Appropriate Human Serum Albumin Fluid Therapy and the Alleviation of COVID-19 Vulnerabilities: An Explanation of the HSA Lymphatic Nutrient Pump

COVID-19 and long COVID-19 vulnerabilities may be caused indirectly by albumin binding deficiency (ABD), which can be corrected by the correct administration of human serum albumin (HSA). The liver is the primary site of nutrient regulation and fluid volume maintenance;control of both is by changes to albumin concentration. In healthy subjects, the HSA lymphatic nutrient pump (HSALNP) ensures continual pumping of nutrients from the liver and that nutrients are appropriately distributed to organs. Nutrients are delivered to cells according to the availability of binding to HSA. The HSALNP, therefore, maintains the correct nutrient and colloidal pressure balance in all tissues independently. In unhealthy tissues, following COVID-19 infection, the passage of HSA/nutrients through the interstitial spaces and lymph will be impeded. Fluid therapy into the periphery leads to the dilution of essential nutrients attached to the protein carriers such as albumin. The levels of albumin being charged by the liver with nutrients is critical in maintaining immune stability by maintaining nutrient support and colloidal pressure of the cellular structures. The site of HSA binding by the liver is of great importance, and direct infusion of albumin into the hepatic portal vein is the most appropriate method of maintaining colloid pressure and cellular nutrient levels.

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

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. ABSTRACT: 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.

SARS-CoV-2 Bound Human Serum Albumin and Systemic Septic Shock.

The emergence of the COVID-19 virus and the subsequent pandemic have driven a great deal of research activity. The effects of COVID-19 are caused by the severe respiratory syndrome coronavirus 2 (SARS-CoV-2) and it is the underlying actions of SARs-CoV-2 virions on the endothelial glycocalyx that we consider here. One of the key factors in COVID-19 infection is its almost unique age-related profile, with a doubling in mortality every 10 years after the age of 50. The endothelial glycocalyx layer is essential in maintaining normal fluid homeostasis, but is fragile and prone to pathophysiological damage. It is physiologically significant in capillary microcirculation and in fluid distribution to the tissues. Human serum albumin (HSA), the most abundant protein in plasma, is created in the liver which also maintains its concentration, but this reduces by 10-15% after 50 years of age. HSA transports hormones, free fatty acids and maintains oncotic pressure, but SARS-CoV-2 virions bind competitively to HSA diminishing its normal transport function. Furthermore, hypoalbuminemia is frequently observed in patients with such conditions as diabetes, hypertension, and chronic heart failure, i.e., those most vulnerable to SARS-CoV-2 infection. Hypoalbuminemia, coagulopathy, and vascular disease have been linked in COVID-19 and have been shown to predict outcome independent of age and morbidity. Hypoalbuminemia is also known factor in sepsis and Acute respiratory distress syndrome (ARDS) occurs when fluids build-up in the alveoli and it is associated with sepsis, whose mechanism is systemic, being associated with the fluid and logistic mechanisms of the circulation. Glycocalyx damage is associated with changes plasma protein concentration, particularly HSA and blockage of albumin transport can produce the systemic symptoms seen in SARS-CoV-2 infection and sepsis. We therefore conclude that albumin binding to SARS-CoV-2 virions may inhibit the formation of the endothelial glycocalyx by inhibition of albumin transport binding sites. We postulate that albumin therapy to replace bound albumin might alleviate some of the symptoms leading to sepsis and that clinical trials to test this postulation should be initiated as a matter of urgency.

Postoperative fever in the time of COVID-19.

Summary: Postoperative fever is common following orthopedic trauma surgery. As the prevalence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection increases in the community, migration into the acute care hospital setting intensifies, creating confusion when fever develops postoperatively. The transmission dynamics of SARS-CoV-2 make it difficult to adequately gauge and pinpoint risk groups with questionnaires at the time of hospital admission. This is particularly problematic when asymptomatic or presymptomatic patients infected with SARS-CoV-2 require urgent surgery and cannot be screened effectively. One approach is to treat every patient as though they were SARS-CoV-2-positive in preparation for surgery, but doing so could exacerbate shortages of personal protective equipment and staffing limitations. Uncertainty regarding the etiology of postoperative fever could be significantly reduced by universal SARS-CoV-2 testing of all surgical patients at the time of hospital admission in addition to routine screening, but testing capacity and a rapid turnaround time would be required.