunity and leads to a sustained microbial-induced inflammatory response in the colon, where the bacterial load is high.[7][48] Another theory is that the inflammation of Crohn’s was caused by an overactive Th1 and Th17 cytokine response.[65][66]

In 2007, the ATG16L1 gene has been implicated in Crohn’s disease, which may induce autophagy and hinder the body’s ability to attack invasive bacteria.[57] Another study has theorized that the human immune system traditionally evolved with the presence of parasites inside the body, and that the lack thereof due to modern hygiene standards has weakened the immune system. Test subjects were reintroduced to harmless parasites, with positive response.[67]


It is hypothesised that maintenance of commensal microorganism growth in the GI tract is dysregulated, either as a result or cause of immune dysregulation.[68] [69]

A number of studies have suggested a causal role for Mycobacterium avium subspecies paratuberculosis (MAP), which causes a similar disease, Johne’s disease, in cattle.[70][71]

NOD2 is a gene involved in Crohn’s genetic susceptibility. It is associated with macrophages’ diminished ability to phagocytize MAP. This same gene may reduce innate and adaptive immunity in gastrointestinal tissue and impair the ability to resist infection by the MAP bacterium.[72] Macrophages that ingest the MAP bacterium are associated with high production of TNF-α.[73][74]

Other studies have linked specific strains of enteroadherent E. coli to the disease.[75] Adherent-invasive Escherichia coli (AIEC), are more common in people with CD,[76][77][78] have the ability to make strong biofilms compared to non-AIEC strains correlating with high adhesion and invasion indices[79][80] of neutrophils and the ability to block autophagy at the autolysosomal step, which allows for intracellular survival of the bacteria and induction of inflammation.[81] Inflammation drives the proliferation of AIEC and dysbiosis in the ileum, irrespective of genotype.[82] AIEC strains replicate extensively inside macrophages inducing the secretion of very large amounts of TNF-α.[83]

Mouse studies have suggested some symptoms of Crohn’s disease, ulcerative colitis, and irritable bowel syndrome have the same underlying cause. Biopsy samples taken from the colons of all three patient groups were found to produce elevated levels of a serine protease.[84] Experimental introduction of the serine protease into mice has been found to produce widespread pain associated with irritable bowel syndrome, as well as colitis, which is associated with all three diseases.[85] Regional and temporal variations in those illnesses follow those associated with infection with the protozoan Blastocystis.[86]

The “cold-chain” hypothesis is that psychrotrophic bacteria such as Yersinia and Listeria species contribute to the disease. A statistical correlation was found between the advent of the use of refrigeration in the United States and various parts of Europe and the rise of the disease.[87][88][89]

There is an apparent connection between Crohn’s disease, Mycobacterium, other pathogenic bacteria, and genetic markers.[90][91] In many individuals, genetic factors predispose individuals to Mycobacterium avium subsp. paratuberculosis infection. This bacterium then produces mannins, which protect both itself and various bacteria from phagocytosis, which causes a variety of secondary infections.[92]

Still, this relationship between specific types of bacteria and Crohn’s disease remains unclear.[93][94]

There is a tentative association between Candida colonization and Crohn’s disease.[95]

Environmental factors[edit]

The increased incidence of Crohn’s in the industrialized world indicates an environmental component. Crohn’s is associated with an increased intake of animal protein, milk protein and an increased ratio of omega-6 to omega-3 polyunsaturated fatty acids.[96] Those who consume vegetable proteins appear to have a lower incidence of Crohn’s disease. Consumption of fish protein has no association.[96] Smoking increases the risk of the return of active disease (flares).[3] The introduction of hormonal contraception in the United States in the 1960s is associated with a dramatic increase in incidence, and one hypothesis is that these drugs work on the digestive system in ways similar to smoking.[97] Isotretinoin is associated with Crohn’s.[98][99][100] Although stress is sometimes claimed to exacerbate Crohn’s disease, there is no concrete evidence to support such claim.[101] Dietary microparticles, such as those found in toothpaste, have been studied as they produce effects on immunity, but they were not consumed in greater amounts in patients with Crohn’s.[102][103]


During a colonoscopy, biopsies of the colon are often taken to confirm the diagnosis. Certain characteristic features of the pathology seen point toward Crohn’s disease; it shows a transmural pattern of inflammation, meaning the inflammation may span the entire depth of the intestinal wall.[1] Ulceration is an outcome seen in highly active disease. There is usually an abrupt transition between unaffected tissue and the ulcer—a characteristic sign known as skip lesions. Under a microscope, biopsies of the affected colon may show mucosal inflammation, characterized by focal infiltration of neutrophils, a type of inflammatory cell, into the epithelium. This typically occurs in the area overlying lymphoid aggregates. These neutrophils, along with mononuclear cells, may infiltrate the crypts, leading to inflammation (crypititis) or abscess (crypt abscess). Granulomas, aggregates of macrophage derivatives known as giant cells, are found in 50% of cases and are most specific for Crohn’s disease. The granulomas of Crohn’s disease do not show “caseation”, a cheese-like appearance on microscopic examination characteristic of granulomas associated with infections, such as tuberculosis. Biopsies may also show chronic mucosal damage, as evidenced by blunting of the intestinal villi, atypical branching of the crypts, and a change in the tissue type (metaplasia). One example of such metaplasia, Paneth cell metaplasia, involves development of Paneth cells (typically found in the small intestine and a key regulator of intestinal microbiota) in other parts of the gastrointestinal system.[105][106]


The diagnosis of Crohn’s disease can sometimes be challenging,[21] and a number of tests are often required to assist the physician in making the diagnosis.[25] Even with a full battery of tests, it may not be possible to diagnose Crohn’s with complete certainty; a colonoscopy is approximately 70% effective in diagnosing the disease, with further tests being less effective. Disease in the small bowel is particularly difficult to diagnose, as a traditional colonoscopy allows access to only the colon and lower portions of the small intestines; introduction of the capsule endoscopy[107] aids in endoscopic diagnosis. Giant (multinucleate) cells, a common finding in the lesions of Crohn’s disease, are less common in the lesions of lichen nitidus.[108]

  • Endoscopic image of Crohn’s colitis showing deep ulceration

  • CT scan showing Crohn’s disease in the fundus of the stomach

  • Endoscopic biopsy showing granulomatous inflammation of the colon in a case of Crohn’s disease.

  • Section of colectomy showing transmural inflammation

  • Resected ileum from a person with Crohn’s disease


Distribution of gastrointestinal Crohn’s disease.

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 that 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.[109] 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.[1]

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.[110] 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.[110][111]


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 colonoscopy can travel past the terminal ileum, but it varies from person to person. 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 30% of Crohn’s disease involves only the ileum,[1] 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.[112] The utility of capsule endoscopy for this, however, is still uncertain.[113] A “cobblestone”-like appearance is seen in approximately 40% of cases of Crohn’s disease upon colonoscopy, representing areas of ulceration separated by narrow areas of healthy tissue.

Radiologic tests[edit]

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. As a result, a barium follow-through X-ray, wherein barium sulfate suspension is ingested and fluoroscopic images of the bowel are taken over time, is useful for looking for inflammation and narrowing of the small bowel.[112][114] Barium enemas, in which barium is inserted into the rectum and fluoroscopy is used to image the bowel, are rarely used in the work-up of Crohn’s disease due to the advent of colonoscopy. They remain useful for identifying anatomical abnormalities when strictures of the colon are too small for a colonoscope to pass through, or in the detection of colonic fistulae (in this case contrast should be performed with iodate substances).[115]

CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols.[116] They are also useful for looking for intra-abdominal complications of Crohn’s disease, such as abscesses, small bowel obstructions, or fistulae.[117] 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.[118] MRI techniques such as diffusion-weighted imaging and high-resolution imaging are more sensitive in detecting ulceration and inflammation compared to CT.[119][120]

Blood tests[edit]

A complete blood count may reveal anemia, which commonly is caused by blood loss leading to iron deficiency or by vitamin B12 deficiency, usually caused by ileal disease impairing vitamin B12 absorption. Rarely autoimmune hemolysis may occur.[121] Ferritin levels help assess if iron deficiency is contributing to the anemia. Erythrocyte sedimentation rate (ESR) and C-reactive protein help assess the degree of inflammation, which is important as ferritin can also be raised in inflammation.[122] Serum iron, total iron binding capacity and transferrin saturation may be more easily interpreted in inflammation. Anemia of chronic disease results in a normocytic anemia. Other causes of anemia include medication used in treatment of inflammatory bowel disease, like azathioprine, which can lead to cytopenia, and sulfasalazine, which can also result in folate deficiency. Testing for Saccharomyces cerevisiae antibodies (ASCA) and antineutrophil cytoplasmic antibodies (ANCA) has been evaluated to identify inflammatory diseases of the intestine[123] and to differentiate Crohn’s disease from ulcerative colitis.[124] Furthermore, increasing amounts and levels of serological antibodies such as ASCA, antilaminaribioside [Glc(β1,3)Glb(β); ALCA], antichitobioside [GlcNAc(β1,4)GlcNAc(β); ACCA], antimannobioside [Man(α1,3)Man(α)AMCA], antiLaminarin [(Glc(β1,3))3n(Glc(β1,6))n; anti-L] and antichitin [GlcNAc(β1,4)n; anti-C] associate with disease behavior and surgery, and may aid in the prognosis of Crohn’s disease.[125][126][127][128]

Low serum levels of vitamin D are associated with Crohn’s disease.[129] Further studies are required to determine the significance of this association.[129]

Comparison with ulcerative colitis[edit]

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.[1][25][26]

Differential diagnosis[edit]

Other conditions with similar symptoms as Crohn’s disease includes intestinal tuberculosis, Behçet’s disease, ulcerative colitis, nonsteroidal anti-inflammatory drug enteropathy, irritable bowel syndrome and celiac disease.[4] Irritable bowel syndrome is excluded when there are inflammatory changes.[4] Celiac disease can’t be excluded if specific antibodies (anti-transglutaminase antibodies) are negative,[134][135] nor in absence of intestinal villi atrophy.[136][137]


Main article: Management of Crohn’s disease

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 and dietary changes, changes to eating habits (eating smaller amounts more often), reduction of stress, moderate activity and exercise. Surgery is generally contraindicated and has not been shown to prevent remission. Adequately controlled, Crohn’s disease may not significantly restrict daily living.[141] Treatment for Crohn’s disease is only when symptoms are active and involve first treating the acute problem, then maintaining remission.

Lifestyle changes[edit]

Certain lifestyle changes can reduce symptoms, including dietary adjustments, elemental diet, proper hydration, and smoking cessation. Diets that include higher levels of fiber and fruit are associated with reduced risk, while diets rich in total fats, polyunsaturated fatty acids, meat, and omega-6 fatty acids may increase the risk of Crohn’s.[142] 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 people should follow a low fiber diet to control acute symptoms especially if fibrous foods cause symptoms.[141] Some find relief in eliminating casein (protein found in cow’s milk) and gluten (protein found in wheat, rye and barley) from their diets. They may have specific dietary intolerances (not allergies).[143]


Acute treatment uses medications to treat any infection (normally antibiotics) and to reduce inflammation (normally aminosalicylate anti-inflammatory drugs and corticosteroids). When symptoms are in remission, treatment enters maintenance, with a goal of avoiding the recurrence of symptoms. Prolonged use of corticosteroids has significant side-effects; as a result, they are, in general, not used for long-term treatment. Alternatives include aminosalicylates alone, though only a minority are able to maintain the treatment, and many require immunosuppressive drugs.[20] It has been also suggested that antibiotics change the enteric flora, and their continuous use may pose the risk of overgrowth with pathogens such as Clostridium difficile.[144]

Medications used to treat the symptoms of Crohn’s disease include 5-aminosalicylic acid (5-ASA) formulations, prednisone, immunomodulators such as azathioprine (given as the prodrug for 6-mercaptopurine), methotrexate, infliximab, adalimumab,[26] certolizumab[145] and natalizumab.[146][147] Hydrocortisone should be used in severe attacks of Crohn’s disease.[148] Biological therapies (biopharmaceuticals) are medications used to avoid long-term steroid use, decrease inflammation, and treat people who have fistulas with abscesses.[24] The monoclonal antibody ustekinumab appears to be a safe treatment option, and may help people with moderate to severe active Crohn’s disease.[149] The long term safety and effectiveness of monoclonal antibody treatment is not known. The monoclonal antibody briakinumab is not effective for people with active Crohn’s disease.[149]

The gradual loss of blood from the gastrointestinal tract, as well as chronic inflammation, often leads to anemia, and professional guidelines suggest routinely monitoring for this.[150][151][152] Adequate disease control usually improves anemia of chronic disease, but iron deficiency may require treatment with iron supplements. Guidelines vary as to how iron should be administered. Besides other, problems include a limitation in possible daily resorption and an increased growth of intestinal bacteria. Some[152] advise parenteral iron as first line as it works faster, has fewer gastrointestinal side effects, and is unaffected by inflammation reducing enteral absorption.

Other guidelines[151] advise oral iron as first line with parenteral iron reserved for those that fail to adequately respond as oral iron is considerably cheaper. All agree that severe anemia (hemoglobin under 10g/dL) should be treated with parenteral iron. Blood transfusion should be reserved for those who are cardiovascularly unstable, due to its relatively poor safety profile, lack of long term efficacy, and cost.[151]


Crohn’s cannot be cured by surgery, as the disease eventually recurs, though it is used in the case of partial or full blockage of the intestine.[153] Surgery may also be required for complications such as obstructions, fistulas, or abscesses, or if the disease does not respond to drugs. After the first surgery, Crohn’s usually comes back at the site where the diseased intestine was removed and the healthy ends were rejoined, however it can come back 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.[154] For patients with an obstruction due to a stricture, two options for treatment are strictureplasty and resection of that portion of bowel. There is no statistical significance between strictureplasty alone versus strictureplasty and resection in cases of duodenal involvement. In these cases, re-operation rates were 31% and 27%, respectively, indicating that strictureplasty is a safe and effective treatment for selected people with duodenal involvement.[155]

Postsurgical recurrence of Crohn’s disease is relatively common. Crohn’s lesions are nearly always found at the site of the resected bowel. The join (or anastomosis) after surgery may be inspected, usually during a colonoscopy, and disease activity graded. The “Rutgeert’s score” is an endoscopic scoring system for post-operative disease recurrence in Crohn’s disease. Mild postsurgical recurrences of Crohn’s disease are graded i1 and i2, moderate to severe recurrences are graded i3 and i4.[156] Fewer lesions result in a lower grade. Based on the score, treatment plans can be designed to give the patient the best chance of managing recurrence of the disease.[157]

Short bowel syndrome (SBS, also short gut syndrome or simply short gut) is caused by the surgical removal of part of the small intestine. It usually develops in those patients who have had half or more of their small intestines removed.[158] Diarrhea is the main symptom, but others may include weight loss, cramping, bloating, and heartburn. Short bowel syndrome is treated with changes in diet, intravenous feeding, vitamin and mineral supplements, and treatment with medications. In some cases of SBS, intestinal transplant surgery may be considered; though the number of transplant centres offering this procedure is quite small and it comes with a high risk due to the chance of infection and rejection of the transplanted intestine.[159]

Bile acid diarrhea is another complication following surgery for Crohn’s disease in which the terminal ileum has been removed. This leads to the development of excessive watery diarrhea. It is usually thought to be due to an inability of the ileum to reabsorb bile acids after resection of the terminal ileum and was the first type of bile acid malabsorption recognized.[160]

Mental health[edit]

Crohn’s may result in anxiety or mood disorders, especially in young people who may have stunted growth or embarrassment from fecal incontinence.[161] Counselling as well as antidepressant or anxiolytic medication may help some people manage.[161]

As of 2017 there is a small amount of research looking at mindfulness-based therapies, hypnotherapy, and cognitive behavioural therapy.[162]

Alternative medicine[edit]

It is common for people with Crohn’s disease to try complementary or alternative therapy.[163] These include diets, probiotics, fish oil and other herbal and nutritional supplements.

  • Acupuncture is used to treat inflammatory bowel disease in China, and is being used more frequently in Western society.[164] At this time, evidence is insufficient to recommend the use of acupuncture.[165]
  • A 2006 survey in Germany, found that about half of people with IBD used some form of alternative medicine, with the most common being homeopathy and a study in France found that about 30% used alternative medicine.[166] Homeopathic preparations are not effective for treating any condition,[167][168][169][168][169] with large-scale studies finding them to be no more effective than a placebo.[170][171][172]
  • There are contradicting studies regarding the effect of medical cannabis on inflammatory bowel disease.[173]


Crohn’s disease is a chronic condition for which there is no known 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. It can vary from being benign to very severe and people with CD could experience just one episode or have continuous symptoms. It usually reoccurs, although some people can remain disease free for years or decades. Most people with Crohn’s live a normal lifespan.[174] However, Crohn’s disease is associated with a small increase in risk of small bowel and colorectal carcinoma (bowel cancer).[175]


Crohn’s disease can lead to several mechanical complications within the intestines, including obstruction,[177] fistulae,[178] and abscesses.[179] Obstruction typically occurs from strictures or adhesions that narrow the lumen, blocking the passage of the intestinal contents. A fistula can develop between two loops of bowel, between the bowel and bladder, between the bowel and vagina, and between the bowel and skin. Abscesses are walled off concentrations of infection, which can occur in the abdomen or in the perianal area. Crohn’s is responsible for 10% of vesicoenteric fistulae, and is the most common cause of ileovesical fistulae.[180]

Endoscopic image of colon cancer identified in the sigmoid colon on screening colonoscopy for Crohn’s disease

Crohn’s disease also increases the risk of cancer in the area of inflammation. For example, individuals with Crohn’s disease involving the small bowel are at higher risk for small intestinal cancer. Similarly, people with Crohn’s colitis have a relative risk of 5.6 for developing colon cancer.[181] Screening for colon cancer with colonoscopy is recommended for anyone who has had Crohn’s colitis for at least eight years.[182] Some studies suggest there is a role for chemoprotection in the prevention of colorectal cancer in Crohn’s involving the colon; two agents have been suggested, folate and mesalamine preparations.[183] Also, immunomodulators and biologic agents used to treat this disease may promote developing extra-intestinal cancers.[184]

Individuals with Crohn’s disease are at risk of malnutrition for many reasons, including decreased food intake and malabsorption. The risk increases following resection of the small bowel. Such individuals may require oral supplements to increase their caloric intake, or in severe cases, total parenteral nutrition (TPN). Most people with moderate or severe Crohn’s disease are referred to a dietitian for assistance in nutrition.[185]

The major significant complications of Crohn’s disease include bowel obstruction, abscesses, free perforation and hemorrhage, which in rare cases may be fatal.[186][187]

Crohn’s disease can be problematic during pregnancy, and some medications can cause adverse outcomes for the fetus or mother. Consultation with an obstetrician and gastroenterologist about Crohn’s disease and all medications facilitates preventative measures. In some cases, remission occurs during pregnancy. Certain medications can also lower sperm count or otherwise adversely affect a man’s fertility.[188]


The percentage of people with Crohn’s disease has been determined in Norway and the United States and is similar at 6 to 7.1:100,000. The Crohn’s and Colitis Foundation of America cites this number as approx 149:100,000; NIH cites 28 to 199 per 100,000.[189][190] Crohn’s disease is more common in northern countries, and with higher rates still in the northern areas of these countries.[191] The incidence of Crohn’s disease is thought to be similar in Europe but lower in Asia and Africa.[189] It also has a higher incidence in Ashkenazi Jews[1][192] and smokers.[193]

Crohn’s disease begins most commonly in people in their teens and 20s, and people in their 50s through to their 70s.[1][25] It is rarely diagnosed in early childhood. It usually affects female children more severely than males.[194] However, only slightly more women than men have Crohn’s disease.[195] Parents, siblings or children of people with Crohn’s disease are 3 to 20 times more likely to develop the disease.[196] Twin studies find that if one has the disease there is a 55% chance the other will too.[197]

The incidence of Crohn’s disease is increasing in Europe[198] and in newly industrialised countries.[199] For example, in Brazil, there has been an annual increase of 11% in the incidence of Crohn’s disease since 1990.[199]


Main article: List of people diagnosed with Crohn’s disease

Inflammatory bowel diseases were described by Giovanni Battista Morgagni (1682–1771) and by Scottish physician T. Kennedy Dalziel in 1913.[200]

Ileitis terminalis was first described by Polish surgeon Antoni Leśniowski in 1904, although it was not conclusively distinguished from intestinal tuberculosis.[201] In Poland, it is still called Leśniowski-Crohn’s disease (Polish: choroba Leśniowskiego-Crohna). Burrill Bernard Crohn, an American gastroenterologist at New York City’s Mount Sinai Hospital, described fourteen cases in 1932, and submitted them to the American Medical Association under the rubric of “Terminal ileitis: A new clinical entity”. Later that year, he, along with colleagues Leon Ginzburg and Gordon Oppenheimer, published the case series as “Regional ileitis: a pathologic and clinical entity”. However, due to the precedence of Crohn’s name in the alphabet, it later became known in the worldwide literature as Crohn’s disease.[18]


Some evidence supports the hypothesis that the bacterium Mycobacterium avium subspecies paratuberculosis (MAP) is a cause of Crohn’s disease (see also Johne’s disease). As a result, researchers are looking at the eradication of MAP as a therapeutic option.[202] Treating MAP using antibiotics has been examined and the results are unclear but tentatively beneficial.[203][204] Vaccination against MAP is also being studied. An anti-MAP vaccine appears effective in mice and cattle with MAP with no apparent side effects.[202][205] Trials in human are pending.[206]

Crohn’s is common in parts of the world where helminthic colonisation is rare and uncommon in those areas where most people carry worms. Infections with helminths may alter the autoimmune response that causes the disease. Trials of extracts from the worm Trichuris suis showed promising results when used in people with IBD.[207][208][209] However these trials (TRUST -I & TRUST -II) failed in Phase 2 clinical trials and were then discontinued after consistent failure in both North America and Europe.[210][211]

Numerous preclinical studies demonstrate that activation of the CB1 and CB2 cannabinoid receptors exert biological functions on the gastrointestinal tract.[212] Activation of CB1 and CB2 receptors in animals has shown a strong anti-inflammatory effect.[213] Cannabinoids and/or modulation of the endocannabinoid system is a novel therapeutic means for the treatment of numerous GI disorders, including inflammatory bowel diseases like Crohn’s disease.[214] A few small trials have looked at medical cannabis but further evidence is required to determine its usefulness.[173]

There is no good evidence that thalidomide or lenalidomide is useful to bring about or maintain remission.[215][216]


  • ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai Baumgart DC, Sandborn WJ; Sandborn (2012). “Crohn’s disease”. The Lancet. 380 (9853): 1590–605. doi:10.1016/S0140-6736(12)60026-9. PMID 22914295. 
  • ^ a b c d e “Crohn’s Disease”. National Digestive Diseases Information Clearinghouse (NDDIC). July 10, 2013. Archived from the original on June 9, 2014. Retrieved June 12, 2014. 
  • ^ a b c Cosnes J (2004). “Tobacco and IBD: Relevance in the understanding of disease mechanisms and clinical practice”. Best Practice & Research Clinical Gastroenterology. 18 (3): 481–96. doi:10.1016/j.bpg.2003.12.003. PMID 15157822. 
  • ^ a b c “Inflammatory Bowel Disease” (PDF). World Gastroenterology Organization. August 2015. Archived (PDF) from the original on March 14, 2016. Retrieved March 13, 2016. 
  • ^ a b Molodecky, NA; Soon, IS; Rabi, DM; Ghali, WA; Ferris, M; Chernoff, G; Benchimol, EI; Panaccione, R; Ghosh, S; Barkema, HW; Kaplan, GG (Jan 2012). “Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review”. Gastroenterology. 142 (1): 46–54.e42; quiz e30. doi:10.1053/j.gastro.2011.10.001. PMID 22001864. 
  • ^ Cho JH, Brant SR (2011). “Recent Insights into the Genetics of Inflammatory Bowel Disease”. Gastroenterology. 140 (6): 1704–12. doi:10.1053/j.gastro.2011.02.046. PMC 4947143 . PMID 21530736. 
  • ^ a b c Dessein R, Chamaillard M, Danese S (2008). “Innate Immunity in Crohn’s Disease”. Journal of Clinical Gastroenterology. 42: S144–7. doi:10.1097/MCG.0b013e3181662c90. PMID 18806708. 
  • ^ Stefanelli T, Malesci A, Repici A, Vetrano S, Danese S (2008). “New Insights into Inflammatory Bowel Disease Pathophysiology: Paving the Way for Novel Therapeutic Targets”. Current Drug Targets. 9 (5): 413–8. doi:10.2174/138945008784221170. PMID 18473770. 
  • ^ a b Marks DJ, Rahman FZ, Sewell GW, Segal AW (2010). “Crohn’s disease: An immune deficiency state”. Clinical reviews in allergy & immunology. 38 (1): 20–31. doi:10.1007/s12016-009-8133-2. PMC 4568313 . PMID 19437144. 
  • ^ Casanova JL, Abel L (August 31, 2009). “Revisiting Crohn’s disease as a primary immunodeficiency of macrophages”. The Journal of Experimental Medicine. 206 (9): 1839–43. doi:10.1084/jem.20091683. PMC 2737171 . PMID 19687225. 
  • ^ Lalande JD, Behr MA (2010). “Mycobacteria in Crohn’s disease: How innate immune deficiency may result in chronic inflammation”. Expert review of clinical immunology. 6 (4): 633–41. doi:10.1586/eci.10.29. PMID 20594136. 
  • ^ Yamamoto-Furusho JK, Korzenik JR (2006). “Crohn’s disease: Innate immunodeficiency?”. World Journal of Gastroenterology. 12 (42): 6751–5. PMID 17106921. Archived from the original on June 6, 2013. 
  • ^ Barrett JC, Hansoul S, Nicolae DL, Cho JH, Duerr RH, Rioux JD, Brant SR, Silverberg MS, Taylor KD, Barmada MM, Bitton A, Dassopoulos T, Datta LW, Green T, Griffiths AM, Kistner EO, Murtha MT, Regueiro MD, Rotter JI, Schumm LP, Steinhart AH, Targan SR, Xavier RJ, Libioulle C, Sandor C, Lathrop M, Belaiche J, Dewit O, Gut I, Heath S, Laukens D, Mni M, Rutgeerts P, Van Gossum A, Zelenika D, Franchimont D, Hugot JP, de Vos M, Vermeire S, Louis E, Cardon LR, Anderson CA, Drummond H, Nimmo E, Ahmad T, Prescott NJ, Onnie CM, Fisher SA, Marchini J, Ghori J, Bumpstead S, Gwilliam R, Tremelling M, Deloukas P, Mansfield J, Jewell D, Satsangi J, Mathew CG, Parkes M, Georges M, Daly MJ (2008). “Genome-wide association defines more than 30 distinct susceptibility loci for Crohn’s disease”. Nature Genetics. 40 (8): 955–62. doi:10.1038/ng.175. PMC 2574810 . PMID 18587394. 
  • ^ Prideaux, L; Kamm, MA; De Cruz, PP; Chan, FK; Ng, SC (Aug 2012). “Inflammatory bowel disease in Asia: a systematic review”. Journal of Gastroenterology and Hepatology. 27 (8): 1266–80. doi:10.1111/j.1440-1746.2012.07150.x. PMID 22497584. 
  • ^ a b Hovde, Ø; Moum, BA (Apr 21, 2012). “Epidemiology and clinical course of Crohn’s disease: results from observational studies”. World Journal of Gastroenterology. 18 (15): 1723–31. doi:10.3748/wjg.v18.i15.1723. PMC 3332285 . PMID 22553396. 
  • ^ a b Burisch, J; Munkholm, P (Jul 2013). “Inflammatory bowel disease epidemiology”. Current Opinion in Gastroenterology. 29 (4): 357–62. doi:10.1097/MOG.0b013e32836229fb. PMID 23695429. 
  • ^ GBD 2015 Mortality and Causes of Death, Collaborators. (October 8, 2016). “Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015”. Lancet. 388 (10053): 1459–1544. doi:10.1016/S0140-6736(16)31012-1. PMC 5388903 . PMID 27733281. 
  • ^ a b Crohn BB, Ginzburg L, Oppenheimer GD (2000). “Regional ileitis: A pathologic and clinical entity. 1932”. The Mount Sinai journal of medicine, New York. 67 (3): 263–8. PMID 10828911. 
  • ^ a b c d e f > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
  • ^ a b c d e Hanauer SB, Sandborn W (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. Retrieved 2009-11-07. 
  • ^ a b Pimentel M, Chang M, Chow EJ, Tabibzadeh S, Kirit-Kiriak V, Targan SR, Lin HC (2000). “Identification of a prodromal period in Crohn’s disease but not ulcerative colitis”. The American Journal of Gastroenterology. 95 (12): 3458–62. doi:10.1111/j.1572-0241.2000.03361.x. PMID 11151877. 
  • ^ “Crohn’s Disease: Get Facts on Symptoms and Diet”. eMedicineHealth. Archived from the original on October 20, 2007. 
  • ^ National Research Council (US) Committee on Diagnosis and Control of Johne’s Disease (2003). Diagnosis and Control of Johne’s Disease. Archived from the original on September 6, 2017. 
  • ^ a b “What I need to know about Crohn’s Disease”. Archived from the original on November 21, 2015. Retrieved December 11, 2015. 
  • ^ a b c d e f g Crohn Disease at eMedicine
  • ^ a b c Podolsky DK (2002). “Inflammatory Bowel Disease”. New England Journal of Medicine. 347 (6): 417–29. doi:10.1056/NEJMra020831. PMID 12167685. 
  • ^ Mueller MH, Kreis ME, Gross ML, Becker HD, Zittel TT, Jehle EC (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. 
  • ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (July 30, 2004). “The Gastrointestinal Tract”. Robbins and Cotran: Pathologic Basis of Disease (7th ed.). Philadelphia, Pennsylvania: Elsevier Saunders. p. 847. ISBN 0-7216-0187-1. 
  • ^ Taylor BA, Williams GT, Hughes LE, Rhodes J (1989). “The histology of anal skin tags in Crohn’s disease: An aid to confirmation of the diagnosis”. International Journal of Colorectal Disease. 4 (3): 197–9. doi:10.1007/BF01649703. PMID 2769004. 
  • ^ Fix OK, Soto JA, Andrews CW, Farraye FA (2004). “Gastroduodenal Crohn’s disease”. Gastrointestinal Endoscopy. 60 (6): 985. doi:10.1016/S0016-5107(04)02200-X. PMID 15605018. 
  • ^ a b Beattie RM, Croft NM, Fell JM, Afzal NA, Heuschkel RB (2006). “Inflammatory bowel disease”. Archives of Disease in Childhood. 91 (5): 426–32. doi:10.1136/adc.2005.080481. PMC 2082730 . PMID 16632672. 
  • ^ Büller HA (1997). “Problems in diagnosis of IBD in children”. The Netherlands Journal of Medicine. 50 (2): S8–11. doi:10.1016/S0300-2977(96)00064-2. PMID 9050326. 
  • ^ O’Keefe SJ (1996). “Nutrition and gastrointestinal disease”. Scand. J. Gastroenterol. Suppl. 220: 52–9. doi:10.3109/00365529609094750. PMID 8898436. 
  • ^ Danese S, Semeraro S, Papa A, Roberto I, Scaldaferri F, Fedeli G, Gasbarrini G, Gasbarrini A (2005). “Extraintestinal manifestations in inflammatory bowel disease”. World Journal of Gastroenterology. 11 (46): 7227–36. PMID 16437620. Archived from the original on July 7, 2007. 
  • ^ a b c d e f g h i j k Trikudanathan G, Venkatesh PG, Navaneethan U (2012). “Diagnosis and therapeutic management of extra-intestinal manifestations of inflammatory bowel disease”. Drugs. 72 (18): 2333–49. doi:10.2165/11638120-000000000-00000. PMID 23181971. 
  • ^ “Arthritis”. Healthline Networks, Inc. October 10, 2008. Archived from the original on July 21, 2010. Retrieved August 16, 2010. 
  • ^ a b Thrash B, Patel M, Shah KR, Boland CR, Menter A (2013). “Cutaneous manifestations of gastrointestinal disease: part II”. Journal of the American Academy of Dermatology. 68 (2): 211 e1–33. doi:10.1016/j.jaad.2012.10.036. PMID 23317981. 
  • ^ Bernstein M, Irwin S, Greenberg GR (2005). “Maintenance Infliximab Treatment is Associated with Improved Bone Mineral Density in Crohn’s Disease”. The American Journal of Gastroenterology. 100 (9): 2031–5. doi:10.1111/j.1572-0241.2005.50219.x. PMID 16128948. 
  • ^ a b c Lomer MC (August 2011). “Dietary and nutritional considerations for inflammatory bowel disease”. The Proceedings of the Nutrition Society. 70 (3): 329–35. doi:10.1017/S0029665111000097. PMID 21450124. 
  • ^ a b c Gerasimidis K, McGrogan P, Edwards CA (August 2011). “The aetiology and impact of malnutrition in paediatric inflammatory bowel disease”. Journal of Human Nutrition and Dietetics (Review). 24 (4): 313–26. doi:10.1111/j.1365-277X.2011.01171.x. PMID 21564345. Archived from the original on February 2, 2017. 
  • ^ a b Crohn’s disease Archived August 5, 2007, at the Wayback Machine.. Retrieved July 13, 2007.
  • ^ MedlinePlus Encyclopedia Small bowel bacterial overgrowth
  • ^ Zadik Y, Drucker S, Pallmon S (2011). “Migratory stomatitis (ectopic geographic tongue) on the floor of the mouth”. Journal of the American Academy of Dermatology. 65 (2): 459–60. doi:10.1016/j.jaad.2010.04.016. PMID 21763590. 
  • ^ a b c d Kornbluth A, Sachar DB (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 (PDF) from the original on April 6, 2008. Retrieved 2009-11-07. 
  • ^ Crohn’s Disease Overview
  • ^ Braat H, Peppelenbosch MP, Hommes DW (August 2006). “Immunology of Crohn’s disease”. Annals of the New York Academy of Sciences. 1072 (1): 135–54. doi:10.1196/annals.1326.039. PMID 17057196. 
  • ^ 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. 
  • ^ a b 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. PMID 16503465. 
  • ^ 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. 
  • ^ Nakagome, S.; Mano, S.; Kozlowski, L.; Bujnicki, JM.; Shibata, H.; Fukumaki, Y.; Kidd, JR.; Kidd, KK.; et al. (Jun 2012). “Crohn’s disease risk alleles on the NOD2 locus have been maintained by natural selection on standing variation”. Mol Biol Evol. 29 (6): 1569–85. doi:10.1093/molbev/mss006. PMC 3697811 . PMID 22319155. 
  • ^ “Crohn’s disease has strong genetic link: study”. Crohn’s and Colitis Foundation of America. April 16, 2007. Archived from the original on May 2, 2007. Retrieved November 7, 2009. 
  • ^ Ogura Y, Bonen DK, Inohara N, Nicolae DL, Chen FF, Ramos R, Britton H, Moran T, Karaliuskas R, Duerr RH, Achkar JP, Brant SR, Bayless TM, Kirschner BS, Hanauer SB, Nuñez G, Cho JH (2001). “A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease”. Nature. 411 (6837): 603–6. doi:10.1038/35079114. PMID 11385577. 
  • ^ Cuthbert AP, Fisher SA, Mirza MM, King K, Hampe J, Croucher PJ, Mascheretti S, Sanderson J, Forbes A, Mansfield J, Schreiber S, Lewis CM, Mathew CG (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. 
  • ^ Kaser A, Lee AH, Franke A, Glickman JN, Zeissig S, Tilg H, Nieuwenhuis EE, Higgins DE, Schreiber S, Glimcher LH, Blumberg RS (September 5, 2008). “XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease”. Cell. 134 (5): 743–56. doi:10.1016/j.cell.2008.07.021. PMC 2586148 . PMID 18775308. 
  • ^ Clevers H (2009). “Inflammatory Bowel Disease, Stress, and the Endoplasmic Reticulum”. New England Journal of Medicine. 360 (7): 726–27. doi:10.1056/NEJMcibr0809591. PMID 19213688. 
  • ^ Vermeire S (2004). “NOD2/CARD15: relevance in clinical practice”. Best Pract Res Clin Gastroenterol (Review). 18 (3): 569–75. doi:10.1016/j.bpg.2003.12.008. PMID 15157828. 
  • ^ a b Prescott NJ, Fisher SA, Franke A, Hampe J, Onnie CM, Soars D, Bagnall R, Mirza MM, Sanderson J, Forbes A, Mansfield JC, Lewis CM, Schreiber S, Mathew CG (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. 
  • ^ Diegelmann, J.; Czamara, D.; Le Bras, E.; Zimmermann, E.; Olszak, T.; Bedynek, A.; Göke, B.; Franke, A.; et al. (2013). “Intestinal DMBT1 expression is modulated by Crohn’s disease-associated IL23R variants and by a DMBT1 variant which influences binding of the transcription factors CREB1 and ATF-2”. PLOS ONE. 8 (11): e77773. doi:10.1371/journal.pone.0077773. PMC 3818382 . PMID 24223725. 
  • ^ Prescott, NJ.; Dominy, KM.; Kubo, M.; Lewis, CM.; Fisher, SA.; Redon, R.; Huang, N.; Stranger, BE.; et al. (May 2010). “Independent and population-specific association of risk variants at the IRGM locus with Crohn’s disease”. Hum Mol Genet. 19 (9): 1828–39. doi:10.1093/hmg/ddq041. PMC 2850616 . PMID 20106866. 
  • ^ Chermesh, I.; Azriel, A.; Alter-Koltunoff, M.; Eliakim, R.; Karban, A.; Levi, BZ. (Jul 2007). “Crohn’s disease and SLC11A1 promoter polymorphism”. Dig Dis Sci. 52 (7): 1632–5. doi:10.1007/s10620-006-9682-3. PMID 17385031. 
  • ^ Jostins L, Ripke S, Weersma RK, et al. (2012). “Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease”. Nature. 491 (7422): 119–24. doi:10.1038/nature11582. PMC 3491803 . PMID 23128233. 
  • ^ Walker MM, Murray JA (Aug 2011). “An update in the diagnosis of coeliac disease”. Histopathology (Review). 59 (2): 166–79. doi:10.1111/j.1365-2559.2010.03680.x. PMID 21054494. Recent genome-wide association studies have shown that chronic inflammatory and autoimmune diseases are linked genetically to coeliac disease; for example, type 1 diabetes mellitus, Grave’s disease and Crohn’s disease. 
  • ^ “A single gene can raise or lower Crohn’s disease risk”. New Scientist. 20 January 2018. 
  • ^ 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. 
  • ^ Cobrin GM, Abreu MT (2005). “Defects in mucosal immunity leading to Crohn’s disease”. Immunol. Rev. 206 (1): 277–95. doi:10.1111/j.0105-2896.2005.00293.x. PMID 16048555. 
  • ^ 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. 
  • ^ Moises Velasquez-Manoff (June 29, 2008). “The Worm Turns”. The New York Times. Archived from the original on January 7, 2017. 
  • ^ Sartor, R Balfour (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. 
  • ^ Dogan B, Scherl E, Bosworth B, Yantiss R, Altier C, McDonough PL, Jiang ZD, Dupont HL, Garneau P, Harel J, Rishniw M, Simpson KW (2013). “Multidrug resistance is common in Escherichia coli associated with ileal Crohn’s disease”. Inflamm. Bowel Dis. 19 (1): 141–50. doi:10.1002/ibd.22971. PMID 22508665. 
  • ^ Naser SA, Collins MT (December 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. 
  • ^ Naser SA, Sagramsingh SR, Naser AS, Naser ST (June 2014). “Mycobacterium avium subspecies paratuberculosis causes Crohn’s disease in some inflammatory bowel disease patients”. World J. Gastroenterol. 20 (23): 7403–7415. doi:10.3748/wjg.v20.i23.7403. PMC 4064085 . PMID 24966610. 
  • ^ Glubb DM, Gearry RB, Barclay ML, Roberts RL, Pearson J, Keenan JI, McKenzie J, Bentley RW (2011). “NOD2 and ATG16L1 polymorphisms affect monocyte responses in Crohn’s disease”. World Journal of Gastroenterology. 17 (23): 2829–37. doi:10.3748/wjg.v17.i23.2829. PMC 3120942 . PMID 21734790. 
  • ^ Clancy R, Ren Z, Turton J, Pang G, Wettstein A (2007). “Molecular evidence for Mycobacterium avium subspecies paratuberculosis (MAP) in Crohn’s disease correlates with enhanced TNF-alpha secretion”. Digestive and Liver Disease. 39 (5): 445–51. doi:10.1016/j.dld.2006.12.006. PMID 17317344. 
  • ^ Nakase H, Tamaki H, Matsuura M, Chiba T, Okazaki K (2011). “Involvement of Mycobacterium avium subspecies paratuberculosis in TNF-α production from macrophage: Possible link between MAP and immune response in Crohn’s disease”. Inflammatory bowel diseases. 17 (11): E140–2. doi:10.1002/ibd.21750. PMID 21990211. 
  • ^ Baumgart M, Dogan B, Rishniw M, Weitzman G, Bosworth B, Yantiss R, Orsi RH, Wiedmann M, McDonough P, Kim SG, Berg D, Schukken Y, Scherl E, Simpson KW (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. 
  • ^ Sasaki M, Sitaraman SV, Babbin BA, Gerner-Smidt P, Ribot EM, Garrett N, Alpern JA, Akyildiz A, Theiss AL, Nusrat A, Klapproth JM (2007). “Invasive Escherichia coli are a feature of Crohn’s disease”. Laboratory Investigation. 87 (10): 1042–54. doi:10.1038/labinvest.3700661. PMID 17660846. 
  • ^ Darfeuille-Michaud A, Boudeau J, Bulois P, Neut C, Glasser AL, Barnich N, Bringer MA, Swidsinski A, Beaugerie L, Colombel JF (2004). “High prevalence of Adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease”. Gastroenterology. 127 (2): 412–21. doi:10.1053/j.gastro.2004.04.061. PMID 15300573. 
  • ^ Baumgart M, Dogan B, Rishniw M, Weitzman G, Bosworth B, Yantiss R, Orsi RH, Wiedmann M, McDonough P, Kim SG, Berg D, Schukken Y, Scherl E, Simpson KW (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. 
  • ^ Nickerson KP, McDonald C (2012). Mizoguchi, Emiko, ed. “Crohn’s Disease-Associated Adherent-Invasive Escherichia coli Adhesion is Enhanced by Exposure to the Ubiquitous Dietary Polysaccharide Maltodextrin”. PLoS ONE (). 7 (12): e52132. doi:10.1371/journal.pone.0052132. PMC 3520894 . PMID 23251695. 
  • ^ Martinez-Medina M, Naves P, Blanco J, Aldeguer X, Blanco JE, Blanco M, Ponte C, Soriano F, Darfeuille-Michaud A, Garcia-Gil LJ (2009). “Biofilm formation as a novel phenotypic feature of adherent-invasive Escherichia coli (AIEC)”. BMC Microbiology. 9 (1): 202. doi:10.1186/1471-2180-9-202. PMC 2759958 . PMID 19772580. 
  • ^ Chargui A, Cesaro A, Mimouna S, Fareh M, Brest P, Naquet P, Darfeuille-Michaud A, Hébuterne X, Mograbi B, Vouret-Craviari V, Hofman P (2012). “Subversion of autophagy in adherent invasive Escherichia coli-infected neutrophils induces inflammation and cell death”. PLoS ONE. 7 (12): e51727. doi:10.1371/journal.pone.0051727. PMC 3522719 . PMID 23272151. 
  • ^ Craven M, Egan CE, Dowd SE, McDonough SP, Dogan B, Denkers EY, Bowman D, Scherl EJ, Simpson KW (2012). “Inflammation drives dysbiosis and bacterial invasion in murine models of ileal Crohn’s disease”. PLoS ONE. 7 (7): e41594. doi:10.1371/journal.pone.0041594. PMC 3404971 . PMID 22848538. 
  • ^ Barnich N, Darfeuille-Michaud A (January 2007). “Adherent-invasive Escherichia coli and Crohn’s disease”. Current Opinion in Gastroenterology. 23 (1): 16–20. doi:10.1097/MOG.0b013e3280105a38. PMID 17133079. 
  • ^ Cenac N, Andrews CN, Holzhausen M, Chapman K, Cottrell G, Andrade-Gordon P, Steinhoff M, Barbara G, Beck P, Bunnett NW, Sharkey KA, Ferraz JG, Shaffer E, Vergnolle N (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. 
  • ^ Cenac N, Coelho AM, Nguyen C, Compton S, Andrade-Gordon P, MacNaughton WK, Wallace JL, Hollenberg MD, Bunnett NW, Garcia-Villar R, Bueno L, Vergnolle N (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. [permanent dead link]
  • ^ Boorom KF, Smith H, Nimri L, Viscogliosi E, Spanakos G, Parkar U, Li LH, Zhou XN, Ok UZ, Leelayoova S, Jones MS (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. 
  • ^ Hugot JP, Alberti C, Berrebi D, Bingen E, Cézard JP (2003). “Crohn’s disease: the cold chain hypothesis”. Lancet. 362 (9400): 2012–5. doi:10.1016/S0140-6736(03)15024-6. PMID 14683664. 
  • ^ “Fridges blamed for Crohn’s disease rise”. Medical News Today. December 12, 2003. Archived from the original on January 3, 2009. 
  • ^ Forbes A, Kalantzis T (2005). “Crohn’s disease: The cold chain hypothesis”. International Journal of Colorectal Disease. 21 (5): 399–401. doi:10.1007/s00384-005-0003-7. PMID 16059694. 
  • ^ Subramanian S, Roberts CL, Hart CA, Martin HM, Edwards SW, Rhodes JM, Campbell BJ (2007). “Replication of Colonic Crohn’s Disease Mucosal Escherichia coli Isolates within Macrophages and Their Susceptibility to Antibiotics”. Antimicrobial Agents and Chemotherapy. 52 (2): 427–34. doi:10.1128/AAC.00375-07. PMC 2224732 . PMID 18070962. 
  • ^ Mpofu CM, Campbell BJ, Subramanian S, Marshall-Clarke S, Hart CA, Cross A, Roberts CL, McGoldrick A, Edwards SW, Rhodes JM (2007). “Microbial Mannan Inhibits Bacterial Killing by Macrophages: A Possible Pathogenic Mechanism for Crohn’s Disease”. Gastroenterology. 133 (5): 1487–98. doi:10.1053/j.gastro.2007.08.004. PMID 17919633. 
  • ^ “New insights into Crohn’s Disease”. Archived from the original on September 23, 2013. 
  • ^ “Possible links between Crohn’s disease and Paratuberculosis” (PDF). European Commission Directorate-General Health & Consumer Protection. Archived from the original (PDF) on December 17, 2008. Retrieved November 7, 2009. 
  • ^ Gui GP, Thomas PR, Tizard ML, Lake J, Sanderson JD, Hermon-Taylor J (1997). “Two-year-outcomes analysis of Crohn’s disease treated with rifabutin and macrolide antibiotics”. Journal of Antimicrobial Chemotherapy. 39 (3): 393–400. doi:10.1093/jac/39.3.393. PMID 9096189. 
  • ^ Kumamoto, Carol A. (August 1, 2011). “Inflammation and gastrointestinal Candida colonization”. Current Opinion in Microbiology. 14 (4): 386–391. doi:10.1016/j.mib.2011.07.015. ISSN 1369-5274. PMC 3163673 . PMID 21802979. 
  • ^ a b Shoda R, Matsueda K, Yamato S, Umeda N (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”. The American Journal of Clinical Nutrition. 63 (5): 741–5. PMID 8615358. 
  • ^ Lesko SM, Kaufman DW, Rosenberg L, Helmrich SP, Miller DR, Stolley PD, Shapiro S (1985). “Evidence for an increased risk of Crohn’s disease in oral contraceptive users”. Gastroenterology. 89 (5): 1046–9. PMID 4043662. 
  • ^ 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. 
  • ^ Borobio E, Arín A, Valcayo A, Iñarrairaegui M, Nantes O, Prieto C (2004). “[Isotretinoin and ulcerous colitis]”. An Sist Sanit Navar (in Spanish). 27 (2): 241–3. doi:10.4321/S1137-66272004000300009. PMID 15381956. 
  • ^ Reniers DE, Howard JM (October 2001). “Isotretinoin-induced inflammatory bowel disease in an adolescent”. Annals of Pharmacotherapy. 35 (10): 1214–6. doi:10.1345/aph.10368. PMID 11675849. [permanent dead link]
  • ^ “Crohn’s Disease”. National Digestive Diseases Information Clearinghouse. Archived from the original on November 8, 2012. Retrieved November 13, 2012. 
  • ^ Lomer MC, Hutchinson C, Volkert S, Greenfield SM, Catterall A, Thompson RP, Powell JJ (December 2004). “Dietary sources of inorganic microparticles and their intake in healthy subjects and patients with Crohn’s disease”. Br. J. Nutr. 92 (6): 947–55. doi:10.1079/bjn20041276. PMID 15613257. 
  • ^ Powell JJ, Thoree V, Pele LC (October 2007). “Dietary microparticles and their impact on tolerance and immune responsiveness of the gastrointestinal tract”. Br. J. Nutr. 98 Suppl 1: S59–63. doi:10.1017/S0007114507832922. PMC 2737314 . PMID 17922962. 
  • ^ 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. 
  • ^ 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.
  • ^ [1]
  • ^ HCP: Pill Cam, Capsule Endoscopy, Esophageal Endoscopy Archived June 16, 2008, at the Wayback Machine.
  • ^ 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. 
  • ^ Tan, WC.; Allan, RN. (Oct 1993). “Diffuse jejunoileitis of Crohn’s disease”. Gut. 34 (10): 1374–8. doi:10.1136/gut.34.10.1374. PMC 1374544 . PMID 8244104. 
  • ^ a b Gasche C, Scholmerich J, Brynskov J, D’Haens G, Hanauer SB, Irvine EJ, Jewell DP, Rachmilewitz D, Sachar DB, Sandborn WJ, Sutherland LR (2007). “A simple classification of Crohn’s disease: Report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998”. Inflammatory Bowel Diseases. 6 (1): 8–15. doi:10.1002/ibd.3780060103. PMID 10701144. 
  • ^ Dubinsky MC, Fleshner PP (2003). “Treatment of Crohn’s disease of inflammatory, stenotic, and fistulizing phenotypes”. Current Treatment Options in Gastroenterology. 6 (3): 183–200. doi:10.1007/s11938-003-0001-1. PMID 12744819. 
  • ^ a b Hara AK, Leighton JA, Heigh RI, Sharma VK, Silva AC, De Petris G, Hentz JG, Fleischer DE (2005). “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. 
  • ^ Triester SL, Leighton JA, Leontiadis GI, Gurudu SR, Fleischer DE, Hara AK, Heigh RI, Shiff AD, Sharma VK (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. 
  • ^ Dixon PM, Roulston ME, Nolan DJ; Roulston; 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. CS1 maint: Multiple names: authors list (link)
  • ^ Carucci LR, Levine MS; Levine (2002). “Radiographic imaging of inflammatory bowel disease”. Gastroenterology Clinics of North America. 31 (1): 93–117, ix. doi:10.1016/S0889-8553(01)00007-3. PMID 12122746. 
  • ^ Rajesh A, Maglinte DD; 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. 
  • ^ Zissin R, Hertz M, Osadchy A, Novis B, Gayer G; Hertz; Osadchy; Novis; 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 (PDF) on April 6, 2008. Retrieved November 7, 2009. CS1 maint: Multiple names: authors list (link)
  • ^ Mackalski BA, Bernstein CN; 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. 
  • ^ Sinha, Rakesh; Rajiah, Prabhakar; Murphy, Paul; Hawker, Peter; Sanders, Scott (2009-10-01). “Utility of High-Resolution MR Imaging in Demonstrating Transmural Pathologic Changes in Crohn Disease”. RadioGraphics. 29 (6): 1847–1867. doi:10.1148/rg.296095503. ISSN 0271-5333. 
  • ^ Sinha, Rakesh; Rajiah, Prabhakar; Ramachandran, Iswaran; Sanders, Scott; Murphy, Paul D. (2013-05-01). “Diffusion-weighted MR Imaging of the Gastrointestinal Tract: Technique, Indications, and Imaging Findings”. RadioGraphics. 33 (3): 655–676. doi:10.1148/rg.333125042. ISSN 0271-5333. 
  • ^ Goh J, O’Morain CA; O’Morain (2003). “Nutrition and adult inflammatory bowel disease”. Alimentary Pharmacology and Therapeutics. 17 (3): 307–20. doi:10.1046/j.1365-2036.2003.01482.x. PMID 12562443. 
  • ^ Chamouard P, Richert Z, Meyer N, Rahmi G, Baumann R; Richert; Meyer; Rahmi; 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. CS1 maint: Multiple names: authors list (link)
  • ^ Kaila B, Orr K, Bernstein CN; Orr; 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. Archived from the original on May 6, 2011. Retrieved July 2, 2006. CS1 maint: Multiple names: authors list (link)
  • ^ Israeli E, Grotto I, Gilburd B, Balicer RD, Goldin E, Wiik A, Shoenfeld Y; Grotto; Gilburd; Balicer; Goldin; Wiik; 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. CS1 maint: Multiple names: authors list (link)
  • ^ Ferrante M, Henckaerts L, Joossens M, Pierik M, Joossens S, Dotan N, Norman GL, Altstock RT, Van Steen K, Rutgeerts P, Van Assche G, Vermeire S; Henckaerts; Joossens; Pierik; Joossens; Dotan; Norman; Altstock; Van Steen; Rutgeerts; Van Assche; Vermeire, S (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. CS1 maint: Multiple names: authors list (link)
  • ^ Papp M, Altorjay I, Dotan N, Palatka K, Foldi I, Tumpek J, Sipka S, Udvardy M, Dinya T, Lakatos L, Kovacs A, Molnar T, Tulassay Z, Miheller P, Norman GL, Szamosi T, Papp J, Lakatos PL; Altorjay; Dotan; Palatka; Foldi; Tumpek; Sipka; Udvardy; Dinya; Lakatos; Kovacs; Molnar; Tulassay; Miheller; Norman; Szamosi; Papp; Hungarian Ibd Study; 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”. The American Journal of Gastroenterology. 103 (3): 665–81. doi:10.1111/j.1572-0241.2007.01652.x. PMID 18047543. CS1 maint: Multiple names: authors list (link)
  • ^ Seow CH, Stempak JM, Xu W, Lan H, Griffiths AM, Greenberg GR, Steinhart AH, Dotan N, Silverberg MS; Stempak; Xu; Lan; Griffiths; Greenberg; Steinhart; Dotan; 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. CS1 maint: Multiple names: authors list (link)
  • ^ 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:10.1586/17474124.1.2.265. PMID 19072419. 
  • ^ a b Del Pinto, Rita; Pietropaoli, Davide; Chandar, Apoorva K.; Ferri, Claudio; Cominelli, Fabio (August 12, 2015). “Association Between Inflammatory Bowel Disease and Vitamin D Deficiency: A Systematic Review and Meta-analysis”. Inflammatory Bowel Diseases. 21: 2708–17. doi:10.1097/MIB.0000000000000546. ISSN 1536-4844. PMC 4615394 . PMID 26348447. 
  • ^ Broomé U, Bergquist A (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. 
  • ^ Baumgart DC, Sandborn WJ (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. Retrieved 2009-11-04. 
  • ^ 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. 
  • ^ 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. 
  • ^ Lewis NR, Scott BB (July 1, 2006). “Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests)”. Aliment Pharmacol Ther (Review). 24 (1): 47–54. doi:10.1111/j.1365-2036.2006.02967.x. PMID 16803602. Archived from the original on May 4, 2016. Both the endomysial antibody and tissue transglutaminase antibody have very high sensitivities (93% for both) and specificities (>99% and >98% respectively) for the diagnosis of typical coeliac disease with villous atrophy. (…) As the detection of at least partial villous atrophy was used to make a diagnosis of coeliac disease in the vast majority of studies, we can’t assume that the same LRs apply to coeliac patients with lesser abnormality such as an increase in intraepithelial lymphocytes or electron-microscopic changes only. In fact, if such lesser abnormalities were used as criteria for diagnosing (and excluding) coeliac disease, the sensitivity of the tests could be lower (i.e. more false negatives), especially since a number of studies suggest that the EMA and tTG antibody tests are less sensitive with lesser degrees of mucosal abnormality 
  • ^ Rodrigo L, Garrote JA, Vivas S (September 6, 2008). “Celiac disease”. Med Clin (Barc) (Review) (in Spanish). 131 (7): 264–70. doi:10.1016/S0025-7753(08)72247-4. PMID 18775218. Archived from the original on March 19, 2016. Estos marcadores presentan en general una elevada sensibilidad y especificidad (cercanas al 90%) en presencia de atrofia marcada de las vellosidades intestinales. Sin embargo, muestran una notable disminución de la sensibilidad (del orden del 40-50%) en casos con atrofia vellositaria leve o cambios mínimos. These markers generally have high sensitivity and specificity (around 90%) in the presence of marked atrophy of the villi. However, they show a marked decrease in sensitivity (of the order of 40-50%) in cases with mild villous atrophy or minimal changes. 
  • ^ Rostami Nejad M, Hogg-Kollars S, Ishaq S, Rostami K (2011). “Subclinical celiac disease and gluten sensitivity”. Gastroenterol Hepatol Bed Bench (Review). 4 (3): 102–8. PMC 4017418 . PMID 24834166. 
  • ^ Bold J, Rostami K (2011). “Gluten tolerance; potential challenges in treatment strategies”. Gastroenterol Hepatol Bed Bench (Review). 4 (2): 53–7. PMC 4017406 . PMID 24834157. 
  • ^ 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. 
  • ^ 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”. Clin. Infect. Dis. 50 (4): 473–80. doi:10.1086/649923. PMID 20067425. 
  • ^ Section “Antibiotics and Ulcerative Colitis” in: Prantera C, Scribano ML (2009). “Antibiotics and probiotics in inflammatory bowel disease: why, when, and how”. Curr. Opin. Gastroenterol. 25 (4): 329–33. doi:10.1097/MOG.0b013e32832b20bf. PMID 19444096. 
  • ^ a b Fries, WS; Nazario, B (May 16, 2007). “Crohn’s Disease: 54 Tips to Help You Manage”. WebMD. Archived from the original on February 8, 2008. Retrieved February 14, 2008. 
  • ^ Hou, Jason K; Abraham, Bincy; El-Serag, Hashem (April 2011). “Dietary Intake and Risk of Developing Inflammatory Bowel Disease: A Systematic Review of the Literature” (PDF). Am. J. Gastroenterol. 106: 563–573. doi:10.1038/ajg.2011.44. PMID 21468064. Archived from the original (PDF) on June 12, 2015. 
  • ^ Escott-Stump, Sylvia (2008). Nutrition and Diagnosis-Related Care, 7th edition. Baltimore, MD: Lippincott Williams & Wilkins. pp. 1020 (pp 431). ISBN 978-1-60831-017-3. 
  • ^ Shanahan, Fergus (January 1, 2002). “Crohn’s disease”. The Lancet. 359 (9300): 62–69. doi:10.1016/S0140-6736(02)07284-7. 
  • ^ “FDA Approves Cimzia to Treat Crohn’s Disease” (Press release). Food and Drug Administration (FDA). April 22, 2008. Archived from the original on October 20, 2009. Retrieved November 5, 2009. 
  • ^ Sandborn WJ, Colombel JF, Enns R, Feagan BG, Hanauer SB, Lawrance IC, Panaccione R, Sanders M, Schreiber S, Targan S, van Deventer S, Goldblum R, Despain D, Hogge GS, Rutgeerts P; Colombel; Enns; Feagan; Hanauer; Lawrance; Panaccione; Sanders; Schreiber; Targan; Van Deventer; Goldblum; Despain; Hogge; Rutgeerts; International Efficacy of Natalizumab as Active Crohn’s Therapy (ENACT-1) Trial Group; Evaluation of Natalizumab as Continuous Therapy (ENACT-2) Trial Group (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. CS1 maint: Multiple names: authors list (link)
  • ^ MacDonald JK, McDonald JW; McDonald (2007). MacDonald, John K, ed. “Natalizumab for induction of remission in Crohn’s disease”. Cochrane Database of Systematic Reviews (1): CD006097. doi:10.1002/14651858.CD006097.pub2. PMID 17253580. CD006097. 
  • ^ Longmore, Murray; Ian Wilkinson; Tom Turmezei; Chee Kay Cheung (2007). Oxford Handbook of Clinical Medicine (7th ed.). Oxford University Press. pp. 266–7. ISBN 0-19-856837-1. 
  • ^ a b Khanna, Reena; Preiss, Jan C.; MacDonald, John K.; Timmer, Antje (May 5, 2015). “Anti-IL-12/23p40 antibodies for induction of remission in Crohn’s disease”. The Cochrane Database of Systematic Reviews (5): CD007572. doi:10.1002/14651858.CD007572.pub2. ISSN 1469-493X. PMID 25942580. 
  • ^ Mowat C, Cole A, Windsor A, Ahmad T, Arnott I, Driscoll R, Mitton S, Orchard T, Rutter M, Younge L, Lees C, Ho GT, Satsangi J, Bloom S; Cole; Windsor; Ahmad; Arnott; Driscoll; Mitton; Orchard; Rutter; Younge; Lees; Ho; Satsangi; Bloom; IBD Section of the British Society of Gastroenterology (May 2011). “Guidelines for the management of inflammatory bowel disease in adults”. Gut. 60 (5): 571–607. doi:10.1136/gut.2010.224154. PMC 1867788 . PMID 21464096. CS1 maint: Multiple names: authors list (link)
  • ^ a b c Goddard AF, James MW, McIntyre AS, Scott BB; James; McIntyre; Scott; British Society of Gastroenterology (2011). “Guidelines for the management of iron deficiency anaemia”. Gut. 60 (10): 1309–1316. doi:10.1136/gut.2010.228874. PMC 1728199 . PMID 21561874. CS1 maint: Multiple names: authors list (link)
  • ^ a b Inflamm Bowel Dis Volume 13, Number 12, December 2007
  • ^ Kristo, Ivan; Stift, Anton; Bergmann, Michael; Riss, Stefan (May 28, 2015). “Surgical recurrence in Crohn’s disease: Are we getting better?”. World Journal of Gastroenterology. 21 (20): 6097–6100. doi:10.3748/wjg.v21.i20.6097. ISSN 2219-2840. PMC 4445088 . PMID 26034346. 
  • ^ Tresca, AJ (January 12, 2007). “Resection Surgery for Crohn’s Disease”. Archived from the original on November 13, 2007. Retrieved February 14, 2008. 
  • ^ Ozuner G, Fazio VW, Lavery IC, Milsom JW, Strong SA; Fazio; Lavery; Milsom; Strong (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. CS1 maint: Multiple names: authors list (link)
  • ^ Rutgeerts P, Geboes K, Vantrappen G, Beyls J, Kerremans R, Hiele M; Geboes; Vantrappen; Beyls; Kerremans; Hiele (October 1990). “Predictability of the postoperative course of Crohn’s disease”. Gastroenterology. 99 (4): 956–63. PMID 2394349. CS1 maint: Multiple names: authors list (link)
  • ^ Yamamoto T, Bamba T, Umegae S, Matsumoto K; Bamba; Umegae; Matsumoto (August 2013). “The impact of early endoscopic lesions on the clinical course of patients following ileocolonic resection for Crohn’s disease: A 5-year prospective cohort study”. United European Gastroenterol J. 1 (4): 294–8. doi:10.1177/2050640613495197. PMC 4040796 . PMID 24917974. CS1 maint: Multiple names: authors list (link)
  • ^ “Short Bowel Syndrome”. Archived from the original on March 21, 2014. 
  • ^ Rhodes, M (October 24, 2006). “Intestinal transplant for Crohn’s disease”. Everyday Health. Archived from the original on October 8, 2008. Retrieved March 22, 2009. 
  • ^ Hofmann AF (1967). “The syndrome of ileal disease and the broken enterohepatic circulation: cholerhetic enteropathy”. Gastroenterology. 52 (4): 752–7. PMID 5337211. 
  • ^ a b Szigethy, E; McLafferty, L; Goyal, A (April 2010). “Inflammatory bowel disease”. Child and adolescent psychiatric clinics of North America. 19 (2): 301–18, ix. doi:10.1016/j.chc.2010.01.007. PMID 20478501. 
  • ^ Ballou, S; Keefer, L (January 19, 2017). “Psychological Interventions for Irritable Bowel Syndrome and Inflammatory Bowel Diseases”. Clinical and Translational Gastroenterology. 8 (1): e214. doi:10.1038/ctg.2016.69. PMC 5288603 . PMID 28102860. 
  • ^ Caprilli R, Gassull MA, Escher JC, Moser G, Munkholm P, Forbes A, Hommes DW, Lochs H, Angelucci E, Cocco A, Vucelic B, Hildebrand H, Kolacek S, Riis L, Lukas M, de Franchis R, Hamilton M, Jantschek G, Michetti P, O’Morain C, Anwar MM, Freitas JL, Mouzas IA, Baert F, Mitchell R, Hawkey CJ; Gassull; Escher; Moser; Munkholm; Forbes; Hommes; Lochs; Angelucci; Cocco; Vucelic; Hildebrand; Kolacek; Riis; Lukas; De Franchis; Hamilton; Jantschek; Michetti; O’Morain; Anwar; Freitas; Mouzas; Baert; Mitchell; Hawkey; European Crohn’s Colitis Organisation (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. CS1 maint: Multiple names: authors list (link)
  • ^ Joos S, Brinkhaus B, Maluche C, Maupai N, Kohnen R, Kraehmer N, Hahn EG, Schuppan D; Brinkhaus; Maluche; Maupai; Kohnen; Kraehmer; Hahn; Schuppan (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. CS1 maint: Multiple names: authors list (link)
  • ^ Caprilli R, Gassull MA, Escher JC, Moser G, Munkholm P, Forbes A, Hommes DW, Lochs H, Angelucci E, Cocco A, Vucelic B, Hildebrand H, Kolacek S, Riis L, Lukas M, de Franchis R, Hamilton M, Jantschek G, Michetti P, O’Morain C, Anwar MM, Freitas JL, Mouzas IA, Baert F, Mitchell R, Hawkey CJ; Gassull; Escher; Moser; Munkholm; Forbes; Hommes; Lochs; Angelucci; Cocco; Vucelic; Hildebrand; Kolacek; Riis; Lukas; De Franchis; Hamilton; Jantschek; Michetti; O’Morain; Anwar; Freitas; Mouzas; Baert; Mitchell; Hawkey; European Crohn’s Colitis Organisation (2006). “The second European evidence-based Consensus on the diagnosis and management of Crohn’s disease: Special situations” (PDF). Gut. 55 (Suppl 1): i36–i58. doi:10.1136/gut.2005.081950c. PMC 1859996 . PMID 16481630. Archived (PDF) from the original on May 26, 2012. 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. CS1 maint: Multiple names: authors list (link) [verification needed]
  • ^ Joos, S (June 2011). “Review on efficacy and health services research studies of complementary and alternative medicine in inflammatory bowel disease”. Chinese journal of integrative medicine. 17 (6): 403–9. doi:10.1007/s11655-011-0758-3. PMID 21660673. 
  • ^ Smith K (2012). “Homeopathy is Unscientific and Unethical”. Bioethics. 26 (9): 508–512. doi:10.1111/j.1467-8519.2011.01956.x. 
  • ^ a b Baran GR, Kiana MF, Samuel SP (2014). Chapter 2: Science, Pseudoscience, and Not Science: How Do They Differ?. Healthcare and Biomedical Technology in the 21st Century. Springer. pp. 19–57. doi:10.1007/978-1-4614-8541-4_2. ISBN 978-1-4614-8540-7. within the traditional medical community it is considered to be quackery 
  • ^ a b Ladyman J (2013). “Chapter 3: Towards a Demarcation of Science from Pseudoscience”. In Pigliucci M, Boudry M. Philosophy of Pseudoscience: Reconsidering the Demarcation Problem. University of Chicago Press. pp. 48–49. ISBN 978-0-226-05196-3. Yet homeopathy is a paradigmatic example of pseudoscience. It is neither simply bad science nor science fraud, but rather profoundly departs from scientific method and theories while being described as scientific by some of its adherents (often sincerely). 
  • ^ Ernst, E. (2002). “A systematic review of systematic reviews of homeopathy”. British Journal of Clinical Pharmacology. 54 (6): 577–82. doi:10.1046/j.1365-2125.2002.01699.x. PMC 1874503 . PMID 12492603. 
  • ^ Shang, Aijing; Huwiler-Müntener, Karin; Nartey, Linda; Jüni, Peter; Dörig, Stephan; Sterne, Jonathan AC; Pewsner, Daniel; Egger, Matthias (2005). “Are the clinical effects of homoeopathy placebo effects? Comparative study of placebo-controlled trials of homoeopathy and allopathy”. The Lancet. 366 (9487): 726–732. doi:10.1016/S0140-6736(05)67177-2. PMID 16125589. 
  • ^ “Evidence Check 2: Homeopathy – Science and Technology Committee”. British House of Commons Science and Technology Committee. February 22, 2010. Retrieved April 5, 2014. 
  • ^ a b Naftali, T; Mechulam, R; Lev, LB; Konikoff, FM (2014). “Cannabis for inflammatory bowel disease”. Digestive diseases (Basel, Switzerland). 32 (4): 468–74. doi:10.1159/000358155. PMID 24969296. 
  • ^ “Crohn’s disease – Prognosis”. University of Maryland Medical Centre. Archived from the original on August 29, 2012. Retrieved October 19, 2012. 
  • ^ Canavan C, Abrams KR, Mayberry J; Abrams; Mayberry (2006). “Meta-analysis: Colorectal and small bowel cancer risk in patients with Crohn’s disease”. Alimentary Pharmacology and Therapeutics. 23 (8): 1097–104. doi:10.1111/j.1365-2036.2006.02854.x. PMID 16611269. CS1 maint: Multiple names: authors list (link)
  • ^ Greenstein AJ, Janowitz HD, Sachar DB (September 1976). “The extra-intestinal complications of Crohn’s disease and ulcerative colitis: a study of 700 patients”. Medicine (Baltimore). 55 (5): 401–12. doi:10.1097/00005792-197609000-00004. PMID 957999. 
  • ^ “Intestinal Obstruction”. MERCK MANUAL Consumer Version. Archived from the original on July 10, 2016. Retrieved June 27, 2016. 
  • ^ “Anorectal Fistula”. MERCK MANUAL Consumer Version. Archived from the original on July 10, 2016. Retrieved June 27, 2016. 
  • ^ “Anorectal Abscess”. MERCK MANUAL Consumer Version. Archived from the original on June 14, 2016. Retrieved June 27, 2016. 
  • ^ Enterovesical Fistula at eMedicine
  • ^ Ekbom A, Helmick C, Zack M, Adami HO; Helmick; Zack; Adami (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. CS1 maint: Multiple names: authors list (link)
  • ^ Collins PD, Mpofu C, Watson AJ, Rhodes JM; Mpofu; Watson; Rhodes (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. CS1 maint: Multiple names: authors list (link)
  • ^ Zisman TL, Rubin DT; Rubin (2008). “Colorectal cancer and dysplasia in inflammatory bowel disease”. World Journal of Gastroenterology. 14 (17): 2662–9. doi:10.3748/wjg.14.2662. PMC 2709054 . PMID 18461651. 
  • ^ Axelrad, JE; Lichtiger, S; Yajnik, V (May 28, 2016). “Inflammatory bowel disease and cancer: The role of inflammation, immunosuppression, and cancer treatment”. World Journal of Gastroenterology (Review). 22 (20): 4794–801. doi:10.3748/wjg.v22.i20.4794. PMC 4873872 . PMID 27239106. 
  • ^ Evans JP, Steinhart AH, Cohen Z, McLeod RS; Steinhart; Cohen; McLeod (2003). “Home Total Parenteral Nutrition an Alternative to Early Surgery for Complicated Inflammatory Bowel Disease”. Journal of Gastrointestinal Surgery. 7 (4): 562–6. doi:10.1016/S1091-255X(02)00132-4. PMID 12763417. CS1 maint: Multiple names: authors list (link)
  • ^ Carrillo, Maria (September 1, 1985). “Man of Many Problems Comes to City for Help”. Richmond Times-Dispatch. Richmond, Virginia, USA. p. B1. 
  • ^ “Kay, Laura Lynn”. Richmond Times-Dispatch. Richmond, Virginia, USA. April 3, 2014. 
    Loebenberg, Priscilla (March 2, 2014). “Doris L. Johnson, 82, of Westminster”. Carroll County Times. Westminster, Maryland, USA. 
    Berrier Jr., Ralph (December 31, 2013). “In memoriam: Dan Hodges Jr”. The Roanoke Times. Roanoke, Virginia, USA. 
    “Cynthia Meredith Routt”. Daily Press. Newport News, Virginia, USA. May 4, 2014. p. A11. 
  • ^ Kaplan, C (October 21, 2005). “IBD and Pregnancy: What You Need to Know”. Crohn’s and Colitis Foundation of America. Archived from the original on February 17, 2012. Retrieved November 7, 2009. 
  • ^ a b Hiatt RA, Kaufman L; Kaufman (1988). “Epidemiology of inflammatory bowel disease in a defined northern California population”. Western Journal of Medicine. 149 (5): 541–6. PMC 1026530 . PMID 3250100. 
  • ^ Moum B, Vatn MH, Ekbom A, Aadland E, Fausa O, Lygren I, Stray N, Sauar J, Schulz T; Vatn; Ekbom; Aadland; Fausa; Lygren; Stray; Sauar; Schulz (1996). “Incidence of Crohn’s disease in four counties in southeastern Norway, 1990-93. A prospective population-based study. The Inflammatory Bowel South-Eastern Norway (IBSEN) Study Group of Gastroenterologists”. Scandinavian Journal of Gastroenterology. 31 (4): 355–61. doi:10.3109/00365529609006410. PMID 8726303. CS1 maint: Multiple names: authors list (link)
  • ^ Shivananda S, Lennard-Jones J, Logan R, Fear N, Price A, Carpenter L, van Blankenstein M; Lennard-Jones; Logan; Fear; Price; Carpenter; Van Blankenstein (1996). “Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD)”. Gut. 39 (5): 690–7. doi:10.1136/gut.39.5.690. PMC 1383393 . PMID 9014768. CS1 maint: Multiple names: authors list (link)
  • ^ Yang H, McElree C, Roth MP, Shanahan F, Targan SR, Rotter JI; McElree; Roth; Shanahan; Targan; Rotter (1993). “Familial empirical risks for inflammatory bowel disease: differences between Jews and non-Jews”. Gut. 34 (4): 517–24. doi:10.1136/gut.34.4.517. PMC 1374314 . PMID 8491401. CS1 maint: Multiple names: authors list (link)
  • ^ Seksik P, Nion-Larmurier I, Sokol H, Beaugerie L, Cosnes J; Nion-Larmurier; Sokol; Beaugerie; Cosnes (2009). “Effects of light smoking consumption on the clinical course of Crohn’s disease”. Inflamm. Bowel Dis. 15 (5): 734–41. doi:10.1002/ibd.20828. PMID 19067428. CS1 maint: Multiple names: authors list (link)
  • ^ “Crohn’s disease manifests differently in boys and girls”. Crohn’s and Colitis Foundation of America. Archived from the original on February 16, 2008. 
  • ^ “Who is affected by Crohn’s disease”. Healthwise. Archived from the original on January 23, 2009. 
  • ^ Satsangi J, Jewell DP, Bell JI; Jewell; Bell (1997). “The genetics of inflammatory bowel disease”. Gut. 40 (5): 572–4. doi:10.1136/gut.40.5.572. PMC 1027155 . PMID 9203931. CS1 maint: Multiple names: authors list (link)
  • ^ Tysk C, Lindberg E, Järnerot G, Flodérus-Myrhed B; Lindberg; Järnerot; Flodérus-Myrhed (1988). “Ulcerative colitis and Crohn’s disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking”. Gut. 29 (7): 990–6. doi:10.1136/gut.29.7.990. PMC 1433769 . PMID 3396969. CS1 maint: Multiple names: authors list (link)
  • ^ Burisch, Johan; Jess, Tine; Martinato, Matteo; Lakatos, Peter L. (2013). “The burden of inflammatory bowel disease in Europe”. Journal of Crohn’s and Colitis. 7 (4): 322–337. doi:10.1016/j.crohns.2013.01.010. ISSN 1873-9946. PMID 23395397. 
  • ^ a b Ng, SC; Shi, HY; Hamidi, N; Underwood, FE; Tang, W; Benchimol, EI; Panaccione, R; Ghosh, S; Wu, JCY; Chan, FKL; Sung, JJY; Kaplan, GG (23 December 2018). “Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies”. Lancet. 390 (10114): 2769–2778. doi:10.1016/S0140-6736(17)32448-0. PMID 29050646. 
  • ^ Kirsner JB (1988). “Historical aspects of inflammatory bowel disease”. J. Clin. Gastroenterol. 10 (3): 286–97. doi:10.1097/00004836-198806000-00012. PMID 2980764. 
  • ^ Lichtarowicz, A.M.; Mayberry, J.F. (August 1, 1988). “Antoni Leśniowski and his contribution to regional enteritis (Crohn’s disease)”. Journal of the Royal Society of Medicine. 81 (8): 468–470. PMC 1291720 . PMID 3047387. 
  • ^ a b Agrawal G, Borody TJ, Chamberlin W; Borody; Chamberlin (2014). “‘Global warming’ to Mycobacterium avium subspecies paratuberculosis”. Future Microbiology. 9 (7): 829–832. doi:10.2217/fmb.14.52. ISSN 1746-0913. PMID 25156371. CS1 maint: Multiple names: authors list (link)
  • ^ Scribano, ML; Prantera, C (Feb 7, 2013). “Use of antibiotics in the treatment of Crohn’s disease”. World Journal of Gastroenterology. 19 (5): 648–53. doi:10.3748/wjg.v19.i5.648. PMC 3574590 . PMID 23429474. 
  • ^ Chamberlin, W; Borody, TJ; Campbell, J (Nov 2011). “Primary treatment of Crohn’s disease: combined antibiotics taking center stage”. Expert review of clinical immunology. 7 (6): 751–60. doi:10.1586/eci.11.43. PMID 22014016. 
  • ^ Bull TJ, Gilbert SC, Sridhar S, Linedale R, Dierkes N, Sidi-Boumedine K, Hermon-Taylor J; Gilbert; Sridhar; Linedale; Dierkes; Sidi-Boumedine; Hermon-Taylor (2007). “‘A novel multi-antigen virally vectored vaccine against Mycobacterium avium subspecies paratuberculosis”. PLoS ONE. 2 (11): e1229. doi:10.1371/journal.pone.0001229. PMC 2082073 . PMID 18043737. CS1 maint: Multiple names: authors list (link)
  • ^ Hultén, K.; Almashhrawi, A.; El-Zaatari, FA.; Graham, DY. (Mar 2000). “Antibacterial therapy for Crohn’s disease: a review emphasizing therapy directed against mycobacteria”. Dig Dis Sci. 45 (3): 445–56. PMID 10749316. 
  • ^ Pommerville, Jeffrey (2014). Fundamentals of microbiology. Burlington, MA: Jones & Bartlett Learning. ISBN 9781449688615. 
  • ^ Elliott, David E.; Weinstock, Joel V. (2012). “Where are we on worms?”. Current Opinion in Gastroenterology. 28 (6): 551–556. doi:10.1097/MOG.0b013e3283572f73. ISSN 0267-1379. PMC 3744105 . 
  • ^ Weinstock, Joel V.; Elliott, David E. (2013). “Translatability of helminth therapy in inflammatory bowel diseases”. International Journal for Parasitology. 43 (3–4): 245–251. doi:10.1016/j.ijpara.2012.10.016. ISSN 0020-7519. Early clinical trials suggested that exposure to helminths such as Trichuris suis or Necator americanus can improve IBD. 
  • ^ Biosciences, Coronado. “Coronado Biosciences Announces Top-Line Results From Its TRUST-I Phase 2 Clinical Trial of TSO for the Treatment of Crohn’s Disease”. Archived from the original on August 16, 2016. Retrieved August 16, 2016. 
  • ^ Biosciences, Coronado. “Coronado Biosciences Announces Independent Data Monitoring Committee Recommendation to Discontinue Falk Phase 2 Trial of TSO in Crohn’s Disease”. Archived from the original on August 16, 2016. Retrieved August 16, 2016. 
  • ^ *Massa F, Monory K; Monory (2007). “Endocannabinoids and the gastrointestinal tract”. Journal of Endocrinological Investigation. 29 (Suppl): 47–57. PMID 16751708. 
  • ^ Massa F, Storr M, Lutz B; Storr; Lutz (2005). “The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract”. Journal of Molecular Medicine. 83 (12): 944–54. doi:10.1007/s00109-005-0698-5. PMID 16133420. CS1 maint: Multiple names: authors list (link)
  • ^ Izzo AA, Coutts AA; Coutts (2005). “Cannabinoids and the digestive tract”. Handbook of Experimental Pharmacology. Handbook of Experimental Pharmacology. 168 (168): 573–98. doi:10.1007/3-540-26573-2_19. ISBN 3-540-22565-X. PMID 16596788. 
  • ^ Srinivasan, R; Akobeng, AK (Apr 15, 2009). “Thalidomide and thalidomide analogues for induction of remission in Crohn’s disease”. The Cochrane Database of Systematic Reviews (2): CD007350. doi:10.1002/14651858.CD007350.pub2. PMID 19370684. 
  • ^ Akobeng, AK; Stokkers, PC (Apr 15, 2009). “Thalidomide and thalidomide analogues for maintenance of remission in Crohn’s disease”. The Cochrane Database of Systematic Reviews (2): CD007351. doi:10.1002/14651858.CD007351.pub2. PMID 19370685. 
  • External links[edit]

    • Crohn’s disease at Curlie (based on DMOZ)

    Lower GI tract:

    GI bleeding/BIS

    • Upper
      • Hematemesis
      • Melena
    • Lower
      • Hematochezia