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)

Desipramine, the monoamine reuptake inhibitor, acts predominantly on noradrenergic neurones, and via alpha-2 receptors brings about the release of growth hormone in normal healthy subjects. Thirteen patients with a diagnosis of irritable bowel syndrome, 10 normal controls and eight patients with peptic ulcer disease were each given a challenge test of desipramine 1 mg/kg body weight. Growth hormone release over a 3 h period was monitored. A blunted response was defined as a failure of growth hormone levels to rise at least 5 mU/l above baseline. Of the 13 patients with irritable bowel syndrome 11 showed such a blunting. The results suggest abnormal central alpha-2 receptor functioning in irritable bowel syndrome.
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PMID:Assessment of central noradrenergic functioning in irritable bowel syndrome using a neuroendocrine challenge test. 217 31

The better understanding of the mechanisms of inflammatory bowel disease has driven our progress into the development of new biological therapies targeting specific molecules. Anti-TNF-alpha biologic compounds have shown great efficacy particularly in Crohn's disease. Infliximab (an IgG1 mouse/human chimeric monoclonal anti-TNF-alpha antibody fragment) is the most efficacious compound in induction and maintenance therapy of active and fistulizing Crohn's disease, being at present the only biological compound approved for therapy, but with the limit of the immunogenicity; CDP-571 (a humanized anti-TNF-alpha antibody) and CDP-870 (a PEGylated anti-TNF-alpha antibody) are less immunogenic, showed some efficacy in induction therapy in Crohn's disease but a rapid loss of response in maintenance therapy. Etanercept and onercept (soluble human recombinant TNF-alpha receptors fusion proteins) seem not to be efficacious in Crohn's disease demonstrating no class-effect for anti-TNF-alpha compounds. In preliminary study, adalimumab (an IgG1 humanized monoclonal anti-TNF-alpha antibody) offers good perspective of efficacy and safety also in infliximab-resistant or allergic patients. Inhibition of lymphocyte trafficking to the gut, through anti-adhesion molecules specific therapies (natalizumab, MLN-02, alicaforsen), has shown promising results: unfortunately, natalizumab, the most effective drug of this class, has recently been suspected to favour serious neurological complications. Other biologic therapies are under evaluation but at present seem to be less promising than infliximab; they consist of antiinflammatory cytokines, inhibitors of proinflammatory cytokines, hormones and growth factors: anti-IL12-antibody, interferon-alpha, interferon-beta, G-CSF, GM-CSF, EGF, growth hormone, anti-interferon-gamma, anti-IL-18, anti-IL-2-receptor and anti-CD3 antibodies. The evaluation of other biological drugs has been suspended for severe side effects as happened for anti-CD40L antibody causing thromboembolism and anti-CD4 antibody causing ly.mphopenia. Other compounds as IL-10 and IL-11 have been proven to be ineffective even if an oral formulation of IL-11 is under evaluation. Among the MAP kinases inhibitors BIRB-796 and RDP58 showed to be ineffective while CNI-1493 is under evaluation. The effort in identifying specific patients features predicting therapy response and the possible combination of different biological therapies represent undoubtedly a very promising perspective. Aim of this article is to review the biological compounds and their efficacy in IBD.
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PMID:Biological therapies for inflammatory bowel disease: research drives clinics. 1684 27

Inflammatory bowel disease is often accompanied by extraintestinal manifestations due to a common autoimmune etiopathogenesis, chronic systemic inflammation, frequent nutrition deficits, and the treatment. Endocrine system changes belong to manifestations too. Interaction is mutual, Crohn's disease and ulcerative colitis cause functional and morphological changes of endocrine tissues. On the other hand the endocrine disorders negatively influence the course of bowel disease. In the article we analyze correlation of IBD with gonadal hormone production and fertility, with adrenal function, with the function and morphology of the thyroid, with growth hormone production and growth disorders in children, and with bone mineral density reduction. This topic is not studied enough and needs more analysis and clarification.
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PMID:[Hormonal changes in inflammatory bowel disease]. 2712 70