While the causes of IBS are still unknown, it is believed that the entire gut–brain axis is affected. Recent findings suggest that an allergy triggered peripheral immune mechanism may underlie the symptoms associated with abdominal pain in patients with irritable bowel syndrome. Risk factors The risk of developing IBS increases six-fold after acute gastrointestinal infection. Postinfection, further risk factors are young age, prolonged fever, anxiety, and depression. Psychological factors, such as depression or anxiety, have not been shown to cause or influence the onset of IBS, but may play a role in the persistence and perceived severity of symptoms. Nevertheless, they may worsen IBS symptoms and quality of life. Antibiotic use also appears to increase the risk of developing IBS. Research has found that genetic defects in innate immunity and epithelial homeostasis increase the risk of developing both post-infectious as well as other forms of IBS. Stress Publications suggesting the role of the brain–gut axis appeared in the 1990s and childhood physical and psychological abuse is often associated with the development of IBS. It is believed that psychological stress may trigger IBS in predisposed individuals. Given the high levels of anxiety experienced by people with IBS and the overlap with conditions such as fibromyalgia and chronic fatigue syndrome, a potential explanation for IBS involves a disruption of the stress system. The stress response in the body involves the hypothalamic–pituitary–adrenal axis (HPA) and the sympathetic nervous system, both of which have been shown to operate abnormally in people with IBS. Psychiatric illness or anxiety precedes IBS symptoms in two-thirds of people with IBS, and psychological traits predispose previously healthy people to developing IBS after gastroenteritis. Post-infectious Approximately 10 percent of IBS cases are triggered by an acute gastroenteritis infection. The CdtB toxin is produced by bacteria causing gastroenteritis and the host may develop an autoimmunity when host antibodies to CdtB cross-react with vinculin. Genetic defects relating to the innate immune system and epithelial barrier as well as high stress and anxiety levels appear to increase the risk of developing post-infectious IBS. Post-infectious IBS usually manifests itself as the diarrhea-predominant subtype. Evidence has demonstrated that the release of high levels of proinflammatory cytokines during acute enteric infection causes increased gut permeability leading to translocation of the commensal bacteria across the epithelial barrier; this in turn can result in significant damage to local tissues, which can develop into chronic gut abnormalities in sensitive individuals. However, increased gut permeability is strongly associated with IBS regardless of whether IBS was initiated by an infection or not. A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved as a cause of post-infectious IBS. Bacteria Small intestinal bacterial overgrowth (SIBO) occurs with greater frequency in people who have been diagnosed with IBS compared to healthy controls. SIBO is most common in diarrhea-predominate IBS but also occurs in constipation-predominant IBS more frequently than healthy controls. Symptoms of SIBO include bloating, abdominal pain, diarrhea or constipation among others. IBS may be the result of the immune system interacting abnormally with gut microbiota resulting in an abnormal cytokine signalling profile. Certain bacteria are found in lower or higher abundance when compared with healthy individuals. Generally Bacteroidota, Bacillota, and Pseudomonadota are increased and Actinomycetota, Bifidobacteria, and Lactobacillus are decreased. Within the human gut, there are common phyla found. The most common is Bacillota. This includes Lactobacillus, which is found to have a decrease in people with IBS, and Streptococcus, which is shown to have an increase in abundance. Within this phylum, species in the class Clostridia are shown to have an increase, specifically Ruminococcus and Dorea. The family Lachnospiraceae presents an increase in IBS-D patients. The second most common phylum is Bacteroidota. In people with IBS, the Bacteroidota phylum has been shown to have an overall decrease, but an increase in the species Bacteroides. IBS-D shows a decrease for the phylum Actinomycetota and an increase in Pseudomonadota, specifically in the family Enterobacteriaceae. Fungus There is growing evidence that alterations of gut microbiota (dysbiosis) are associated with the intestinal manifestations of IBS, but also with the psychiatric morbidity that coexists in up to 80% of people with IBS. The role of the gut mycobiota, and especially of the abnormal proliferation of the yeast Candida albicans in some people with IBS, was under investigation as of 2005. Protozoa Prevalence of protozoal infections in industrialized countries (United States and Canada) in the 21st century Protozoal infections can cause symptoms that mirror specific IBS subtypes, e.g., infection by certain substypes of Blastocystis hominis (blastocystosis). As of 2017, evidence indicates that blastocystis colonisation occurs more commonly in IBS affected individuals and is a possible risk factor for developing IBS. Dientamoeba fragilis has also been considered a possible organism to study, though it is also found in people without IBS. Vitamin D Vitamin D deficiency is more common in individuals affected by irritable bowel syndrome. Vitamin D is involved in regulating triggers for IBS including the gut microbiome, inflammatory processes and immune responses, as well as psychosocial factors. Genetics SCN5A mutations are found in a small number of people who have IBS, particularly the constipation-predominant variant (IBS-C). The resulting defect leads to disruption in bowel function, by affecting the Nav1.5 channel, in smooth muscle of the colon and pacemaker cells.
complications of Interstitial cystitis
complications of Bladder stone
symptom of Urethral cancer
symptoms of Bladder cancer
symptom of Interstitial cystitis
medical cause of Dysmenorrhea
symptom of Bladder cancer
medical cause of Pyelonephritis