Bowel symptoms in patients that receive proton pump inhibitors. Results of a multicenter survey in Mexico. / Síntomas intestinales en pacientes que reciben inhibidores de bomba de protones (IBP). Resultados de una encuesta multicéntrica en México.

INTRODUCTION: Proton pump inhibitors (PPIs) have been associated with small intestinal bacterial overgrowth (SIBO), which increases with prolonged PPI use, and SIBO has been associated with irritable bowel syndrome (IBS). OBJECTIVE: The aim of the present study was to study the prevalence of bowel symptoms in patients treated with PPIs in Mexico. METHODS: Gastroenterologists in 36 cities surveyed patients treated with PPIs, utilizing an ad hoc questionnaire to determine the presence of bowel symptoms and IBS. RESULTS: Two hundred and fifteen physicians interviewed 1,851 patients. PPI indications were gastritis (48.8%), gastroesophageal reflux (38.5%), peptic ulcer (6.2%), and others (6.5%). A total of 77.5% of the patients received treatment for ≤6 months and 11.9% for ≥1 year. Symptoms were reported in 92.3% of the patients: abnormal bowel habits (90%), bloating (82%), abdominal pain (63%), flatulence (58%), and abdominal discomfort (53%). A total of 67.5% of the patients fit the Rome III criteria for IBS. Symptoms presented in 55.9% of the patients before PPI intake and in 44.1% of the patients after PPI use (P<.005). Constipation (63.8%) predominated in the former, and diarrhea (56.5%) in the latter (P<.0001). The treatments prescribed for managing those symptoms were antispasmodics, antibiotics, prokinetics, and antiflatulents, but patients stated greater satisfaction with antibiotics (mainly rifaximin) (P<.0001). CONCLUSION: The association of PPIs with bowel symptoms and IBS is frequent in Mexico. Diarrhea and bloating predominate, and antibiotics produce the greatest treatment satisfaction, suggesting that SIBO or dysbiosis is the cause of the PPI-related bowel symptoms. However, that remains to be confirmed.

Colonic immune cells in irritable bowel syndrome: A systematic review and meta-analysis.

BACKGROUND & AIMS: Increases in mucosal immune cells have frequently been observed in irritable bowel syndrome (IBS) patients. However, this finding is not completely consistent between studies, possibly due to a combination of methodological variability, population differences and small sample sizes. We performed a meta-analysis of case-control studies that compared immune cell counts in colonic biopsies of IBS patients and controls. METHODS: PubMed and Embase were searched in February 2017. Results were pooled using standardized mean difference (SMD) and were considered significant when zero was not within the 95% confidence interval (CI). Heterogeneity was assessed based on I2 statistics where I2  ≤ 50% and I2  > 50% indicated fixed and random effect models, respectively. KEY RESULTS: Twenty-two studies on 706 IBS patients and 401 controls were included. Mast cells were increased in the rectosigmoid (SMD: 0.38 [95% CI: 0.06-0.71]; P = .02) and descending colon (SMD: 1.69 [95% CI: 0.65-2.73]; P = .001) of IBS patients. Increased mast cells were observed in both constipation (IBS-C) and diarrhea predominant IBS (IBS-D). CD3+ T cells were increased in the rectosigmoid (SMD: 0.53 [95% CI: 0.21-0.85]; P = .001) and the descending colon of the IBS patients (SMD: 0.79, 95% CI [0.28-1.30]; P = .002). This was possibly in relation to higher CD4+ T cells in IBS (SMD: 0.33 [95% CI: 0.01-0.65]; P = .04) as there were no differences in CD8+ T cells. CONCLUSIONS & INFERENCES: Mast cells and CD3+ T cells are increased in colonic biopsies of patients with IBS vs non-inflamed controls. These changes are segmental and sometimes IBS-subtype dependent. The diagnostic value of the quantification of colonic mucosal cells in IBS requires further investigation.

The Mexican consensus on irritable bowel syndrome. / Consenso mexicano sobre el síndrome de intestino irritable.

BACKGROUND: Since the publication in 2009 of the Guidelines on the Diagnosis and Treatment of Irritable Bowel Syndrome of the Asociación Mexicana de Gastroenterología (2009 Guidelines), there have been significant advances in our knowledge of the epidemiology, pathophysiology, diagnosis, and treatment of this disease. AIMS: To present a consensus review of the most current knowledge of IBS, updating the 2009 Guidelines by incorporating new internationally published scientific evidence, with a special interest in Mexican studies. METHODS: The PubMed literature from January 2009 to March 2015 was reviewed and complemented through a manual search. Articles in English and Spanish were included and preference was given to consensuses, guidelines, systematic reviews, and meta-analyses. Statements referring to the different aspects of the disease were formulated and voted upon by 24 gastroenterologists employing the Delphi method. Once a consensus on each statement was reached, the quality of evidence and strength of recommendation were determined through the GRADE system. RESULTS: Forty-eight statements were formulated, updating the information on IBS and adding the complementary data that did not appear in the 2009 Guidelines regarding the importance of exercise and diet, diagnostic strategies, and current therapy alternatives that were analyzed with more stringent scientific vigor or that emerged within the last 5 years. CONCLUSIONS: We present herein a consensus review of the most relevant advances in the study of IBS, updating and complementing the 2009 Guidelines. Several studies conducted in Mexico were included.

Brain-gut interaction in irritable bowel syndrome: new findings of a multicomponent disease model.

Knowledge on the pathophysiology of irritable bowel syndrome has evolved, beginning with disturbances in motility to visceral hypersensitivity, and ultimately to alterations in brain-gut bi-directional communication, where neurotransmitters such as serotonin play a key role. Recently, a multicomponent disease model that integrates all these alterations was proposed. This model is divided into physiological, cognitive, emotional and behavioral components that explain the gastrointestinal as well as the constitutional symptoms. In recent years there has been an explosion of research together with new developments in pharmacological treatments for IBS that support each component of this model. This review presents recent data in favor of these alterations in IBS.

Perceptual responses in patients with inflammatory and functional bowel disease.

BACKGROUND AND AIMS: Enhanced visceral sensitivity following a transient inflammatory process in the gut has been postulated as an aetiological mechanism of irritable bowel syndrome (IBS). In this study we compared perceptual responses to rectosigmoid distension in patients with mild chronic inflammation of the rectum (ulcerative colitis (UC)) and patients without mucosal inflammation (IBS) to determine if chronic low grade mucosal inflammation may be a plausible explanation for rectosigmoid hypersensitivity reported in both IBS and UC patients. METHODS: UC disease activity was quantified using activity index scores. Perception thresholds for discomfort during rectosigmoid distension were compared between 11 UC patients with quiescent or mild disease activity, 18 IBS patients, and 13 healthy controls. RESULTS: Although UC activity index scores negatively correlated with perceptual thresholds for discomfort (r=-0.76, p=0.016), UC patients had higher discomfort thresholds compared with IBS patients and controls before (p=0.02) and after (p<0.001) a noxious sigmoid conditioning stimulus. CONCLUSIONS: Rectal perception was attenuated in UC but enhanced in IBS. In chronic mild inflammation, activation of antinociceptive mechanisms may prevent the development of visceral hyperalgesia. Low grade mucosal inflammation alone is unlikely to be responsible for symptoms in functional gastrointestinal disorders.

Evolving concepts in irritable bowel syndrome.

Converging evidence from investigations of the peripheral and central aspects of bidirectional brain-gut interactions is beginning to shape a pathophysiological model of irritable bowel syndrome (IBS) and related functional gastrointestinal (GI) disorders. This neurobiological model includes alterations in autonomic, neuroendocrine, and pain modulatory mechanisms. The frequent association of IBS and other functional GI disorders with co-morbid affective disorders and temporal association of symptom exacerbation with psychosocial or physical stressors are consistent with alterations in the neurobiological mechanisms underlying the central stress response. Renewed interest in drug development for IBS has resulted in development of instruments for the better assessment of the impact of global symptoms on quality of life and in the development of candidate compounds undergoing clinical evaluation.

Gastrointestinal sensory abnormalities in functional dyspepsia.

Symptoms of functional dyspepsia, such as epigastric pain, bloating or early satiety and nausea, are non-specific and are likely to arise from different mechanisms. Current evidence suggests the presence of at least two subgroups: patients who respond to a prolonged course of acid suppression and patients who show a significant overlap of symptoms with other functional gastrointestinal disorders such as irritable bowel syndrome. An enhanced sensitivity of visceral afferent pathways with or without associated autonomic dysregulation appears to play an important role in the aetiology of symptoms in the second group. In the absence of visceral hypersensitivity, neither the slowing of gastric emptying nor the presence of chronic gastritis appears to be sufficient to cause symptoms of functional dyspepsia. The mechanisms and aetiology of visceral hypersensitivity are incompletely understood. An alteration in the interplay between vagal and spinal afferents, and the inadequate activation of antinociceptive systems in response to tissue irritation, may play a role in symptom generation.

Helicobacter pylori infection among patients with alcoholic and nonalcoholic cirrhosis.

BACKGROUND: The prevalence of Helicobacter pylori in patients with alcoholic and nonalcoholic cirrhosis is uncertain. The present study was aimed at determining the prevalence of H. pylori infection among cirrhotic patients and to explore its relationship to demography, etiology of cirrhosis, and liver function. MATERIALS AND METHODS: Thirty-three cirrhotic patients were included. H. pylori infection was determined by the 14C urea breath test (n = 30) and endoscopy with antral biopsy (n = 4). Etiology of cirrhosis was classified as alcoholic or nonalcoholic. The rate of H. pylori infection was related to age, gender, etiology, Child-Pugh grading, portal hypertension, and portal-systemic encephalopathy (PSE). None of the patients received antibiotics for at least the last 3 months. RESULTS: Twelve alcoholic and 21 nonalcoholic cirrhotics, with a median age of 57 years and a male:female ratio of 1:1.4 were studied. Overall H. pylori prevalence was 45.5%. This prevalence varied from 47.1% to 43.8% in those younger and older than the median age, and from 35.7% to 52.6% in men and women, respectively. Fifty percent of alcoholic and 42.9% of nonalcoholic cirrhotics were H. pylori-positive. According to Child-Pugh grading, 69% of grade A, 40% of grade B, and 0% of grade C were infected (p = .03). Among patients with PSE, 25% were H. pylori-positive compared to 52% of those without PSE (p = .24). CONCLUSIONS: The prevalence of H. pylori infection in cirrhotics is 45.5%. Prevalence was unrelated to age, gender, and etiology of cirrhosis. An inverse relation to the Child-Pugh grading and a tendency to a lower prevalence in PSE was found.