Irritable Bowel Syndrome

Irritable Bowel Syndrome

Irritable bowel syndrome refers to a complex disorder of the lower intestinal tract. It is mainly characterized by a pattern of symptoms that is often worsened by emotional stress. The condition involves hypersensitivity to pain in the gut, combined with altered bowel habits resulting in diarrhea, constipation, or both.
Research suggests that people with IBS seem to have a colon that is more sensitive and reactive than usual to a variety of things, including certain foods and stress. Some evidence indicates that the immune system, which fights infection, is also involved.
Predisposing factors may include a low-fiber diet, emotional stress, use of laxatives, a bout of infectious diarrhea, or other temporary bowel inflammation.
The objective of treatment is to relieve symptoms. Changes in diet may help alleviate symptoms in some patients. Increasing dietary fiber and eliminating gastrointestinal stimulants such as caffeine may be beneficial.
A healthy, balanced immune system is ideal in dealing with this condition. For optimal immune support, normal transfer factors at 4-6 capsules per day would be suggested. Digestive Enzymes & Probiotics™ with EnzyGuard-D™ would also be suggested to give your body the necessary tools to digest and process your food, promote a healthy balance of bacteria, and protect your body against harmful invading microorganisms.

 

Bacillary dysentery as a causative factor of irritable bowel syndrome and its pathogenesi


IBS Immune System Clinical Summaries
Gut. 2004 Aug;53(8):1096-101.
Wang LH, Fang XC, Pan GZ.
Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.

BACKGROUND AND AIMS: The incidence of irritable bowel syndrome (IBS) or functional bowel disorders (FBD) after bacillary dysentery (BD) has not been extensively evaluated, and little is known of the pathogenesis of post-infective (PI) IBS. Therefore, we investigated the incidence of IBS and FBD in a Chinese patient population who had recovered from BD. To further elucidate its pathogenesis, neuroimmunological changes, including interleukins (IL), mast cells, neuropeptides, and the relationship between mast cells and intestinal nerves, were investigated. METHODS: A cohort study of 295 patients who had recovered from BD (shigella identified from stool in 71.4%) and 243 control subjects consisting of patient siblings or spouses who had not been infected with BD were included in the study. All subjects were followed up using questionnaires for 1-2 years to explore the incidence of FBD and IBS, as defined by the Rome II criteria. In 56 cases of IBS (PI and non-PI) from another source, the number of mast cells in biopsy specimens from the intestinal mucosa were stained with antitryptase antibody and counted under light microscopy. Also, the relationship of mast cells to neurone specific enolase (NSE), substance P (SP), 5-hydroxytryptamine (5-HT), or calcitonin gene related peptide positive nerve fibres was observed using double staining with alcian blue and neuropeptide antibodies. In 30 cases of IBS (PI-IBS, n = 15) taken at random from the 56 cases, expression of interleukin (IL)-1alpha, IL-1beta, and IL-1 receptor antagonist (IL-1ra) mRNAs in intestinal mucosa were identified using reverse transcription-polymerase chain reaction. The above results were compared with 12 non-IBS controls. RESULTS: In the BD infected cohort, the incidences of FBD and IBS were 22.4% and 8.1% (in total)-10.2% (among those in who shigella were identified) respectively, which were significantly higher (p<0.01) than the incidences of FBD (7.4%) and IBS (0.8%) in the control cohort. A longer duration of diarrhoea (>or=7 days) was associated with a higher risk of developing FBD (odds ratio 3.49 (95% confidence interval 1.71-7.13)). Expression of IL-1beta mRNA in terminal ileum and rectosigmoid mucosa was significantly higher in PI-IBS patients (p<0.01). The number of mast cells in the terminal ileum mucosa in PI-IBS (11.19 (2.83)) and non-PI-IBS patients (10.78 (1.23)) was significantly increased compared with that (6.05 (0.51)) in control subjects (p<0.01). Also, in the terminal ileum and rectosigmoid mucosa of IBS patients, the density of NSE, SP, and 5-HT positively stained nerve fibres increased (p<0.05) and appeared in clusters, surrounding an increased number of mast cells (p<0.01 compared with controls). CONCLUSIONS: BD is a causative factor in PI-IBS. The immune and nervous system may both play important roles in the pathogenesis of PI-IBS.
                   

[Intestinal infection and irritable bowel syndrome]

Zhonghua Nei Ke Za Zhi. 2002 Feb;41(2):90-3. [Article in Chinese]
Wang L, Fang X, Pan G.
Department of Gastroenterology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, Beijing 100730, China.
 
OBJECTIVE:
To determine whether intestinal infection plays a role on the pathogenesis of irritable bowel syndrome (IBS).
 
METHODS:
295 patients who had no previous history of functional bowel disorder had received treatment for dysentery (n = 235) or for acute bowel infection at the hospital between April-October, 1998, were followed up for 1 - 2 years and evaluated for their subsequent bowel habits. A cohort study of 243 subjects using their siblings, husbands or wives who did not have dysentery or acute bowel infection at the same period was taken as control. Furthermore, the contents of mRNAs of IL-1alpha, IL-1beta and IL-1ra in the mucosa at the terminal ileum and recto-sigmoid junctions were determined and compared using RT-PCR method in 30 IBS patients and 12 controls. RESULTS: (1) Sixty-six (22.4%) patients were reported to have functional bowel disturbance, and 24 (8.1% total and 10.2% among cases of dysentery) developed IBS in the study group, whereas, only 7.4% had altered bowel habit and 0.8% had IBS in the control group (P < 0.01). (2) The risk of having functional bowel disturbance was higher in patients who suffered from a longer duration (> 8 d, OR = 3.5) of dysentery. (3) The IL-1beta mRNA level in the mucosa of terminal ileum and recto-sigmoid junction of IBS patients with dysentery was higher than that of controls and IBS patients without dysentery (P < 0.01).
 
CONCLUSION: Intestinal infection plays a role on the pathogenesis of IBS through some immunological factors.

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