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Crohn's Disease


About Crohn's Disease

Crohn's Disease (CD) is an ailment that creates Chronic Inflammation in the digestive system; it can affect any part of the digestive system from the mouth to the Anus and affects approximately one million people in the United States and 27–48 per 100,000 people in Europe with numbers in all areas rising. Crohn's Disease, along with Ulcerative Colitis are commonly referred to as Inflammatory Bowel Disease, or IBD.

The exact cause and disease mechanisms are not fully understood, but it is thought to be caused by multiple factors. Microbes, environment, genetic status, and immunology are factors that can affect Crohn's Disease susceptibility and disease progression.

Crohn's Disease has a Genetic link (over 30 genes have been discovered so far); if a close family member has Crohn's Disease, you are at increased risk of having an IBD. Studies indicate a risk between 10%-20% [this number can vary depending on gene mutation(s)].

Crohn's Disease is most common in Caucasians and less often diagnosed in Asians and African Americans. [14]

Crohn's Disease is NOT Irritable Bowel Syndrome (IBS) (see IBD v IBS). Crohn's Disease must be differentiated from other conditions which on the surface may have similar symptoms such as: Ulcerative Colitis, IBS, Clostridium difficile Infection, Parasite Infection, etc. See Also: Crohn's Disease vs. Ulcerative Colitis.

It is yet unknown how important a role diet plays in Crohn's Disease but certain foods definitely aggravate symptoms. Crohn's Disease was once portrayed as an autoimmune disease but many researchers are moving away from that categorization. Crohn's Disease is now widely considered a disease of Immune System Deficiency or Immune System Dysregulation.[3]


Crohn's Disease symptoms tend to first manifest in the teens or twenties, but can occur at any age. Crohn's Disease is typically a chronic, relapsing condition that cycles through periods of Remission and "Flare-Ups". Crohn's Disease often exhibits a high patient-to-patient variability in terms of symptoms and disease course. Crohn's Disease is often difficult to diagnose because many symptoms are common to other conditions. While symptoms can vary significantly between sufferers, typical symptoms of Crohn's Disease often include:
*(Independent conditions / diseases that often co-occur with Crohn's Disease are listed in parentheses and italics)

Anus / Rectal
Blood Tests**For Other Blood Tests Check the Wiki Page: Blood test codes and results explained

Bones / Joints
Bowel Movements / Defecation / Stool
Mouth / Oral
Psychiatric / Mental State / Mood / Affect
Stomach / Upper GI
Systemic / Body as a Whole
* Some people have all these symptoms, some only have one or two.

Types of Crohn's Disease

Ileocolitis - Ileocolitis is the most common type of Crohn's disease and affects the ileum, terminal ileum, and colon. Those with Ileocolitis frequently experience diarrhea, pain and cramping in the lower right quadrant of the abdomen and periumbilical region (around the belly button), and weight loss. Due to the nature of Ileocolitis, it is important to have Vitamin B12 and Folate levels checked regularly to test for deficiency. As Inflammation between the ileum and colon is usually continuous, the ileocecal valve is usually also diseased.

Ileitis - Ileitis is much like Ileocolitis but only affects the ileum and terminal ileum. Those with Ileitis, like Ileocolitis, frequently experience diarrhea (large volume), pain in the lower right abdomen and periumbilical region, and weight loss. Those with Ileitis should have their Vitamin B12 and Folate levels tested.

Gastroduodenal Crohn's Disease - Gastroduodenal Crohn's Disease is characterized by inflammation in the stomach and duodenum. Common symptoms include weight loss, nausea, loss of appetite, pain in the middle of the abdomen, and occasionally vomiting. Gastroduodenal Crohn's Disease is often misdiagnosed as normal ulcer disease and a correct diagnosis is not made until symptoms worsen. As the jejunum is where most nutrients are absorbed, those with Gastroduodenal Crohn's Disease often experience malnutrition due to malabsorption. [1]

Jejunoileitis - Jejunoileitis occurs when there is inflammation in the jejunum. It is characterized by diarrhea, pain following eating, and abdominal pain.

Crohn's Colitis - Crohn's Colitis (Granulomatous Colitis) is Crohn's Disease that only affects the colon. It is characterized by bleeding from the rectum and diarrhea (lower volume but greater frequency). It differs from Ulcerative Colitis in that the inflammation will be patchy whereas Ulcerative Colitis is continuous as Crohn's Colitis doesn't necessarily involve the rectum whereas Ulcerative Colitis always does.

Categories of Crohn's Disease

There are three categories that each type of Crohn's Disease can fall into. These are:
  • Stricturing - Stricturing Crohn's Disease can lead to strictures or narrowing of the intestine. This can in turn lead to Intestinal Obstruction.
  • Penetrating - Penetrating Crohn's Disease can lead to Fistulae which are tunnels from the intestines to other areas of the body including the skin, bladder, and vagina.
  • Inflammatory (sometimes referred to as non-penetrating, non-stricturing) - this category of disease produces Inflammation but no strictures of fistulae.

Extraintestinal Manifestations

There are often symptoms which occur outside of the digestive system. These are termed Extraintestinal Manifestations. These issues can be caused by Inflammation or Crohn's-induced Vitamin and Mineral Deficiencies.

Diagnosing Crohn's Disease

Crohn's disease can be difficult to diagnose. If you think you may be suffering from Crohn's disease, or another IBD, it may be helpful to keep a diary (see diary inclusions) as this will help your doctor build up a picture of your symptoms, and ensure they take your concerns seriously.

Diagnostic Tests

Histologic Findings
Often a series of biopsies will be taken when a colonoscopy or like procedure is performed. The histologic findings of Crohn's Disease are highly variable and not all characteristics are usually seen.[13] Findings may include:
  • Areas of chronic inflammation, comprising increased lamina propria plasma cells and lymphocytes, in association with chronic architectural distortion with patchy, mild to severe, neutrophilic inflammation, including neutrophilic cryptitis, crypt abscesses, or erosions/ulcers
  • Skip lesions comprising focal, patchy erosions or ulcers, vertical fissures, and fistulas
  • The hint of "skip lesions" – Mucosal fragments from the same level of the colon have variable microscopic findings.
  • Transmural inflammation with multiple lymphoid aggregates
  • Granulomas - Granulomas are seen in only 10-40% of Crohn's Disease patients and can also be found in patients with tuberculosis or yersiniosis.
  • Submucosal fibrosis and neuromuscular hyperplasia of submucosa

Blood Tests

There are a variety of blood tests that can help your doctor determine if you have Crohn's Disease or not. While none are 100% accurate, they can help pinpoint what is transpiring.

Other Tests

Disease Course

Crohn's Disease Symptomology is Often Cyclic -

The course of Crohn's Disease varies dramatically between patients. Often, symptoms wax and wane between "Flare" and Remission. Some patients have extended periods of remission, while others may live in a continuous flare and never fully achieve remission.

Dysregulated Immune Response Stimulates Inflammatory Processes -

In Crohns Disease, cells of the Innate Immune System often do not respond appropriately to Antigens in the GI Tract. Different gene mutations can cause the error in immune response to occur at different steps in the pathway, and some genetic factors implicated in Crohn's Disease are yet unknown. The general disease trend is an error (or errors) within the innate immune response to antigen which results in a dysregulation of the balance between pro-inflammatory Cytokines [such as Interleukin 1 (IL1), Interleukin 6 (IL6), Interleukin 12 (IL12), Tumor Necrosis Factor alpha (TNF α), IFN-gamma] and anti-inflammatory cytokines [such as Interleukin 4 (IL4), Interleukin 10 (IL10), Interleukin 11 (IL11)]. During a "flare" the inflammatory response goes unchecked and results in large amounts of pro-inflammatory factors to be activated.
Normal Immune Response to Pathogens:
In a normally functioning immune system, there exists a balance between pro-inflammatory and anti-inflammatory factors that are expressed at a baseline level (Figure 1A).

Upon stimulation with an infectious agent, the pro-inflammatory responders are co-activated- or followed shortly thereafter with upregulation of anti-inflammatory factor activity, and leads to a delicate interplay between pro-inflammatory and anti-inflammatory responses (Figure 1B).

When the threat (pathogen) has been cleared, the pro-inflammatory signals subside and the balance is slowly normalized (Figure 1C).

Crohn's Disease Response to Pathogens:
In Crohn's Disease, the immune response is dysregulated. The immune system may be stimulated inappropriately (i.e. to normal intestinal flora) and/or can ineffectively over-activate in response to a pathogen. Often, one or more of the mechanisms utilized for killing and removal of pathogens is ineffective. This can be in combination with an inefficient feedback mechanism to dampen the inflammatory/immune responses. The result of reduced pathogen-destruction combined with less effective anti-inflammatory signaling can trigger a vicious "pro-inflammatory cycle" typically seen in Crohn's Disease symptomatic "flares" (Figure 1D).

In the normally functioning immune response the activation of innate immunity in turn activates the adaptive immune system allowing a more specific (although delayed) response to the infecting agent. The adaptive immune system activates additional factors to stimulate both adaptive and innate immune responses. In Crohn's Disease, the anti-inflammatory mechanisms are reduced causing this pro-inflammatory cycling effect. Chronically active pro-inflammatory responses can cause tissue destruction and certain inflammatory factors can increase growth rates of microorganisms.

Crohn's Disease can Cause Strictures -

Many Patients Require Surgical Intervention


There are many treatments available to alleviate the symptoms of Crohn's disease, reduce inflammation, induce remission, and minimize the likelihood of relapse. Unfortunately there is no cure as yet.

Drug Treatments

There are a variety of drug treatments available to control symptoms, help induce remission, and prevent relapse.


This is a class of drugs which are similar to aspirin, and have a similar anti-inflammatory effect. These drugs are poorly absorbed into the body, therefore they act on the surface of the intestines. This makes them relatively mild, and less likely to have side effects.

Mesalazine / mesalamine (Apriso, Asacol, Lialda, Pentasa)


Immune System Suppressors

Biological Therapies

Traditional methods of Crohn's Disease treatment have a high rate of side-effects and offer sub-optimal results. In order to obtain a more favorable treatment outcome, Biological Therapies were developed. Biological therapies work with the body's immune system to combat disease. Popular treatments include the use of monoclonal antibodies which neutralize pro-inflammatory factors, such as: Tumor Necrosis Factor (TNF) or Alpha-4-Integrin.

TNF - Based Biological Therapy:
Infliximab (Remicade)
Adalimumab (Humira)
Certolizumab (Cimzia)
Ustekinumab (Stelara)

Alpha - 4 Integrin - Based Biological Therapy:
Natalizumab (Tysabri) [5]



Over The Counter (OTC) Drug Treatments

There are also over the counter drugs and remedies to make living with the symptoms easier.


In some cases, surgery may be required to remove particularly diseased sections of bowel. Half of adults with Crohn's Disease will require surgery with 10 years of diagnosis. In children, surgical rates are much higher, 34% of children undergo surgery within 5 years of diagnosis.[4]

Check out this external website for more information about Surgery for IBD. HERE


Some people may choose to use supplements and complementary therapies, either as a stand alone treatment or to enhance other treatments.


Likewise, different diets can be used to alleviate symptoms, or as a main course of treatment.

Alternative Treatments

Some people may choose to use alternative treatments, either because they feel more comfortable doing so, or because conventional treatments have failed.

New and Future Treatments for Crohn's Disease

Various new and emerging treatments are currently being explored as possible effective treatments for Crohn's Disease and Crohn's-related symptoms.
- Stem Cell (SC) Therapy
- An Opioid Antagonist, Low Dose Naltrexone (LDN), previously used for treating Substance Abuse has shown promise in the treatment of Crohn's Disease.
It is important to discuss the different options with your doctor before deciding which course of treatment(s) to follow.

Risk of Relapse in Crohn's Disease

Patients with Crohn's Disease have extremely variable rates of symptom return following remission. There are multiple factors which contribute to a higher risk of relapse.

Gene Mutation(s) -
Certain genetic mutations correlate with more aggressive disease. For example, certain mutations in the Nod2 / Card15 Gene is associated with earlier onset of symptoms and higher rates of surgery.

Age of Onset -
An earlier age of onset of symptoms (especially in young children) often correlates with more aggressive disease.

Treatment Course - "Top-Down" strategies in treating Crohn's Disease versus the traditional "Step-Up" approach, using aminosalicylates, antibiotics, immunosuppressants, to TNF - inhibitors.

Treatment Compliance - Higher rates of relapse were seen in patients that were less compliant with drug regimens.

Smoking - Smoking, or exposure to second-hand smoke is a well-established factor in decreasing periods of remission.

Blood Test Predictors -
Certain blood test predictors correlate with greater probability of relapse, these include:
- 1). Elevated CRP (C-Reactive Protein) - Levels 20mg/L and above.
- 2). Elevated Neutrophils - 4 x 10^9 /L and above.
- 3). Low Hemoglobin (Hgb) - Below 12.0 g/dL.

Living with Crohn's disease

Although there is no cure, a diagnosis of Crohn's disease is not a death sentence. With medication and adjustments to their lifestyle, many sufferers go on to live perfectly normal lifes, while others may find that their symptoms have a minor impact on everyday life.

How to Travel with Crohn's disease
Going to school with Crohn's disease
Working with Crohn's disease
Disability and Crohn's disease
What to eat with Crohn's disease
Making life easier with Crohn's disease
Crohn's and Colitis Associations
US Health Care
UK Health Care
Eating Out
Explaining Crohn's disease to children
If a loved one has IBD


3. Korzenik JR. Is Crohn's disease due to defective immunity? Gut. 2007;56(:2-5.
4. Lakatos PL and Kiss LS. Current status of thiopurine analogues in the treatment in Crohn's disease. World J Gastroenterol. 2011;17(39):4372-4381.
6. Crohn's Disease. National Association for Colitis and Crohn's Disease (NACC). 2010.
6. Singh UP. Singh NP. Singh B. et al. Stem cells as potential therapeutic targets for inflammatory bowel disease. Front Biosci (Schol Ed).;2:993-1008.
7. Cottone M. and Criscuoli V. Infliximab to treat Crohn’s disease: an update. Clin Exp Gastroenterol. 2011; 4: 227–238.
8. Bosani M, Ardizzone S, and Porro GB. Biologic targeting in the treatment of inflammatory bowel diseases.Biologics. 2009; 3: 77–97.
9. Caviglia R, Boškoski I, and Cicala M. Maintenance treatment with infliximab for the management of Crohn’s disease in adults. Biologics: Targets and Therapy 2009, 3:39-49.
10. Goulas SS. Management of refractory Inflammatory Bowel Disease. Annals of Gastroenterology. 2006;19(2): 168-173.
11. Oliva-Hemker M, Escher JC, Moore D, et al. Journal of Pediatric Gastroenterology and Nutrition
14. Cho JH. Inflammatory bowel disease: Genetic and epidemiologic considerations. World J Gastroenterol 2008; 14(3): 338-347.

Popular Threads Discussing Crohn's Disease

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05-11-2011, 10:51 PM   #1
New Member
Join Date: May 2011
my mom had crohns disease and got a illeostomy a couple years back will she also found out she had colon cancer during the surgery will she get her crohns disease back ?
05-12-2011, 07:37 AM   #2
itsMeFred's Avatar
Join Date: Apr 2011
Crohn's is an autoimmune disease like lupus, rheumatoid arthritis or MS. It never goes away.
It can go into remission for years, though...
~*~ Erin ~*~
05-12-2011, 08:04 PM   #3
New Member
Join Date: May 2011
thanks not what i wanted to hear but thanks
11-14-2012, 11:31 AM   #4
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Location: west chester, Ohio
08-20-2015, 12:24 PM   #5
Join Date: Aug 2015
Thanks for the useful wiki on Crohn’s. I’ve been educating myself on the topic for some time now, and I think that some additional references would help make some recent advances more widely known. I’m not a medical professional, but all the sources I cite are from medical journals except for the two web pages associated with Epi-Br. I would provide links to all of these, but this web forum will not let me post web links.

In section 1, I suggest the following edits:
The exact cause and disease mechanisms are not fully understood, but it is thought to be caused by multiple factors. Microbes, environment, genetic status, and immunology are factors that can affect Crohn's Disease susceptibility and disease progression. Mycobacterium avium subspecies paratuberculosis (MAP) is associated with many cases of Crohn’s disease (1, 2), although it’s specific role as a cause of Crohn’s disease remains to be defined (2). Numerous genetic loci have been associated with Crohn’s Disease, Ulcerative Colitis, or both diseases, and there is considerable overlap between loci for these diseases, other immune-mediated disorders, and mycobacterial infection (3).

In section 6, Diagnostic Tests, I suggest adding the following
MAP – Mycobacterium avium paratuberculosis (MAP) is difficult to detect, but where proper methods have been used most people with Crohn’s Disease have been found to be infected with MAP (1; see especially the section "MAP in humans" and references 35-39 therein).

In section 8.1.5, Treatment, antibiotics, I suggest adding the following:
Some patients have responded well to anti-MAP treatments involving rifabutin and clarithromycin (1); or a three-drug treatment including rifabutin, clarithromycin, and clofazimine (4). Anti-MAP therapy is reviewed by (1), in the section “Can anti-MAP treatment heal Crohn's disease?”

In section 8.7, New and Future Treatments, I suggest adding two paragraphs:
A modern vaccine against MAP has been developed and is awaiting clinical trial; this vaccine would both treat existing MAP-infected Crohn’s Disease patients and prevent new MAP infections (reference: on the web at crohnsmapvaccine [dot] com [slash] vaccine/)


Testing of a formulation of 16-bromoepiandrosterone (Epi-Br) for the treatment of MAP / Crohn’s Disease is being pursued by Immunikas (references: search for web page titled: “Immune Modulating Drug Stimulates Innate Immunity, Down-Regulates Unproductive Inflammation and Promotes Th1 Immunity” by Dr. William Chamberlain; and www [dot] immunikas [dot] com). This drug “enhances innate immunity and rebalances the immune network to limit excessive, destructive, inappropriate inflammation.” (reference web page: “Immune Modulating Drug Stimulates Innate Immunity, Down-Regulates Unproductive Inflammation and Promotes Th1 Immunity” by Dr. William Chamberlain)

1. Hermon-Taylor, J. Mycobacterium avium subspecies paratuberculosis, Crohn's disease and the Doomsday scenario. Gut Pathogens 2009, 1, (1), 1-6.
2. Feller, M.; Huwiler, K.; Stephan, R.; Altpeter, E.; Shang, A.; Furrer, H.; Pfyffer, G. E.; Jemmi, T.; Baumgartner, A.; Egger, M. Mycobacterium avium subspecies paratuberculosis and Crohn's disease: a systematic review and meta-analysis. The Lancet Infectious Diseases 2007, 7, (9), 607-613.
3. Jostins, L.; Ripke, S.; Weersma, R. K.; Duerr, R. H.; McGovern, D. P.; Hui, K. Y.; Lee, J. C.; Philip Schumm, L.; Sharma, Y.; Anderson, C. A.; Essers, J.; Mitrovic, M.; Ning, K.; Cleynen, I.; Theatre, E.; Spain, S. L.; Raychaudhuri, S.; Goyette, P.; Wei, Z.; Abraham, C.; Achkar, J.-P.; Ahmad, T.; Amininejad, L.; Ananthakrishnan, A. N.; Andersen, V.; Andrews, J. M.; Baidoo, L.; Balschun, T.; Bampton, P. A.; Bitton, A.; Boucher, G.; Brand, S.; Buning, C.; Cohain, A.; Cichon, S.; D/'Amato, M.; De Jong, D.; Devaney, K. L.; Dubinsky, M.; Edwards, C.; Ellinghaus, D.; Ferguson, L. R.; Franchimont, D.; Fransen, K.; Gearry, R.; Georges, M.; Gieger, C.; Glas, J.; Haritunians, T.; Hart, A.; Hawkey, C.; Hedl, M.; Hu, X.; Karlsen, T. H.; Kupcinskas, L.; Kugathasan, S.; Latiano, A.; Laukens, D.; Lawrance, I. C.; Lees, C. W.; Louis, E.; Mahy, G.; Mansfield, J.; Morgan, A. R.; Mowat, C.; Newman, W.; Palmieri, O.; Ponsioen, C. Y.; Potocnik, U.; Prescott, N. J.; Regueiro, M.; Rotter, J. I.; Russell, R. K.; Sanderson, J. D.; Sans, M.; Satsangi, J.; Schreiber, S.; Simms, L. A.; Sventoraityte, J.; Targan, S. R.; Taylor, K. D.; Tremelling, M.; Verspaget, H. W.; De Vos, M.; Wijmenga, C.; Wilson, D. C.; Winkelmann, J.; Xavier, R. J.; Zeissig, S.; Zhang, B.; Zhang, C. K.; Zhao, H.; Silverberg, M. S.; Annese, V.; Hakonarson, H.; Brant, S. R.; Radford-Smith, G.; Mathew, C. G.; Rioux, J. D.; Schadt, E. E.; Daly, M. J.; Franke, A.; Parkes, M.; Vermeire, S.; Barrett, J. C.; Cho, J. H. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 2012, 491, (7422), 119-124.
4. Borody, T. J.; Leis, S.; Warren, E. F.; Surace, R. Treatment of severe Crohn's disease using antimycobacterial triple therapy — approaching a cure? Digestive and Liver Disease 2002, 34, (1), 29-38.

My notes on above papers:
1. John Hermon-Taylor is a giant in the Crohn’s field, and his research & review papers bear looking at.
2. This is a landmark paper -- a meta-analysis of 28 studies that analyzed for MAP in Crohn's patients and non-Crohn's controls (including some ulcerative colitis patients). IMO, this paper is one of many nails in the coffin of naysayers who doubt a MAP - Crohn's link. Figure 1: 16 of 18 studies that used PCR found odds ratios > 1, meaning MAP more likely to be detected in Crohn's patients than controls. Overall odds ratio of 7 (7x more likely to detect MAP in Crohn's than non-Crohn's patients, and that average ratio includes the two studies w/ OR's < 1). Figure 2 shows ELISA-based studies (a different technique that's quicker & cheaper to get results, but less sensitive). A little less compelling than the PCR studies, but still the average odds ratio is 1.72 (almost twice as likely to detect MAP in Crohn's versus non-Crohn's controls). This meta-analysis is a major piece of work. Anyone doubting the MAP-Crohn's link is ignoring a mountain of evidence. Whether it's causative or not is not addressed by the paper.
3. Another landmark paper on the genetic predisposition of Crohn’s, and the overlap between Crohn’s predisposition and predisposition to mycobacterial infections (of which mycobacterium avium paratuberculosis is one key example).
4. Borody has published numerous papers on treatment of Crohn’s via anti-MAP therapy.
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