Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 32-year-old female was suffering from intractable lupus nephritis (LN). Prednisolone at 30 mg per day had been prescribed for two months because of massive proteinuria and edema. After that, anasarca and orthopnea were induced, and hypoproteinemia, hypercholesteremia, and anti-cardiolipin antibody were observed. Prednisolone at a dose of 60 mg per day was necessary. However, there was no improvement of the nephrotic state and renal pathological changes shown as diffuse proliferative lupus nephritis were followed by moderate crescent formation as determined by serial needle biopsy. Cyclophosphamide (CYP) pulse therapy was started and marked improvement of LN was obtained clinically and serologically without significant adverse effects.
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PMID:Effect of cyclophosphamide pulse therapy in a patient with intractable lupus nephritis. 227 25

A young woman presented with high fever and edema in January, 1984, and was diagnosed as having systemic lupus erythematosus. Prednisolone administration failed to improve her symptoms. In May she was admitted to hospital because of elevated erythrocyte sedimentation rate (ESR), hypoproteinemia, hypogammaglobulinemia, hypocomplementemia, positive antinuclear antibody, elevated immune complex level, and diarrhea. Edema disappeared following administration of diuretics and albumin, although the pathogenesis was still undetermined. In September, she was referred to our institution because of severe watery diarrhea and hypoproteinemia. Endoscopic examination showed a diffuse inflammatory lesion in the duodenum and the colon. Radioisotopic 51Cr-albumin study results were compatible with protein-losing enteropathy. Hypoproteinemia and inflammatory changes of the intestine were improved by antibiotics, suggesting that the inflammatory lesion was caused by bacterial infection. Despite the improvements in clinical symptoms and laboratory findings, the serum IgA level was still low and the thrombocytopenia remained. The morphological characteristics of the megakaryocytes were consistent with idiopathic thrombocytopenic purpura. In May, 1986, the thrombocytopenia deteriorated, causing purpura. Prednisolone was administered again, and this resulted in normalization of the platelet count, although the IgA level remained low. Finally the prednisolone was stopped, and the IgA level gradually recovered, with the improvement of the enterocolitis. The exact pathogenesis of the whole picture in this case is unclear, but an 8-year-long clinical course suggests that the protein-losing was caused by an infectious enterocolitis superimposed on IgA deficiency.
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PMID:A case of protein-losing enteropathy in idiopathic thrombocytopenic purpura with decreased IgA. 806 5

A 76-year-old woman with a 5-mo history of recurrent diarrhea and generalized edema was admitted to our hospital. Colonoscopy revealed edematous mucosa, and histopathological examination was compatible with collagenous colitis. Protein leakage from the colon, particularly in the ascending portion, was identified on 99mTc-human serum albumin scintigraphy. Collagenous colitis associated with protein-losing enteropathy (PLE) without small bowel disease was diagnosed. Prednisolone treatment ameliorated diarrhea and hypoproteinemia. Collagenous colitis should be included in the differential diagnosis of chronic diarrhea with hypoproteinemia for appropriate management.
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PMID:A unique case of collagenous colitis presenting as protein-losing enteropathy successfully treated with prednisolone. 1893 90

A 24-year-old man presented with abdominal distension, diarrhea, and nausea. Blood tests showed eosinophilia (WBC 14400/microl, Eos 36%) and slight hypoproteinemia (TP 6.4 mg/dl, Alb 3.7 mg/dl). Ultrasonography and computed tomography revealed massive ascites (WBC 11500/microl, Eos 95%, protein 4.7 g/dl) and wall thickening of the small intestine. Endoscopic and histological examinations showed mucosal redness and edema with eosinophilic infiltration throughout the digestive tracts. Fecal alpha1- antitrypsin clearance was increased (44.6 ml/day). A diagnosis of eosinophilic gastroenteritis with ascites and protein-losing gastroenteropathy was made, and was classified as mixed type of both predominant subserosal and mucosal disease. Prednisolone therapy improved all the symptoms and findings. Measurements of serum levels of several cytokines and chemokines showed that interleukin-5 and soluble interleukin-2 receptor, but not eotaxin, were possible indicators of the disease activity. It should be kept in mind that eosinophilic gastroenteritis is one of the causes of ascites.
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PMID:[A case of eosinophilic gastroenteritis with ascites and protein-losing gastroenteropathy]. 1989 93