FACTORS ALTERING CONCENTRATION OF BLOOD LIPIDS 459 



i. The Blood Lipids in Hepatic Disease, (a) In Cholelithiasis. When 

 gallstones are formed which do not become lodged in the bile ducts, no 

 abnormalities in lipid metabolism or in the level of blood lipids can be 

 noted. Since the gallstones are frequently composed of cholesterol, it 

 has been postulated that they result from an abnormally high amount of 

 cholesterol in the bile. However, it has been demonstrated that non-ob- 

 structive cholelithiasis is not associated with hypercholesterolemia. 671-673 

 Turner et al. 67i reported that the activity of the cholesterol-esterifying 

 enzyme was normal in cholelithiasis and stricture of the common bile duct, 

 as well as in cholecystitis. 



(6) In Obstruction of the Common Bile Duct. It is obvious that, when 

 the common bile duct is occluded by calculi or by a tumor, the absorption 

 of lipids will be retarded, due to the lack of bile acids in the intestine. 

 The effect of such a condition would be akin to that described for steator- 

 rhea, in which there is a considerable excretion of fat in the stools. One 

 would expect that, in the event of bile stoppage, the alimentary lipemic 

 response would be largely abolished. 



However, the retention of cholesterol caused by the inability to excrete 

 it in the bile causes a pronounced increase in serum cholesterol, 215 ' 671,673 ' 675 ' 676 

 which may reach as high as 1000 milligram per cent. 672 Heinlein 676 sug- 

 gests that the hypercholesterolemia occurring in obstructive jaundice is 

 due not to a defect in excretion but to a disturbance of the storage function 

 of the liver. The higher levels of cholesterolemia are generally found in 

 cases of long-standing obstruction. Albrink et a?. 677 reported that an in- 

 crease in the ratio of free to esterified cholesterol obtained in this condi- 

 tion. However, if the obstruction is not relieved, the blood cholesterol 

 falls prior to death. 672 Byers and co-workers 678 reported that the rapid 

 and marked increase in the cholesterol content of the plasma of rats after 



666 N. Poczka and W. Fischel, Deut. Arch. klin. Med., 177, 14-28 (1934). 



666 D. Adlersberg and H. Sobotka, /. Nutrition, 25, 255-263 (1943). 



667 W. H. Barker and C. P. Rhoads, Am. J. Med. Set., 194, 804-810 (1937). 



668 C. E. Kellett, Lancet, 1932, II, 1270-1272. 



669 T. E. H. Thaysen, Quart. J. Med., n.s. 4, 359-395 (1935). 



670 P. Vogt-M0ller and B. Lawaetz, Acta Med. Scand., 92, 105-134 (1937). 



671 E. Z. Epstein, Arch. Internal Med., 50, 203-222 (1932). 



672 E. Z. Epstein and E. B. Greenspan, Arch. Internal Med., 58, 860-890 (1936). 



673 J. A. Gardner and H. Gainsborough, Quart. J. Med., 23, 465-483 (1930). 



674 K. B. Turner, G. H. McCormack, Jr., and A. Richards, J. Clin. Invest., 32, 801-806 

 (1953). 



676 W. B. Hawkins and A. Wright, J. Exptl. Med., 59, 427^39 (1934). 



676 H. Heinlein, Z. ges. exptl. Med., 91, 638 (1933). 



677 M. J. Albrink, E. B. Man, and J. P. Peters, J. Clin. Invest., 29, 781-788 (1950). 



678 S. O. Byers, M. Friedman, and F. Michaelis, J. Biol. Chern., 188, 637-641 (1951). 



