It could be that these groups are more likely to have genes associated with IBD as well as live in industrialized areas. However, the ethnicity gap seems to be narrowing. IBD symptoms may also differ among various racial groups, though this is an area that needs more research, Dr. Some studies suggest that African Americans are more likely than white people to need surgery because of IBD. The gastrointestinal tract contains trillions of bacteria that help digest your food. These are "good" germs.
However, infections with "bad" germs, such as salmonella and campylobacter, have been associated with a greater risk of IBD. Both types of bacteria can be ingested through contaminated food, and they are responsible for thousands of cases of food poisoning each year.
By Alyssa Sparacino Updated March 27, Save Pin More. Research has given us some hints as to the causes of IBD. It has been found that a combination of genes and environmental exposures is probably to blame. Here are some factors that may affect IBD risk. Start Slideshow. MRIs use magnetic fields to form images of the body. MRIs are especially helpful in examining soft tissues and detecting fistulas.
Anti-inflammatory drugs are the first step in IBD treatment. These drugs help decrease inflammation of the digestive tract. However, they have many side effects. Glucocorticoids , a subcategory of corticosteroids , are examples of anti-inflammatory drugs used for IBD. They include:. These drugs are available in a variety of forms, from oral tablets to injections to rectal foams. For this group, they strongly recommended:.
They prevent the immune system from attacking the bowel and causing inflammation. However, your doctor may prescribe them anyway. This is referred to as off-label drug use. However, a doctor can still use the drug for that purpose. This is because the FDA regulates the testing and approval of drugs, but not how doctors use drugs to treat medical conditions in their patients. Biologics are genetically designed drugs that may be a choice for people with moderate to severe IBD.
Some biologics block tumor necrosis factor TNF. TNF is a chemical that causes inflammation and is produced by the immune system. Biosimilars, which are cheaper and have been reverse-engineered to produce the same results as biologics, are available for some of these drugs, though. Adalimumab is less effective. Adalimumab can be self-administered, which may make it more convenient than the other drugs.
Other drugs block separate pathways causing inflammation, including the UC drug tofacitinib Xeljanz. Due to safety concerns, the AGA recommends that this oral drug only be taken during a clinical or registry study.
Antidiarrheal medications and laxatives can also be used to treat IBD symptoms. Shop for antidiarrheal medications and laxatives online. Drinking plenty of fluids helps to compensate for those lost in your stool. Avoiding dairy products and stressful situations also improves symptoms. Exercising and quitting smoking , if you smoke, can further help improve your health. Vitamin and mineral supplements can help with nutritional deficiencies. For example, iron supplements can help treat anemia.
Shop for iron supplements online. Routine colonoscopy is used to monitor for colorectal cancer, since those with IBD are at a higher risk for developing it. However, you may be able to reduce your risk for developing IBD or prevent a relapse by:. IBD can cause some discomfort, but there are ways you can manage the disease and still live a healthy, active lifestyle. IBD Healthline is a free app that connects you with others living with IBD through one-on-one messaging and live group chats while also providing access to expert-approved information on managing IBD.
Download the app for iPhone or Android. Male gender RR: 2. In contrast, deployment during the surveillance period was associated with a decreased risk of IBD RR: 0. Estimates of CD and UC incidence were quite similar No other rate ratio estimates were significantly different when the non-IBS cohort was stratified by acute or chronic illnesses matching data not shown. While the time to meeting the IBD outcome definition was more prolonged for subjects without an antecedent IBS diagnosis median: 2.
This effect was apparent for all IGE infection diagnosis groups e. Among those with IBS who reported diarrhea during deployment Similarly, Garcia-Rodriguez et al. Using a case—control design, we previously reported on this association in a comparable population, albeit at a lower magnitude than reported by Garcia-Rodriguez et al.
This retrospective cohort study builds on these two initial reports using a more well-defined study population and detailed evaluation of medical encounters for IBS and non-IBS subjects. The association between IBS and IBD is well-recognized; however, the mechanism s underlying this association is a source of ongoing research. Some have argued that IBS and IBD represent clinical presentations on a pathophysiologic spectrum of disease given the considerable overlap between symptoms in patients with IBS and IBD, whereby IBS symptoms represent sub-clinical inflammation and immune activation that progress in severity towards the expression of IBD [ 4 , 13 ].
Increased mucosal barrier defects in some patients with IBS may also contribute to the increase passage of luminal antigens of dietary and bacterial origin into the sub-mucosal which may result in the further activation of mucosal immune responses involved in the genesis of IBD [ 14 ].
Another common link between these two disorders is the independent associations with antecedent Campylobacter jejuni infection which have been described [ 9 , 10 , 15 — 17 ]. This disruption in intestinal barrier function may prime the intestine for chronic inflammatory responses in susceptible individuals.
Follow-on genetic studies of the Walkerton, Ontario STEC-Campylobacter outbreak found that subjects with single nucleotide polymorphisms for genes encoding proteins involved in epithelial cell barrier function and the innate immune response to enteric bacteria TLR9, IL6, and CDH1 were independently associated with development of IBS following acute gastroenteritis [ 21 ]. Interestingly, recent experimental and clinical evidence implicate aberrant CDH1 function related to maintenance of epithelial barrier integrity with increased risk of IBD as well [ 22 , 23 ].
Furthermore, Chae et al. Finally, recent findings have suggested that there may be similarities in serotonin signaling between IBS and UC patients that could explain the altered motility, secretion, and sensation common to both [ 25 ]. Clearly, more studies are needed to evaluate the potential overlap in pathogenesis between these two disorders in terms of genetic, host and environmental interactions which may support the observed epidemiological findings.
In fact, in a number of patients with IBS, the colonic mucosa appears normal; however, there are histopathological changes in the rectum, a region not commonly biopsied during colonoscopy for IBS symptoms.
In total, these data suggest that IBS patients are at increased risk of IBD and additional studies are needed to ascertain whether certain genetic or immunologic abnormalities underlie both of these conditions, and determine which subset of IBS patients may be at higher IBD risk. We found a median IBD onset time of 2.
In contrast, Pimentel et al. A possible explanation for the apparent discrepancy in prodromal periods between the two studies may be the method by which these data were obtained or differences in healthcare access or health-seeking behavior between study populations. While the study by Pimentel et al. Both methodologies have inherent limitations and potential sources of bias.
We also found a 4-fold increased risk of IBD among subjects with more than 1 documented episode of IGE after controlling for other important covariates. The consistency of this finding seems to point to a direct association, though a causal link has not yet been established.
Other covariates were associated with differential IBD risk. Specifically, males had a slightly higher risk of IBD than females. In contrast, a population-based study of IBD incidence in a Canadian province showed a significantly higher rate of CD in women than in men, and a similar rate of UC in both genders [ 28 ].
A report on IBD incidence in participants in a specific managed care organization found similar rates of UC and CD among men and women [ 28 ]. One possible explanation is that the population based study did not control for comorbid IBS, a FGD that is known to be more common in females [ 29 ].
Deployment during the study period was associated with a decreased IBD risk. At first glimpse, this appears contradictory to what may be expected given that deployments are frequently to regions at high risk of IGE, often associated with bacterial pathogens linked to an increased IBD risk [ 9 , 10 ].
However, the likely explanation of this inverse association is that of a healthy worker effect. As stated previously, there is a recognized prodrome for IBD.
It is reasonable to assume that subjects with such a complex of symptoms may be less likely to be deployed due to undiagnosed health concerns precluding one from adequately performing in a deployed setting. A similar finding has been reported with non-specific arthralgia and arthropathy [ 30 ]. Alternatively, there may be an inherent delay in the diagnosis of IBD in military populations, as this and similar diagnoses can result in medical discharge, [ 6 ] and military personnel who are motivated to deploy may be of a type that are less likely to seek care for chronic underlying diseases in order to avoid diagnosis and separation.
DuPont et al. We were limited in our assessment of infectious gastroenteritis IGE to only episodes associated with a medical encounter, and it has been well-established that only a small proportion of IGE episodes actually seek medical care [ 32 ].
Therefore, it is possible that the observation of an increased rate of IGE in the IBS cohort may be related to the fact that those subjects were more likely to seek care for an incident IGE episode than their non-IBS counterparts.
Thus, this observation may be solely due to differences in care seeking behavior or differences in the severity of diarrheal and non-diarrheal symptoms such as abdominal pain or cramps, nausea, malaise or myalgia. An alternative explanation is that due to the common clinical features, IBS symptoms may have been misdiagnosed as being of infectious etiology. Unfortunately, inadequate sample collection and microbiology is commonplace with infectious gastroenteritis [ 32 ], so we are unable to assess this potential bias.
First, in patients with IBS, there is a modification of genetic expression and secretion of important chemokines such as interleukin 8 IL-8 , which is decreased in those with IBS [ 33 ]. Another possibility is that the modified intestinal microbiome in a subset of IBS patients may influence subsequent IGE risk [ 35 ]. Furthermore, in a subset of IBS patients evidence of mucosal barrier dysfunction is apparent which could increase susceptibility to enteric infection [ 36 — 38 ].
Of note, we found a significantly higher incidence of protozoal-attributed IGE than was seen for either bacterial or viral-associated IGE though the lack of pathogen-specific data in this study precludes an assessment of pathogen-specific risks. These findings need validation in a different population, and if found to be consistent would have certain implications on considerations regarding management of patients with IBS in situations where IGE risk is high.
If the association between IBS, IGE and IBD is found in additional studies of other populations, increased emphasis on preventive efforts may be needed in those subpopulations with IBS to include consideration of antibiotic chemoprophylaxis as currently recommend for high-risk groups [ 41 , 42 ].
As previously stated, there are inherent limitations to the data presented herein and the results should be interpreted with caution. First, the use of a medical encounter database is a potential source for misclassifications of exposure, outcome and other covariates due to inaccurate ICD-9 or CPT coding.
We attempted to reduce the impact of this misclassification by requiring multiple medical encounters to document both the exposure and outcome of interest as has been described previously [ 43 ]. Importantly, as part of the military screening process, potential servicemembers are screened to ensure they are in good general health. Screening for functional bowel disorders is not done, nor would it be exclusionary.
Thus we cannot necessarily rule out someone with pre-existing IBS; however, it does minimize the potential impact of this limitation inherent in this study design.
0コメント