Upper gastrointestinal bleeding: an ammoniagenic and catabolic event due to the total absence of isoleucine in the haemoglobin molecule

Upper gastrointestinal bleeding causes increased urea concentrations in pat ients with normal liver function and high ammonia concentrations in patient s with impaired liver function. This ammoniagenesis may precipitate encepha lopathy. The haemoglobin molecule is unique because it lacks the essential amino acid isoleucine and has high amounts of leucine and valine. Upper gas trointestinal bleeding therefore presents the gut with protein of very low biologic value, which may be the stimulus to induce a cascade of events cul minating in net catabolism, This may influence the function of rapidly divi ding cells and short half-life proteins. We hypothesize that, following a v ariceal bleed in a cirrhotic patient, the lack of isoleucine in blood prote in is the cause of the exaggerated ammoniagenesis and catabolism, We propos e that intravenous administration of isoleucine may serve as a simple thera peutic that transforms blood protein in a balanced protein, resulting in on ly a short-lived rise in ammonia and urea production, and preventing interf erence with protein synthesis.