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)

Pyothorax is a serious disease process which requires both medical and surgical intervention. Late recognition, management problems, and likely recurrence make successful treatment difficult and often frustrating. Aims of therapy should be to avoid undue stress to the patient, to relieve respiratory distress by thoracocentesis, to eliminate infectious agents with antimicrobials, to remove pleural exudate, and to provide supportive care. Close monitoring of the patient is necessary to prevent iatrogenic complications such as pneumothorax, hemothorax, hypothermia, or hypoproteinemia. Exploratory thoracotomy for removal of granulomatous material and fibroelastic pleural "peels" is occasionally necessary to resolve compressive cardiopulmonary lesions.
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PMID:Management of pyothorax. 31 57

The postoperative problems and management of 8 patients following right hepatic lobectomy for blunt liver injury are discussed. Multiple injury and in particular chest injury are of importance. Respiratory distress may be insidious in onset and must be anticipated. Most patients require at least temporary positive pressure ventilation. Liver regeneration is rapid and histological evidence of regenerative hyperplasia is present within 3 days of injury. Hypoglycaemia of a degree sufficient to threaten life may occur postoperatively, particularly in the first 48 hours. Jaundice may be a worrying postoperative feature, but the use of T-tube drainage after hepatic lobectomy will enable any possible extrahepatic obstruction to be excluded. Hypoproteinaemia and hypo-albuminaemia occur in the immediate postoperative period, and recovery rapidly follows the peak period of regenerative activity of the liver. Normal levels are regained by the fourth to sixth postoperative weeks. Prophylactic antibiotics have no place in the postoperative management of blunt liver injury. Haemorrhagic diathesis is common after hepatic resection and is of a complex nature. Intravascular coagulation may occur and factor V deficiency is common. The mainstay of treatment is transfusion of fresh blood.
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PMID:Postoperative problems and management after hepatic resection for blunt injury to the liver. 112 57

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

Nephropathia epidemica (NE) is a hemorrhagic fever with renal syndrome (HFRS) normally taking a benign clinical course. The etiologic agent, Puumala hantavirus is genetically closely related to Sin Nombre virus, which causes a frequently lethal febrile syndrome with pulmonary involvement (hantavirus pulmonary syndrome, HPS). HPS is characterized by acute respiratory distress, non-cardiogenic pulmonary edema and severe and hypotension, but usually no significant renal involvement. Pulmonary involvement and respiratory symptoms also occur in NE. To understand the mechanisms of pulmonary involvement in NE, we studied the clinical records and chest X-rays of 125 hospital-treated acutely ill NE patients. Twenty-eight percent of the patients had disease-related changes in their chest radiographs. Pleural effusion and atelectasis were the most common X-ray findings, whereas frank pulmonary edema was rare. The patients with pathologic X-ray findings had a more marked hypoproteinemia (lowest measured serum protein concentration 54 +/- 1 g/l) than those with normal X-ray (62.1 +/- 0.9 g/l, p < 0.001) and leukocytosis (highest measured blood leukocyte count 14.1 +/- 0.9 x 10(9)/l vs. 10.6 +/- 0.6 x 10(9)/l, p < 0.001) and more severe renal insufficiency (highest measured serum creatinine 590 +/- 60 mumol/l vs. 356 +/- 29 mumol/l, p < 0.05). Hypoproteinemia best predicted the occurrence of abnormal chest X-ray findings in NE. This suggests, that capillary leakage and inflammation may play a role in the pathogenesis of NE lung involvement, similarly as in HPS. Differently from HPS, the fluid volume overload associated with renal insufficiency seemed to contribute strongly to the chest X-ray changes in NE.
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PMID:Pulmonary involvement in nephropathia epidemica: radiological findings and their clinical correlations. 898 52

Systemic capillary leak syndrome (SCLS) is a rare disorder with a high mortality rate, characterized by rapidly developing edema, weight gain and hypotension, hemoconcentration and hypoproteinemia. This syndrome is caused by sudden, reversible capillary hyperpermeability with a rapid extravasation of plasma from the intravascular to the interstitial space. Even though SCLS has been suggested to be the pathogenic mechanism for the pulmonary toxicity of gemcitabine (GCB), a new deoxycytidine analogue with structural similarities to cytosine arabinoside, a direct correlation between GCB and SCLS has never been reported. We describe a case of repeated SCLS after GCB administration in a 51-year-old male with locally-advanced non-small-cell lung cancer treated with a combination of cisplatin and GCB. The detection of GCB-induced SCLS supports the hypothesis that SCLS could be the pathogenic way of GCB pulmonary toxicity. This finding can help to better understand and treat the potentially deadly GCB-related acute respiratory distress syndrome that is being recognized.
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PMID:Gemcitabine-induced systemic capillary leak syndrome. 1182 67