Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235886 (leg edema)
 674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 41-year-old man presented with physical signs of leg oedema and a laboratory value of decreased serum albumin of 2.4 g.dl-1. Loss of protein via the gastrointestinal tract was demonstrated by an increased faecal excretion of 51-chromium-labelled-albumin and by elevated stool clearance of alpha 1-antitrypsin. No anatomical lesions or intestinal disease were found to explain this protein loss. Constrictive pericarditis was suspected as the cause of protein-losing enteropathy but could not be confirmed by right heart catheterization, in which normal filling pressures and no sign of 'dip and plateau' pressure pattern were found. However, magnetic resonance imaging clearly demonstrated a thickening of the pericardium over the right heart and a tubular-shaped right ventricle as signs of constrictive pericarditis. Peripheral oedema disappeared and serum protein concentration returned to normal after pericardectomy. This demonstrates that moderate pericardial constriction not resulting in discernible pressure abnormalities in the right heart can be associated with protein-losing enteropathy and thus result in hypoproteinaemic peripheral oedema. In this condition a morphological investigation by magnetic resonance imaging is of importance in order not to miss the diagnosis of a potentially treatable disease.
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PMID:Constrictive pericarditis without typical haemodynamic changes as a cause of oedema formation due to protein-losing enteropathy. 178 39

A 47 year-old man with selective IgA deficiency (SIgAD) consulted us in November 1981, with complaints of leg edema and common cold-like symptoms and was diagnosed as SIgAD based on data of his serum protein (IgG 2,160 mg/dl, IgM 65 mg/dl, no detectable IgA). Later in July 1989, he was admitted with edema and ascites. Laboratory examinations showed; total protein 4.6 g/dl, albumin 1.26 g/dl, IgG 2,375 mg/dl, IgM 38 mg/dl, no detectable IgA. C3 22 mg/dl, C4 6 mg/dl, antinuclear antibody 80X, anti dsDNA antibody 4.5 U/ml, anti IgA antibody 258%, and lymphocytopenia. Co-culture of lymphocytes from the patient and normal subject revealed deficiency of IgA synthesis in his B cell populations. Systemic lupus erythematosus was suggested based on the findings of skin biopsy, renal damage, oral ulcer, decreased complements, autoantibody and lymphocytopenia. We could not give him conventional products of albumin and frozen plasma because he had anti IgA antibody. Instead, we administered concentrated autogenous ascitic fluid and prednisolone. His ascitic fluid disappeared and complements and albumin in his serum normalized. He has continued in good condition and is being treated as an outpatient.
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PMID:[Reinfusion of concentrated autogenous ascitic fluid in a patient with selective IgA deficiency]. 845 Jun 6

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

Primary intestinal lymphangiectasia (PIL) is a protein-losing, exsudative gastroenteropathy causing lymphatic obstruction. Diagnosis depends on clinical examination and histological findings. Conservative treatment modalities include a low-fat diet and enteral nutritional therapy in order to reduce enteric protein loss and to improve fat metabolism. Other treatment options consist of administration of antiplasmin or octreotide to lower lymph flow and secretion. We report on a 58-year-old patient who underwent exploratory laparotomy due to a worsening physical status, recurrent chylaskos and leg oedema under conservative dietary therapy. Intraoperative findings showed a typical PIL of the jejunum about 20 cm distal to the Treitz's ligament. Histological examinations confirmed this diagnosis. One year after segmental small bowel resection (105 cm) with end-to-end anastomosis the patient is healthy, free of symptoms, has gained weight and his serum protein level has increased. Intraabdominal ascites and leg oedema have not reoccurred since.
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PMID:[Surgical therapy of segmental jejunal, primary intestinal lymphangiectasia]. 2322 60