490 PATHOLOdlCAL I'IGMEXTATION 



they may fail to pass into the tissues; hence we may have cholemia 

 without icterus or chohiria, because of the tirmness with wliich tlie pig- 

 ments are bound in the plasma (Hoover -^). 



The question whether in icterus the skin may be colored by other 

 pigments than bilirubin, especially by its reduction product, urobilin, 

 seems to have been decided negatively. Hile-pignient is probably not 

 absorbed as such from the intestine in sufficient quantity to cause 

 icterus. Such bile-pigment as enters tlie blood from the liver is ex- 

 creted through the kidneys chiefly, but also in the sweat. Ordinarily, 

 other secretions (milk, tears, saliva, sputum) are not colored in jaun- 

 dice, but if the secretions are mixed with inflammatory exudations, 

 they may then be colored (e. g., pneumonic sputum). When the bile- 

 pigment is resorbed from the skin, it may be in part transformed into 

 urobilin, which appears in the urine in increased amounts during the 

 period of recovery from jaundice. Part of the bile-pigment is prob- 

 ably eliminated by the liver after the cause of obstruction has been 

 removed from the bile-passages. 



Urobilin ^-'^ is probably formed chiefly, if not solely, from bile pig- 

 ments by the action of reducing bacteria in the intestine. It is ex- 

 creted in the urine only as its chromogen, urobilinogen, but in the 

 feces both urobilin and urobilinogen may be found ; when exposed to 

 air the chromogen oxidizes quickly to urobilin. Addis ^^ states that 

 bilirubin is reduced to urobilinogen, in the bowel and is then largely 

 absorbed, to be at once oxidized and polymerized into urobilin, two 

 molecules of urobilinogen uniting under the influence of oxygen to 

 form one of urobilin. In the liver the urobilin is largely worked over 

 to form new hemoglobin, and hence the functional capacity of the 

 liver is indicated by the completeness with which it utilizes the uro- 

 bilin, except in cases of excessive formation of urobilinogen as a re- 

 sult of hemolysis. The amount of urobilinogen in the urine will be 

 found increased, therefore, in hemolytic icterus, and decreased in ob- 

 structive icterus. However, with advanced renal disease the kidneys 

 may become unable to excrete the urobilinogen brought to them in the 

 blood. Exceptionally, urobilinogen may be fonned from blood dis- 

 integrated in bloody effusions without evident participation of the 

 liver, e. g., urobilinogenuria in hemorrhagic ascites, with hemolytic 

 poisons, etc. AVith a normal liver urobilinogeiuiria is found only 

 when there is excessive hemolysis, otherwise urobilinogenuria occurs 

 only with an injury to the liver parenchynui (Ilildebrant). Occlu- 

 sion of the bile ducts stops an existing urobilinogenuria by prevent- 

 ing the formation of urobilinogen in the intestine. Normally there is 

 a very small amount of urobilinogen and related substances in the 

 urine, which disappears when there is no bile in the intestine. From- 



"ii T>il)lio<rrapliv and review bv INfever-Botz, Erffpli. inn. ^lod., litl."] (12). 734; 

 Willnir and Addis, Arcli. Int. Med., "l 014 (13), 235. 

 ai^Arcli. Fnt. Med.. IOI.t (15), 412. 



