COVID-19 vulnerabilities are intensified by declining human serum albumin levels.

Abstract

What is the topic of this review? Human serum albumin (HSA) a common factor in COVID‐19 vulnerabilities. What advances does it highlight? Understanding of HSA capacity, and systemic vulnerabilities to COVID‐19. Raising HSA in COVID‐19 patients may alleviate systemic injury caused by diminished native HSA binding. A change in fluid therapy administration into the portal system of the liver is proposed to safely raise HSA levels. The specific nature of the vulnerabilities to COVID‐19 are an intrinsic part of COVID‐19 infection in many patients. This paper proposes that vulnerabilities to COVID‐19 may be intensified by a decrease in human serum albumin (HSA) as a ligand carrier for nutrients. A mechanism for COVID‐19 vulnerabilities is evident from consideration of ligand carriers such as HSA as intermediaries. We hypothesise that low levels of pool HSA binding, caused for whatever reason, affect the performance of albumin as a carrier protein reducing the availability of nutrients. Hypoalbuminaemia (low HSA) has been implicated as an indicator of COVID‐19 and long‐COVID‐19. The levels of HSA directly affect the immune system and vulnerabilities to age, diabetes and obesity in COVID‐19. Any slight reduction in available HSA has profound effects on ligand concentrations in the small capillaries where damage occurs in COVID‐19. The clinical implication is that attempts should be made to return HSA to clinical levels to compensate for the additional ligands caused by infection (SARS‐CoV‐2 virions, antibodies and cellular breakdown products). Therapeutic albumin is usually given peripherally, and usual preparations are unbound to ligands, but we suggest that a clinical trial of HSA therapy via the hepatic portal vein should be considered.