748 JAUNDICE. [BOOK n. 



absorption of the glycin and taurin respectively. From which 

 we may conclude that the presence of these bodies stirs up the 

 hepatic cell to an increased formation of cholalic acid. 



480. As a general rule the formation of bile acids runs 

 parallel with the formation of bile pigment, an increase or de- 

 crease of bile meaning an increase or decrease of both constituents. 

 But there are some facts which seem to shew that the two 

 actions may be dissociated. The condition or symptom known as 

 'jaundice ' is essentially an excess of bilirubin in the blood, whereby 

 the tissues such as the skin, and the fluids such as the urine are 

 coloured with the yellow pigment. In most of the maladies of which 

 jaundice is a symptom, there is evidence of an obstruction to the 

 flow of bile through the bile passages ; and the presence of bile in 

 the blood and hence in the tissues at large is in such cases due 

 to the fact that the bile after secretion by the hepatic cells is 

 reabsorbed from the bile ducts, see 256. 



But in certain cases where jaundice is a prominent symptom, 

 no evidence of any obstruction whatever to the flow of bile can be 

 obtained. This is the case in the jaundice of yellow fever and of a 

 peculiar allied malady known as ' acute yellow atrophy of the 

 liver.' Now in these cases there is no evidence of an accumu- 

 lation in the blood or elsewhere of bile-acids as there is of bile- 

 pigment. And in the obscure malady known as simple or idio- 

 ]i;ithic jaundice, in which though tin- anatomical conditions are 

 unknown there is at least no sign of obstruction, the urine though 

 loaded with bile pigment is said to contain no bile acids. 



It has been supposed that these cases afford proof that the bile 

 may be formed elsewhere than in the liver. In face however of the 

 arguments brought forward in the preceding paragraphs, they cannot 

 be accepted as proof that the normal formation of bilirubin is so 

 carried on ; nor is there any evidence to shew that in these cases 

 bilirubin is formed on a plan wholly different from the normal. 

 And a different explanation seems possible. We may suppose that 

 in these cases the metabolic activity of the hepatic cells is modified, 

 and, further, so modified as while affecting largely the formation of 

 bile salts and other functions of the hepatic cells, only partially to 

 affect the formation and discharge of bilirubin, to affect indeed its 

 discharge rather than its formation. That in acute yellow atrophy 

 the functions of the cells are greatly affected is not only indicated 

 by post mortem histological appearances, but is also shewn, as we 

 shall presently have occasion to point out, by the substitution of 

 leucin and tyrosin for urea in the urine. We have already 

 commented on the fact that there is something peculiar in the 

 action of the hepatic cell in secreting bilirubin inasmuch as the 

 bilirubin so formed may, under certain circumstances, in part pass 

 from the cell itself into the blood instead of into the bile passages. 

 And we may perhaps explain the jaundice of the diseases under 

 discussion by supposing that the morbid changes of the hepatic 



