Indication
Hypoalbuminemia
Hypoalbuminemia is a clinical state and laboratory finding defined by abnormally low circulating levels of serum albumin, typically below 3.5 g/dL, affecting the cardiovascular and extracellular fluid compartments. Read more about Hypoalbuminemia
40 drugs 13 manufacturers
Drugs that treat it
Common Hypoalbuminemia therapies.
PLASBUMIN-5 (albumin human)
ALBUMINAR-25 (albumin human)
ALBUMINAR-5 (albumin human)
FLEXBUMIN (albumin human)
ALBUTEIN (albumin human)
ALBUTEIN (albumin human)
BUMINATE (albumin human)
ALBUKED-25 (albumin human)
News & literature
Coming soonRelated codes
Coming soonRelated conditions & guidelines
Coming soonHypoalbuminemia is a clinical state and laboratory finding defined by abnormally low circulating levels of serum albumin, typically below 3.5 g/dL, affecting the cardiovascular and extracellular fluid compartments.
It most frequently arises from systemic inflammation, critical illness, severe hepatic dysfunction leading to decreased synthesis, or excessive protein wasting via nephrotic syndrome, protein-losing enteropathy, or extensive burns.
Pathophysiologically, the reduction in serum albumin diminishes intravascular colloid oncotic pressure and alters vascular permeability, predisposing patients to interstitial fluid extravasation, peripheral edema, ascites, and impaired transport of endogenous molecules and drugs.
- nih.gov
Hypoalbuminemia is a clinical state and laboratory finding defined by abnormally low circulating levels of serum albumin, typically below 3.5 g/dL, affecting the cardiovascular and extracellular fluid compartments
- nih.gov
Hypoalbuminemia is a clinical state and laboratory finding defined by abnormally low circulating levels of serum albumin, typically below 3.5 g/dL, affecting the cardiovascular and extracellular fluid compartments Pathophysiologically, the reduction in serum albumin diminishes intravascular colloid oncotic pressure and alters vascular permeability, predisposing patients to interstitial fluid extravasation, peripheral edema, ascites, and impaired transport of endogenous molecules and drugs
- nih.gov
It most frequently arises from systemic inflammation, critical illness, severe hepatic dysfunction leading to decreased synthesis, or excessive protein wasting via nephrotic syndrome, protein-losing enteropathy, or extensive burns Pathophysiologically, the reduction in serum albumin diminishes intravascular colloid oncotic pressure and alters vascular permeability, predisposing patients to interstitial fluid extravasation, peripheral edema, ascites, and impaired transport of endogenous molecules...
- nih.gov
It most frequently arises from systemic inflammation, critical illness, severe hepatic dysfunction leading to decreased synthesis, or excessive protein wasting via nephrotic syndrome, protein-losing enteropathy, or extensive burns
- nih.gov
It most frequently arises from systemic inflammation, critical illness, severe hepatic dysfunction leading to decreased synthesis, or excessive protein wasting via nephrotic syndrome, protein-losing enteropathy, or extensive burns
- scribd.com
It most frequently arises from systemic inflammation, critical illness, severe hepatic dysfunction leading to decreased synthesis, or excessive protein wasting via nephrotic syndrome, protein-losing enteropathy, or extensive burns Pathophysiologically, the reduction in serum albumin diminishes intravascular colloid oncotic pressure and alters vascular permeability, predisposing patients to interstitial fluid extravasation, peripheral edema, ascites, and impaired transport of endogenous molecules...
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