Serum albumin, a good indicator of persistent organ failure in acute pancreatitis

Acute pancreatitis (AP) is known to be an inflammatory disorder which has a process observed clinically from local pancreatitis through the systemic inflammatory response, organ dysfunction and death. Minority patients will develop a severe disease with local or systemic complications even organ failure (OF) while most patients suffer from a mild, self-limiting inflammatory process [1]. The severe AP (SAP) has been redefined as AP with persistent organ failure (OF lasts more than 48 h) with a lethality rate of 20–50% according to 2012 revised Atlanta classification for AP [2‐7].

It is vital for the determination of therapeutic strategy to have an early assessment of disease severity because effective treatment could significantly decrease mortality of patients with severe pancreatitis [8, 9]. Some invasive or non-invasive methods, including scoring systems, radiological imaging modalities, and biochemical parameters are used for diagnosing and evaluating disease severity of AP.

Abnormal low-level of albumin signals act as a pivotal starter in the pathogenesis of AP. The hypoproteinemia has been observed in AP patients and the mechanism was studied too. There are also some therapy aimed at albumin having been used on AP patients [10]. However, with the publication of revised Atlanta classification for AP, the relationship between incidence of POF in the AP pathophysiology and serum albumin has not been assessed yet. Our study was aimed to evaluate the value of serum albumin on admission of hospital in correlation with the incidence of POF in AP.

Acute pancreatitis is one of the most serious emergencies in abdominal surgery department. Although we have met amount of patients with acute pancreatitis who got satisfactory results, we still have to pay attention to this disease for its high mortality especially in severe type. We designed our research according to 2012 revision of the Atlanta Classification of acute pancreatitis, and we found the level of albumin in acute pancreatitis patients with POF is much lower than patients without POF.

Albumin, with 585 residues, and three domains of similar size, each one containing two sub-domains, is a stable and very flexible heart-shape-molecule [11]. It’s a natural plasma protein of which the median half-life is around 18 to 19 days and synthesized only by liver at a rate of 9 to 14 g per day in healthy individuals [12]. However, albumin can be catabolized in most organs of the body at a similar rate by uptake into endocytotic vesicles on the endothelial surface and finally turn into amino acids as breakdown products [12, 13].

Albumin has well-known effects on maintaining fluid balance, being responsible for 75 to 80% of colloid osmotic pressure in the basal physiological state [12, 14]. Albumin can bind to an extremely wide range of endogenous and exogenous ligands, to transport them to specific tissues and organs, to increase their solubility in plasma, or to dispose of them when they are toxic. The chemical structure of albumin can be altered by some specific processes (oxidation, glycation) leading to rapid clearance and catabolism [11].

In the progress of many diseases, including cancer, infection, inflammation, a low-level of serum albumin has been identified [15‐18]. According to the researches into the phenomenon of low-level of serum albumin in those diseases, abnormal metabolism of albumin led by inflammation response may be an important reason for that, as well as a low intake of albumin [19]. The mechanism is not clear yet, however, IL-6 and other inflammatory cytokines may play an important role in it [11, 18]. Similarly, this phenomenon has also been found in AP, especially obvious in severe acute pancreatitis patients. The mechanism is complicated and not so clear yet. But some researches also gave explanation, that (a) The reaction in the progress of SAP, including infection, will lead to insulin resistance, which may at last result in metabolic disorders. Thus, the degradation of albumin gets much more for the reason of lower using-rate of glucose and fat; (b) The ability of biosynthesis of albumin in liver is weak for low intake and stimulate of inflammatory factors; (c) In the progress of stress response, vasopermeability become higher so that albumin will permeate into tissue space [11, 13, 15, 20, 21].

POF, which develops in 10–20% of AP patients with a mortality rate between 20 and 50%, is the most important cause of death within the first 2 weeks of disease onset [2, 3]. It’s critical to have the ability to assess the risk of AP patients developing POF earlier upon hospitalization, both for triaging patients to the appropriate grade of care and for designing appropriate intervention and medical treatment [22]. Lots of invasive or non-invasive methods, including biochemical parameters, severity scores and radiological imaging modalities have been applied for predicting POF in patients with AP. In a systemic review for prospective studies, the Bedside Index of Severity in Acute Pancreatitis (BISAP) and the Japanese Severity Score were identified as the best predictors evaluating predictors of POF within 48 h of admission [23]. The Japanese Severity Scale showed a specificity of 0.90 with a cutoff value of 1. But they were too cumbersome to be applied in the individual patient. The Japanese Severity Scale was made up of 21 parameters, and the BISAP included a total of 8 parameters. This highlights the need to develop approaches to prediction of POF that have early practical utility while still providing a performance sufficient to be applied in the individual patient. Another study found that the Glasgow score is the best classifier at 48 h of admission for predicting POF in patients with AP by using a head-to-head comparison between the Ranson, APACHE II, Glasgow and the BISAP scoring systems [24]. Mounzer et al. compared several existing clinical scoring systems and found that these scores showed modest accuracy (AUC at admission of 0.6 to 0.8 in both the training and the validation cohorts) and seemed to have reached their maximal efficacy to predict POF in patients with AP [25].

Though the boxplot showed that low-level of ALB2 also had a closely relation to the development of POF on AP patients, the prediction function of ALB2 is not reliable: (1). Patient with low-level serum albumin 48 h after admission may have been in POF state, that is low-level ALB 48 h later could be the result of POF rather than an indicator. (2). During the 48 h in hospital, different therapies were used including infusion of human serum albumin, which can lead to error in our research. (3). The indicator of POF need to help us make decision as soon as we checked our patients, 48-h is quite a long time.

However, the intra-individual variation in albumin value can be another interesting study to be addressed.

There are several limitations of the present study. The sample size of our study is a bit small. And the causality role of POF and albumin in AP, however, requires to be investigated further in a prospective validation study as it is an observational study.

In conclusion, our present study reveals that serum albumin on admission is independently associated with POF in AP. We suggest that albumin is a valuable tool for a rapid assessment of POF in patients with AP.