BILIARY CALCULI 457 



because these colloids deposit in that form {e. g., corpora amylacea 

 and other protein concretions). These considerations explain the for- 

 mation of gall-stones in the gall-bladder from either inflammation, 

 or stagnation without inflammation. 



Aschoff and Bacmeister,**** however, hold that the usual series of 

 events in the formation of gall-stones is first the formation of a pure 

 cholesterol stone without inflammatory cause, because of actual in- 

 creased excretion of cholesterol by the liver, because of cholesterolemia; 

 or because of resorption of solvent substances from stagnating bile: 

 these primary cholesterol stones then cause inflammation and occlu- 

 sion, leading to the formation of the common mixed stones. Bac- 

 meister ascribes more importance to calcium than do most o<"her 

 investigators, in which he is supported by Rosenbloom,*^ while Kuru^" 

 states that fibrin is usually present. Boscnbloom reports a small 

 series in which concretions composed chiefly of calcium were found in 

 all cases with a history of infection, while in cases without infection 

 the stones we;*e cholesterol. 



More recent studies of the cholesterol content of the blood and bile 

 also have reacted against the concept that all the cholesterol of gall- 

 stones comes from the wall of the bile tract through inflammatory 

 changes. It has been found that patients with gall-stones often show 

 a hypercholesterolemia;^^ that pregnancy, which seems to be a predis- 

 posing cause of cholelithiasis, is accompanied by hypercholesterolemia; 

 that in races subject to cholelithiasis there is more cholesterol in the 

 diet and in the blood than in those races that seldom have gall-stones 

 (DeLangen) ; that with hypercholesterolemia there is an increased out- 

 put of cholesterol in the bile, and that experimental hypercholester- 

 olemia may lead to the formation of gall-stones without evident 

 infection of the bile tracts (Dewey^^). 



As far as the existing evidence permits one to draw conclusions, it 

 would seem probable that both local and systemic conditions are of 

 iniyortance iii gall-stone formation. Apparently, gall-stones may form 

 from cholesterol derived from the inflamed bile tract walls, independent 

 of the amount of cholesterol present in the bile; but presumably they 

 may derive part if not all the cholesterol from the bile in some cases. 

 In either event, a hj^percholesterolemia will favor their formation, 

 and hence any given condition of injury to the gall bladder will more 

 often give rise to concretions in persons with a high cholesterol content 

 in the blood. ^^ Changes in the bile itself may be produced by disease 



88 Ziegler's Beitr., 1908 (44), 528. 



89 Jour. Amer. Med. Assoc, 1917 (69), 1765. 

 »" Virchow's Arch., 1912 (210), 433. 



»i Henes, Surji., Gyn. and Obst., 1916 (23), 91. 



»2 Arch. Int. Med., 1916 (17), 757; see also Aoyama, Deut. Zeit. Chir., 1914 

 (132), 234. 



9^ This relation of hypercholesterolemia and infection to cholelithiasis is sup- 

 ported by the extensive observations of Rothschild and Wilensky (Anier. Jour. 

 Med. Sci., 1918 (156), 239, 404, 564; Arch. Int. Med., 1919 (24), 520), who find 

 some types of cases accompanied by cholesterol increase, which is missing in 

 many cases of inflammatory cholelithiasis. (See also Reimann and Magown, 

 Surg., Gynec. and Obst., 1918 (26), 282; Fasiani, Arch. Sci. Med., 1918 (41), 144. 



