Postinfectious irritable bowel syndrome

A small but significant subgroup of patients with irritable bowel syndrome (IBS) report a sudden onset of their IBS symptoms after a bout of gastroenteritis. Population-based surveys show that although a history of neurotic and psychologic disorders, pain-related diseases, and gastroenteritis are all risk factors for developing IBS, gastroenteritis is the most potent. More toxigenic organisms increase the risk 11-fold, as does an initial illness lasting more than 3 weeks. Hypochondriasis and adverse life events double the risk for postinfective (PI)-IBS and may account for the increased proportion of women who develop this syndrome. PI-IBS is associated with modest increases in mucosal T lymphocytes and serotonin-containing enteroendocrine cells. Animal models and some preliminary human data suggest this leads to excessive serotonin release from the mucosa. Both the histologic changes and symptoms in humans may last for many years with only 40% recovering over a 6-year follow-up. Celiac disease, microscopic colitis, lactose intolerance, early stage Crohn's disease, and bile salt malabsorption should be excluded, as should colon cancer in those over the age of 45 years or in those with a positive family history. Treatment with Loperamide, low-fiber diets, and bile salt- binding therapy may help some patients. Serotonin antagonists are logical treatments but have yet to be evaluated.     

Postinfectious irritable bowel syndrome--a meta-analysis

OBJECTIVES: Irritable bowel syndrome (IBS) is a heterogeneous disorder affecting 12% of the population worldwide. Several studies identify IBS as a sequela of infectious gastroenteritis (IGE) with reported prevalence ranging from 4% to 31% and relative risk from 2.5 to 11.9. This meta-analysis was conducted to explore the differences between reported rates and provide a pooled estimate of risk for postinfectious irritable bowel syndrome (PI-IBS). DATA SOURCES: Electronic databases (MEDLINE, OLDMEDLINE, EMBASE, Cochrane database of clinical trials) and pertinent reference lists (including other review articles). REVIEW METHODS: Data were abstracted from included studies by two independent investigators; study quality, heterogeneity, and publication bias were assessed; sensitivity analysis was performed; and a summative effect estimate was calculated for risk of PI-IBS. RESULTS: Eight studies were included for analysis and all reported elevated risk of IBS following IGE. Median prevalence of IBS in the IGE groups was 9.8% (IQR 4.0-13.3) and 1.2% in control groups (IQR 0.4-1.8) (sign-rank test, p= 0.01). The pooled odds ratio was 7.3 (95% CI, 4.7-11.1) without significant heterogeneity (chi2 heterogeneity statistic, p= 0.41). Subgroup analysis revealed an association between PI-IBS risk and IGE definition used. CONCLUSIONS: This study provides supporting evidence for PI-IBS as a sequela of IGE and a pooled risk estimate revealing a sevenfold increase in the odds of developing IBS following IGE. The results suggest that the long-term benefit of reduced PI-IBS may be gained from primary prevention of IGE.     

Post-infectious irritable bowel syndrome

Post-infectious irritable bowel syndrome （PI-IBS） is a common disorder wherein symptoms of IBS begin after an episode of acute gastroenteritis. Published studies have reported incidence of PI-IBS to range between 5% and 32%. The mechanisms underlying the development of PI-IBS are not fully understood, but are believed to include persistent sub-clinical inflammation, changes in intestinal permeability and alteration of gut flora. Individual studies have suggested that risk factors for PI-IBS include patients＇ demographics, psychological disorders and the severity of enteric illness. However, PI-IBS remains a diagnosis of exclusion with no specific disease markers and, to date, no definitive therapy exists. The prognosis of PI- IBS appears favorable with spontaneous and gradual resolution of symptoms in most patients.     

The irritable bowel syndrome

The irritable bowel syndrome (IBS) is a familiar problem in the clinic, but as a disease entity it remains ill defined. Much confusion has arisen in the past, because of the inappropriate inclusion within the category of IBS of almost any patient with unexplained abdominal discomfort. Recent work has established that IBS patients can be positively identified by a cluster of specific symptoms. With the use of these criteria, it seems likely that IBS patients suffer from a diffuse motor abnormality of the gut associated with visceral hypersensitivity; although there is no associated psychopathology, a central nervous system component to the disorder is possible. Better insight into IBS promises more effective management.     

Diagnosing irritable bowel syndrome

It is often possible to positively diagnose irritable bowel syndrome (IBS) based on a combination of multiple symptoms and their chronic nature. Both the Manning criteria and the ROME 1999 Consensus Working Party Diagnostic Criteria help in diagnosing IBS. It is important that, during the first visit, possible contributing factors, such as associated psychosocial stress or a history of mental, physical, or sexual abuse, are considered as part of the patient evaluation. Patients need to receive a clear explanation of the possible causes of symptoms, the benign nature of IBS, and the low likelihood of serious underlying disease. An interactive, positive physician-patient relationship has a beneficial effect on the course of IBS and may be associated with a decreased need for future health care visits.     

Post-infectious irritable bowel syndrome

Irritable bowel syndrome (IBS) is a common disorder associated with abdominal pain or discomfort and altered bowel habits. The majority of patients describe an insidious onset of symptoms; however, a subset report a fairly precise time of onset following an attack of acute gastroenteritis. Typically, the potential acute infectious symptoms, such as fever and vomiting, resolve after several days, but abdominal discomfort, bloating, and diarrhea persist. Although the underlying mechanism of post-infectious IBS (PI-IBS) has not been established, ongoing inflammation appears to play a role, with an increase in serotonin-containing enterochromaffin cells, T lymphocytes, mast cells, proinflammatory cytokines, and intestinal permeability. Psychiatric comorbidities are less common in PI-IBS, compared with IBS patients in general; however, the prevalence of psychological disorders is still higher compared with that in the general population and is associated with a poorer prognosis. Overall, patients with PI-IBS have a slightly improved prognosis compared with those with IBS without an infectious onset.     

Post-infectious irritable bowel syndrome

Irritable bowel syndrome (IBS) affects 8% to 22% of the general population. Although patients describe an insidious onset of symptoms, including abdominal pain relieved with bowel movements, excessive intestinal gas, variable bowel habits, and abdominal bloating, a subgroup of individuals describe the onset of IBS symptoms following an episode of acute gastroenteritis, known as post-infectious IBS (PI-IBS). Several studies have demonstrated the development of IBS following infection. Risk factors for the development of PI-IBS are female sex and longer duration of initial illness. Although the underlying mechanism of PI-IBS is unclear, ongoing inflammation is clearly a factor in the pathogenesis. The underlying inflammatory process results in increased enterochromaffin cells, T-lymphocytes, intestinal permeability, colonic transit time, and a variety of immunologic abnormalities. PI-IBS patients tend to have a better prognosis than do those with idiopathic IBS, with resolution of symptoms within 5 to 6 years. Treatment is similar to that of idiopathic IBS.     

老年肠易激综合征

肠易激综合征是由腹部不适或腹痛伴排便异常组成的一组肠功能障碍性综合征,不能用任何结构异常或生化异常来解释。过去曾被称之谓“过敏性结肠”、“易激结肠”或“黏液性结肠炎”等,现规范统称之谓“肠易激综合征”（irritable bowel syndrome。IBS）^[1]。这是一种发病率高,时常影响终生的胃肠道疾病。流行病学研究提示年龄增长伴随IBS发病率减低（可能和老年人痛觉改变有关）,但1BS始终是老年人常见的胃肠道疾病。     

肠易激综合征的研究方向

肠易激综合征 (ｉｒｒｉｔａｂｌｅｂｏｗｅｌｓｙｎｄｒｏｍｅ ,ＩＢＳ)是由腹部不适或腹痛伴排便异常组成的一组肠功能紊乱综合征 ,无任何器质性或异常的生化指标。过去曾被称为“过敏性结肠”、“易激结肠”或“黏液性结肠炎”等 ,现规范统称为“肠易激综合征”。国际上对该病的诊断标准曾多次研究制订 ,于 2 0 0 0年公布了最新的罗马Ⅱ诊断标准[1] 。其要点为 :(1)诊断本病首先需排除有组织结构或生化异常的器质性疾病 ;(2 )1年内至少要累积 3个月有反复发作的腹痛或腹部不适并伴有下列排便异常中的 2项指标 :①便后腹痛缓解或减轻 ,②…     

感染后肠易激综合征

越来越多的流行病学和临床资料表明早期胃肠道感染与肠易激综合征(irritable bowel syndrome,IBS)的关系密切。大部分胃肠道感染患者能够很快恢复并且无后遗症,但是仍有一部分患者会有持续性的症状,符合IBS的诊断标准,即为感染后肠易激综合征(post-infectious irritable bowel syndrome,PI-IBS)。本文综合国内外有关PI-IBS的研究进展,从PI-IBS的流行病学特征、相关危险因素、病理生理学改变以及临床特征等方面进行作一概述。     

Abnormal electroencephalogram in irritable bowel syndrome.

BACKGROUND: Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by abdominal pain and abnormal bowel habits. IBS patients sometimes complain of sleep disturbance, depression, and various autonomic symptoms. Our hypothesis is that the central nervous system (CNS) might play a role in the pathogenesis of IBS. METHODS: We conducted two experiments using an electroencephalogram (EEG) to evaluate brain activity while at rest and during mental arithmetic stress with pharmacologic neostigmine administered to IBS patients. The first experiment was conducted on 48 conscious and relaxed patients (24 IBS patients and 24 normal controls). EEG recordings were evaluated for visual and power spectrum data. In the second experiment colonic manometric studies combined with EEG recordings were performed in 21 of 24 IBS patients and 8 of 24 normal controls under mental arithmetic stress and the administration of neostigmine. RESULTS: Inspection of the EEG showed significantly greater EEG abnormality in the IBS patients (29.2%) than in the controls (4.2%) (P < 0.02). In the power spectrum analysis of the EEG the IBS patients showed significantly greater beta power percentage than did the normal subjects (P < 0.02). A significant positive correlation was observed between the colonic motility index and beta power percentage after the administration of neostigmine, 10 microg/kg, only in the IBS patients (P < 0.05). CONCLUSION: A brain dysfunction as indexed by the EEG suggests an electrophysiologic brain-gut interaction in IBS.     

Hypothalamic digoxin and irritable bowel syndrome.

BACKGROUND: The hypothalamus produces an endogenous membrane Na+-K+ ATPase inhibitor digoxin that can modulate neurotransmitter transport and may play a role in hemispheric dominance. It can also modulate glycoconjugate synthesis and thus affect synaptic connectivity in the bowel wall. Digoxin could play a role in the genesis of irritable bowel syndrome (IBS). AIM: To study digoxin status in IBS and to correlate it with hemispheric dominance. METHODS: The isoprenoid pathway, tryptophan/tyrosine catabolic patterns and glycoconjugate metabolism were assessed in patients with IBS and in right hemispheric dominant/left hemispheric dominant/bihemispheric dominant individuals. RESULTS: The isoprenoid pathway was upregulated in IBS, with increased HMG CoA reductase activity (0.8 [0.07] vs 0.4 [0.06] in controls; p<0.01), serum digoxin (14.8 [1.0] vs 29.0 [1.2] ng/dL; p<0.01) and dolichol levels (63.8 [3.0] vs 120.3 [3.6] mg/dL; p<0.01). RBC membrane Na+-K+ ATPase activity (3.0 [0.2] vs 1.0 [0.1] microg/p/mg protein; p<0.01), serum magnesium (1.7 [0.1] vs 1.0 [0.1] mg/dL; p<0.01) and ubiquinone (86.4 [5.9] vs 39.8 [1.2] microg/dL; p<0.01) were reduced. There was increase in tryptophan catabolites and reduction in tyrosine catabolites. Serum total glycosaminoglycan and carbohydrate component of glycoproteins were increased in IBS. The activity of glycosaminoglycan degrading enzymes and glycohydrolases were increased. This pattern correlated with those obtained in right hemispheric chemical dominance. CONCLUSION: Hypothalamic digoxin and right hemispheric dominance could play a role in the genesis of irritable bowel syndrome.     

The genetics of irritable bowel syndrome.

Because of the heterogeneity in symptoms and diagnostic findings, patients with irritable bowel syndrome (IBS) remain a challenge to treat and to study. This difficulty stems from lack of understanding of the pathophysiology of this disorder. Environmental factors likely play an important role in the pathogenesis and clinical manifestations of IBS. Several recent studies suggest a genetic basis for IBS, either in etiology or predicting response to therapy. Because of interest in studying the genetic contributors to this and other functional gastrointestinal disorders, we review the literature on genetic risk factors that might explain the familial clustering of IBS. Familial aggregation studies and twin studies suggest a modest contribution of genetics to the development of IBS. Pharmacogenomic and association studies provide stronger, although far from conclusive, evidence for genetic variants that affect expression of IBS. Together, these studies suggest that a multidisciplinary approach with clinical and psychological tools, epidemiologic methods, and genetic techniques might help elucidate the molecular components leading to the common symptoms of IBS and result in better treatments for those with IBS.