Ileocolitis can result from a complicated interaction of the immune and digestive systems or from a primary digestive disease such as Crohn's disease. The main causes in adults are unknown and the diagnosis usually is based on colonoscopy and biopsy. Most sufferers have no evidence of a previous diagnosis and are treated based on empirical therapy for one year. The exact cause is unknown and treatment options are limited so that the most appropriate therapy can be obtained and the condition is best managed.
Most common treatments for ileocolitis include discontinuing any oral or parenteral food, using probiotics and antibiotics as the last resort, or a combination of the above. Surgery is not an option in ileocolitis, and all patients are managed symptomatically.
The incidence of ileocolitis is low in the U.S. in contrast to Denmark, where one tenth of all patients with Crohn's disease need to be treated with systemic corticosteroids each year. The low incidence in Denmark may be explained by the fact that only patients who need systemic corticosteroids are admitted to hospital for a colostomy or colectomy. The high incidence of ileocolitis in Denmark may perhaps be caused by a larger use of systemic corticosteroids in both patients with Crohn's disease and ulcerative colitis, since the use of corticosteroids is not restricted to patients with ileocolitis.
Patients with severe ileocolitis are at risk of perforation. However, ileic pouch surgery with diversionary ileostomy can be offered to patients with disabling disease who are not candidates for pouch substitution surgery. The use of ileostomy in a subset of pouch surgery patients can be associated with some reduction in the rate of pouch-related complications and hospital admissions.
To rule out inflammatory bowel disease, physicians must consider symptoms such as diarrhea, rectal bleeding, anemia, and abdominal distension. Also, an ileocecal valve of >30 cm can be an indicator of ileocolitis. When evaluating a patient for inflammatory bowel disease, physicians should consider a workup of colonic and fecal examinations, stool histologic examination, evaluation of inflammatory indices, and evaluation of inflammatory bowel disease-specific tests.
There was no statistical difference between groups after the 1-month follow-up in scores for SISSI-FI and IBS symptom improvement or quality of life as perceived by patients. A large placebo effect is assumed in clinical trials of medications (in this case, a subgroup of patients with a severe form of ileocolitis were treated by the placebo only).
In a recent study, findings has quantified the mean age of onset for IC. There was no statistical difference for males or females as well as right- and left-side onset as seen in other studies. Younger individuals have a longer onset of IC than those diagnosed with age.
Therapeutic brazikumab 20 mg was well tolerated and efficacious in the treatment of pouchitis and pouch failure. The use of brazikumab in the treatment of pouchitis may be comparable or superior to conventional therapy with oral metronidazole or methotrexate, although a randomized comparative study is needed.
The dose of B-ABZ used in the present study was found to be safe and effective. Given a higher incidence of adverse events with higher rates observed in the placebo arm after two years, a study on a longer duration of follow up would be warranted. However, this prospective study was only a pilot study and a full-scale study with an extended data collection period is required in order to establish safety and efficacy of B-ABZ.
While most patients with colitis are treated surgically with one of the medications used in the clinical trials, the clinical trials and their data are the basis for this treatment. In this review we have only highlighted the most relevant trials and have not covered all of the ileocolitis trials. We hope that this review will lead to the inclusion of more trials investigating this area of chronic gut disease and the advancement of therapy.
Recent findings showed no evidence for an increased risk of IBD in families with other members with a similar phenotype, suggesting that an autoimmune mechanism is unlikely to be responsible for susceptibility in these families.