Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assist the radiologist in differentiating the colitis in children, this review proposes a systematic US approach to the disease, presents the US aspect of the normal colon and describes three distinctive US patterns reflecting the intramural extension of the histopathological changes. Each pattern corresponds to one or several diseases producing alterations in the same layer(s). Stratified thickening suggests an inflammatory mucosal process resulting from infection (as in advanced appendicitis or in infectious colitis) or to inflammation (as in IBD). Nonstratified thickening with loss of the haustral folds reflects a marked submucosal infiltrate. Color Doppler is required to distinguish between an inflammatory disease (as advanced CD or neutropenic colitis) and an ischemic colitis (HUS in children). Nonstratified thickening with preservation of the length of the haustral folds is the sign of an intraluminal deposit due to PMC. Correlating the sonographic pattern and the anatomic distribution of the disease with the clinical and laboratory findings often permits to propose a specific diagnosis.
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PMID:Sonographic diagnosis of colitis in children. 1523 10

It is common knowledge that dysfunction of the immune and neuroendocrine systems, in addition to neuroplasticity, is among the pathways that underlie irritable bowel syndrome (IBS) and depression. From as early as the 1950s, the association of IBS with psychiatric disease was postulated; however, the exact mechanism remains elusive. There has been considerable research into the association of IBS and depression over the last years; research into the gut-brain axis and alterations in gut microbes have gained momentum to spell out the relationship between depression and IBS. Evidence from these researchers indicate the dysfunction of homeostatic coping mechanisms; corticotropin-releasing factor appears to be at the core of this dysfunction. The multifactorial etiology of both depression and IBS hinders a universal, one-strategy-fits-all treatment approach to patients with comorbid depression and IBS. This review analyzes the pathophysiology that associates these two conditions; it explores the bidirectional communication between the brain and the gastrointestinal tract, and how these influence the endocrine and immune systems. Review articles, clinical trials and randomized controlled trials that analyzed the association of depression and IBS were identified by searching PubMed, Google Scholar, and articles in PMC databases. Full texts written in English and available via these search engines were selected for the synthesis of this review. Alterations to the gut-brain axis, intestinal microbiota, and the neuro-immune system may be the cornerstone to the association of IBS and depression. This literature review opens alternate therapeutic approaches to comorbid IBS and depression and encourages further research into this topic.
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PMID:Irritable Bowel Syndrome and Depression: A Shared Pathogenesis. 3035 38