Cannabinoids Relieve Colitis Symptoms


Colitis is a term used to describe inflammation of the colon.  There are a variety of causes of colitis including infections, poor blood supply, and autoimmune reactions.
The colon is located in the abdominal cavity and is divided into the following parts:  the cecum, the ascending colon, the transverse, the descending colon, the sigmoid, the rectum, and the anus.  The right colon includes the cecum and ascending colon.  The left colon includes the transverse segment to the sigmoid.
The colon (large bowel or large intestine) is responsible for collecting and storing the waste products of digestion.  A long muscular tube pushes undigested food towards the anus for eventual elimination as a bowel movement.  Food is digested in the stomach into liquid slurry that passes through the small intestine where the nutrients are absorbed into the body for use.  When the liquid mixture enters the colon, it mixes with mucus and normal bacteria that reside in the colon.  The wall of the colon has numerous layers.  A smooth muscle layer wraps the outside and is responsible for squeezing the undigested food through the length of the colon.  The inner layer, or mucosa, meets the fluid and allows the absorption of water and electrolytes, which help to solidify the feces (poop).  The mucosal layer is where the colon inflammation occurs and is responsible for the symptoms of colitis.

As with any other organ, the colon has a blood supply with arteries delivering oxygen rich blood and nutrients to it, and veins that drain carbon dioxide and lactic acid from it.  Diseases that decrease blood supply can cause inflammation of the colon. 

What are the symptoms of colitis?

Inflammation of the colon causes the muscle layers to go into intermittent spasm and cause cramp-like pain, which is pain that comes and goes.  The pain usually is in the lower abdomen.  Since the muscles fail to contract in a normal pattern and the colonic contents move through the colon rapidly, there is little opportunity for water to be reabsorbed.  This leads to watery diarrhea.  If the lining of the colon is inflamed and breaks down, bleeding may occur.
With colitis, particularly colitis involving the distal colon (rectum and sigmoid colon), the pain often crescendos and precedes a diarrheal bowel movement.  After the bowel movement, the pain may relent but then returns with the next episode of pain.
Depending upon the cause of the colitis, fever, and possibly malaise may or may not be present.

The signs and symptoms of colitis are quite variable and dependent on the etiology (or cause) of the given colitis and factors that modify its course and severity.
Symptoms of colitis may include abdominal pain, loss of appetite, fatigue, diarrhea, cramping, urgency and bloating.
Signs may include:  abdominal tenderness, weight loss, changes in bowel habits (increased frequency), fever, bleeding (overt or occult)/bloody stools, diarrhea and distension.
Signs seen on colonoscopy include colonic mucosal erythema (redness of the inner surface of the colon), ulcers, bleeding.


There are many types of colitis.  They are usually classified by the etiology.
Infectious Colitis
Viruses and bacteria can cause colon infections.  Most are food-borne illnesses or "food poisoning.”  Common bacterial causes include Shigella, E Coli, Salmonella and Campylobacter.  These infections may cause bloody diarrhea and can result in significant dehydration.

Parasites such as giardia can cause significant diarrhea.  The parasite can enter the body when infected water is swallowed.  The source may be from recreational water such as rivers, lakes, and swimming pools.  It may also be contaminated from a water well or cistern.
Pseudo membranous colitis is caused by the bacteria Clostridium difficile (C. difficile).  This disorder often seen in patients who have recently been taking antibiotics for an infection.  The antibiotic alters the normal bacteria present in the colon and allows an overgrowth of the Clostridium bacteria.  Clostridium bacteria produce a toxin that causes diarrhea.  This is an infection, and often there is a fever present.  The diarrhea is usually not bloody.

Ischemic Colitis

The arteries that supply blood to the colon are like any other artery in the body.  They have the potential to become narrow due to atherosclerosis (just as if blood vessels in the heart, which can cause angina, or narrowed vessels in the brain can cause a stroke).  When these arteries become narrow, the colon may lose its blood supply and become inflamed.
The colon can also lose its blood supply for mechanical reasons.  A couple of examples include volvulus, where the bowel twists on itself, or an incarcerated hernia, where a portion of the colon gets trapped in an out pouching of the abdominal wall, which prevents blood from flowing to the affected portion.
In individuals who are at risk for decreased blood flow to the colon, ischemic colitis can occur if the blood pressure falls.  This may occur with dehydration, anemia, or shock.
Ischemia or lack of blood supply causes significant pain, fever, and bloody bowel movements.

Inflammatory Bowel Disease

There are two types of inflammatory bowel disease, ulcerative colitis, and Crohn's disease.
Ulcerative colitis is thought to be an autoimmune illness in which the body's immune system attacks the colon and causes inflammation.  Ulcerative colitis begins in the rectum and may gradually spread throughout the colon.  The signs and symptoms include abdominal pain and bloody bowel movements.
Crohn's disease may involve any part of the digestive tract from the esophagus and stomach, through to the small and large intestine all the way to the rectum.  It often has skip lesions, that is diseased areas are interspersed with healthy areas of tissue.

Microscopic Colitis

Two diseases make up this group of colon inflammation, collagenous colitis and lymphocytic.  In these diseases, the inflammation is caused when the colon wall becomes engorged with either collagen or lymphocytes.  Watery, non-bloody diarrhea is the most common symptom.
This uncommon illness is seen more frequently in older women.  The cause is unknown but an autoimmune potential may exist.

Chemical Colitis

If chemicals are instilled into the colon, inflammation and damage can occur.  One of the complications of an enema is inflammation of the mucosal lining of the colon caused by harsh chemicals.

The treatment of colitis depends on the cause.

Often the initial treatment no matter what the cause of colitis is to rehydrate the patient and assist with the control of pain.  Rehydration may occur by mouth; however, in patients who cannot tolerate fluids orally, are too dehydrated, or have severe electrolyte abnormalities, intravenous fluids may be required.


How a given colitis is treated is dependent on its etiology, e.g., infectious colitis' are usually treated with antimicrobial agents (e.g. antibiotics); autoimmune mediated colitis is treated with immune modulators/immune suppressants.  Severe colitis can be life threatening and may require surgery.

Severity of colitis

Fulminant colitis is any colitis that becomes worse rapidly.  In addition to the diarrhea, fever, and anemia seen in colitis, the patient has severe abdominal pain and presents a clinical picture similar to that of septicemia, where shock is present.  About half of human patients require surgery.  In horses, the fulminant colitis known as colitis X usually results in death within 24 hours.
Irritable bowel syndrome, a separate disease, has been called spastic colitis.  This name may lead to confusion, since colitis is not always a feature of irritable bowel syndrome.  Since the etiology of IBS is currently unknown and possibly multifactorial, there may be some overlap in symptoms between IBS and the various forms of colitis.


Infectious colitis.
A well-known subtype of infectious colitis is pseudomembranous colitis, which results from infection by a toxigenic (produces toxins) strain of Clostridium difficile
Enterohemorrhagic colitis may be caused by Shiga toxin in Shigella dysenteriae or Shigatoxigenic group of Escherichia coli (STEC), which includes serotype O157:H7 and other enterohemorrhagic E. coli.
Parasitic infections, like those caused by Entamoeba histolytica, can also cause colitis.

Unclassifiable Colitis

Indeterminate colitis is a term used for a colitis that has features of both Crohn's disease and ulcerative colitis.  Indeterminate colitis' behavior is usually closer to ulcerative colitis than Crohn's disease.
Atypical colitis is a phrase that is occasionally used by physicians for a colitis that does not conform to criteria for accepted types of colitis.  It is not an accepted diagnosis as such, a colitis that cannot be definitively classified.

Call your health care provider if you have symptoms such as:

  • Abdominal pain that does not get better
  • Blood in the stool or stools that look black
  • Diarrhea or vomiting that does not go away
  • Swollen (distended) abdomen

What is the prognosis for a patient with colitis?

Patients with infectious diarrhea tend to get better relatively quickly with supportive care.  Most infections will resolve with or without specific treatment such as antibiotics.
Patients with inflammatory bowel disease probably will require lifelong treatment to help control their symptoms.  The goal (as with any long-term illness) is to allow the patient to live a normal life with minimal symptoms from the disease.

Patients with ischemic colitis need to minimize their risk factors for progressive narrowing of the arteries.  These are the same risks as for heart disease, including controlling high blood pressure, diabetes, and high cholesterol;   and stopping smoking.  Patients with severe ischemia that leads to dead (gangrenous) colon require surgery to remove the gangrenous segment.

Cannabis Studies:

Cannabidiol, a safe and non-psychotropic ingredient of the marijuana plant Cannabis sativa, is protective in a murine model of colitis.
Borrelli F, Aviello G, Romano B, Orlando P, Capasso R, Maiello F, Guadagno F,Petrosino S, Capasso F, Di Marzo V, Izzo AA.
Department of Experimental Pharmacology, University of Naples Federico II, via D Montesano 49, 80131 Naples, Italy.

Inflammatory bowel disease affects millions of individuals, PHARMACOLOGICAL TREATMENT IS DISAPPOINTINGLY UNSATISFACTORY.  Cannabidiol, a safe and non-psychotropic ingredient of marijuana, exerts pharmacological effects (e.g., antioxidant) and mechanisms (e.g., inhibition of endocannabinoids enzymatic degradation) potentially beneficial for the inflamed gut.  Thus, we investigated the effect of cannabidiol in a murine model of colitis.  Colitis was induced in mice by intracolonic administration of dinitrobenzene sulfonic acid.  Inflammation was assessed both macroscopically and histologically.  In the inflamed colon, cyclooxygenase-2 and inducible nitric oxide synthase (iNOS) were evaluated by Western blot, interleukin-1beta and interleukin-10 by ELISA, and endocannabinoids by isotope dilution liquid chromatography-mass spectrometry.  Human colon adenocarcinoma (Caco-2) cells were used to evaluate the effect of cannabidiol on oxidative stress.  Cannabidiol reduced colon injury, inducible iNOS (but not cyclooxygenase-2) expression, and interleukin-1beta, interleukin-10, and endocannabinoid changes associated with 2, 4, 6-dinitrobenzene sulfonic acid administration.  In Caco-2 cells, cannabidiol reduced reactive oxygen species production and lipid peroxidation.  In conclusion, cannabidiol, a likely safe compound, prevents experimental colitis in mice.

Cannabinoids are known to reduce intestinal inflammation.  Atypical cannabinoids produce pharmacological effects via unidentified targets.  We were interested in whether the atypical cannabinoid O-1602, reportedly an agonist of the putative cannabinoid receptor GPR55, reduces disease severity of dextran sulfate sodium (DSS) and trinitrobenzene sulfonic acid (TNBS)-induced colitis in C57BL/6N and CD1 mice.
Our data demonstrate that O-1602 is protective against experimentally induced colitis and inhibits neutrophil recruitment independently of CB1, CB2, and GPR55 receptors.  Thus, atypical cannabinoids represent a novel class of therapeutics that may be useful for the treatment of inflammatory bowel diseases.  (Inflame Bowel Dis 2010 ;)
Potential of cannabinoids to modulate the inflammatory response in colitis
Violeta Zaric, 1Brandon Busbee, 1Prakash Nagarkatti, 1 and Mitzi Nagarkatti1
1Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC

Recent studies have suggested the role for cannabinoid (CB) type 1 and CB2 receptors in modulating gastrointestinal inflammation in animal models of experimental colitis.  Our preliminary studies using delta-9-tetrahydrocannabinol (THC) showed promising results in a 2, 4, 6-trinitrobenzene sulfonic acid TNBS-induced colitis.  50mg/kg body weight of TNBS/ethanol was administered in 10 female BALB/c mice.  Each group received intraperitoneal injections of vehicle or THC (10 mg/kg) once every other day.  At day six, mice were sacrificed and cells from spleen and MLN were analyzed for the expression of surface markers for T-cells, myeloid-derived suppressor cells (MDSC) and regulatory T-cells (Treg) by flow cytometry.  The body weight increased in TNBS-treated mice administered THC when compared to vehicle.  THC improved the survival up to 60% of mice in TNBS-induced colitis when compared to vehicle treated mice (30%).  In the spleen and MLN, the ratio of T-cells is lower in THC-treated mice compared to vehicle-treated group whereas the ratio of Treg is increased in THC-treated mice.  THC also reduced the ratio of MDSCs in TNBS-treated mice.  THC treatment ameliorated colitis by modulating the immune response towards Treg and altering the T-cells and their subsets.  Future experiments will address the potential of other cannabinoids in modulating the inflammatory response in colitis THC-treated mice.  THC also reduced the ratio of MDSCs in TNBS-treated mice.  THC treatment ameliorated colitis by modulating the immune response towards Treg and altering the T-cells and their subsets. 
THC treatment ameliorated colitis by modulating the immune response towards Treg and altering the T-cells and their subsets. 

The atypical cannabinoid O-1602 protects against experimental colitis and inhibits neutrophil recruitment.

Cannabidiol may represent a good candidate to normalize motility in patients with inflammatory bowel disease.”

Researchers investigating anecdotal evidence that cannabis relieves some of the symptoms of inflammatory bowel disease (IBD) have discovered a potential new target for cannabis-derived drugs for treatment of the disease.

Cannabis Helps Ulcers and Crohn’s Disease
“Researchers claim that cannabis may help combat problems such as intestinal ulcers and Crohn’s disease”.

In the Human Colon:  Cannabinoids Promote Epithelial Wound Healing
“CB1 receptors are expressed in normal human colon and colonic epithelium is responsive biochemically and functionally to cannabinoids.  Increased epithelial CB2-receptor expression in human inflammatory bowel disease tissue implies an immunomodulatory role that may impact on mucosal immunity.”
Mayo Study:  Marijuana’s THC Reduces Stomach Cramping
“THC may relax the colon and reduce stomach cramping after eating, according to a study presented at the 71st Annual Scientific Meeting of the American College of Gastroenterology.  The study compared the effects of dronabinol (THC) and placebo on colonic motility and sensation in healthy adults.”
Cannabinoids are known to reduce intestinal inflammation.  Activation of cannabinoid 2 receptor (CB2) protects against experimental colitis.”  Inflammatory bowel diseases.  15.11 (2009): 1678-85.

Cannabis helps combat cramping that accompanies many GI disorders because cannabinoids relax contractions of the smooth muscle of the intestines. Research shows that the body’s own cannabinoids, known as anandamides, affect neurological systems that control the gastrointestinal system. External and internal cannabinoids strongly control gastrointestinal motility and inflammation. They also have the ability to decrease gastrointestinal fluid secretion and inflammation. This means that cannabis can be useful to stop ulcers and other syndromes.

The chronic pain and spasms that accompany many gastrointestinal disorders are a life hindrance to those who suffer from IBS and other diseases. Medical cannabis is a very effective pain reliever. It blocks spinal, peripheral and gastrointestinal mechanisms that promote pain in IBS and related disorders. It also can be used against gastroesophageal reflux disease (acid reflux). When acid reflux occurs, gastric acids attack the esophagus. The pharmaceutical medicines that doctors prescribe for this condition are in some ways as bad as the condition itself. They prescribe drugs like atropine, for example, which have severe side-effects.

Cannabis is also an adaptogenic immune system modulator that can increase or decrease immune systems function in ways that almost always contribute to healthier outcomes. Studies indicate that cannabinoids in marijuana bind with cannabinoid receptors in the digestive tract, especially the small and large intestine, causing muscle relaxation, reduction of inflammation, analgesia, increased nerve-muscle coordination, anti-emesis, and relief of spasms such as those that cause nausea. 

Pharmaceutical drugs commonly prescribed to combat GI disorders include:  all come with substantial side effects!

  • Megestrol acetate (Megace), an anticachectic. This substance can cause high blood pressure, diabetes, inflammation of the blood vessels, congestive heart failure, seizures, and pneumonia. Less serious side effects of this medicine include diarrhea, flatulence, nausea, vomiting, constipation, heartburn, dry mouth, increased salivation, and thrush; impotence, decreased libido, urinary frequency, urinary incontinence, urinary tract infection, vaginal bleeding and discharge; disease of the heart, palpitation, chest pain, chest pressure, and edema; pharyngitis, lung disorders, and rapid breathing; insomnia, headache, weakness, numbness, seizures, depression, and abnormal thinking.
  • Metronidazole (Flagyl) is carcinogenic. Patients treated with Metronidazole have reported convulsive seizures and peripheral neuropathy. Ironically, this medicine causes problems in the gastrointestinal tract; nausea is reported by about 12% of patients, and is sometimes accompanied by headache, anorexia, and occasionally vomiting; diarrhea; epigastric distress, and abdominal cramping. Constipation has also been reported.
  • Sulfasalazine (Azulfidine) -Common adverse reactions associated with sulfasalazine are anorexia, headache, nausea, vomiting, gastric distress, and apparently reversible oligospermia. These occur in about one-third of the patients. Less frequent adverse reactions are pruritus, urticaria, fever, Heinz body anemia, hemolytic anemia and cyanosis, which may occur at a frequency of one in every thirty patients or less.
  • Chlordiazepoxide/Clidinium (Librax) - Drowsiness, ataxia and confusion have been reported in some patients, particularly the elderly and debilitated. Adverse effects reported with use of Librax are those typical of anticholinergic agents, i.e., dryness of the mouth, blurring of vision, urinary hesitancy and constipation. Withdrawal symptoms, similar in character to those noted with barbiturates and alcohol (convulsions, tremor, abdominal and muscle cramps, vomiting and sweating), have occurred following abrupt discontinuance of chlordiazepoxide. Hyoscyamine Sulfate (Levsin) - Adverse reactions may include dryness of the mouth; urinary hesitancy and retention; blurred vision; tachycardia; palpitations; mydriasis; cycloplegia; increased ocular tension; loss of taste; headache; nervousness; drowsiness; weakness; dizziness; insomnia; nausea; vomiting; impotence; suppression of lactation; constipation; bloated feeling; allergic reactions or drug idiosyncrasies; urticaria and other dermal manifestations; ataxia; speech disturbance; some degree of mental confusion and/or excitement (especially in elderly persons); and decreased sweating.
  • Mesalamine CR (Pentasa) - Common side effects are diarrhea, headache, nausea, abdominal pain, dyspepsia, vomiting, and rash
  • Phosphorated carbohydrate (Emetrol) - Side effects include: fainting; swelling of face, arms, and legs; unusual bleeding; vomiting; weight loss; yellow eyes or skin. Less common-more common with large doses: Diarrhea; stomach or abdominal pain.
  • Dicyclomine (Bentyl) - Can cause blurred vision, dry mouth, heart problems, seizures, impotence, and difficulty in urinating, among other effects.
  • Ciprofloxacin (Cipro) - The most frequent side effects include nausea, vomiting, diarrhea, abdominal pain, rash, headache, and restlessness. Rare allergic reactions have been described, such as hives and anaphylaxis (shock). Methotrexate (Rheumatrex, Trexall) – Is very toxic, depending on dose. The most frequent reactions include mouth sores, stomach upset, and low white blood counts. Methotrexate can cause severe toxicity of the liver and bone marrow, which require regular monitoring with blood testing. It can cause headache and drowsiness, which may resolve if the dose is lowered. Methotrexate can cause itching, skin rash, dizziness, and hair loss.
  • Diphenoxylate and atropine (Lotomil) - Bad effects include drowsiness, dizziness, and headache, nausea or vomiting, and dry mouth. Euphoria, depression, lethargy, restlessness, numbness of extremities, loss of appetite, and abdominal pain or discomfort has been reported less frequently. Although the dose of atropine in Lomotil is too low to cause side effects when taken in the recommended doses, side effects of atropine (including dryness of the skin and mucous membranes, increased heart rate, urinary retention, and increased body temperature) have been reported, particularly in children under 2.
  • Prednisone (Delatasone). This is a steroid drug that can have serious adverse musculoskeletal, gastrointestinal, dermatologic, neurological, endocrine, and ophthalmic side effects. These include: congestive heart failure in susceptible patients, potassium loss, hypokalemic alkalosis, sodium retention, and hypertension. Muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, tendon rupture, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fracture of long bones. Peptic ulcer with possible perforation and hemorrhage; pancreatitis; abdominal distention; ulcerative esophagitis. Impaired wound healing, thin fragile skin, petechiae and ecchymoses, facial erythema. Increased intracranial pressure, usually after treatment, convulsions, vertigo, and headache. Menstrual irregularities; development of Cushingoid state; secondary adrenocortical and pituitary unresponsiveness; decreased carbohydrate tolerance; manifestations of latent diabetes mellitus. Posterior subcapsular cataracts, increased intraocular pressure, glaucoma, and exophthalmos.

Recommendation:  Indica dominant hybrid (high CBD levels).

Dynamite, Aunti Em, Blue Fruit, Strawberry Cough, Michael Phelps, Gran Daddy Purple

Vaporization, Extracts  (under the tongue).

Oral administration is absorbed more slowly and it goes through the liver (lasts longer).  Systemically administered (smoking or vaporizing) enters the system quicker.  Better to vaporize for spasms.


Grotenhermen, Franjo. 2001. Practical hints. In Cannabis and Cannabinoids: Pharmacology, toxicology and therapeutic potential, edited by F. Grotenhermen and E. Russo. Binghamton, NY: Haworth Press.
Iversen, Leslie L. 2000. The science of marijuana. Oxford ; New York: Oxford University Press.
McPartland, J. M., and P. L. Pruitt. 1999. Side effects of pharmaceuticals not elicited by comparable herbal medicines: the case of tetrahydrocannabinol and marijuana. Altern Ther Health Med 5 (4):57-62.
McPartland, John M., and Vito Mediavilla. 2001. Non-cannabinoids in cannabis. In Cannabis and cannabinoids, edited by F. Grotenhermen and E. B. Russo. Binghamton, NY: Haworth Press
1. a b Ulcerative colitis at eMedicine
2. Orholm M, Binder V, Sørensen TI, Rasmussen LP, Kyvik KO (2000). "Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study". Scand. J. Gastroenterol. 35 (10): 1075–81. doi:10.1080/003655200451207. PMID 11099061.
3. Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B (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): 990–996. doi:10.1136/gut.29.7.990. PMC 1433769.PMID 3396969.
4. a b c Baumgart DC, Carding SR (2007). "Inflammatory bowel disease: cause and immunobiology". The Lancet 369 (9573): 1627–1640.doi:10.1016/S0140-6736(07)60750-8. PMID 17499605.
5. Cho JH, Nicolae DL, Ramos R, et al. (2000). "Linkage and linkage disequilibrium in chromosome band 1p36 in American Chaldeans with inflammatory bowel disease". Hum. Mol. Genet. 9 (9): 1425–32. doi:10.1093/hmg/9.9.1425. PMID 10814724.
6. Järnerot G, Järnmark I, Nilsson K (1983). "Consumption of refined sugar by patients with Crohn's disease, ulcerative colitis, or irritable bowel syndrome". Scand. J. Gastroenterol. 18 (8): 999–1002. doi:10.3109/00365528309181832. PMID 6673083.
7. Corrao G, Tragnone A, Caprilli R, et al. (1998). "Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC)". Int J Epidemiol 27 (3): 397–404. doi:10.1093/ije/27.3.397. PMID 9698126.
8. Voreacos, David (2007-05-29). "Roche Found Liable in First Of 400 Suits Over Accutane". Washington Post. Retrieved 2010-05-26.
9. Reddy D, Siegel CA, Sands BE, Kane S (2006). "Possible association between isotretinoin and inflammatory bowel disease". Am. J. Gastroenterol.101 (7): 1569–73. doi:10.1111/j.1572-0241.2006.00632.x. PMID 16863562.
10. Borobio E, Arín A, Valcayo A, Iñarrairaegui M, Nantes O, Prieto C (2004). "[Isotretinoin and ulcerous colitis]" (in Spanish; Castilian). An Sist Sanit Navar 27 (2): 241–3. PMID 15381956.
11. Reniers DE, Howard JM (2001). "Isotretinoin-induced inflammatory bowel disease in an adolescent". Ann Pharmacother 35 (10): 1214–6.doi:10.1345/aph.10368. PMID 11675849.
12. Heather WonTesoriero (2008-04-23). "Jury Awards $10.5 Million Over Accutane". Wall St Journal.
13. Baumgart DC, Sandborn WJ (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.
14. a b Fauci et al. Harrison's Internal Medicine, 17th ed. New York: McGraw-Hill Medical, 2008. ISBN 0071599916
15. a b c d e f g Kornbluth A, Sachar DB (2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee". Am. J. Gastroenterol. 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x. PMID 15233681.[dead link]
16. a b Roediger WE, Moore J, Babidge W (1997). "Colonic sulfide in pathogenesis and treatment of ulcerative colitis". Dig. Dis. Sci. 42 (8): 1571–9.doi:10.1023/A:1018851723920. PMID 9286219.
17. Levine J, Ellis CJ, Furne JK, Springfield J, Levitt MD (1998). "Fecal hydrogen sulfide production in ulcerative colitis". Am. J. Gastroenterol. 93 (1): 83–7. doi:10.1111/j.1572-0241.1998.083_c.x. PMID 9448181.
18. a b c d Kornbluth, Asher; David B. Sachar (July 2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee" (PDF). American Journal of Gastroenterology 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x. PMID 15233681. Archived from the original on April 6, 2008. Retrieved 2009-11-07.
19. Crohn's Disease Overview
20. 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. doi:10.1053/j.gastro.2007.03.104. PMID 17570211.
21. a b Hanauer SB; Hanauer, Stephen B. (1996). "Inflammatory bowel disease". N. Engl. J. Med. 334 (13): 841–8.doi:10.1056/NEJM199603283341307. PMID 8596552.
22. a b Podolsky DK (2002). "Inflammatory bowel disease". N. Engl. J. Med. 347 (6): 417–29. doi:10.1056/NEJMra020831. PMID 12167685.
23. Shivananda S, Lennard-Jones J, Logan R, et al. (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.
24. Sonnenberg A, McCarty DJ, Jacobsen SJ (January 1991). "Geographic variation of inflammatory bowel disease within the United States".Gastroenterology 100 (1): 143–9. PMID 1983816.
25. NEJM 2001;344:808.
26. NEJM 1987;316:707.
27. a b c d e f > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
28. a b c d Hanauer, Stephen B.; William Sandborn (2001-03-01). "Management of Crohn's disease in adults" (PDF). American Journal of Gastroenterology 96 (3): 635–43. doi:10.1111/j.1572-0241.2001.03671.x. PMID 11280528. Retrieved 2009-11-07.
29. Broomé, Ulrika; Annika Bergquist (February 2006). "Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer". Seminars in Liver Disease 26 (1): 31–41. doi:10.1055/s-2006-933561. PMID 16496231.
30. 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.
31. 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.
32. Prevalence defined as at least 5 health care contacts in a 10 year period for the condition, according to: Greenstein, AJ; Janowitz, HD; Sachar, DB (1976). "The extra-intestinal complications of Crohn's disease and ulcerative colitis: a study of 700 patients". Medicine 55 (5): 401–12.PMID 957999. edit
33. Leighton JA, Shen B, Baron TH, et al. (2006). "ASGE guideline: endoscopy in the diagnosis and treatment of inflammatory bowel disease".Gastrointest. Endosc. 63 (4): 558–65. doi:10.1016/j.gie.2006.02.005. PMID 16564852.
34. Olsson R, Danielsson A, Järnerot G, et al. (1991). "Prevalence of primary sclerosing cholangitis in patients with ulcerative colitis". Gastroenterology100 (5 Pt 1): 1319–23. PMID 2013375.
35. Page 481 in: Colonic diseases. By Timothy R. Koch. 2003. ISBN 0896039617, 9780896039612
36. S. Kane (2006). "Asacol - A Review Focusing on Ulcerative Colitis".
37. "Millennium Resumes Clinical Program For MLN0002". 18 May 2007. Retrieved 5 February 2010.
38. 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.
39. Feller, M.; Huwiler, K.; Schoepfer, A.; Shang, A.; Furrer, H.; Egger, M. (2010). "Long-term antibiotic treatment for Crohn's disease: systematic review and meta-analysis of placebo-controlled trials". Clinical Infectious Diseases 50 (4): 473–480. doi:10.1086/649923. PMID 20067425. edit
40. [1] Section "Antibiotics and Ulcerative Colitis" in: Prantera, C.; Scribano, M. (2009). "Antibiotics and probiotics in inflammatory bowel disease: why, when, and how". Current opinion in gastroenterology 25 (4): 329–333. doi:10.1097/MOG.0b013e32832b20bf. PMID 19444096. edit
41. Bensoussan M, Jovenin N, Garcia B, et al. (January 2006). "Complementary and alternative medicine use by patients with inflammatory bowel disease: results from a postal survey". Gastroenterol. Clin. Biol. 30 (1): 14–23. doi:10.1016/S0399-8320(06)73072-X. PMID 16514377.
42. Shah S (2007). "Dietary factors in the modulation of inflammatory bowel disease activity". MedGenMed 9 (1): 60. PMC 1925010.PMID 17435660.
43. Terry PD, Villinger F, Bubenik GA, Sitaraman SV (January 2009). "Melatonin and ulcerative colitis: evidence, biological mechanisms, and future research". Inflamm. Bowel Dis. 15 (1): 134–40. doi:10.1002/ibd.20527. PMID 18626968.
44. Calkins BM (1989). "A meta-analysis of the role of smoking in inflammatory bowel disease". Dig. Dis. Sci. 34 (12): 1841–54.doi:10.1007/BF01536701. PMID 2598752.
45. Lakatos PL, Szamosi T, Lakatos L (2007). "Smoking in inflammatory bowel diseases: good, bad or ugly?". World J Gastroenterol. 13 (46): 6134–9.doi:10.3748/wjg.13.6134. PMID 18069751.
46. cite paper |author=Dr M. Guslandi |title=Nicotine treatment for ulcerative colitis |journal= |volume= |issue= |pages= |year= |pmid= |doi= |url=
47. cite paper |author=Sandborn WJ, Tremaine WJ, Offord KP, Lawson GM, Petersen BT, Batts KP, Croghan IT, Dale LC, Schroeder DR, Hurt RD |title=Transdermal nicotine for mildly to moderately active ulcerative colitis |journal= |volume= |issue= |pages= |year= |pmid= |doi= |url=
48. Akhtar MS, Munir M (1989). "Evaluation of the gastric anti-ulcerogenic effects of Solanum nigrum, Brassica oleracea and Ocimum basilicum in rats.". Journal of ethnopharmacology 27 (1-2): 163–76. doi:10.1016/0378-8741(89)90088-3. PMID 2515396. "Brassica oleracea (leaf) powder did not affect the ulcer index significantly but its aqueous extract lowered the index and increased hexosamine levels, suggesting gastric mucosal protection.".
49. "Omega-3 fatty acids, fish oil, alpha-linolenic acid". MedlinePlus Herbs and Supplements.
50. Brzezinski A, Rankin G, Seidner D, Lashner B (1995). "Use of old and new oral 5-aminosalicylic acid formulations in inflammatory bowel disease.".Cleve Clin J Med 62 (5): 317–23. PMID 7586488.
51. Salim A (1992). "Role of sulphydryl-containing agents in the management of recurrent attacks of ulcerative colitis. A new approach.". Pharmacology45 (6): 307–18. doi:10.1159/000139016. PMID 1362613.
52. Gupta, I.; Parihar, A.; Malhotra, P.; Singh, G.; Lüdtke, R.; Safayhi, H.; Ammon, H. (1997). "Effects of Boswellia serrata gum resin in patients with ulcerative colitis". European journal of medical research 2 (1): 37–43. PMID 9049593. edit
53. Bibiloni R, Fedorak RN, Tannock GW, et al. (2005). "VSL#3 probiotic-mixture induces remission in patients with active ulcerative colitis". Am. J. Gastroenterol. 100 (7): 1539–46. doi:10.1111/j.1572-0241.2005.41794.x. PMID 15984978. VSL#3 company site
54. Borody TJ, Warren EF, Leis SM, Surace R, Ashman O, Siarakas S (2004). "Bacteriotherapy using fecal flora: toying with human motions". J. Clin. Gastroenterol. 38 (6): 475–83. doi:10.1097/01.mcg.0000128988.13808.dc. PMID 15220681. Fulltext(PDF)
55. Borody TJ, Warren EF, Leis S, Surace R, Ashman O (2003). "Treatment of ulcerative colitis using fecal bacteriotherapy". J. Clin. Gastroenterol. 37(1): 42–7. doi:10.1097/00004836-200307000-00012. PMID 12811208. Fulltext(PDF)
56. {cite journal |author= MICHAEL S. SILVERMAN,*,‡ IAN DAVIS,§ and DYLAN R. PILLAI*|title= Success of Self-Administered Home Fecal Transplantation for Chronic Clostridium difficile Infection |journal=CLIN GASTROENTEROLOGY AND HEPATOLOGY| volume=8 |issue=5 |pages=471–473 |year=2010 | pmid=20117243 |doi=doi:10.1016
57. Summers RW, Elliott DE, Urban JF, Thompson RA, Weinstock JV (2005). "Trichuris suis therapy for active ulcerative colitis: a randomized controlled trial". Gastroenterology 128 (4): 825–32. doi:10.1053/j.gastro.2005.01.005. PMID 15825065.
Ulcerative colitis at the Open Directory Project
National Digestive Diseases Information Clearinghouse

George F Longstreth, MD, Department of Gastroenterology, Kaiser Permanente Medical Care Program San Diego, California. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

Traffic Roots Pixel