PrealbuminEdit
Prealbumin is a small transport protein produced mainly by the liver and, in humans, is more formally known as transthyretin. It participates in the transport of critical molecules in the bloodstream by binding thyroxine (T4) and forming a complex with retinol-binding protein to shuttle vitamin A. This dual role places prealbumin at the intersection of endocrine and nutritional physiology, making it of interest to clinicians who monitor metabolic status in various settings transthyretin thyroxine retinol-binding protein.
Because prealbumin has a relatively short half-life—about two days—it responds more quickly than many other circulating proteins to changes in hepatic synthesis and nutritional intake. In clinical practice, this has made prealbumin a candidate marker for short-term changes in nutritional status or acute illness affecting protein production. Typical reference ranges in adults are roughly 15–36 mg/dL (0.15–0.36 g/L), though exact values depend on the assay and the laboratory. Clinicians frequently interpret prealbumin alongside other indicators of nutrition and health, such as albumin, body weight trends, and dietary assessment, rather than relying on it in isolation.
Biology and function
Prealbumin is synthesized primarily in the liver and circulates in the plasma as a carrier protein for small hydrophobic molecules. In particular, it serves as a chaperone for thyroxine and, in tandem with retinol-binding protein, participates in the transport of vitamin A. Its name reflects historical protein separation techniques; in modern terms, its designation is most often linked to transthyretin in the literature. The protein’s stability and short half-life contribute to its sensitivity to acute physiological changes, which is both an advantage for tracking rapid shifts and a limitation when interpreting results in the presence of inflammatory processes.
Clinical use
In nutrition and clinical medicine, prealbumin has been explored as a marker of protein-energy status and as a surrogate for the body’s response to nutritional therapy. Because of its rapid turnover, prealbumin can decline quickly with undernutrition or catabolic states and can rise with adequate nutritional rehabilitation. It is commonly measured in hospital settings to help gauge whether a patient is responding to enteral or parenteral nutrition. However, prealbumin is not a perfect measure of nutritional status on its own; it is influenced by factors beyond protein intake, including liver function, renal disease, and the systemic inflammatory response. Inflammation, infection, sepsis, and other acute conditions can suppress hepatic synthesis of prealbumin, lowering levels even when nutrition is adequate. For this reason, many guidelines recommend using prealbumin in conjunction with other markers and clinical assessment rather than as a sole determinant of nutritional status. See also the discussion of how prealbumin relates to overall nutrition assessment alongside albumin and other clinical indicators.
The measurement of prealbumin is typically done on serum using immunoassay–based methods, with results reported in mg/dL or g/L. Some laboratories employ nephelometry or immunoturbidimetric assays. The interpretation of results depends on the assay type and reference ranges provided by the testing laboratory.
Measurement and interpretation
Prealbumin testing is most informative when interpreted within the broader clinical context. Important considerations include: - Inflammatory status: As a negative acute-phase protein, prealbumin levels can fall during inflammation or acute illness independent of nutritional intake, potentially masking the presence of adequate nutrition. In such cases, concurrent markers of inflammation (for example, C-reactive protein) help clarify the picture. - Liver and kidney function: Hepatic synthetic capacity directly affects prealbumin production. Renal diseases, nephrotic syndrome, and critical illness can also alter circulating levels. - Nutrition therapy: In patients receiving targeted nutrition support, rising prealbumin over days to weeks may indicate an evolving positive response to therapy, while persistently low levels warrant a broader evaluation of catabolic stress, infection, or organ dysfunction.
Because prealbumin responds to multiple physiological processes, contemporary practice often uses it as part of a panel rather than a stand-alone test. This integrated approach is reflected in nutrition guidelines and expert consensus from professional bodies such as ESPEN and ASPEN.
Limitations and controversies
The use of prealbumin as a stand-alone marker of nutritional status has been debated in the literature. Critics point out that its sensitivity to inflammatory states and hepatic function can confound assessment, particularly in hospitalized or chronically ill populations. Some studies have found limited correlation between prealbumin levels and caloric intake or body composition in certain groups, leading to caution against overreliance on this marker. Proponents emphasize its short half-life as a practical advantage for monitoring rapid changes, provided the interpretation accounts for inflammation and organ function. In practice, most guidelines advocate a multi-parameter approach that combines clinical assessment, anthropometrics, and a panel of biomarkers, rather than using prealbumin alone to diagnose malnutrition or to guide therapy.