Published online Dec 27, 2015. doi: 10.4240/wjgs.v7.i12.370
Peer-review started: July 14, 2015
First decision: September 22, 2015
Revised: October 12, 2015
Accepted: November 10, 2015
Article in press: November 11, 2015
Published online: December 27, 2015
Processing time: 167 Days and 12.9 Hours
Albumin is the single most abundant protein in the human serum. Its roles in physiology and pathology are diverse. Serum albumin levels have been classically thought to reflect the nutritional status of patients. This concept has been challenged in the last two decades as multiple factors, such as inflammation, appeared to affect albumin levels independent of nutrition. In general, cancer patients have a high prevalence of hypoalbuminemia. As such, the role of hypoalbuminemia in patients with colorectal cancer has received significant interest. We reviewed the English literature on the prognostic value of pretreatment albumin levels in colorectal cancer. We also consolidated the evidence that led to the current understanding of hypoalbuminemia as an inflammatory marker rather than as a nutritional one among patients with colorectal cancer.
Core tip: Early studies had shown a prognostic value of hypoalbuminemia in colorectal cancer. The relationship between albumin levels and survival was more consistent when the former was coupled to C-reactive protein, a classic inflammatory marker, in the modified Glasgow prognostic score (mGPS). This relationship also appeared to be independent of nutrition on multivariate analyses. The superiority of mGPS in predicting survival supports inflammation as the major culprit of poorer outcomes. A number of studies showing an association of lower albumin-to-globulin ratios with poorer survival are also in favor of a tilt towards proinflammatory states as the cause of morbidity and mortality. Cancer cachexia is a downstream consequence of the systemic inflammation brought in by colorectal cancer. In this view, albumin is a negative acute phase reactant rather than a nutritional marker. Interventions aimed to halt cancer cachexia should therefore target inflammation.