HPE Human albumin handbook | Page 11

returns to the systemic circulation through the lymphatic system . Albumin in extracellular fluid enters the interstitial space by endothelial cell endocytosis . It is mainly degraded by lysosomes in muscle , liver and kidney before being released into the extracellular fluid . The rate of dynamic exchange is maintained with a rate of 5 % per hour . Circulation half-life is about 16 – 18 hours . Under physiological conditions , the overall half-life in healthy young adults is approximately 12 – 19 days . Synthesis and degradation proceed almost simultaneously to maintain a balance . ^{7 , 8}

Function of albumin As the most important regulator of body fluid distribution among plasma colloids , albumin contributes to 70 %– 80 % of osmotic pressure . The effect is primarily explained by the smaller molecular weight and higher plasma concentration as well as its water retention effect due to the negative charge on its surface to adsorb sodium ions . ^{7 , 8} It is estimated that 1g can reabsorb approximately 18ml of fluid from the interstitial space . ⁹ In addition to its well-known function of maintaining colloid osmotic pressure , albumin has many physiological functions related to its special tertiary structure , such as binding and transporting various hydrophobic endogenous molecules ( such as cholesterol , fatty acids , bilirubin , thyroxine , etc ) and exogenous molecules ( including non-steroidal antiinflammatory drugs , warfarin , antibacterial drugs , furosemide , etc ). It binds with ROS , reactive nitrogen species ( RNS ), nitric oxide and metal ions as an antioxidant . It regulates immune and inflammatory responses ( for example , binding endotoxin , prostaglandins and pro-inflammatory cytokines ) and maintains functional integrity of microcirculation ( for example , endothelial stability and anti-platelet aggregation ). ¹⁰

It should be emphasised that albumin is only distributed in body fluids and not stored in tissues . Therefore , depletion and degradation upon starvation and stress is not elevated . The serum albumin level is affected by many factors such as changes in body fluid distribution volume , disease loss , substrate supply , and liver function . It is not an ideal indicator for nitrogen balance and nutritional status of the body . ¹¹

Albumin treatment in cirrhosis : Basic rationale Hypoalbuminaemia is one of the manifestations of cirrhosis and is an independent risk factor for poor prognosis . It is not only explained by decrease in albumin synthesis by liver cells , but also by dilution of extracellular fluid albumin due to water and sodium retention blood volume increase , elevated albumin catabolism and albumin permeation through capillaries to the interstitial space . ^{7 , 8} In addition to changes in the amount of albumin , the pro-inflammatory and pro-oxidative status of advanced cirrhosis also induce changes in the structure and function of albumin . As the severity of the disease escalates , extensive post-transcriptional changes of albumin gradually occur . Physiological functions such as the ability to sequester cobalt and the ability to bind and transport are

12 , 13 compromised .

FIGURE 2

Potential role of albumin in liver cirrhosis and complications

Cirrhosis

Endothelial stabilisation Portal hypertension

Immunomodulation

Splanchnic vasodilation

Bacterial translocation Endotoxaemia Inflammation

Effective arterial hypovolaemia

Activation vasoconstrictor systems Renin-angiotensin-aldosterone system Sympathetic nervous system Antidiuretic hormone

Oncotic pressure Endothelial stabilisation Capillary permeability

Oncotic pressure