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inflammation of the colon, or large intestineintestine,
muscular hoselike portion of the gastrointestinal tract extending from the lower end of the stomach (pylorus) to the anal opening. In humans this fairly narrow (about 1 in./2.
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. The term "colitis" may be used to refer to any of a number of disorders involving the colon. Symptoms include diarrhea (often with blood and mucus), abdominal pain, and fever.

Ulcerative colitis is a serious chronic inflammation and ulceration of the lining of the colon and rectum. Another form of colitis, called Crohn's disease, has similar signs and includes thickening of the intestinal wall. The disease typically occurs in the small intestine near the point where it joins the colon, but the colon and other parts of the gastrointestinal tract may be affected as well. The term "inflammatory bowel disease" has been used to refer to both ulcerative colitis and Crohn's disease, the causes of which are unknown. A less severe disorder, known as irritable bowel syndromeirritable bowel syndrome
(IBS), condition characterized by constipation, diarrhea, or alternating constipation and diarrhea in the absence of any disease process. It is usually accompanied by abdominal pain, especially in the lower left quadrant, bloating, and flatulence.
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, or IBS, was formerly called mucous colitis.

Colitis is sometimes caused by infections with viruses, parasites, or bacteria. For example, two distinct types of dysenterydysentery
, inflammation of the intestine characterized by the frequent passage of feces, usually with blood and mucus. The two most common causes of dysentery are infection with a bacillus (see bacteria) of the Shigella group, and infestation by an ameba,
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 are caused by amebas and bacteria. Infectious forms of colitis are often the result of poor hygienic practices. Prolonged use of antibiotics can also cause colitis, either by direct irritation of the colon or by killing bacteria that normally live in the intestine, allowing the toxin-producing bacterium Clostridium difficile to proliferate. Colitis is also sometimes caused by diverticulitis (see under diverticulosisdiverticulosis,
a disorder characterized by the presence of diverticula, which are small, usually multiple saclike protrusions through the wall of the colon (large intestine).
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) or by colon cancercolon cancer,
cancer of any part of the colon (often called the large intestine). Colon cancer is the second most common cancer diagnosed in the United States. Epidemiological evidence has shown that a diet high in fat and low in fruits, vegetables, and fiber contributes to the
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The Columbia Electronic Encyclopedia™ Copyright © 2013, Columbia University Press. Licensed from Columbia University Press. All rights reserved.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.



inflammation of the colon.

Colitis is one of the commonest diseases of the gastrointestinal tract. It may be caused by infection (dysentery bacilli, salmonellas, amoebas, balantidia), poor food habits, or poisoning (by mercury and other chemicals). It can result from uremic autointoxication or as an independent disease of autoimmune nature (for example, nonspecific ulcerative colitis); in addition, it can arise secondarily from digestive disorders of the stomach and small intestine (gastric achylia, pancreatitis, gastroenteritis). Depending on the cause and severity of the colitis, the changes in the colon may vary from superficial catarrh to necrotic-ulcerative inflammation.

Colitis may be either acute or chronic. Acute colitis is accompanied by general malaise, loss of appetite, spastic abdominal pains, diarrhea, and, sometimes (especially in dysentery), painful straining at stool (tenesmus). The temperature may rise in acute colitis of infectious origin. The feces are pulpy or liquid and mixed with mucus (in severe cases, with mucus and blood). Acute colitis may become chronic.

Chronic colitis is accompanied by loss of appetite, nausea, and general weakness. Dull or paroxysmal abdominal pains often appear before or after defecation. Stool disturbances generally appear as an alternation of constipation and diarrhea. There is a sensation that the abdomen will burst, accompanying borborygmus and copious gas formation. With diarrhea, stools may be passed three or four times a day; they are generally pulpy or liquid and, in severe cases, mixed with mucus and streaks of blood. In spastic colitis, the fecal matter takes the form of small hard lumps. The abdomen is somewhat distended and tender upon palpation along the colon (with spastic constriction). The diagnosis of colitis is confirmed by X-ray examination, proctosigmoidoscopy, and laboratory analysis of the fecal matter.

The treatment of acute colitis (and exacerbations of chronic colitis) involves a starvation or semistarvation diet for one or two days, followed by a mostly protein diet, if fermentative processes are predominant in the intestine, or a carbohydrate diet, if putrefactive processes are predominant. Thereafter, a special colitis diet is recommended (strained, steamed, nourishing foods, with the exception of fruits, vegetables, and fresh milk). Antimicrobial and antiparasitic preparations and preparations that normalize the intestinal flora are indicated for infectious colitis. Therapeutic enemas are prescribed to act on the mucosae in cases of inflammation of the rectum and sigmoid colon. Antispasmodic and cholinolytic agents are used for spasms. Physical therapy (thermal procedures) and sanatorium-health resort treatment (Essentuki, Zheleznovodsk, Piatigorsk, Borzhomi, Morshin) are prescribed for patients with chronic colitis. Surgery is sometimes performed in cases of severe ulcerative colitis. The prevention of gastrointestinal infections, the treatment of diseases of the alimentary canal, and proper diet are helpful in preventing the occurrence of the condition.


Men’shikov, F. K. Bolezni kishechnika. Moscow, 1962.
Bolezni organov pishchevareniia. Edited by S. M. Ryss. Leningrad, 1966.


The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.


Inflammation of the large bowel, or colon.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.


, colonitis
inflammation of the colon
Collins Discovery Encyclopedia, 1st edition © HarperCollins Publishers 2005
References in periodicals archive ?
Colitic groups had a lower body weight compared to control rats (P < 0.01) at day 2 but there is no difference among colitic groups (Figure 1(b)).
It indicates the presence of a higher number of granulocytes in the intestine of colitic males compared to females.
Mice were assigned to different experimental groups (n = 6): a non-colitic group and five DNBS colitic groups, including an untreated group, three that received AFC treatment (25, 50, or 100 mg/kg), and the remaining administered with dexamethasone (2.4 mg/kg); all treatments were dissolved in 0.2 ml of phosphate buffer saline (PBS).
Resveratrol attenuated colitic inflammation in IL-[10.sup.-/-] mice by down-regulating Th1 responses (Singh et al.
Hypermethylation of p14 (ARF) may be predictive of colitic cancer in patients with ulcerative colitis.
Our study revealed reduced colonic levels of active TGF-[beta]1 in colitic [Eng.sup.+/-] mice, associated with lower expression of thrombospondin-1 (TSP-1), an angiostatic factor capable of activating TGF-[beta]1 [beta]1 [26].
Villous dysplasia: an ominous histologic sign in colitic patients.
The signs of diarrhoea were detected in 80% of the colitic animals (Table 1).
Gln supplementation had no influence on blood leukocyte or MLN lymphocyte populations in normal or colitic mice (Table 2).
They state that "the interpretation of the microscopic findings was based on previously published definitions" and they refer to an article by Riddell et al6 that was published in 1983 and dealt not with Barrett mucosa, including dysplasias, but with colitis, mainly ulcerative colitis and colitic dysplasias.
Raine et al., "Cutting edge: regulator of G protein signaling-1 selectively regulates gut T cell trafficking and colitic potential," The Journal of Immunology, vol.
reported that VEGF-A is upregulated in tissues involved in IBD in humans and in colitic mice, as is its receptor VEGFR-2; whereas VEGFR1 expression is not upregulated [12].