LAUSR

Could Albumin Be a Biomarker to Monitor the Effect of Intravenous Immunoglobulin on Guillain-Barré Syndrome? To the Editor Fokkink and colleagues1 reported that hypoalbuminemia was associated with a severe clinical course and poor outcomes among patients with Guillain-Barré syndrome (GBS) who received intravenous immunoglobulin treatment. They proposed that the serum albumin could be a potential biomarker to monitor the treatment responses to intravenous immunoglobulin among patients with GBS.1 However, we have several concerns about the study. Several causes of hypoalbuminemia have been identified, including reduced synthesis, increased catabolism, an alteration in distribution, and increased loss through kidney/ skin/bowel.2 In this regard, we believe that selection bias may have confounded the results of this study. The serum samples were collected from patients at different time points.1 In particular, the status of the patients when the blood was drawn was not specified. It is strongly suggested that blood from patients who have been fasting should be collected for an analysis.2 Were the patients in a supine or upright position when the blood was drawn? Serum albumin is a relatively sensitive laboratory index, and food intake/position could influence the synthesis/distribution of the albumin,2 which could consequently influence the concentration of the albumin in the patient’s blood. Second, we remain cautious about the potential of serum albumin as a biomarker. Albumin may be oversensitive to be a biomarker to monitor the treatment effect of intravenous immunoglobulin. When hypoalbuminemia occurs, several alternative causes of hypoalbuminemia should be ruled out. Third, 2 alternative interpretations of the results are available. Infection is able to influence the level of serum albumin by increasing the transcapillary escape rate of albumin, and inflammation could reduce the hepatic synthesis of albumin.2 Various antecedent infections have been identified in GBS, and the disturbance of immune balance is long observed in GBS.3 Thus, the reduced level of albumin before treatment may be caused by the antecedent infection or inflammation. Moreover, albumin is synthesized by the liver, and hypoalbuminemia could be attributed to different liver diseases. A previous study has identified liver function disturbance among patients with GBS.4 Considering this, hypoalbuminemia may also result from a temporal liver function disturbance in GBS.