Inflammatory bowel disease ( IBD ) is a group of conditions of inflammation of the large intestine and small intestine. Crohn's disease and ulcerative colitis are the main types of inflammatory bowel disease. It is important to note that not only Crohn's disease affects the small intestine and colon, it can also affect the mouth, esophagus, stomach and anus while ulcerative colitis mainly affects the colon and rectum.
Video Inflammatory bowel disease
Signs and symptoms
Apart from Crohn's and UC being a very different disease, both can present with one of the following symptoms: abdominal pain, vomiting, diarrhea, rectal bleeding, severe internal cramping/muscle spasms in the pelvic area and weight loss. Anemia is the most common extraintestinal complication of inflammatory bowel disease. Related complaints or diseases include arthritis, pyoderma gangrenosum, primary sclerosing cholangitis, and non-thyroidal illness syndrome (NTIS). Associations with deep vein thrombosis (DVT) and bronchiolitis obliterans organizing pneumonia (BOOP) have also been reported. Diagnosis is generally by assessment of inflammatory markers in the stools followed by colonoscopy with biopsy of pathologic lesions.
Maps Inflammatory bowel disease
Cause
IBD is a complex disease that arises as a result of the interaction of environmental and genetic factors that cause immunologic and inflammatory responses in the gut.
Diet
Dietary pattern is associated with risk of ulcerative colitis. Specifically, subjects who were in the highest tertile of a healthy diet had a 79% lower risk of ulcerative colitis.
Gluten sensitivity is common in IBD and is associated with flareup. Gluten sensitivity was reported in 23.6 and 27.3% of Crohn's disease and patients with ulcerative colitis, respectively.
High protein diet, certain animal protein, may be associated with an increased risk of inflammatory bowel disease and relapse.
Microbiota
As a result of symbiosis and microbial immunity, changes in enteral bacteria may contribute to inflammatory bowel disease. Individuals affected by IBD have been found to have a 30-50 percent reduction in the biodiversity of commensal bacteria, such as decreased Firmicutes (ie Lachnospiraceae) and Bacteroidetes. Further evidence of the role of intestinal flora in the causes of inflammatory bowel disease is that IBD-affected individuals are more likely to have been prescribed antibiotics within the next 2-5 years before their diagnosis than unaffected individuals. Enteral bacteria can be altered by environmental factors, such as concentrated milk fats (common ingredients from processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.
Intestinal obstruction violations
The loss of intestinal epithelial integrity plays a key pathogenic role in IBD. Congenital immune dysfunction through biased TLR signaling contributes to acute and chronic inflammatory processes in IBD colitis and related cancers. Changes in the composition of the intestinal microbiota are important environmental factors in the development of IBD. Adverse changes in the intestinal microbiota induce an inappropriate (uncontrolled) immune response that causes damage to the intestinal epithelium. Violation of this critical barrier (the intestinal epithelium) allows further microbiota infiltration which, in turn, leads to further immune responses. IBD is a multifactorial disease that is somehow driven in part by an excessive immune response to intestinal microbiota that causes defects in the epithelial barrier function.
Genetics
Genetic contributions are poorly understood and appear to arise from the small contributions of dozens of genes. In 2012, 163 IBD susceptibility loci were confirmed, which means 163 alleles that can increase susceptibility to disease have been found. These 163 loci explained from 8.2% to 13.6% variants in Crohn's disease and 4.1% to 7.5% in ulcerative colitis.
The 163 loci were linked to 300 known genes. The functional enrichment analysis of this gene group using gene ontology shows that there are many genes associated with cytokine production, lymphocyte activation and response to bacterial infections. In an effort to identify possible genes, probabilistic probabilistic gene tissue was constructed. Here, subnetworks including NOD2, Il10 and CARD9 seem to show a close relationship between IBD and the genes associated with host interaction with bacteria. Particular relevance is the presence of HCK genes that seem to play an important role of anti-inflammation. In the picture on the side, there is a cluster that focuses on NOD2 in the subgroup of the causal gene.
Diagnosis
Diagnosis is usually confirmed by a biopsy on colonoscopy. Calprotectin feces is useful as a preliminary investigation, which may indicate a possible IBD, since the test is sensitive but not specific to IBD.
Differential diagnosis
Other diseases may cause increased excretion of calprotectin stool, such as infectious diarrhea, untreated celiac disease, necrotizing enterocolitis, cystic fibrosis of the intestine and neoplastic pediatric tumor cells.
Conditions with the same symptoms as Crohn's disease include intestinal tuberculosis, BehÃÆ'§et disease, ulcerative colitis, nonsteroidal anti-inflammatory drug enteropathy, irritable bowel syndrome and celiac disease.
Conditions with the same symptoms as ulcerative colitis include acute colitis, amebic colitis, schistosomiasis, Crohn's disease, colon cancer, irritable bowel syndrome, intestinal tuberculosis and nonsteroidal anti-inflammatory drug enteropathy.
Classification
The main types of inflammatory bowel disease are Crohn's disease and ulcerative colitis (UC). Inflammatory bowel disease falls into the class of autoimmune disease, where the immune system itself attacks the elements of the digestive system.
Accounting for fewer cases is another form of IBD, which is not always classified as a typical IBD:
- Microscopic colitis is divided into collagen colitis and lymphocytic colitis
- Rescue Colitis
- BehÃÆ'§et's Disease
- Indefinite colitis
There is no specific marker of the disease currently known in the blood, allowing reliable separation of Crohn's disease and patients with ulcerative colitis. The way doctors can know the difference between Crohn's disease and UC is the location and nature of inflammatory changes. Crohn may affect any part of the gastrointestinal tract, from the mouth to the anus (bypassing the lesion), although most cases begin in the ileal terminal. Ulcerative colitis, on the other hand, is confined to the colon and rectum. Microscopically, ulcerative colitis is limited to the mucosa (the lining of the intestinal epithelium), whereas Crohn's disease affects the full thickness of the intestinal wall ("transmural lesion"). Finally, Crohn's disease and ulcerative colitis present with extra-intestinal manifestations (such as liver problems, arthritis, skin manifestations and eye problems) in different proportions.
In 10-15% of cases, a definitive diagnosis of both Crohn's disease and ulcerative colitis can be done because of idiosyncrasies in the presentation. In this case, the diagnosis of indefinite colitis can be done. Despite the recognized definition, not all centers refer to this.
Treatment
Surgery
CD and UC are chronic inflammatory diseases, and can not be cured medically. However, ulcerative colitis in most cases can be cured by proctocolectomy, although this may not relieve extra-intestinal symptoms. An ileostomy will collect dirt in the bag. Alternatively, the bag can be made from the small intestine; this serves as the rectum and prevents the need for permanent ileostomy. A small percentage of patients with ileo-anal bags should manage occasional or chronic pouchitis.
Surgery can not cure Crohn's disease but may be needed to treat complications such as abscesses, strictures or fistulas. Severe cases may require surgery, such as bowel resection, strictureplasty or temporary or permanent colostomy or ileostomy. In Crohn's disease, surgery involves the removal of the most inflamed parts of the intestine and connecting healthy areas, but unfortunately, it does not cure Crohn's or eliminate the disease. At some point after the first operation, Crohn's disease may reappear in healthy parts of the intestine, usually in resection sites. (For example, if a patient with Crohn's disease has an ileocecal anastomosis, where the terminal caecum and ileum are removed and the ileum joins to the ascending colon, Crohn's will almost always light up near anastomosis or in the rest of the ascending colon).
Medical therapy
IBD medical care is individualized for each patient. Which drug selection to use and which route to administer (oral, rectal, injection, infusion) depends on factors including the type, distribution, and severity of the patient's illness, as well as other historical and biochemical prognostic factors, and patient preferences. For example, mesalazine is more useful in ulcerative colitis than in Crohn's disease. Generally, depending on severity, IBD may require immunosuppression to control symptoms, with drugs such as prednisone, TNF inhibitor, azathioprine (Imuran), methotrexate, or 6-mercaptopurine.
Steroids, such as glucocorticoid prednisone, are often used to control disease flares and have been accepted as maintenance medications. Biological therapy for inflammatory bowel disease, particularly TNF inhibitors, is used in people with more severe or resistant Crohn's disease and occasionally on ulcerative colitis.
Treatment usually begins with the administration of drugs with high anti-inflammatory effects, such as prednisone. Once the inflammation is successfully controlled, other drugs to keep the disease in remission, such as mesalazine in UC, are the main treatment. If further treatment is required, a combination of immunosuppressive drugs (such as azathioprine) with mesalazine (which may also have anti-inflammatory effects) may be necessary, depending on the patient. Controlled release Budesonide is used for mild ileal Crohn's disease.
Nutritional and dietetic therapy
Lack of nutrition plays an important role in IBD. Malabsorption, diarrhea, and GI blood loss are common features of IBD. Lack of vitamin B, fat-soluble vitamins, essential fatty acids, and major minerals such as magnesium, zinc, and selenium are very common and benefit from replacement therapy. Dietary interventions, including certain dietary exceptions, low fiber diets, and low FODMAP diets have several benefits.
Anemia is commonly found in ulcerative colitis and Crohn's disease. Because of elevated levels of inflammatory cytokines leading to increased hepcidin expression, parenteral iron is the preferred treatment option because it passes through the gastrointestinal system, has a lower incidence of adverse events and allows for faster treatment. Hepcidin itself is also an anti-inflammatory agent. In the murine model, very low iron levels limit the synthesis of hepcidin, exacerbating existing inflammation. Enteral nutrition has been shown to be efficient in improving hemoglobin levels in patients with inflammatory bowel disease, especially in combination with erythropoietin.
Microbiome
There is evidence of the contribution of infection to inflammatory bowel disease in some patients and this subgroup of patients may benefit from antibiotic therapy.
Stool microbiota transplantation is a relatively new treatment option for IBD that has attracted attention since 2010. Some preliminary studies have demonstrated benefits similar to those in Clostridium difficile infection but a review of use in IBD suggests that FMT is safe, but variable efficacy. A 2014 review states that randomized controlled trials are required.
Alternative medicine
Complementary and alternative treatment approaches have been used in intestinal inflammatory disorders. Evidence from a controlled study of this therapy has been reviewed; the risk of bias is quite heterogeneous. The best supporting evidence is found for herbal therapy, with Plantago ovata and curcumin in UC maintenance therapy, wormwood on the CD, mind/body therapy and self-intervention at UC, and acupuncture on UC and CD.
The novel approaches
Stem cell therapy is undergoing research as a possible treatment for IBD. The study review shows promising roles, despite substantial challenges, including cost and characterization of securities, which limit current use in clinical practice.
Prognosis
While IBD may limit the quality of life due to pain, vomiting, diarrhea, and other undesirable social symptoms, it is rarely fatal by itself. Deaths due to complications such as toxic megacolons, bowel perforations and surgical complications are also rare.
About one-third of individuals with IBD develop persistent gastrointestinal symptoms similar to irritable bowel syndrome (IBS) in the absence of objective evidence of disease activity. Despite the side effects of long-term therapy, this group has a quality of life that does not differ significantly with individuals with uncontrolled disease, is objectively active, and escalation of therapy against biological agents is usually not effective in resolving their symptoms. The cause of IBS-like symptoms is unclear, but it has been suggested that changes in the intestinal-gut axis, epithelial barrier dysfunction, and intestinal flora may be partly responsible.
While IBD patients do have an increased risk of colorectal cancer, this is usually caught much earlier than the general population in regular surveillance of colon by colonoscopy, and therefore patients are far more likely to survive.
New evidence suggests that patients with IBD may have an increased risk of endothelial dysfunction and coronary artery disease.
Latest literature review by Gandhi et al. it was explained that IBD patients over age 65 and women are at an increased risk of coronary artery disease despite the lack of traditional risk factors.
The goal of treatment is to achieve remission, after which the patient usually switches to a milder drug with fewer side effects. Often, reappear acute original symptoms; this is known as "flare-up". Depending on the circumstances, it can disappear by itself or require treatment. The time between flare-ups can occur anywhere from week to year, and varies between patients - some never experience flare-ups.
Living with IBD can be challenging; However, many patients live a relatively normal life. Although living with IBD can be difficult, there are many resources available to help families navigate the IBD ins and outs, such as Crohn's and the Colitis Foundation of America (CCFA).
Epidemiology
IBD produced a global total of 51,000 deaths by 2013 and 55,000 deaths in 1990. Increased IBD incidence since World War 2 has been associated with increased meat consumption worldwide, supporting claims that animal protein intake is associated with IBD. Inflammatory bowel disease is increasing in Europe.
Research
The following treatment strategies are not routinely used, but appear promising in some forms of inflammatory bowel disease.
Initial reports indicate that "worm therapy" not only prevents, but also controls IBD: drinks with about 2,500 ova of the Trichuris suis worm taken twice a month, decreasing the obvious symptoms in many patients. It even speculated that an effective "immunization" procedure could be developed - by consuming cocktails at an early age.
Prebiotics and probiotics focus on increased interest as a treatment for IBD. Currently, there is evidence to support the use of certain probiotics in addition to standard care in people with ulcerative colitis but there is not enough data to recommend probiotics in people suffering from Crohn's disease. Further research is needed to identify specific probiotic strains or combinations and prebiotic agents for the treatment of intestinal inflammation. Currently, probiotic strains, frequency, dosage and duration of probiotic therapy have not been established. In people with severe illness with IBD there is a risk of passage of live bacteria from the gastrointestinal tract to internal organs (bacterial translocation) and subsequent bacteraemia, which can cause serious adverse health consequences. Live bacteria may not be important because the beneficial effects of probiotics appear to be mediated by their DNA and by dissolved soluble factors, and their therapeutic effects can be obtained by systemic administration rather than oral administration.
In 2005, New Scientist published a joint study by Bristol University and the University of Bath on the power of healing marijuana at IBD. Reports that cannabis relieve the symptoms of IBD suggest possible presence of cannabinoid receptors in the lining of the intestine, which responds to molecules in chemicals derived from plants. CB1 cannabinoid receptors - known to exist in the brain - exist in endothelial cells lining the intestines, it is thought that they are involved in repairing the lining of the intestine when damaged.
The team deliberately destroys cells to cause inflammation of the intestinal lining and then adds synthetically produced cannabinoids; the result is the intestines begin to heal: damaged cells repaired and brought back together to repair tears. It is believed that in the healthy gut, natural endogenous kanabinoids are released from endothelial cells when they are injured, which then binds to the CB1 receptor. This process seems to trigger a wound healing reaction, and when people use cannabis, cannabinoids bind to these receptors in the same way.
Previous research has shown that CB1 receptors located in nerve cells in the intestine respond to cannabinoids by slowing bowel motility, thus reducing painful muscle contractions associated with diarrhea. CB2, another cannabinoid receptor that is predominantly expressed by immune cells, was detected in the IBD bowel at higher concentrations. These receptors, which also respond to chemicals in cannabis, appear to be linked to programmed cell death - are programmed - and may have a role in suppressing an overactive immune system and reducing inflammation by clearing excess cells.
Alicaforsen is the first generation antigen-oligodeoxinucleotide designed to bind specifically to human ICAM-1 messenger RNA through the interaction of a Watson-Crick base pair to conquer the expression of ICAM-1. ICAM-1 spreads an inflammatory response promoting extravasation and activation of leukocytes (white blood cells) into inflamed tissues. Increased expression of ICAM-1 has been observed in the inflamed intestinal mucosa of ulcerative colitis, pouchitis and Crohn's patients where ICAM-1 on production is correlated with disease activity. This suggests that ICAM-1 is a potential therapeutic target in the treatment of this disease.
In 2014, an alliance between Broad Institute, Amgen and Massachusetts General Hospital was formed with the intent to "collect and analyze patient DNA samples to identify and validate further genetic targets."
By 2015, the meta-analysis of 938 IBD and 953 control patients, IBD was significantly associated with a higher likelihood of vitamin D deficiency.
Gram-positive bacteria present in the lumen can be associated with prolonged relapse time for ulcerative colitis.
See also
- Inflammatory bowel disease-22
References
External links
- Inflammatory bowel disease in Curlie (based on DMOZ)
- European Crohn and Colitis Organization - A professional organization dedicated to improving patient care with IBD.
- Crohn & amp; Colitis Foundation of America - Information and education provider for IBD patients and their families.
- IBDrelief - Education to help people live better with IBD.
Source of the article : Wikipedia
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