The primary symptoms of IBS are abdominal pain or discomfort in association with frequent diarrhea or constipation, a change in bowel habits. There may also be urgency for bowel movements, a feeling of incomplete evacuation (tenesmus), bloating or abdominal distention. People with IBS, more commonly than others, have gastro-esophageal reflux, symptoms relating to the genitourinary system, chronic fatigue syndrome, fibromyalgia, headache, backache and psychiatric symptoms such as depression and anxiety. Some studies indicate that up to 60% of persons with IBS also have a psychological disorder, typically anxiety or depression and anxiety.
The cause of IBS is unknown, but several hypotheses have been proposed. The risk of developing IBS increases six-fold after acute gastrointestinal infection. Post-infection, further risk factors are young age, prolonged fever, anxiety, and depression. Publications suggesting the role of brain-gut “axis” appeared in the 1990s, such as a study entitled Brain-gut response to stress and cholinergic stimulation in IBS published in the Journal of Clinical Gastroenterology in 1993. A 1997 study published in Gut magazine suggested that IBS was associated with a “derailing of the brain-gut axis.” Psychological factors may be important in the etiology of IBS.
Active infections: Prevalence of protozoal infections in industrialized countries (United States and Canada) in 21st century:
There is research to support IBS being caused by an as-yet undiscovered active infection. Other researchers have focused on an unrecognized protozoal infection as a cause of IBS as certain protozoal infections occur more frequently in IBS patients. Two of the protozoa investigated have a high prevalence in industrialized countries and infect the bowel, but little is known about them as they are recently emerged pathogens.
Blastocystis is a single-cell organism that has been reported to produce symptoms of abdominal pain, constipation and diarrhea in patients though these reports are contested by some physicians. Studies from research hospitals in various countries have identified high Blastocystis infection rates in IBS patients, with 38% being reported from London School of Hygiene & Tropical Medicine, 47% reported from the Department of Gastroenterology at Aga Khan University in Pakistan and 18.1% reported from the Institute of Diseases and Public Health at University of Ancona in Italy. Reports from all three groups indicate a Blastocystis prevalence of approximately 7% in non-IBS patients. Researchers have noted that clinical diagnostics fail to identify infection, and Blastocystis may not respond to treatment with common antiprotozoals.
Dientamoeba fragilis is a single-cell organism that produces abdominal pain and diarrhea. Studies have reported a high incidence of infection in developed countries, and symptoms of patients resolve following antibiotic treatment. One study reported on a large group of patients with IBS-like symptoms who were found to be infected with Dientamoeba fragilis, and experienced resolution of symptoms following treatment. Researchers have noted that methods used clinically may fail to detect some Dientamoeba fragilis infections. It is also found in people without IBS.
There is no specific laboratory or imaging test that can be performed to diagnose irritable bowel syndrome. Diagnosis of IBS involves excluding conditions that produce IBS-like symptoms, and then following a procedure to categorize the patient’s symptoms. Ruling out parasitic infections, lactose intolerance, small intestinal bacterial overgrowth and celiac disease is recommended for all patients before a diagnosis of irritable bowel syndrome is made. In patients over 50 years old it is recommended that they undergo a screening colonoscopy.
Colon cancer, inflammatory bowel disease, thyroid disorders and giardiasis can all feature abnormal defecation and abdominal pain. Less common causes of this symptom profile are carcinoid syndrome, microscopic colitis, bacterial overgrowth, and eosinophilic gastroenteritis. IBS is, however, such a common presentation and testing for these conditions would yield such low numbers of positive results that it is considered difficult to justify the expense. Because there are many causes of diarrhea that give IBS-like symptoms, the American Gastroenterological Association published a set of guidelines for tests to be performed to rule out other causes for these symptoms. These include gastrointestinal infections, lactose intolerance, and coeliac disease. Research has suggested that these guidelines are not always followed. Physicians may choose to use one of these guidelines, or may simply choose to rely on their own anecdotal experience with past patients. The guidelines may include additional tests to guard against misdiagnosis of other diseases as IBS. Such “red flag” symptoms may include weight loss, gastrointestinal bleeding, anemia, or nocturnal symptoms. However, researchers have noted that red flag conditions may not always contribute to accuracy in diagnosis — for instance, as many as 31% of IBS patients have blood in their stool many possibly from hemorrhoidal bleeding.
The diagnostic algorithm identifies a name that can be applied to the patient’s condition based on the combination of the patient’s symptoms of diarrhea, abdominal pain, and constipation. For example, the statement “50% of returning travelers had developed functional diarrhea while 25% had developed IBS” would mean that half the travelers had diarrhea while a quarter had diarrhea with abdominal pain. While some researchers believe this categorization system will help physicians understand IBS, others have questioned the value of the system and suggested that all IBS patients have the same underlying disease but with different symptoms. On this line is a recent study, which showed that constipation and/or diarrhea seems to be different manifestations of the same underlying condition, that is a build-up of fecal retention reservoirs in the colon. Abdominal X-rays were analyzed for colon transit time and fecal distribution, which correlated significantly with bloating and abdominal pain. Thus a group of patients were identified with an increased fecal loading compared to controls, but having a colon transit time equal or less to the controls. This suggests that defecation patterns do not reflect the amount of feces in the colon and is called hidden constipation. This phenomenon may be linked to bacterial overgrowth.
Published research has demonstrated that some poor patient outcomes are due to treatable causes of diarrhea being misdiagnosed as IBS. Common examples include infectious diseases, coeliac disease, Helicobacter pylori, and parasites.
Celiac disease in particular is often misdiagnosed as IBS. The American College of Gastroenterology recommends that all patients with symptoms of IBS be tested for celiac disease. Chronic use of certain sedative-hypnotic drugs especially the benzodiazepines may cause irritable bowel like symptoms that can lead to a misdiagnosis of irritable bowel syndrome.
Researchers have identified several medical conditions, or comorbidities, which appear with greater frequency in patients diagnosed with IBS.
Headache, Fibromyalgia, Chronic fatigue syndrome and Depression: A study of 97,593 individuals with IBS identified co-morbidities as headache, fibromyalgia, and depression. A systematic review found that IBS occurs in 51% of chronic fatigue syndrome patients and 49% of fibromyalgia patients, and psychiatric disorders were found to occur in 94% of IBS patients.
Inflammatory bowel disease (IBD): Some researchers have suggested that IBS is a type of low-grade inflammatory bowel disease. Researchers have suggested that IBS and IBD are interrelated diseases, noting that patients with IBD experience IBS-like symptoms when their IBD is in remission. A 3-year study found that patients diagnosed with IBS were 16.3 times more likely to be diagnosed with IBD during the study period. Serum markers associated with inflammation have also been found in patients with IBS (see Causes).
Abdominal surgery: A recent (2008) study found that IBS patients are at increased risk of having unnecessary cholecystectomy (gall bladder removal surgery) not due to an increased risk of gallstones, but rather to abdominal pain, awareness of having gallstones, and inappropriate surgical indications. A 2005 study reported that IBS patients are 87% more likely to undergo abdominal and pelvic surgery, and three times more likely to undergo gallbladder surgery. A study published in Gastroenterology came to similar conclusions, and also noted IBS patients were twice as likely to undergo hysterectomy.
Endometriosis: One study reported a statistically significant link between migraine headaches, IBS, and endometriosis.
Other chronic disorders: Interstitial cystitis may be associated with other chronic pain syndromes, such as irritable bowel syndrome and fibromyalgia.
Some people with IBS are likely to have food intolerances. In 2007 the evidence base was not strong enough to recommend restrictive diets.
Many different dietary modifications have been attempted to improve the symptoms of IBS. Some are effective in certain sub-populations. As lactose intolerance and IBS have such similar symptoms a trial of a lactose free diet is often recommended. A diet restricting fructose and fructan intake has been shown to successfully treat the symptoms in a dose-dependant manner in patients with fructose mal-absorption and IBS.
While many IBS patients believe they have some form of dietary intolerance, tests attempting to predict food sensitivity in IBS have been disappointing. One study reported that an IgG antibody test was effective in determining food sensitivity in IBS patients, with patients on the elimination diet experiencing 10% greater symptom reduction than those on a sham diet.
There is no evidence that digestion of food or absorption of nutrients is problematic for those with IBS at rates different from those without IBS. However, the very act of eating or drinking can provoke an overreaction of the gastrocolic response in some patients with IBS due to their heightened visceral sensitivity, and this may lead to abdominal pain, diarrhea, and/or constipation.
Gibson and Shepherd state a diet restricted in fermentable oligo di and monosaccharides and polyols (FODMAPS) now has an evidence base sufficiently strong to recommend its widespread application in conditions such as IBS and IBD. They also state the restriction of FODMAPs globally, rather than individually, controls the symptoms of functional gut disorders (e.g., IBS), and the majority of IBD patients respond just as well. It is more successful than restricting only fructose and fructans, which are also FODMAPs, as is recommended for those with fructose malabsorption. Longer term compliance with the diet was high.
A randomized controlled trial on IBS patients found relaxing an IgG-mediated food intolerance diet led to a 24% greater deterioration in symptoms compared to those on the elimination diet and concluded food elimination based on IgG antibodies may be effective in reducing IBS symptoms and is worthy of further biomedical research.
Further information: NIH funding of IBS Research
One of the first references to the concept of an “irritable bowel” appeared in the Rocky Mountain Medical Journal in 1950.
The term was used to categorize patients who developed symptoms of diarrhea, abdominal pain, constipation, but where no well-recognized infective cause could be found. Early theories suggested that the irritable bowel was caused by a psychosomatic or mental disorder since no physical manifestation was found.
IBS can be classified as either diarrhea-predominant (IBS-D), constipation-predominant (IBS-C) or IBS with alternating stool pattern (IBS-A or pain-predominant). In some individuals, IBS may have an acute onset and develop after an infectious illness characterized by two or more of the following: fever, vomiting, diarrhea, or positive stool culture. This post-infective syndrome has consequently been termed “post-infectious IBS” (IBS-PI).
About Crohn’s Disease:
Crohn’s disease, also known as regional enteritis, is an inflammatory disease of the intestines that may affect any part of the gastrointestinal tract from mouth to anus, causing a wide variety of symptoms. It primarily causes abdominal pain, diarrhea (which may be bloody if inflammation is at its worst), vomiting, or weight loss, but may also cause complications outside the gastrointestinal tract such as skin rashes, arthritis, and inflammation of the eye, tiredness, and lack of concentration.
Crohn’s disease is thought to be an autoimmune disease, in which the body’s immune system attacks the gastrointestinal tract, causing inflammation; it is classified as a type of inflammatory bowel disease. There is evidence of a genetic link to Crohn’s disease, putting individuals with siblings afflicted with the disease at higher risk. It is thought to have a large environmental component as evidenced by a higher incidence in western industrialized nations compared to other parts of the world. Males and females are equally affected. Smokers are two times more likely to develop Crohn’s disease than nonsmokers. Crohn’s disease effects between 400,000 and 600,000 people in North America. Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000. Crohn’s disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age.
There is no known pharmaceutical or surgical cure for Crohn’s disease. Treatment options are restricted to controlling symptoms, maintaining remission, and preventing relapse.
Many people with Crohn’s disease have symptoms for years prior to the diagnosis. The usual onset is between 15 and 30 years of age, but can occur at any age. Because of the ‘patchy’ nature of the gastrointestinal disease and the depth of tissue involvement, initial symptoms can be more subtle than those of ulcerative colitis. People with Crohn’s disease experience chronic recurring periods of flare-ups and remission.
Abdominal pain may be the initial symptom of Crohn’s disease. It is often accompanied by diarrhea, especially in those who have had surgery. The diarrhea may or may not be bloody. People who have had surgery or multiple surgeries often end up with short bowel syndrome of the gastrointestinal tract. The nature of the diarrhea in Crohn’s disease depends on the part of the small intestine or colon involved. Ileitis typically results in large-volume, watery feces. Colitis may result in a smaller volume of feces of higher frequency. Fecal consistency may range from solid to watery. In severe cases, an individual may have more than 20 bowel movements per day and may need to awaken at night to defecate. Visible bleeding in the feces is less common in Crohn’s disease than in ulcerative colitis, but may be seen in the setting of Crohn’s colitis. Bloody bowel movements are typically intermittent, and may be bright or dark red in color. In the setting of severe Crohn’s colitis, bleeding may be copious. Flatulence and bloating may also add to the intestinal discomfort.
Symptoms caused by intestinal stenosis are also common in Crohn’s disease. Abdominal pain is often most severe in areas of the bowel with stenosis. In the setting of severe stenosis, vomiting and nausea may indicate the beginnings of small bowel obstruction. Although the association is greater in the context of ulcerative colitis, Crohn’s disease may also be associated with primary sclerosing cholangitis, a type of inflammation of the bile ducts.
Perianal discomfort may also be prominent in Crohn’s disease. Itchiness or pain around the anus may be suggestive of inflammation, fistulization or abscess around the anal area or anal fissure. Perianal skin tags are also common in Crohn’s disease. Fecal incontinence may accompany perianal Crohn’s disease. At the opposite end of the gastrointestinal tract, the mouth may be affected by non-healing sores (aphthous ulcers). Rarely, the esophagus, and stomach may be involved in Crohn’s disease. These can cause symptoms including difficulty swallowing (dysphagia), upper abdominal pain, and vomiting.
Crohn’s disease, like many other chronic, inflammatory diseases, can cause a variety of systemic symptoms. Among children, growth failure is common. Many children are first diagnosed with Crohn’s disease based on inability to maintain growth. As it may manifest at the time of the growth spurt in puberty, up to 30% of children with Crohn’s disease may have retardation of growth. Fever may also be present, though fevers greater than 101.3 ?F are uncommon unless there is a complication such as an abscess. Among older individuals, Crohn’s disease may manifest as weight loss, usually related to decreased food intake, since individuals with intestinal symptoms from Crohn’s disease often feel better when they do not eat and might lose their appetite. People with extensive small intestine disease may also have malabsorption of carbohydrates or lipids, which can further exacerbate weight loss.
In addition to systemic and gastrointestinal involvement, Crohn’s disease can effect many other organ systems. Inflammation of the interior portion of the eye, known as uveitis, can cause eye pain, especially when exposed to light (photophobia). Inflammation may also involve the white part of the eye (sclera), a condition called episcleritis. Both episcleritis and uveitis can lead to loss of vision if untreated.
Crohn’s disease is associated with a type of rheumatologic disease known as seronegative spondyloarthropathy. This group of diseases is characterized by inflammation of one or more joints (arthritis) or muscle insertions (enthesitis). The arthritis can affect larger joints, such as the knee or shoulder, or may exclusively involve the small joints of the hands and feet. The arthritis may also involve the spine, leading to ankylosing spondylitis if the entire spine is involved or simply sacroiliitis if only the lower spine is involved. The symptoms of arthritis include painful, warm, swollen, stiff joints and loss of joint mobility or function.
Crohn’s disease may also involve the skin, blood, and endocrine system. One type of skin manifestation, erythema nodosum, presents as red nodules usually appearing on the shins. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue, and is characterized by septal panniculitis. Another skin lesion, pyoderma gangrenosum, is typically a painful ulcerating nodule. Crohn’s disease also increases the risk of blood clots; 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, pallor, 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 may cause osteoporosis, or thinning of the bones. Individuals with osteoporosis are at increased risk of bone fractures.
Crohn’s disease can also cause neurological complications (reportedly in up to 15% of patients). The most common of these are seizures, stroke, myopathy, peripheral neuropathy, headache and depression.
Crohn’s patients often also have issues with small bowel bacterial overgrowth syndrome, which has similar symptoms.
Crohn’s disease can lead to several mechanical complications within the intestines, including obstruction, fistulae, and abscesses. Obstruction typically occurs from strictures or adhesions that narrow the lumen, blocking the passage of the intestinal contents. Fistulae 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 collections of infection, which can occur in the abdomen or in the perianal area in Crohn’s disease sufferers. Crohn’s is responsible for 10% of vesicoenteric fistulae, and is the most common cause of ileovesical fistulae.
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. Screening for colon cancer with colonoscopy is recommended for anyone who has had Crohn’s colitis for at least eight years. 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.
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.
Crohn’s disease can cause significant complications, including bowel obstruction, abscesses, free perforation and hemorrhage.
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 allows preventative measures to be taken. In some cases, remission can occur during pregnancy. Certain medications can also impact sperm count or may otherwise adversely affect a man’s ability to conceive.
Although the exact cause of Crohn’s disease is still unknown, a combination of environmental factors and genetic predisposition seems to cause the disease. The genetic risk factors have now more or less been comprehensively elucidated, making Crohn’s disease the first genetically complex disease of which the genetic background has been resolved. The relative risks of contracting the disease when one has a mutation in one of the risk genes, however, are actually very low (approximately 1:200). In broad terms, the genetic data indicate the innate immune systems in patients with Crohn’s disease malfunction, and direct assessment of patient immunity confirms this notion. This had led to the notion Crohn’s disease should be viewed as innate immune deficiency, chronic inflammation being caused by adaptive immunity trying to compensate for the reduced function of the innate immune system.
Some research has indicated Crohn’s disease may have a genetic link. The disease runs in families and those with a sibling with the disease are 30 times more likely to develop it than the general population.
Mutations in the CARD15 gene (also known as the NOD2 gene) are associated with Crohn’s disease and with susceptibility to certain phenotypes of disease location and activity. In earlier studies, only two genes were linked to Crohn’s, but scientists now believe over thirty genes show genetics play a role in the disease, either directly through causation or indirectly, as with a mediator variable. Anomalies in the XBP1 gene have recently been identified as a factor, pointing towards a role for the unfolded protein response pathway of the endoplasmatic reticulum in inflammatory bowel diseases.
Diet is believed to be linked to its higher prevalence in industrialized parts of the world. A positive correlation has been found between the incidence of the disease and an increased intake of animal protein, milk protein and an increased ratio of omega-6 to omega-3 polyunsaturated fatty acids. Negative correlation of the disease incidence was found to the increased consumption of vegetable protein, and no correlation to fish protein. Smoking has been shown to increase the risk of the return of active disease, or “flares”. The introduction of hormonal contraception in the United States in the 1960s is linked with a dramatic increase in the incidence rate of Crohn’s disease. Although a causal linkage has not been effectively shown, there remain fears these drugs work on the digestive system in ways similar to smoking. Several scientific studies have posited isotretinoin is a possible cause of Crohn’s disease in some individuals.
Abnormalities in the immune system have often been invoked as being causes of Crohn’s disease. It is thought to be an autoimmune disease, with inflammation stimulated by an overactive Th1 cytokine response. However, more recent evidence has shown Th17 is of greater importance in the disease. The most recent gene to be implicated in Crohn’s disease is ATG16L1, which may induce autophagy and hinder the body’s ability to attack invasive bacteria.
Contrary to the prevailing view that Crohn’s disease is a primary T cell autoimmune disorder, there is an increasing body of evidence in favor of the hypothesis that Crohn’s disease results from an impaired innate immunity. The immunodeficiency, which has been shown to be due (at least in part) to impaired cytokine secretion by macrophages, is thought to lead to a sustained microbial-induced inflammatory response, in particular, in the colon where the bacterial load is especially high.
A variety of pathogenic bacteria were initially suspected of being causative agents of Crohn’s disease. However, most healthcare professionals now believe a variety of microorganisms are taking advantage of their host’s weakened mucosal layer and inability to clear bacteria from the intestinal walls, both symptoms of the disease. Some studies have suggested Mycobacterium avium subspecies paratuberculosis (MAP) plays a role in Crohn’s disease, in part because it causes a very similar disease, Johne’s disease, in cattle. The mannose-bearing antigens (mannins) from yeast may also elicit an antibody response. Other studies have linked specific strains of enteroadherent E. coli to the disease. Still, this relationship between specific types of bacteria and Crohn’s disease remains unclear.
Some 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. 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. The authors of that study were unable to identify the source of the protease, but a separate review noted regional and temporal variations in those illnesses follow those associated with infection with a poorly understood protozoan, Blastocystis.
A study in 2003 put forth the “cold-chain” hypothesis 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. Later studies have provided support for this hypothesis.
Studies done at the University of Liverpool have offered ideas to explain the apparent connection between Crohn’s disease, Mycobacterium, other pathogenic bacteria, and genetic markers. 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.
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. Ulceration is an outcome seen in highly active disease. There is usually an abrupt transition between unaffected tissue and the ulcer. 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) in other parts of the gastrointestinal system.
The diagnosis of Crohn’s disease can sometimes be challenging, and a number of tests are often required to assist the physician in making the diagnosis. 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 aids in endoscopic diagnosis. Multinucleated giant cells, a common finding in the lesions of Crohn’s disease, are less common in the lesions of lichen nitidus.
A colonoscopy is the best test for making the diagnosis of Crohn’s disease, as it allows direct visualization of the colon and the terminal ileum, identifying the pattern of disease involvement. On occasion, the colonoscope can travel past the terminal ileum, but it varies from patient to patient. During the procedure, the gastroenterologist can also perform a biopsy, taking small samples of tissue for laboratory analysis, which may help confirm a diagnosis. As 30% of Crohn’s disease involves only the ileum, cannulation of the terminal ileum is required in making the diagnosis. Finding a patchy distribution of disease, with involvement of the colon or ileum, but not the rectum, is suggestive of Crohn’s disease, as are other endoscopic stigmata. The utility of capsule endoscopy for this, however, is still uncertain.
A 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. 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.
CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols.They are also useful for looking for intra-abdominal complications of Crohn’s disease, such as abscesses, small bowel obstructions, or fistulae. Magnetic resonance imaging (MRI) is another option for imaging the small bowel as well as looking for complications, though it is more expensive and less readily available
Multiphase white blood cell scans have been shown to be effective in detecting the locations of active Crohn’s disease, particularly in hard to diagnose patients suffering with the early stages or a mild form of the disease with negative endoscopic and radiologic findings. The procedure, a type of nuclear medicine, uses white blood cells removed from the patient; they are tagged with a radioisotope, and then injected intravenously into the patient, and later scanned at several intervals to detect any abnormal white blood cell accumulation, such as pooling in the intestinal tract. Studies have also suggested such scans are useful to monitor the disease and evaluate the effectiveness of therapy.
Comparison with ulcerative colitis
The most common disease that mimics the symptoms of Crohn’s disease is ulcerative colitis, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases, since the course of the diseases and treatments may be different. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis.
At the present time, there is no cure for Crohn’s disease and remission may not be possible or prolonged if achieved. In cases where remission is possible, relapse can be prevented and symptoms controlled with medication, lifestyle changes, and, in some cases, surgery. Adequately controlled, Crohn’s disease may not significantly restrict daily living. Treatment for Crohn’s disease is only when symptoms are active and involve first treating the acute problem, then maintaining remission.
Certain lifestyle changes can reduce symptoms, including dietary adjustments [Elemental diet], proper hydration, and smoking cessation. Smoking may increase Crohn’s disease; stopping is recommended. Eating small meals frequently instead of big meals may also help with a low appetite. To manage symptoms have a balanced diet with proper portion control. Fatigue can be helped with regular exercise, a healthy diet, and enough sleep. A food diary may help with identifying foods that trigger symptoms. Some patients should follow a low dietary fiber diet to control symptoms especially if fibrous foods cause symptoms.
Crohn’s cannot be cured by surgery, though it is used when partial or a full blockage of the intestine occurs. Surgery may also be required for complications such as obstructions, fistulas and/or abscesses, or if the disease does not respond to drugs. After the first surgery, Crohn’s usually shows up at the site of the resection, however it can appear in other locations. After a resection, scar tissue builds up, which can cause strictures, which form when the intestines become too small to allow excrement to pass through easily, which can lead to a blockage. After the first resection, another resection may be necessary within five years. For patients with an obstruction due 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 patients with duodenal involvement.
Short bowel syndrome (SBS, also short gut syndrome or simply short gut) can be caused by the surgical removal of the small intestines. It usually develops in those having had half or more of their small intestines removed. Diarrhea is the main symptom of short bowel syndrome, however other symptoms may include cramping, bloating, and heartburn. Short bowel syndrome is treated with changes in diet, intravenous feeding, vitamin and mineral supplements, and treatment with medications. Another complication following surgery for Crohn’s disease in which the terminal ileum has been removed is the development of excessive watery diarrhea. This is due to an inability of the ileum to reabsorb bile acids after resection of the terminal ileum.
In some cases of SBS, intestinal transplant surgery may be considered; though the number of transplant centers 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.
Complementary and alternative medicine
Crohn’s disease is a chronic condition for which there is currently no cure. It is characterized by periods of improvement followed by episodes when symptoms flare up. With treatment, most people achieve a healthy height and weight, and the mortality rate for the disease is relatively low. However, Crohn’s disease is associated with an increased risk of small bowel and colorectal carcinoma, including bowel cancer.
Researchers at University College London have questioned the wisdom of suppressing the immune system in Crohn’s, as the problem may be an underactive rather than an overactive immune system: Their study found that Crohn’s patients showed an abnormally low response to an introduced infection, marked by a poor flow of blood to the wound.
Since Crohn’s is an auto-immune disease it is thought that the body is attacking itself and thusly cannot fight off infection or wounds because it is busy mistakenly fighting itself.
The disease was named for American gastroenterologist Burrill Bernard Crohn, who, in 1932, together with two colleagues, described a series of patients with inflammation of the terminal ileum, the area most commonly affected by the illness. For this reason, the disease has also been called regional ileitis or regional enteritis. The condition, however, has been independently identified by others in the literature prior, the most notable one being in 1904 by Polish surgeon Antoni Leśniowski for whom the condition is additionally named (Leśniowski-Crohn’s disease) in the Polish literature.
Ileitis terminalis was first described by Polish surgeon Antoni Leśniowski in 1904, however, due to the precedence of Crohn’s name in the alphabet, it became later to be known in the worldwide literature as Crohn’s disease. Only in Poland it continues to be named Leśniowski-Crohn’s disease. Burrill Bernard Crohn, an American gasteroenterologist 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”.
Distribution of gastrointestinal Crohn’s disease, based on data from American Gastroenterological Association:
Crohn’s disease is one type of inflammatory bowel disease (IBD). It typically manifests in the gastrointestinal tract and can be categorized by the specific tract region affected. A disease of both the ileum (the last part of the small intestine, which connects to the large intestine), and the large intestine, Ileocolic Crohn’s accounts for fifty percent of cases. Crohn’s ileitis, manifest in the ileum only, accounts for thirty percent of cases, and 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 (MedlinePlus 2010). The disease can attack any part of the digestive tract, from mouth to anus. However individuals affected by the disease rarely fall outside these three classifications with presentations in other areas.
Crohn’s disease may also be categorized by the behavior of disease as it progresses. These categorizations formalized in the Vienna classification of the disease. There are three categories of disease presentation in Crohn’s disease: stricturing, penetrating, and inflammatory. Stricturing disease causes narrowing of the bowel that may lead to bowel obstruction or changes in the caliber of the feces. Penetrating disease creates abnormal passageways (fistulae) between the bowel and other structures, such as the skin. Inflammatory disease (or nonstricturing, nonpenetrating disease) causes inflammation without causing strictures or fistulae.