• Plasma proteins, except immunoglobulins and complement;
• Most coagulation factors, including fibrinogen and factors II (prothrombin), V, VII, IX, X, XI, XII and XIII. Of these prothrombin (II) and factors VII, IX and X cannot be synthesized without vitamin K;
• The lipoproteins, VLDL and HDL;
• Primary bile acids.
The liver has a very large functional reserve. Deficiencies in synthetic function can only be detected if liver disease is extensive; such abnormalities are more often due to nonhepatic factors. For example, before a fall in plasma albumin concentration is attributed to advanced liver disease extrahepatic causes must be excluded, such as the loss of protein through the kidney, gut or skin, or across capillary membranes into the interstitial space as in even mild inflammation or infection.
Prothrombin levels, assessed by measuring the prothrombin time, may be reduced because of impaired hepatic synthesis, whether due to failure to absorb vitamin K or to hepatocellular damage. If hepatocellular function is adequate, parenteral administration of vitamin K will reverse the abnormality.