Ulcerative Colitis Treatment

Standard treatment for ulcerative colitis depends on ''extent of involvement'' and disease ''severity''. The goal is to induce remission initially with medications, followed by the administration of maintenance medications to prevent a relapse of the disease. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing a remission which involves relief of symptoms and mucosal healing of the lining of the colon and then longer term treatment to maintain the remission.

Drugs used

Aminosalicylates

Sulfasalazine has been a major agent in the therapy of mild to moderate UC for over 50 years. In 1977 Mastan S.Kalsi et al. determined that 5-aminosalicylic acid (5-ASA and mesalazine) was the therapeutically active compound in sulfasalazine. Since then many 5-ASA compounds have been developed with the aim of maintaining efficacy but reducing the common side effects associated with the sulfapyridine moiety in sulfasalazine.

Mesalazine, also known as 5-aminosalicylic acid, mesalamine, or 5-ASA. Brand name formulations include Asacol, Pentasa, Mezavant, Lialda, and Salofalk.
Sulfasalazine, also known as Azulfidine.
Balsalazide, also known as Colazal or Colazide (UK).
Olsalazine, also known as Dipentum.

Corticosteroids

Cortisone
Prednisone
Prednisolone
Cortifoam
Hydrocortisone
Methylprednisolone
Beclometasone
Budesonide - under the brand name of Entocort

Immunosuppressive drugs

Mercaptopurine, also known as 6-Mercaptopurine, 6-MP and Purinethol.
Azathioprine, also known as Imuran, Azasan or Azamun, which metabolises to 6-MP.
Methotrexate, which inhibits folic acid
Tacrolimus

Biological treatment

Infliximab
Visilizumab

Low Molecular Weight Heparin (LMWH) e.g. clexane is used in acute management of the flare of UC.

Surgery

Unlike Crohn's disease, ulcerative colitis can generally be cured by surgical removal of the large intestine. This procedure is necessary in the event of: exsanguinating hemorrhage, frank perforation or documented or strongly suspected carcinoma. Surgery is also indicated for patients with severe colitis or toxic megacolon. Patients with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life.

Ulcerative colitis is a disease that affects many parts of the body outside the intestinal tract. In rare cases the extra-intestinal manifestations of the disease may require removal of the colon. A variety of dietary treatments show promise, but they require further research before they can be recommended.

In vitro research, animal evidence, and limited human study suggest that melatonin may be beneficial.

Smoking

Unlike Crohn's disease, ulcerative colitis has a lesser prevalence in smokers than non-smokers. Nonetheless, the risks of smoking contraindicate using cigarettes as a treatment for ulcerative colitis. Patients who choose to use smoking as a treatment should give serious consideration to the links between smoking cessation and the onset or relapse of ulcerative colitis.

Dietary modification

Dietary fibre, meaning indigestible plant matter, has been recommended for decades in the maintenance of bowel function. Of peculiar note is fibre from brassica, which seems to contain soluble constituents capable of reversing ulcers along the entire human digestive tract before it is cooked. Oatmeal is also commonly prescribed.

Fats and oils

Fish oil. Eicosapentaenoic acid (EPA), derived from fish oil. This is an Eicosanoid that inhibits leukotriene activity, the latter which may be a key factor of inflammation. As an IBD therapy, there are no conclusive studies in support and no recommended dosage. But dosages of EPA between 180 to 1500 mg/day are recommended for other conditions, most commonly cardiac.
Short chain fatty acid (butyrate) enema. The colon utilizes butyrate from the contents of the intestine as an energy source. The amount of butyrate available decreases toward the rectum. Inadequate butyrate levels in the lower intestine have been suggested as a contributing factor for the disease. This might be addressed through butyrate enemas. The results however are not conclusive.

Herbals

Herbal medications are used by patients with ulcerative colitis. Compounds that contain sulphydryl may have an effect in ulcerative colitis (under a similar hypothesis that the sulpha moiety of sulfasalazine may have activity in addition to the active 5-ASA component). One randomized control trial evaluated the over-the-counter medication methionine-methyl sulphonium chloride (abbreviated MMSC, but more commonly referred to as Vitamin U) and found a significant decreased rate of relapse when the medication was used in conjunction with oral sulfasalazine.

Bacterial recolonization

Probiotics may have benefit. One study which looked at a probiotic known as VSL#3 has shown promise for people with ulcerative colitis.

Fecal bacteriotherapy involves the infusion of human probiotics through fecal enemas. It suggests that the cause of ulcerative colitis may be a previous infection by a still unknown pathogen. This initial infection resolves itself naturally, but somehow causes an imbalance in the colonic bacterial flora, leading to a cycle of inflammation which can be broken by "recolonizing" the colon with bacteria from a healthy bowel. There have been several reported cases of patients who have remained in remission for up to 13 years.

Intestinal parasites

Inflammatory bowel disease is less common in the developing world. Some have suggested that this may be because intestinal parasites are more common in underdeveloped countries. Some parasites are able to reduce the immune response of the intestine, an adaptation that helps the parasite colonize the intestine. The decrease in immune response could reduce or eliminate the inflammatory bowel disease.

Helminthic therapy using the whipworm ''Trichuris suis'' has been shown in a randomized control trial from Iowa to show benefit in patients with ulcerative colitis. The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of patients in the developed world may lead to inflammation. Both helminthic therapy and fecal bacteriotherapy induce a characteristic Th2 white cell response in the diseased areas, which is somewhat paradoxical given that ulcerative colitis immunology was thought to classically involve Th2 overproduction.