Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All patients admitted to an Intensive Care Unit were assigned randomly to one of two groups, A and B. Group A received colloid volume replacement as 4.5% albumin whilst group B received a synthetic colloid, polygeline. This study describes the changes in serum albumin concentration in survivors and nonsurvivors in the two groups during their stay in the Intensive Care Unit. The incidences of renal failure and pulmonary oedema were also assessed. Serum albumin concentration decreased in all nonsurvivors. In survivors the serum albumin concentration decreased to a greater extent in the synthetic colloid group than in the albumin group. Despite the differences in serum albumin concentration there were no significant differences between the groups in the incidences of pulmonary oedema or renal failure.
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PMID:Colloid solutions in the critically ill. A randomised comparison of albumin and polygeline 2. Serum albumin concentration and incidences of pulmonary oedema and acute renal failure. 153 12

Endogenous lung surfactant, and lung surfactant replacements used to treat respiratory distress syndrome, can be inactivated during lung edema, most likely by serum proteins. Serum albumin shows a concentration-dependent surface pressure that can exceed the respreading pressure of collapsed monolayers in vitro. Under these conditions, the collapsed surfactant monolayer can not respread to cover the interface, leading to higher minimum surface tensions and alterations in isotherms and morphology. This is an unusual example of a blocked phase transition (collapsed to monolayer form) inhibiting bioactivity. The concentration-dependent surface activity of other common surfactant inhibitors including fibrinogen and lysolipids correlates well with their effectiveness as inhibitors. These results show that respreading pressure may be as important as the minimum surface tension in the design of replacement surfactants for respiratory distress syndrome.
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PMID:A concentration-dependent mechanism by which serum albumin inactivates replacement lung surfactants. 1180 25

Cardiovascular disease is the leading cause of death worldwide. Conceptually, endothelial dysfunction, inflammatory conditions and oxidative stress are at the forefront of the onset and development of most cardiovascular diseases, particularly coronary artery disease and heart failure. Serum albumin has many physiological properties, including in particular antioxidant, anti-inflammatory, anticoagulant and anti-platelet aggregation activity. It also plays an essential role in the exchange of fluids across the capillary membrane. Hypoalbuminemia is a powerful prognostic marker in the general population as well as in many disease states. In the more specific context of cardiovascular disease, low serum albumin is independently associated with the development of various deleterious conditions such as coronary artery disease, heart failure, atrial fibrillation, stroke and venous thromboembolism. Low serum albumin has also emerged as a potent prognostic parameter in patients with cardiovascular disease regardless of usual prognostic markers. Remarkably, its potent prognostic value persists after adjusting for causative confounders such as malnutrition and inflammation. This prognostic value probably refers primarily to the syndrome of malnutrition-inflammation and the severity of comorbidities. Nevertheless, several recent meta-analyses strongly support the hypothesis that hypoalbuminemia may act as an unrecognized, potentially modifiable risk factor contributing to the emergence and progression of cardiovascular disease, primarily by exacerbating oxidative stress, inflammation and platelet aggregation, and by favouring peripheral congestion and pulmonary edema. Currently, it is unknown whether prevention and correction of low serum albumin offers a benefit to patients with or at risk for cardiovascular disease, and further studies are critically needed in this setting.
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PMID:Serum albumin and cardiovascular disease: State-of-the-art review. 3279 38