Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent literature data have given emphasis to the relationship between gastrointestinal (GI) disorders and neurologic diseases, underlying a new pathogenic pathway: The so-called "gut-brain axis." Herein, authors report a case of a 10-month-old male infant, admitted for drug-resistant epilepsy, associated with irritable behavior and GI discomfort, secondary to cow's milk protein allergy. Seizures were described by parents as upward eye movements that were mostly deviated to the right and were associated with slight extension of his neck. They were infrequent at first, but had increased gradually during the course of 3 days (up to 15-20 times/day). No anticonvulsant therapy was effective. Only a cow's milk protein-free diet, accidentally started during a gastroenteritis episode, was effective in stopping seizures. Our case underlines the peculiar vulnerability of the blood-brain barrier under 1 year of age, for which children of this age group experience neurologic manifestations during episodes of systemic inflammation.
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PMID:The Gut-brain Axis: A New Pathogenic View of Neurologic Symptoms - Description of a Pediatric Case. 2855 99

Irritable bowel syndrome (IBS) is a complex, functional gastrointestinal disorder characterized by chronic abdominal pain or discomfort and altered bowel habits. Despite the global prevalence and disease burden of IBS, its underlying pathophysiology remains unclear. Inflammation may play a pathogenic role in IBS. Studies have highlighted the persistence of mucosal inflammation at the microscopic and molecular level in IBS, with increased recruitment of enteroendocrine cells. Substantial overlaps between IBS and inflammatory bowel disease have also been reported. This review thus aimed to discuss the body of evidence pertaining to the presence of mucosal inflammation in IBS, its putative role in the disease process of IBS, and its clinical relevance. Increased mast cell density and activity in the gut may correlate with symptoms of visceral hypersensitivity. As evidenced by patients who develop postinfectious IBS, infective gastroenteritis could cause systemic inflammation and altered microbiome diversity, which in turn perpetuates a cycle of chronic, low-grade, subclinical inflammation. Apart from mucosal inflammation, neuroinflammation is probably involved in the pathophysiology of IBS via the "gut-brain" axis, resulting in altered neuroendocrine pathways and glucocorticoid receptor genes. This gives rise to an overall proinflammatory phenotype and dysregulated hypothalamic-pituitary-adrenal axis and serotonergic (5-HT) functioning, which could, at least in part, account for the symptoms of IBS. Although a definite and reproducible pattern of immune response has yet to be recognized, further research into anti-inflammatories may be of clinical value.
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PMID:The role of inflammation in irritable bowel syndrome (IBS). 3028 77


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