Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under the aspect of systemic diseases and their manifestation in the gut the following conclusions can be drawn: 1. The skin is the mirror of the intestinal tract; not only in primary gastroenterological disorders one should look for dermatological complications, but should also think in chronic skin lesions of concomitant intestinal alterations. 2. In all patients with collagen diseases a gastrointestinal involvement is very common. 3. In all endocrine disorders except in hypothyroidism diarrhea is a very common finding. 4. Infiltrations of gastrointestinal tract can be demonstrated in many cases by gastric, small bowel or rectal biopsy. 5. In all forms of dysgammaglobulinemia giardiasis is very common. 6. In right heart failure protein-losing enteropathy should be considered, in left ventricular insufficiency bowel ischemia.
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PMID:[Manifestations of systemic diseases in the gastrointestinal tract]. 96 97

Diffuse mucosal granularity was reported recently in small bowel Crohn's disease. The radiographic appearance corresponded on histopathologic examination to villous hypertrophy, fusion, or epithelial bridge formation. We have observed similar granularity in Crohn's disease but also in several other conditions, including radiation enteritis, pancreatic glucagonoma, protein-losing enteropathy, and small bowel ischemia. Histopathologic examination demonstrated various alterations in villous morphology, such as edema, hyperplasia, clubbing, or fusion. In Crohn's disease, this appearance was sometimes an indication of early inflammatory disease but was also seen following extensive small bowel resection, possibly due to villous enlargement resulting from intestinal adaptation. These findings suggest that granular mucosa in the small bowel is a nonspecific finding reflecting an alteration in villous structure.
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PMID:Granular small bowel mucosa: a reflection of villous abnormality. 359 39

A 10-year-old boy developed internal herniation of the small intestine associated with significant ischemia, which was reduced without resection. Severe diarrhea, hypoalbuminemia, and lymphopenia ensued while he was receiving total parenteral nutrition. Resolution of symptoms occurred only after resection of an area of ileum, which revealed persistent inflammation and atrophy. Postischemic epithelial cell regeneration of the intestine is discussed in light of this patient's protein-losing enteropathy.
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PMID:Protein-losing enteropathy in prolonged post-ischemic ileitis. 372 76

A 64-year-old man presented with leg edema and hypoproteinemia. His alpha-1 antitrypsin clearance rate of 174 mL/day indicated the presence of protein-losing enteropathy (PLE). Computed tomographic scans demonstrated thickened ileal wall and mesenteric edema. Angiography revealed occlusion in a peripheral branch of the superior mesenteric vein. Furthermore, both the patient and his son had low protein C levels. The patient was treated successfully with partial resection of the ileum. Histologic examination of the resected ileum revealed multiple erosions and submucosal fibrosis with organized venous thrombi in the mesenteric veins. This is the first case report of PLE caused by mesenteric venous thrombosis, and our findings suggest that serum protein was lost through erosion of the ileum caused by ischemia due to mesenteric venous thrombosis.
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PMID:Protein-losing enteropathy caused by mesenteric venous thrombosis with protein C deficiency. 1063 22

An ultrasound pattern of corrugated, and sometimes thickened, bowel wall has been associated with pancreatitis and small intestinal lymphangiectasia. In a retrospective study, records of dogs and cats with an ultrasound diagnosis of corrugated bowel were examined for age, breed, gender, presenting complaint, abdominal radiographic results, and final diagnosis. Eighteen dogs and six cats had an ultrasound diagnosis of corrugated bowel. The final diagnosis was pancreatitis (12 of 24), peritonitis (4 of 24), enteritis (2 of 24), pancreatic neoplasia (2 of 24), diffuse abdominal neoplasia (1 of 24), lymphocytic-plasmacytic enteritis (1 of 24), thrombosis/infarction (1 of 24), and protein-losing enteropathy and acute renal failure (1 of 24). The presence of bowel wall corrugation, although a nonspecific finding, should alert one-to the possibility of pancreatitis, enteritis, peritonitis, neoplasia, or bowel wall ischemia.
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PMID:Ultrasonographic appearance and etiology of corrugated small intestine. 1271 56

We report an unusual case of systemic lupus erythematosus presented with protein-losing enteropathy. A 24-year-old girl was referred to our hospital with generalized edema, thrombocytopenia, hypoalbuminemia, hypercholesterolemia, hypocomplementemia, antinuclear antibody (ANA) (speckled pattern) and anti- SSA/Ro positivities, and elevated CA125 antigen appeared in the blood examination. On the radiological studies, she had mild pleural effusion and moderate ascites which were transudate. A diagnosis of protein-losing enteropathy was made on the basis of increased 99mTc-labelled human immunoglobulin scintigram showing abnormal radioactivity. Endoscopic gastric, duodenal and jejunal biopsies showed chronic inflammation, but vasculitis and immune complex deposition findings were not present. Renal biopsy revealed no definitive findings of lupus nephritis. By the administration of corticosteroids, hypoalbuminemia began to improve, but steroid doses were decreased due to steroid-induced myopathy. Temporary hemiparesis and facial paralysis developed in the patients' follow up. Her cranial magnetic resonance imaging revealed chronic ischemia, and the patient was considered to have neurological involvement due to systemic lupus erythematosus. protein-losing enteropathy and other symptoms then improved dramatically after monthly intravenous cyclophosphamide (three times) combined with oral low-dose corticosteroids. The combination of azathioprine and low-dose steroids was used as maintenance medication. Although about 30 protein-losing enteropathy -associated systemic lupus erythematosus cases have been reported, the patients having initial symptoms as protein-losing enteropathy are rare in the literature. Protein-losing enteropathy -associated systemic lupus erythematosus cases probably represent a subgroup of systemic lupus erythematosus, the characteristics of which are hypocomplementemia, protein-losing enteropathy, ANA positivity showing speckled pattern and anti-ds DNA negativities. In the patients with systemic lupus erythematosus with edema and hypoalbuminemia without renal protein loss, protein-losing enteropathy-associated systemic lupus erythematosus should be kept in mind.
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PMID:A case of systemic lupus erythematosus presenting with protein-losing enteropathy. 1694 Dec 61

In this review of the gastrointestinal (GI) and hepatic manifestations of systemic lupus erythematosus (SLE), 180 articles from the English literature, found using a medline search from January 1965 to December 2010, were examined. Vasculitis may cause ulcerations, bleeding, stricture formation, and perforation from ischemia and infarction. Otherwise, GI symptoms, occurring in about 50% of patients, are usually mild. Esophageal dysmotility may result in heartburn, regurgitation, and dysphagia. Occasionally, pneumatosis cystoides intestinalis may develop, sometimes associated with benign pneumoperitoneum. Patients are prone to salmonella bacteremia, presenting more commonly with fever and abdominal pain than with diarrhea. Intestinal pseudoobstruction usually is found with active lupus serology, preferentially involving small rather than the large bowel. Protein-losing enteropathy, characterized by diarrhea, edema, and hypoalbuminemia, can be the initial presentation of SLE. Malabsorption with a prevalence of 9.5% is occasionally associated with celiac disease. Pancreatitis, with an annual incidence of 0.4 to 1/1000, has an overall mortality of 27% that is decreased with corticosteroid therapy. Acute and chronic ascites may be due to lupus peritonitis or to associated diseases, such as pancreatitis, nephrotic syndrome, heart failure, or infections. Abnormal liver function tests may be due to steatosis from lupus or from corticosteroid therapy. Only about 10% of patients with autoimmune hepatitis have lupus. Up to 4.7% of patients with SLE have chronic active hepatitis correlating strongly with the presence of antibody to ribosomal P protein. SLE can involve the entire GI tract and the liver. Treatment with corticosteroids, cytotoxic agents, and/or immunosuppressants is often successful.
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PMID:Gastrointestinal and hepatic manifestations of systemic lupus erythematosus. 2142 47