Our mission is to empower awareness about Crohn's Disease for those affected, the world over. 

Living with Crohn's can be difficult, but by working together we can affect global change and foster the support we all need!

Rare

Fewer than 200,000 US cases per year

Can't be cured, but treatment may help

Requires a medical diagnosis

Lab tests or imaging often required

Chronic: can last for years or be lifelong

Crohn's disease can sometimes causes life-threatening complications.

Crohn's disease can cause abdominal pain, diarrhea, weight loss, anemia, and fatigue. Some people may be symptom free most of their lives, while others can have severe chronic symptoms that never go away.

Crohn's disease cannot be cured. Medications such as steroids and immunosuppressants are used to slow the progression of disease. If these aren't effective, a patient may require surgery. Additionally, patients with Crohn's disease may need to receive regular screening for colorectal cancer due to increased risk.

 

What is Crohn disease?                          

Crohn disease is a complex, chronic disorder , named after Dr. Burril B. Crohn that primarily affects the digestive system. This condition typically involves abnormal inflammation of the intestinal walls, particularly in the lower part of the small intestine (the ileum) and portions of the large intestine (the colon). Inflammation can occur in any part of the digestive system, however. The inflamed tissues become thick and swollen, and the inner surface of the intestine may develop open sores (ulcers).

Crohn disease most commonly appears in a person's late teens or twenties, although the disease can appear at any age. Signs and symptoms tend to flare up multiple times throughout life. The most common features of this condition are persistent diarrhea, abdominal pain and cramping, loss of appetite, weight loss, and fever. Some people with Crohn disease have chronic bleeding from inflamed tissues in the intestine; over time, this bleeding can lead to a low number of red blood cells (anemia). In some cases, Crohn disease can also cause medical problems affecting the joints, eyes, or skin.

Intestinal blockage is a common complication of Crohn disease. Blockages are caused by swelling or a buildup of scar tissue in the intestinal walls. Some affected individuals also develop fistulae, which are abnormal connections between the intestine and other tissues. Fistulae occur when ulcers break through the intestinal wall to form passages between loops of the intestine or between the intestine and nearby structures (such as the bladder, vagina, or skin).

Crohn disease is one common form of inflammatory bowel disease (IBD). Another type of IBD, ulcerative colitis, also causes chronic inflammation of the intestinal lining. Unlike Crohn disease, which can affect any part of the digestive system, ulcerative colitis typically causes inflammation only in the colon. In addition, the two disorders involve different patterns of inflammation.

 

How common is Crohn disease? Could I develop Crohn’s?

Crohn disease is most common in western Europe and North America, where it affects 100 to 150 in 100,000 people. About one million Americans are currently affected by this disorder. Crohn disease occurs more often in whites and people of eastern and central European (Ashkenazi) Jewish descent than among people of other ethnic backgrounds.

Crohn’s tends to run in families, so if you or a close relative have the disease, your family members have a significantly increased chance of developing Crohn’s. Studies have shown that 5% to 20% of affected individuals have a first – degree relative (parents, child, or sibling) with one of the diseases. The risk is greater with Crohn’s disease than ulcerative colitis. The risk is also substantially higher when both parents have IBD. The disease is most common among people of eastern European backgrounds, including Jews of European descent. In recent years, an increasing number of cases have been reported among African American populations.Now, Individuals of any age, gender or race can develop Crohn’s disease, especially if a blood relative or has it or another type of IBD. Crohn’s commonly affects adolescents and young adults ages 15-35. Studies show that Crohn’s is more common in Urban communities than Rural areas based on an increase of reports among African American populations in the last several years. 

 

 what causes Crohn’s?

There’s no concrete proof as to what causes Crohn’s, however, researchers have discovered a strong possibility. The immune system is our body’s natural system of defense. When unknown bacteria or viruses enter the body, the immune system goes into attack mode. The bacteria in the digestive tract, or Gastrointestinal (GI) tract, triggers the immune system causing it to believe it is constantly under attack. This overreaction leads to the inflammation and ulcers which in turn damages the intestines. Stress, diet and smoking are factors that can cause Crohn’s as well. 

What are the genetic changes related to Crohn disease?

Crohn disease is related to chromosomes 5 and 10.

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A variety of genetic and environmental factors likely play a role in causing Crohn disease. Although researchers are studying risk factors that may contribute to this complex disorder, many of these factors remain unknown. Cigarette smoking is thought to increase the risk of developing this disease, and it may also play a role in periodic flare-ups of signs and symptoms.

Studies suggest that Crohn disease may result from a combination of certain genetic variations, changes in the immune system, and the presence of bacteria in the digestive tract. Recent studies have identified variations in specific genes, including ATG16L1IL23RIRGM, and NOD2, that influence the risk of developing Crohn disease. These genes provide instructions for making proteins that are involved in immune system function. Variations in any of these genes may disrupt the ability of cells in the intestine to respond normally to bacteria. An abnormal immune response to bacteria in the intestinal walls may lead to chronic inflammation and the digestive problems characteristic of Crohn disease.

Researchers have also discovered genetic variations in certain regions of chromosome 5 and chromosome 10 that appear to contribute to Crohn disease risk. One area of chromosome 5, known as the IBD5 locus, contains several genetic changes that may increase the risk of developing this condition. Other regions of chromosome 5 and chromosome 10 identified in studies of Crohn disease risk are known as "gene deserts" because they include no known genes. Instead, these regions may contain stretches of DNA that regulate nearby genes. Additional research is needed to determine how genetic variations in these chromosomal regions are related to a person's chance of developing Crohn disease.

 

Can Crohn disease be inherited?

The inheritance pattern of Crohn disease is unclear because many genetic and environmental factors are likely to be involved. This condition tends to cluster in families, however, and having an affected family member is a significant risk factor for the disease.

Where can I find information about diagnosis or management of Crohn disease?

These resources address the diagnosis or management of Crohn disease and may include treatment providers.

·         Genetic Testing Registry: Inflammatory bowel disease 1

·         MedlinePlus Encyclopedia: Crohn's disease

You might also find information on the diagnosis or management of Crohn disease in Educational resourcesand Patient support.

General information about the diagnosis and management of genetic conditions is available in the Handbook. Read more about genetic testing, particularly the difference between clinical tests and research tests.

To locate a healthcare provider, see How can I find a genetics professional in my area? in the Handbook.

 

·         Specific Risk Factors for Inflammatory Bowel Disease (Table 1)

·         Numerous environmental risk factors of IBD have been explored, including smoking, oral contraceptive pills (OCPs), appendectomy, diet, breastfeeding, and nonsteroidal anti-inflammatory drugs (NSAIDs); however, none of these factors completely explain the environmental determinants of IBD

·         IBD has been primarily characterized as a disease of industrialized nations, with increased prevalence in the developed world. Since the 19th century, the incidence of IBD has increased steadily in North America and Europe until stabilizing in the middle and latter parts of the 20th century for UC (2–15/100,000 person-years) and CD (3–15/100,000 person-years), respectively. Although developing regions have traditionally reported lower prevalence of IBD, the incidence of IBD is rising in many of these nations (eg, India and China) as they have become industrialized.8,9 Furthermore, migrant studies have demonstrated that individuals immigrating from regions with low prevalence to countries with higher prevalence are at an increased risk of developing IBD, particularly among first-generation children.5,6 Thus, environmental exposures are thought to contribute to the development of IBD.

·         Many microorganisms have been considered as possible causes of IBD. Several candidate organisms have been proposed in the pathogenesis of IBD, including Mycobacterium avium subspecies paratuberculosis(MAP), the measles virus, and adherent-invasive strains of Escherichia coli (AIEC).

 

·           Multiple theories have been proposed to explain the unknown environmental exposures that may interact with the immune system and result in an abnormal inflammatory response to intestinal microflora.10 The most predominant theory is the hygiene hypothesis. This hypothesis proposes that the rising frequency of immunologic disorders can be attributed to a lack of childhood exposure to enteric pathogens.5,11 Improved sanitation and hygiene, along with decreased exposure to enteric organisms during early childhood, may lead to a greater susceptibility to develop an inappropriate immunologic response upon exposure to new antigens (eg, a gastrointestinal infection) later in life.12 Many factors have been examined as proxy markers of environmental exposures in early life, including Helicobacter pylori infection, family size, sibship, birth order, urban upbringing, and pet exposure.10,13-15

  

·         Helicobacter pylori

·         H. pylori is an infection often acquired early in childhood. Colonization has been correlated to sibship size, household crowding, and poor sanitary facilities.16 IBD is more prevalent in developed nations where H. pylori infection is less common.17 A meta-analysis of 23 studies concluded that H. pylori infection was negatively associated with both CD and UC.17 Furthermore, colonization may protect against other immune conditions such as asthma.17 H. pylori infection may protect against the development of IBD by increasing the expression of genes (eg, FOXP3) that are involved in T-regulatory cell function.17 However, reduced colonization of H. pylori in IBD patients may be secondary to antibiotic and mesalamine use,18 which could eradicate H. pylori infection in some IBD patients.    

Family Size, Sibship, and Birth Order

·         Individuals raised with fewer siblings may have fewer opportunities to acquire the enteric infections during childhood that are necessary to program the immune system of the gut to respond appropriately to bowel infections later in life.12,18 

 

·         Specific Risk Factors for Inflammatory Bowel Disease (Table 1)

·         Numerous environmental risk factors of IBD have been explored, including smoking, oral contraceptive pills (OCPs), appendectomy, diet, breastfeeding, and nonsteroidal anti-inflammatory drugs (NSAIDs); however, none of these factors completely explain the environmental determinants of IBD.

·         Smoking

·         A paradoxical relationship has been consistently demonstrated between smoking and IBD. A meta-analysis concluded that active smokers were less likely to develop UC compared to individuals who were never smokers or ex-smokers; in contrast, active smokers, followed by ex-smokers, were at an increased risk for acquiring CD.31 A dose-response relationship between smoke exposure and IBD has been described.32-34 The exact mechanisms by which smoking influences the development of IBD are unknown. Nicotinic acetylcholine receptors (nAChRs) are present in mucosal epithelial cells of the bowel.35,36The expression of nAChRs has also been found on T cells, indicating that nicotine may directly regulate T-cell function.37However, clinical trials of nicotine replacement in UC have yielded only a modest benefit at best; thus, nicotine alone may not be the driving factor.35 Other proposed mechanisms have included modulating cellular immunity,38 altering cytokine levels,39modifying colonic mucus production,40 and predisposing patients to microvascular thrombi.35,41 Although the relationship between smoking and IBD is well documented, a paradox exists in that the highest incidence of smoking is found in countries with the lowest incidence of IBD. For example, the incidence of IBD is higher in Canada42 compared to South Korea43; however, the prevalence of smoking in Canada (22%)44,45 is lower than in South Korea (65%).45

·         A similar relationship has also been proposed with passive smoke exposure.32,34 However, a meta-analysis did not demonstrate an association for childhood passive smoke exposure or prenatal smoke exposure.32 A possible explanation for these findings could be the presence of a dose-response relationship between smoking and IBD,32in which passive smoking may represent a lower level of exposure, leading to nonsignificant associations.32

·         Oral Contraceptive Pills

·         In 1995, a meta-analysis of 2 cohort studies and 7 case-control studies suggested that OCPs may marginally increase the risk of developing CD, but not UC.46 This paper was limited by small sample sizes, and only 1 of the 9 included studies had a significant association. Additionally, the meta-analysis did not investigate a dose-response effect, as the majority of studies were performed before the introduction of lower OCP estrogen preparations.47A meta-analysis conducted in 2008 demonstr

 

 

·         Breastfeeding

·         Breastfeeding, which protects infants against many other immune-mediated diseases,76 may also reduce the risk of developing IBD. Although several studies support a protective role between breastfeeding and IBD,76-79 other studies have failed to find an association,22,74,80 while still others have shown a positive relationship.18,81 A metaanalysis of 14 case-control studies found a protective role for breastfeeding in both CD and UC.76 The mechanism by which breastfeeding may have a beneficial effect is likely multifactorial. Breastfeeding is important for acquiring oral tolerance to microflora and food antigens,10,76 which may prevent IBD development.76 Infant formula lacks lactoferrin, which is found in breastmilk10and may have antibacterial and antiviral effects,82 as well as anti-inflammatory properties.82Although the metaanalysis found a negative association between breastfeeding and IBD, subsequent studies have produced conflicting evidence in which breastfeeding was found to be a significant risk factor for pediatric CD.18

·         Antibiotics

·         Exposure to antibiotics in childhood is hypothesized to interfere with the normal process of developing tolerance to enteric bacteria, which may lead to IBD.83 Card and coworkers demonstrated a positive association between antibiotic use and the development of CD.84 This finding is supported by evidence from other studies demonstrating a similar relationship.74,83

·         Nonsteroidal Anti-Inflammatory Drugs

·          A case-control study by Felder and colleagues investigating the effects of NSAIDs on IBD found a positive association for both UC and CD.85 NSAIDs can cause damage to the intestinal mucosa of the stomach, small bowel, and colon.85,86 NSAIDs can also increase intestinal permeability by inhibiting cyclooxygenase, which reduces prostaglandin production.85,86 Inhibition of prostaglandins has been implicated in IBD due to immunoregulatory effects.

 

How can I tell if I might have Crohn’s?

The symptoms for each person varies, however, the most common are diarrhea (persistent) , pain and cramps in the abdomen and weight loss. These are symptoms shared with other IBD’s such as Ulcerative Colitis and Celiac so a professional diagnosis is recommended.

 

So how do I find out if I have it?

A physical exam is necessary to diagnose Crohn’s. There are several different tests a doctor could perform. The most commonly used is a colonoscopy because is more specific in diagnosing Crohn’s. Blood tests can be done to determine the white blood cell count. A high count can indicate chronic inflammation. A stool sample, CT scans, Capsule endoscopy (a pill with a mini camera to see inside), upper GI x-rays and upper enteroscopy are several other useful exams.  

Ok, I’ve been diagnosed. Now what?

 Seek a knowledgeable Gastroenterologist. There is no cure but treatment is available, one of which may include surgery. Surgery typically only becomes necessary when medication and other treatment no longer helps. These doctors specialize in IBD’s and can help you set up your personal treatment plan. The main objective is to decrease the inflammation, relieve abdominal pain and other symptoms like rectal bleeding. Anti-inflammation medicines like Pentasa (mesatamine), immune system suppressors and antibiotics are some medicinal options. But like any other illness or condition, diet and nutrition are the key factors to effective treatment. Researchers haven’t found any food that directly cause Crohn’s or for the intestine to become inflamed. However, to avoid worsening symptoms, stay clear of spicy foods, diary products, greasy foods and alcoholic beverages. If needed, consult a dietician for assistance with meal planning. 

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