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

GI protein loss can result from a heterogeneous group of diseases, including lymphangiectasia, IBD, neoplasia, ulceration, intussusception, and histoplasmosis. PLE should be suspected in any hypoalbuminemic patient with no evidence of exudative protein loss, proteinuria, or HI. A minimum laboratory database for the suspected PLE patient should include a complete blood cell count, a biochemical and electrolyte profile, urinalysis (+/- urine protein:cretinine ratio), and pre- and postprandial bile acid determinations. Fecal alpha 1-PI concentrations may be used to confirm the presence of GI protein loss in cases with concurrent renal or hepatic disease. Because PLE is a syndrome and not a specific disease, the most effective therapy must be directed at the underlying cause. Multiple high-quality endoscopic biopsies are sufficient to diagnose most patients with PLE, although full-thickness biopsies are required in some cases. Patients with PLE are often clinically "fragile," and careful symptomatic therapy must be integrated with dietary and medical management strategies in most cases.
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PMID:Protein-losing enteropathies. 1455 61

In many ways, infliximab has drastically altered expectations for medical therapy in IBD, and it is expected that adalimumab and certolizumab pegol with ultimately have a similar role. Patients initiating such therapy should be made cognizant of the potential risks of serious infection including opportunistic ones, such as TB and histoplasmosis; demyelinating disorders; CHF; and lymphoma. Proper selection of candidates for anti-TNF-alpha therapy is critical in maintaining a proper benefit-to-risk ratio.
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PMID:Safety of infliximab and other biologic agents in the inflammatory bowel diseases. 1712 16