by Mary Ellen Posthauer, RDN, CD, LD, FAND
Several years ago when my nutrition blog began, I discussed the issue of relying on laboratory values – in particular albumin, pre-albumin and transthyretin – as markers of nutritional status. Recently, during a discussion of nutrition and wound care, a dietitian expressed her frustration with a surgeon who kept postponing corrective abdominal surgery until a patient's nutritional status improved, as evidenced by the albumin being in the normal range. However, the patient was receiving adequate calories per enteral feeding and had gained weight. The albumin level was not reflective of the nutritional status. This discussion prompted me to revisit the issue of serum proteins as markers of nutritional status.
Albumin as a Marker of Nutritional Status
Albumin is a serum protein with a large body pool size distributed between the vascular and interstitial spaces, with 50% located extravascular. The liver synthesizes only 5% of albumin daily, so protein intake doesn't affect the albumin pool on a daily basis. The majority of the changes in albumin are caused by redistribution between the intravascular and extravascular spaces. For example, edema, ascites, and over-hydration depress albumin levels and dehydration falsely elevates albumin. Albumin's long half-life of 14-20 days has resulted in clinicians promoting this as a marker of chronic nutritional status. Albumin functions as a carrier protein and assists in maintaining oncotic pressure.
Pre-albumin as a Marker of Nutritional Status
Pre-albumin (transthyretin) is also a visceral protein with a small body pool size, compared to albumin, and is affected by many of the same factors as albumin. Pre-albumin is a transport protein for thyroxine and a carrier for retinal binding protein. Pre-albumin levels are elevated in acute renal failure as the kidneys degrade it. It is also affected by some of the same factors as albumin.
Transferrin as a Marker of Nutritional Status
Transferrin has been touted as a marker of nutritional status but since it is involved in iron transport, its levels are affected by iron status. Total iron binding capacity is an indirect measurement of transferrin stores except in cases of iron overload.
Albumin, pre-albumin and transferrin are negative acute phase reactants that are stimulated by the inflammatory process including infection, trauma, surgery, autoimmune processes, burns, etc. Acute-phase proteins change by approximately 25% during inflammation and are expected to return to normal once the inflammatory response resolves. The response in acute and chronic inflammation is a release of cytokines such as interleukin-6 that is responsible for the production of most acute-phase proteins. Cytokines are responsible for fever, inflammation of chronic disease and cachexia.
Decreasing nutrient intake does not correlate with a decrease in albumin, pre-albumin or transferrin levels and increased ingestion doesn't always result in increasing their levels. However, the current body of research indicates that acute-phase proteins reflect the severity of the inflammatory response rather than nutritional status. Nutrition care should focus on ensuring the individual receives and consumes appropriate meals and/or supplements, plus any therapy (speech, physical or occupational) ordered to strengthen their clinical status.
Serum hepatic protein levels should be evaluated in the context of the individual's overall medical condition. The significance of biochemical tests using acute-phase proteins as an indicator for malnutrition is limited.
About The Author
Mary Ellen Posthauer RDN, CD, LD, FAND is an award winning dietitian, consultant for MEP Healthcare Dietary Services, published author, and member of the Purdue University Hall of Fame, Department of Foods and Nutrition, having held positions on numerous boards and panels including the National Pressure Ulcer Advisory Panel and the American Dietetic Association's Unintentional Weight Loss work group.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, Kestrel Health Information, Inc., its affiliates, or subsidiary companies.