Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review the authors focus on the adverse GIT events during long-term treatment with non-steroid anti-inflammatory drugs, and explain pathogenesis of the NSA induced gastropathy and enteropathy. The risk groups of patients and prophylactic and therapeutic modalities are discussed. There are indices that most of the NSA gastric ulcers don't induce clinical symptoms, and massive bleeding may be the first clinical manifestation. This is why the clinical symptoms cannot be used as predictors of NSA gastropathy. It seems, on the author's clinical experience, that more than half cases of massive non-variceal bleeding from upper GIT is induced by non-steroid anti-inflammatory drugs and acetylsalicylic acid. NSA-gastropathy often presents with multifocal ulcers and erosions in the antrum of the stomach. The course of massive bleeding induced by NSA is associated with high rate of lethality.
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PMID:[Adverse effects of nonsteroidal antirheumatic agents on the digestive tract]. 1268 51

Protein losing enteropathy (PLE) is a gastrointestinal disorder that is associated with excessive loss of plasma protein into the gut resulting from abnormal mucosal permeability. The disease is usually caused by inflammation. The loss of protein in PLE is a nonselective process affecting albumin, globulin and transferrin. Abdominal scintigraphy with human serum albumin marked by Tc99m seems to be an easy and sensitive method for diagnosing PLE. An 4-year-old girl was presented to an outside Pediatric Department due to hypoproteinemia and recurrent pneumonia which had caused several prior hospitalizations. The laboratory tests revealed hypoproteinemia, hypoalbuminemia, low level of IgG, sideropenia, and a decreased level of T lymphocytes. The loss of protein into the gut was confirmed by fecal clearance of alfa-1 antitrypsin. Only nonspecific inflammation was detected by biopsy of the small intestine. These clinical and laboratory findings, quickly decreasing IgG and albumin levels in spite of i.v. supplementation and the lack of proteinuria permitted PLE diagnosis. The abdominal scintigraphy was planned to assess and localise protein losing through GIT and for strategy of possible surgical treatment. Abdominal dynamic scintigraphy was performed immediately after the injection of 300 MBq Tc99m human albumin. 90 images were taken within 180 minutes. Delayed abdominal images were obtained 6 and 24 hours after the tracer injection. Anterior abdominal scintigraphy showed pathological activity of Tc99m-albumin in small bowel in the upper left segment of the abdomen in the 40th minute after injection. Extensive accumulation of albumin was seen in the 160th minute. Delayed images, after 3 and 6 hours, revealed translocation of the tracer into the lower right abdominal segment. The further passage and tracer concentration was detected in ascendant and transverse colon. Based on the laboratory tests and scintigraphic images the girl was suspected to have segmental lymphangiectasia of small intestine and was qualified for laparatomy and, possibly, for surgical resection of the pathologically changed bowel. However, diffuse pathological changes revealed in the guts during the operation, rendered the operation impossible. Tc99m-labelled human serum albumin scintigraphy may be considered the method-of-choice in the diagnosis of protein-losing enteropathy. However, in this test the assessment of the enteropathy dimension is difficult and surgical treatment should be planned with caution.
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PMID:[Protein losing enteropathy (PLE) detected by Tc99m-labelled human serum albumin abdominal scintigraphy--case report]. 1506 43