The prognosis for lymphocytic colitis and collagenous colitis is good, and both conditions are considered to be benign. The majority of people afflicted with the conditions recover from their diarrhea, and their histological abnormalities resolve, although relapses commonly occur if maintenance treatment is not continued.

Symptoms suggestive of colitis are worked-up by obtaining the medical history, a physical examination and laboratory tests (CBC, electrolytes, stool culture and sensitivity, stool ova and parasites et cetera). Additional tests may include medical imaging (e.g. abdominal computed tomography, abdominal X-rays) and an examination with a camera inserted into the rectum (sigmoidoscopy, colonoscopy).

An important investigation in the assessment of colitis is biopsy. A very small piece of tissue (usually about 2mm) is removed from the bowel mucosa during endoscopy and examined under the microscope by a histopathologist. It can provide important information regarding the cause of the disease and the extent of bowel damage.

The initial diagnostic workup for ulcerative colitis includes the following:

- A complete blood count is done to check for anemia; thrombocytosis, a high platelet count, is occasionally seen

- Electrolyte studies and renal function tests are done, as chronic diarrhea may be associated with hypokalemia, hypomagnesemia and pre-renal failure.

- Liver function tests are performed to screen for bile duct involvement: primary sclerosing cholangitis.

- X-ray

- Urinalysis

- Stool culture, to rule out parasites and infectious causes.

- Erythrocyte sedimentation rate can be measured, with an elevated sedimentation rate indicating that an inflammatory process is present.

- C-reactive protein can be measured, with an elevated level being another indication of inflammation.

- Sigmoidoscopy a type of endoscopy which can detect the presence of ulcers in the large intestine after a trial of an enema.

Although ulcerative colitis is a disease of unknown causation, inquiry should be made as to unusual factors believed to trigger the disease.

The simple clinical colitis activity index was created in 1998 and is used to assess the severity of symptoms.

Diagnosis may be simple in cases where the patient's signs and symptoms are idiopathic to a specific cause. However this is generally not the case, considering that many pathogens which cause enteritis may exhibit the similar symptoms, especially early in the disease. In particular, "campylobacter, shigella, salmonella" and many other bacteria induce acute self-limited colitis, an inflammation of the lining of the colon which appears similar under the microscope.

A medical history, physical examination and tests such as blood counts, stool cultures, CT scans, MRIs, PCRs, colonoscopies and upper endoscopies may be used in order to perform a differential diagnosis. A biopsy may be required to obtain a sample for histopathology.

The diagnosis is usually confirmed by biopsies on colonoscopy. Fecal calprotectin is useful as an initial investigation, which may suggest the possibility of IBD, as this test is sensitive but not specific for IBD.

Some people may be admitted into the hospital following the colonoscopy depending on results. It is sometimes necessary to get the patient started on a steroid to speed up the healing of the colon. It may also be necessary to get the patient hydrated from the fluid loss and iron replaced from the loss of blood. After a hospital stay, the patient may be put on a daily medication to manage their chronic colitis. The medication can be an anti-inflammatory or an immunosuppressant. There are many different types of medication used and the doctor will prescribe the one they see fit. If the patient doesn't respond, new medications will be tried until there is a good fit.

Moreover, several studies recently have found significant relationship between colitis and dairy allergy (including: cow milk, cow milk UHT and casein), suggesting some patients may benefit from an elimination diet.

Biopsies of the mucosa are taken to definitively diagnose UC and differentiate it from Crohn's disease, which is managed differently clinically. Microbiological samples are typically taken at the time of endoscopy. The pathology in ulcerative colitis typically involves distortion of crypt architecture, inflammation of crypts (cryptitis), frank crypt abscesses, and hemorrhage or inflammatory cells in the lamina propria. In cases where the clinical picture is unclear, the histomorphologic analysis often plays a pivotal role in determining the diagnosis and thus the management. By contrast, a biopsy analysis may be indeterminate, and thus the clinical progression of the disease must inform its treatment.

Lymphocytic and collagenous colitis have both been shown in randomized, placebo-controlled trials to respond well to budesonide, a glucocorticoid. Budesonide formulated to be active in the distal colon and rectum is effective for both active disease and in the prevention of relapse. However, relapse occurs frequently after withdrawal of therapy.

Studies of a number of other agents including antidiarrheals, bismuth subsalicylate (Pepto-Bismol), mesalazine/mesalamine (alone or in combination with cholestyramine), systemic corticosteroids, cholestyramine, immunomodulators, and probiotics have shown to be less effective than budesonide for treating both forms of microscopic colitis.

Anti-TNF inhibitors. split ileostomy, diverting ileostomy, and subtotal colectomy are options for management of steroid-dependent or refractory microscopic colitis. Currently, the need to resort to surgery is limited considering the improvement of drug therapy options. However, surgery is still considered for patients with severe, unresponsive microscopic colitis.

There may be signs of septic shock. A physical examination reveals abdominal tenderness and possible loss of bowel sounds. An abdominal radiography shows colonic dilation. White blood cell count is usually elevated. Severe sepsis may present with hypothermia or leukopenia.

Other diseases may cause an increased excretion of fecal calprotectin, such as infectious diarrhea, untreated coeliac disease, necrotizing enterocolitis, intestinal cystic fibrosis and neoplastic pediatric tumor cells.

Conditions with similar symptoms as Crohn's disease includes intestinal tuberculosis, Behçet's disease, ulcerative colitis, nonsteroidal anti-inflammatory drug enteropathy, irritable bowel syndrome and coeliac disease.

Conditions with similar symptoms as ulcerative colitis includes acute self-limiting colitis, amebic colitis, schistosomiasis, Crohn's disease, colon cancer, irritable bowel syndrome, intestinal tuberculosis and nonsteroidal anti-inflammatory drug enteropathy.

A small bowel follow-through may suggest the diagnosis of Crohn's disease and is useful when the disease involves only the small intestine. Because colonoscopy and gastroscopy allow direct visualization of only the terminal ileum and beginning of the duodenum, they cannot be used to evaluate the remainder of the small intestine. As a result, a barium follow-through X-ray, wherein barium sulfate suspension is ingested and fluoroscopic images of the bowel are taken over time, is useful for looking for inflammation and narrowing of the small bowel. Barium enemas, in which barium is inserted into the rectum and fluoroscopy is used to image the bowel, are rarely used in the work-up of Crohn's disease due to the advent of colonoscopy. They remain useful for identifying anatomical abnormalities when strictures of the colon are too small for a colonoscope to pass through, or in the detection of colonic fistulae (in this case contrast should be performed with iodate substances).

CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols. They are also useful for looking for intra-abdominal complications of Crohn's disease, such as abscesses, small bowel obstructions, or fistulae. Magnetic resonance imaging (MRI) is another option for imaging the small bowel as well as looking for complications, though it is more expensive and less readily available. MRI techniques such as diffusion-weighted imaging and high-resolution imaging are more sensitive in detecting ulceration and inflammation compared to CT.

Symptoms of pouchitis include Increased stool frequency, urgency, incontinence, nocturnal seepage, abdominal cramping, pelvic discomfort, and arthralgia.

Symptom severity does not always correlate with severity of endoscopically- or histologically-evaluated pouch inflammation. Additionally, these symptoms are not necessarily specific for pouchitis, asthey may arise from other inflammatory or functional pouch disorders such as Crohn's disease of the pouch, cuffitis, pouch sinus, or irritable pouch syndrome. The most reliable tool for diagnosis is endoscopy combined with histologic features (derived from tissue biopsies obtained during endoscopy).

Ileitis is an inflammation of the ileum, a portion of the small intestine. Crohn's ileitis is a type of Crohn's disease affecting the ileum. Ileitis is caused by the bacterium "Lawsonia intracellularis".

Inflammatory bowel disease does not associate with "Lawsonia intracellularis" infection.

A complete blood count may reveal anemia, which commonly is caused by blood loss leading to iron deficiency (a microcytic anemia) or by vitamin B deficiency (a macrocytic anemia), usually caused by ileal disease impairing vitamin B absorption. Rarely autoimmune hemolysis may occur. Ferritin levels help assess if iron deficiency is contributing to the anemia. Erythrocyte sedimentation rate (ESR) and C-reactive protein help assess the degree of inflammation, which is important as ferritin can also be raised in inflammation. Serum iron, total iron binding capacity and transferrin saturation may be more easily interpreted in inflammation. Anemia of chronic disease results in a normocytic anemia. Other causes of anemia include medication used in treatment of inflammatory bowel disease, like azathioprine, which can lead to cytopenia, and sulfasalazine, which can also result in folate deficiency. Testing for "Saccharomyces cerevisiae" antibodies (ASCA) and antineutrophil cytoplasmic antibodies (ANCA) has been evaluated to identify inflammatory diseases of the intestine and to differentiate Crohn's disease from ulcerative colitis. Furthermore, increasing amounts and levels of serological antibodies such as ASCA, antilaminaribioside [Glc(β1,3)Glb(β); ALCA], antichitobioside [GlcNAc(β1,4)GlcNAc(β); ACCA], antimannobioside [Man(α1,3)Man(α)AMCA], antiLaminarin [(Glc(β1,3))3n(Glc(β1,6))n; anti-L] and antichitin [GlcNAc(β1,4)n; anti-C] associate with disease behavior and surgery, and may aid in the prognosis of Crohn's disease.

Low serum levels of vitamin D are associated with Crohn's disease. Further studies are required to determine the significance of this association.

Mild cases usually do not require treatment and will go away after a few days in healthy people. In cases where symptoms persist or when it is more severe, specific treatments based on the initial cause may be required.

In cases where diarrhoea is present, replenishing fluids lost is recommended, and in cases with prolonged or severe diarrhoea which persists, intravenous rehydration therapy or antibiotics may be required. A simple oral rehydration therapy (ORS) can be made by dissolving one teaspoon of salt, eight teaspoons of sugar and the juice of an orange into one litre of clean water. Studies have shown the efficacy of antibiotics in reducing the duration of the symptoms of infectious enteritis of bacterial origin, however antibiotic treatments are usually not required due to the self-limiting duration of infectious enteritis.

The objective of treatment is to decompress the bowel and to prevent swallowed air from further distending the bowel. If decompression is not achieved or the patient does not improve within 24 hours, a colectomy (surgical removal of all or part of the colon) is indicated. When surgery is required the recommended procedure is a subtotal colectomy with end ileostomy. Fluid and electrolyte replacement help to prevent dehydration and shock. Use of corticosteroids may be indicated to suppress the inflammatory reaction in the colon if megacolon has resulted from active inflammatory bowel disease. Antibiotics may be given to prevent sepsis.

Often, a diagnosis can be made based on the patient's description of their symptoms, but other methods which may be used to verify gastritis include:

- Blood tests:

- Blood cell count

- Presence of "H. pylori"

- Liver, kidney, gallbladder, or pancreas functions

- Urinalysis

- Stool sample, to look for blood in the stool

- X-rays

- ECGs

- Endoscopy, to check for stomach lining inflammation and mucous erosion

- Stomach biopsy, to test for gastritis and other conditions

Bile acid malabsorption is common in Crohn's disease but not always recognised. Most patients with previous ileal resection and chronic diarrhea will have abnormal SeHCAT tests and can benefit from bile acid sequestrants.

Patients with primary bile acid diarrhea are frequently misdiagnosed as having the irritable bowel syndrome as clinicians fail to recognize the condition. When SeHCAT testing is performed, the diagnosis of primary bile acid diarrhea is commonly made. In a review of 18 studies of the use of SeHCAT testing in diarrhea-predominant irritable bowel syndrome patients, 32% of 1223 patients had a SeHCAT 7-day retention of less than 10%, and 80% of these reported a response to cholestyramine, a bile acid sequestrant.

Estimates of the population prevalence taken from this review suggest that 1% of the adult population could have primary bile acid diarrhea (Type 2 bile acid malabsorption).

With most infections, the key is to block the spread of the organism.

- Wash hands frequently

- Eat properly prepared and stored food.

- Bleach soiled laundry

- Vaccinations for "Vibrio cholerae" and rotavirus have been developed. Rotavirus vaccination is recommended for infants in the U.S. Vaccines for "V. cholerae" may be administered to individuals traveling to at-risk areas

There is no clinically approved treatment for pouchitis.

First line treatment is usually with antibiotics, specifically with ciprofloxacin and metronidazole. Ampicillin or Piperacillin can also be considered as alternatives to empiric Ciprofloxacin and metronidazole). Administration of metronidazole at a high daily dose of 20 mg/kg can cause symptomatic peripheral neuropathology in up to 85% of patients. This can be a limiting factor in the use of maintenance metronidazole to suppress chronic pouchitis.

Other therapies which have been shown to be effective in randomised clinical trials include probiotic therapy, the application of which usually begins as soon as any antibiotic course is completed so as to re-populate the pouch with beneficial bacteria. Biologics, such as anti-TNF antibodies, may also be useful but the evidence for their use is largely anecdotal. In addition, discussion by patients using related internet forums appears to give evidence of benefits (again, after cessation of antibiotics) from certain diets, such as the Specific Carbohydrate Diet, Paleolithic Diet, and Low FODMAP Diet. In particular, attention has been drawn to the exclusion of complex carbohydrates, as well as other foods with high starch content (such as grains, rice, and potatoes) and certain dairy products including milk and soft cheese.

There is no cure for short bowel syndrome except transplant. In newborn infants, the 4-year survival rate on parenteral nutrition is approximately 70%. In newborn infants with less than 10% of expected intestinal length, 5 year survival is approximately 20%. Some studies suggest that much of the mortality is due to a complication of the total parenteral nutrition (TPN), especially chronic liver disease. Much hope is vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower.

Although promising, small intestine transplant has a mixed success rate, with postoperative mortality rate of up to 30%. One-year and 4-year survival rate are 90% and 60%, respectively.

Diagnosis is generally made by endoscopy with biopsy to evaluate histology. Review of symptoms and associated conditions is important.

The doctor will take a medical history to make sure that nothing else is causing the symptoms. Also, the doctor might perform a rectal or abdominal examination to exclude the possibilities of inflammatory bowel disease (e.g., Crohn’s disease) and pelvic abscesses (pockets of pus). A stool culture (a laboratory test to identify bacteria and other organisms from a sample of feces) can be used to determine the specific virus or germ that is causing gastroenteritis.

Other radiological studies frequently used to assess patients with chronic stomach problems include a barium swallow, where a dye is consumed and pictures of the esophagus and stomach are obtained every few minutes. Other tests include a 24-hour pH study, CT scans or MRI.

Several methods have been developed to identify the disorder but there are difficulties with all of them. Fecal bile acid quantification is unpleasant for both the patient and laboratory. Diagnosis of bile acid malabsorption is easily and reliably made by the SeHCAT test. This nuclear medicine test involves two scans a week apart and so measures multiple cycles of bile acid excretion and reabsorption. There is limited radiation exposure (0.3 mSv). Retention of SeHCAT at 7 days is normally above 15%; values less than 15%, 10% and 5% predict respectively mild, moderate and severe abnormal retention and an increasing likelihood of response to bile acid sequestrants. This test is not licensed in the USA, and is underutilized even where it is available.

Older methods such as the C-glycocholic breath test are no longer in routine clinical use.

Measurement of 7α-Hydroxy-4-cholesten-3-one, a bile acid precursor, in serum, shows the increased bile acid synthesis found in bile acid malabsorption. This test is an alternative diagnostic means when available. Fasting blood FGF19 values may have value in the recognition of the disease and prediction of response.

Currently, there are two tests for evaluating BAM in the U.S. One test, currently available only for research purposes, measures serum levels of the marker 7α-hydroxy-4-cholesten-3-one (C4), a downstream product of CYP7A1. Plasma C4 levels increase when bile acid synthesis increases, and C4 levels are substantially elevated in BAM patients with a sensitivity and specificity of 90 percent and 79 percent, respectively. C4 levels have also been shown to correlate well with SeHCAT retention. This makes fasting serum C4 attractive as a screening test for BAM, although it can produce false-positives and false-negatives in patients who have liver disease or are taking statins.

The second test, which can now be clinically ordered, is the fecal bile acid excretion test. It quantifies individual and total bile acids in a 48-hour stool collection. Increased total fecal bile acids are seen in patients with chronic functional diarrhea and higher levels of CA and CDCA are associated with IBS-D.

A clinical validation involving 94 healthy volunteers, 60 patients with IBS-D and 28 patients with IBS with constipation (IBS-C) found that the sum of CA and CDCA concentrations above 3.7 percent were indicative of IBS-D with 72 percent sensitivity and 90 percent specificity. In addition, the upper limit of normal total fecal bile acid excretion over the 48 hours has been defined.