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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen years after its recognition, outbreaks and sporadic infections attributed to Escherichia coli O157 continue to increase. Acute gastrointestinal, and the systemic complications haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP), are frequent and severe. Current challenges that face clinicians are the early recognition of infection, identification of risk factors for poor prognosis, determination of appropriate monitoring for the development of complications, establishment of a therapeutic strategy and, finally, advice for patients about their long-term prognosis. Clinical features which, in combination, have been shown to distinguish E. coli O157 infection from other enteric pathogens are a history of bloody diarrhoea, visibly bloody stools, absence of fever, a leucocyte count greater than 10 x 10(9) l(-1) and abdominal tenderness on physical examination. The most consistent risk factors for the development of HUS/TTP are the extremes of age and a raised leucocyte count. Bloody diarrhoea and 'antimotility' drugs are also likely to be important risk factors. Recent evidence from the central Scotland outbreak suggests that individuals who are taking drugs that reduce gastric acidity or antibiotics at the time of infection with E. coli O157, or who have a short incubation period, may also be at increased risk of progression to HUS/TTP. Clinical management, in particular the role of antibiotics in gastrointestinal infection, remains controversial, and retrospective assessment of the 1996 outbreaks from central Scotland and Japan only adds to this controversy. Therapeutic plasma exchange is a promising treatment for adults who develop HUS/TTP, but its role has yet to be determined definitively, either in a randomized controlled trial or by an international register of cases. Significant chronic sequelae of infection occur, particularly irritable bowel syndrome after uncomplicated gastrointestinal infection, and renal failure after HUS/TTP. Their frequency and severity are likely to become evident over the next decade.
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PMID:Clinical presentation, complications and treatment of infection with verocytotoxin-producing Escherichia coli. Challenges for the clinician. 1088 Jan 76

Irritable bowel syndrome affects 10% of adults with an unexplained female predominance. Although only a few people see their family doctor, the disease causes reduced quality of life and represents a multi-billion pound health-care problem. The disorder clusters in families, which is possibly because of intra-familial learning and a genetic predisposition. Visceral hypersensitivity is a key feature in most patients. Results of imaging studies of regional cerebral blood flow during rectal distension suggest underlying disturbances of central processing of afferent signals, though this is not unique to the disorder, since it is seen in other chronic pain syndromes. Environmental factors that are strongly implicated in at least some patients include gastrointestinal infection and inflammation and chronic stress. Diagnosis is based on positive symptoms and absence of any alarm indicators. Treatment remains unsatisfactory and hinges on an excellent doctor-patient relationship, with drugs for symptom exacerbations. Cognitive behavioural treatment, psychotherapy, and hypnosis could provide long-lasting benefit in some patients. Tricyclic antidepressants in low doses seem to be the most effective class of drugs for the disorder on the basis of limited data.
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PMID:Irritable bowel syndrome: a little understood organic bowel disease? 1224 74

Irritable bowel syndrome (IBS) is a functional, multifactorial disease characterized by abdominal pain and erratic bowel habit. Changes in gastrointestinal motor function, enhanced perception of stimuli arising from the gut wall and psychosocial factors are thought to be major contributors for symptom generation. In recent years, several additional factors have been identified and postulated to interact with these classical mechanisms. Reduced ability to expel intestinal gas with consequent gas trapping and bowel distension may contribute to abdominal discomfort/pain and bloating. Abnormal activation of certain brain regions following painful stimulation of the rectum suggests altered processing of afferent signals. An acute gastrointestinal infection is now a recognized aetiological factor for symptom development in a subset of IBS patients (i.e. post-infectious IBS), who are probably unable to down-regulate the initial inflammatory stimulus efficiently. Furthermore, low-grade inflammatory infiltration and activation of mast cells in proximity to nerves in the colonic mucosa may also participate in the frequency and severity of perceived abdominal pain in post-infectious and non-specific IBS. Initial evidence suggests the existence of changes in gut microflora, serotonin metabolism and a genetic contribution in IBS pathophysiology. These novel mechanisms may aid a better understanding of the complex pathophysiology of IBS and to develop new therapies.
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PMID:New pathophysiological mechanisms in irritable bowel syndrome. 1533 8

There is increasing evidence indicating health benefits by consumption of foods containing microorganisms, i.e. probiotics. A number of clinical trials have been performed to evaluate the effects in the prevention and treatment of gastrointestinal diseases caused by pathogenic microorganisms or by disturbances in the normal microflora. Gastrointestinal infections caused by Helicobacter pylori, traveller's diarrhoea, rotavirus diarrhoea, antibiotic-associated diarrhoea (AAD) and Clostridium difficile-induced diarrhoea are conditions that have been studied. There are also studies performed on the preventive effect of probiotics on radiation-induced diarrhoea and diarrhoea in tube-fed patients. Inflammatory bowel disease and irritable bowel syndrome, two idiopathic conditions where alterations in the normal microflora have been implicated as responsible for initiation, are two further areas where the use of probiotics has been regarded as promising. The results from clinical studies have not been conclusive in that the effects of probiotics have been strain-dependent and different study designs have been used. Treatment of acute diarrhoea in children and prevention of AAD are the two most justified areas for the application of probiotics.
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PMID:Probiotics and gastrointestinal diseases. 1560 79

Irritable Bowel Syndrome (IBS) is multifactorial in its etiology and heterogeneous in its clinical presentation and pathogenesis. It is recognized that inflammation plays an important role in symptom generation, at least in a subset of patients with IBS. Previous gastroenteritis has been identified as the most important risk factor for IBS, and several studies reported that a substantial proportion of patients with gastrointestinal infection develops IBS symptoms,which can persist for several years. Recent studies have demonstrated that a proportion of IBS patients without any history of enteritis has signs of immune activation in the gut. There is clinical overlap between IBS and inflammatory bowel disease (IBD), with IBS-like symptoms frequently reported in patients before the diagnosis of IBD, and a higher than expected percentage reports of IBS symptoms in patients in remission from established IBD. Thus,these conditions may coexist with a higher than expected frequency, or may exist on a continuum, with IBS and IBD at different ends of the same spectrum. This article examines these relation-ships using immune activation and inflammation as a common pathogenic process to IBD and a subset of IBS patients.
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PMID:Is irritable bowel syndrome a low-grade inflammatory bowel disease? 1586 32

Functional dyspepsia (FD) is one of the most common gastrointestinal disorders. This review summarizes recent progress in our understanding of the pathogenesis and therapy for FD. Although distinction among FD, irritable bowel syndrome, and reflux disease is difficult in population-based studies, separate entities can be recognized in patients who seek medical attention. The pathogenesis of FD remains unclear, but recent studies have demonstrated a role for acute gastrointestinal infection in triggering FD and in genetic polymorphisms of G-proteins in predisposing to FD. The role of abnormalities in gastric motor function, visceral hypersensitivity, and psychosocial factors in the pathophysiology of dyspeptic symptoms has been the topic of multiple studies. Treatment options for FD remain limited. Recent studies have focused on acid-suppressive drugs and on novel prokinetics. Progress in our understanding of the pathogenesis and pathophysiology of FD may lead to new or improved treatment modalities. Areas of major advances are the role of infection and genetic predisposition and studies on the role of abnormalities in gastric motility and sensitivity.
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PMID:Pathogenesis and therapy for idiopathic dyspepsia. 1631 72

Postinfectious functional gastrointestinal disorders (FGIDs) may not be specific to gastroenteritis. This pilot study aimed to ascertain the 3- and 6-month incidence of functional gut disorders in people with non-gastrointestinal (GI) infection, gastroenteritis and healthy controls. This was a prospective study of three cohorts recruited from hospital (non-GI infections) and the community (others). FGIDs were diagnosed using self-completed Rome II modular questionnaires administered at baseline, 3 and 6 months. Thirty-six subjects with non-GI infection, 219 healthy subjects and 108 with bacterial gastroenteritis participated. No difference in incidence of FGID was detected between the GI and non-GI infection cohorts. Any FGID was more frequent in people who had a non-GI infection than in controls at both 3 [odds ratio: 4.34 (95% CI: 3.60-16.45)] and 6 months [4.76 (4.42-27.92)]. Irritable bowel syndrome (IBS) alone was more frequent in people with non-GI infections than in controls at 3 months (6.12 [1.30-29.12]) but did not quite reach statistical significance at 6 months (4.58 [0.79-26.46]). Our findings were unexpected. Postinfectious FGIDs may be related to non-GI and GI infection, although not all potential biases were controlled in study design. Further studies need to explore these preliminary findings and, if confirmed, the underlying mechanisms.
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PMID:Postinfectious irritable bowel syndrome may occur after non-gastrointestinal and intestinal infection. 1691 63

Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder. It is associated with cardiovascular disorders and irritable bowel syndrome (IBS). Besides stressful life-events, a prior history of gastrointestinal infection is a predisposing factor for the development of IBS. Only a proportion of persons exposed to traumatic events develop PTSD. Several factors, like genetic predisposition, stressor intensity, cognitive appraisal mechanisms and coping processes influence the likelihood of developing PTSD after exposure to a trauma. We used a single session of footshocks in rats, an animal model with a high degree of validity for PTSD, to study whether transient colonic inflammation alters local and distal visceral sensitivity, and whether reactivity to the open-field (low (LA) or high (HA) active) predicts long-term stress-induced behavioural and cardiovascular sensitisation and altered visceral pain sensitivity. A distention series and noise challenge were given 2 weeks after foot-shocks, followed by a transient colonic inflammation period and a second distention series and noise challenge 4 weeks after foot-shocks. During exposure to noise, both before and after inflammation, footshocked rats showed increased immobility compared to controls, which was significantly greater in LA rats than in HA rats. LA preshocked rats also showed a greater blood pressure response to the noise test, but this only became evident in the second noise-test. Neither footshocks nor colonic inflammation affected duodenal pain sensitivity. The results provide additional evidence for long-lasting cardiovascular hyperresponsivity after a stressful event and indicate that its degree is predicted by personality traits or coping style.
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PMID:Individual reactivity to the open-field predicts the expression of cardiovascular and behavioural sensitisation to novel stress. 1692 56

Functional gastrointestinal disorders, such as functional dyspepsia (FD) and irritable bowel syndrome, are common pathologies of the gut. FD is a clinical syndrome defined as chronic or recurrent pain or discomfort of unknown origin in the upper abdomen. The pathophysiological mechanisms responsible for FD have not been fully elucidated, but new ideas regarding its pathophysiology and the significance of the pathophysiology with respect to the symptom pattern of FD have emerged. In particular, there is growing interest in alterations in gastric motility, such as accommodation to a meal or gastric emptying, and visceral sensation in FD. The mechanisms underlying impaired gastroduodenal motor function are unclear, but possible factors include abnormal neurohormonal function, autonomic dysfunction, visceral hypersensitivity to acid or mechanical distention, Helicobacter pylori infection, acute gastrointestinal infection, psychosocial comorbidity, and stress. Although the optimum treatment for FD is not yet clearly established, acid-suppressive drugs, prokinetic agents, eradication of H. pylori, and antidepressants have been widely used in the management of patients with FD. The therapeutic efficacy of prokinetics such as itopride hydrochloride and mosapride citrate in the treatment of FD is supported by the results of relatively large and well-controlled studies. In addition, recent research has yielded new therapeutic agents and modalities for dysmotility in FD, including agonists/antagonists of various sensorimotor receptors, activation of the nitrergic pathway, kampo medicine, acupuncture, and gastric electric stimulation. This review discusses recent research on the pathophysiology of and treatment options for FD, with special attention given to digestive dysmotility.
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PMID:Recent insights into digestive motility in functional dyspepsia. 1716 May 14

The present report describes a young woman with no previous gastrointestinal complaints who was initially diagnosed with postinfective irritable bowel syndrome (IBS) after a confirmed case of Campylobacter jejuni enteritis. However, because of persistent diarrhea, new-onset bloating and the development of iron and vitamin deficiencies, serological markers for celiac disease (CD) were evaluated. A positive tissue transglutaminase immunoglobulin A antibody test and repeat endoscopy with duodenal biopsy showing a Marsh IIIa lesion confirmed the diagnosis of CD. Infectious gastroenteritis is a well-established risk factor for the development of IBS, and there is recent evidence that it could play a role in the initiation and exacerbation of inflammatory bowel disease. The present case suggests that the clinical expression of CD can be unmasked by an acute gastrointestinal infection and supports the hypothesis that environmental factors other than gliadin may play a role in the clinical onset of CD in a genetically susceptible host. The increasing availability of serological testing and upper endoscopy has led to increasingly frequent diagnoses of CD and recognition that it may mimic IBS. The present case findings suggest that CD should be considered in the differential diagnosis of persistent IBS-like symptoms after an episode of infectious gastroenteritis.
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PMID:Clinical onset of celiac disease after an episode of Campylobacter jejuni enteritis. 1763 49


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