Biomedical subjects

M J Schmulson

Publications and source records attributed to M J Schmulson.

5 recordsLinked to original sources

PubMed2001

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.

Brain↗

PubMed2000

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.

Adult↗

PubMed1999

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.

Journal Article↗

PubMed1998

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.

Dyspepsia↗

PubMed1997

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.

Adult↗