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)

We herein report the case of a 65-year old man with gastrojejunocolic fistula. The patient was admitted to our hospital because of edema of the lower limbs, diarrhea, and weight loss. His history included a distal gastric resection and Billroth II reconstruction for a duodenal ulcer 20 years previously. The laboratory data on admission revealed hypoproteinemia and hypoalbuminemia. An upper gastrointestinal X-ray series revealed a fistula between the transverse colon and upper jejunum. After improving his state of malnutrition, a partial resection of the remnant stomach, transverse colon, and jejunum, which were involved in the fistula, was performed. The postoperative course was uneventful and the patient was discharged on the 26th postoperative day. Gastrojejunocolic fistula is one of the severe complications of a stomal ulcer after a gastric resection with Billroth II reconstruction, which is considered to be induced by an inadequate resection of the stomach. As a result of the recent development of improved agents for the treatment of peptic ulcers, the occurrence of gastrojejunocolic fistula has decreased remarkably. However, gastrojejunocolic fistula should be recognized as one of the late severe complications observed after a gastrectomy with Billroth II reconstruction, since this disease may occur even 20 years after the first operation for peptic ulcer.
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PMID:Gastrojejunocolic fistula after gastrectomy with Billroth II reconstruction: report of a case. 1202 5

The prognosis of patients with end-stage renal disease has been improved by the recent remarkable advances in medical and engineering technology. However, there are still many unsolved problems in the clinical field. One of the problems is an intractable malnutrition characterized by clinical manifestations including hypoproteinemia and decrease in muscular volume, which is associated with deterioration in the quality of the patient's life. Malnutrition in hemodialysis patients involves abnormal energy metabolism and aberrant amino acid metabolism. In the most malnourished patients, immunodefense mechanisms and homeostasis are disrupted, greatly influencing the prognosis. Moreover, when the performance of dialyzer used is too high, the dialysis treatment might remove a necessary nutrient for the patient. There is also a possibility that the protein catabolism is accelerated when the biocompatibility is inferior. On the other hand, in malnutri-tion, the circulating level of insulin-like growth factor-1 (IGF-1) falls while the level of insulin-like growth factor binding protein-1 (IGFBP-1) is remarkably increased. It has been recognized that IGF-1 and IGFBP-1 are indicators reflecting the initiation of a malnutritional state in patients with chronic renal failure, although there are many indicators such as albumin, prealbumin, and anthropometric measurement for nutritional assessment. We have suggested that r-hGH and IGF-1 improve the malnutritional state by alleviating hypoproteinemia and abnormality of serum amino acid profile in uremic patients on hemodialysis. The serum IGF-1/IGFBP-1 ratio is useful not only as a nutritional parameter but also as a predicting index of responsiveness to r-hGH. It is necessary to examine the problem from various angles to improve malnutrition in the dialysis patient, while considering the above mentioned.
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PMID:Nutritional effect of dialysis therapy. 1266 6

Authors monitored a case of a 25 years old woman who was admitted for swelling of lower limbs. Laboratory results showed hypoproteinemia, elevation of liver enzymes, and prolonged prothrombin time. Ultrasound examination proved hepatomegalia with diffusely hyperechogenic liver without central lesion. Computer tomography confirmed hepatomegalia with diffusely hyperechogenic liver and a suspicion of liver steatosis was expressed. Liver biopsy confirmed serious diffuse large droplet steatosis of unclear genesis. Carried out examinations excluded infectious and autoimmune liver diseases, metabolic diseases, and congenital liver diseases (Wilson's disease, porphyria, haemochromatosis etc.). Laboratory results showed gliadin, endomysin, and reticulin antibodies. An enteroscopy picture showed villi decrease. Histology examination of a biopsy specimen confirmed total villi atrophy with non-differentiated enterocytes and round-cell cellulisation of epithelium and proprium. Histology and histochemical findings were distinct proves of coeliac disease. A patient was prescribed a gluten free diet. Her metabolic parameters (normalisation of albumine levels, prothrombine time, and trace elements) and anino transferase levels gradually improved. This case documents development of a serious liver disorder as a result of malnutrition which developed in a young woman as a result of unrecognised coeliac disease.
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PMID:[Large-droplet liver steatosis in celiac disease]. 1512 78

One hundred and twenty-six cancer patients admitted consecutively to the Istituto Nazionale Tumori, Milan, were examined. Within 48 h of hospital admission and again after one week, each patient underwent a nutritional assessment including standard anthropometric and biochemical indices (weight loss, serum proteins, serum albumin, total iron binding capacity (TIBC), cholinesterase (CHE) and lymphocyte count). Calorie and protein intake were also calculated. Each patient was classified with respect to a threshold of normality for each variable (< 10% for weight loss, > 6 g/dL for serum proteins, 3.4 g/dL for serum albumin, >/= 250 mmg/dL for TIBC, >/= 1900 mU/dL for CHE, >/= 1500/nm for total lymphocytes count and 90% Recommended Dietary Allowances (RDA) for nutritional intake). The Mann-Whitney test was performed to assess the statistical significance of the variation between all the nutritional variables at admission and after 7 days of hospitalisation. The relative risk of developing malnutrition regarding a nutritional index after 7 days of hospitalisation was then calculated with reference to each nutritional variable at admission. The significance was tested by the chi square test. The analysis showed that patients who developed deterioration of a nutritional index during hospitalisation had, at admission, worse values of the variable which subsequently deteriorated. In particular, low levels of serum albumin and total iron binding capacity were the variables associated with the higher number of nutritional indices which deteriorated after 7 days of hospitalisation. These were followed by low values of cholinesterase, body weight, serum proteins and lymphocytes. No significant relationship was found between change of a nutritional variable and protein and calorie intake. The risk of developing relevant weight loss (relative risk (RR) = 3.52), hypoalbuminemia (RR = 2.38) and hypoproteinemia (RR = 2.6) during hospitalisation was significantly higher when CHE was below 1900 mU/mL at admission.
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PMID:Predictability of deterioration in marginally malnourished cancer patients during hospitalisation. 1683 90

Protein-losing enteropathy (PLE) is a rare but severe complication of Crohn's disease (CD) and hypoalbuminemia can be one of the presenting symptoms of this illness. The diagnosis of PLE can only be made after exclusion of malnutrition and liver or kidney failure. Significant intestinal leakage can be caused by mucosal injury, increased lymphatic pressure or dilated lymphatics and has been reported in a large number of diseases. The protein-losing can be diagnosed by assessing the excretion of different radiolabeled macromolecules in the faeces or by the clearance of alpha-1-antitrypsine in stools. The primary approach should be the optimization of the nutritional status. Medical treatment of the underlying disease is primordial. In other cases surgical resection of the most affected areas is inevitable. We report a case of a 21-year-old male with a 4 year history of CD, who developed significant hypoproteinemia with pitting oedema, initially in the absence of any other sign of severe disease activity. A "Cr-chloride albumin excretion confirmed our hypothesis of protein-losing enteropathy. Because of sub-obstruction signs some months later, a laparotomy was performed which revealed a severely affected loop with dilatation of the proximal jejunum. Interestingly, multiple large lymph nodes and dilated lymphatics were seen. A partial jejunal resection was performed for stricturing Crohn's disease. Histology showed severe mesenteric granulomatosis, dilated lymph vessels and granulomatous vasculitis. After the resection our patient improved without further albumin infusions and the oedema resolved.
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PMID:Protein-losing enteropathy in Crohn's disease. 1734 81

Chylopericardium is a very rare complication after open heart surgery that is performed by median sternotomy. It is defined as uncontrollable chylous fluid loss, and may lead to hypoproteinemia, malnutrition, and immune deficiency; hence, overall increases postoperative morbidity. In this report, we present a case in which chylopericardium developed after coronary artery bypass grafting. The patient has been successfully treated; however, postoperative course was majorly complicated with the consequences of chylous fluid loss. Interestingly, the cause of the drainage was a lymphatic channel in the mediastinum. To the best of our knowledge, this is the first report in the literature in which a lymphatic channel has been demonstrated sporadically in the mediastinum as a cause of chylopericardium following open heart surgery in the adulthood.
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PMID:An interesting cause of chylopericardium after open heart surgery: a lymphatic channel. 1843 47

Twin-to-twin transfusion syndrome (TTTS) has been related to unbalanced unidirectional arteriovenous anastomoses in the placenta of monochorionic diamniotic (DiMo) twin gestations. As maternal malnutrition accounting for hypoproteinemia and anemia has been detected in severe cases of TTTS, the purpose of this study was to evaluate the impact of early diet supplementation on TTTS. Fifty-one DiMo twin pregnancies were given commercially available oral nutritional diet supplements and then compared in a retrospective cohort study to 52 twin gestations with the same chorionicity but not subjected to nutritional supplementation. Diet supplementation was associated with lower overall incidence of TTTS (20/52 versus 8/51, P = 0.02) and with lower prevalence of TTTS at delivery (18/52 versus 6/51, P = 0.012) when compared with no supplementation. Nutritional intervention also significantly prolonged the time between the diagnosis of TTTS and delivery (9.4 +/- 3.7 weeks versus 4.6 +/- 6.5 weeks; P = 0.014). The earlier nutritional regimen was introduced, the lesser chance of detecting TTTS ( P = 0.001). Although not statistically significant, dietary intervention was also associated with lower Quintero stage, fewer invasive treatments, and lower twin birth weight discordance. Diet supplementation appears to counter maternal metabolic abnormalities in DiMo twin pregnancies and improve perinatal outcomes in TTTS when combined with the standard therapeutic options.
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PMID:Nutritional supplementation in monochorionic diamniotic twin pregnancies: impact on twin-twin transfusion syndrome. 1894 43

Protein-losing enteropathy (PLE) is a rare syndrome of gastrointestinal protein loss that may complicate a variety of diseases. The primary causes can be divided into erosive gastrointestinal disorders, nonerosive gastrointestinal disorders, and disorders involving increased central venous pressure or mesenteric lymphatic obstruction. The diagnosis of PLE should be considered in patients with hypoproteinemia after other causes, such as malnutrition, proteinuria, and impaired protein synthesis due to cirrhosis, have been excluded. The diagnosis of PLE is most commonly based on the determination of fecal alpha-1 antitrypsin clearance. Treatment of PLE targets the underlying disease but also includes dietary modification, supportive care, and maintenance of nutritional status. In this article, cases illustrating a variety of clinical presentations and etiologies of PLE are presented, and its diagnostic approach and treatment are reviewed.
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PMID:Protein-losing enteropathy: case illustrations and clinical review. 1978 26

When blood plasma proteins are depleted by bleeding with return of red cells suspended in saline (plasmapheresis) it is possible to bring dogs to a steady state of hypoproteinemia and a constant level of plasma protein production if the diet nitrogen intake is controlled and limited. Such dogs are outwardly normal but have a lowered resistance to infection and intoxication and probably to vitamin deficiency. When the diet nitrogen is provided by certain mixtures of the ten growth essential amino acids plus glycine, given intravenously at a rapid rate, plasma protein production is good. The same mixture absorbed subcutaneously at a slower rate may be slightly better utilized. Fed orally the same mixture is better utilized and associated with a lower urinary nitrogen excretion. An ample amino acid mixture for the daily intake of a 10 kilo dog may contain in grams dl-threonine 1.4, dl-valine 3, dl-leucine 3, dl-isoleucine 2, l(+)-lysine.HCl.H(2)O 2.2, dl-tryptophane 0.3, dl-phenylalanine 2, dl-methionine 1.2, l(+)-histidine.HCl.H(2)O 1, l(+)-arginine.HCl 1, and glycine 2. Half this quantity is inadequate and not improved by addition of a mixture of alanine, serine, norleucine, proline, hydroxyproline, and tyrosine totalling 1.4 gm. Aspartic acid appears to induce vomiting when added to a mixture of amino acids. The same response has been reported for glutamic acid (8). Omission from the intake of leucine or of leucine and isoleucine results in negative nitrogen balance and rapid weight loss but plasma protein production may be temporarily maintained. It is possible that leucine may be captured from red blood cell destruction. Tryptophane deficiency causes an abrupt decline in plasma protein production. No decline occurred during 2 weeks of histidine deficiency but the urinary nitrogen increased to negative balance. Plasma protein production may be impaired during conditions of dietary deficiency not related to the protein or amino acid intake. Skin lesions and liver function impairment are described. Unidentified factors present in liver and yeast appear to be involved.
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PMID:PLASMA PROTEIN PRODUCTION INFLUENCED BY AMINO ACID MIXTURES AND LACK OF ESSENTIAL AMINO ACIDS : A DEFICIENCY STATE RELATED TO UNKNOWN FACTORS. 1987 90

Protein-losing enteropathy (PLE) is a rare complication of a variety of intestinal disorders characterized by an excessive loss of proteins into the gastrointestinal tract due to impaired integrity of the mucosa. The clinical presentation of patients with PLE is highly variable, depending upon the underlying cause, but mainly consists of edema due to hypoproteinemia. While considering PLE, other causes of hypoproteinemia such as malnutrition, impaired synthesis, or protein loss through other organs like the kidney, liver, or skin, have to be excluded. The disorders causing PLE can be divided into those due to protein loss from intestinal lymphatics, like primary intestinal lymphangiectasia or congenital heart disease and those with protein loss due to an inflamed or abnormal mucosal surface. The diagnosis is confirmed by increased fecal concentrations of alpha-1-antitrypsin. After PLE is diagnosed, the underlying cause should be identified by stool cultures, serologic evaluation, cardiac screening, or radiographic imaging. Treatment of PLE consists of nutrition state maintenance by using a high protein diet with supplement of fat-soluble vitamins. In patients with lymphangiectasia, a low fat with medium chain triglycerides (MCT) diet should be prescribed. Besides dietary adjustments, appropriate treatment for the underlying etiology is necessary and supportive care to avoid complications of edema. PLE is a rare complication of various diseases, mostly gastrointestinal or cardiac conditions that result into loss of proteins in the gastrointestinal tract. Prognosis depends upon the severity and treatment options of the underlying disease.
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PMID:Clinical practice. Protein-losing enteropathy in children. 2057 26


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