452 CALCIFICATION, CONCRETIOXS, .l.VZ) IXCRl'STATIOyS 



masses, consisting chiefly of cholesterol and bilirubin-calcium. From 

 this material calculi may eventually form, and by their irritation lead 

 to further formation of cholesterol and increased o:rowth.''*'^ But 

 bacterioloo-ical studies indicate that generally an infectious influence 

 is present in cholelithiasis, and bacilli may be found alive in gall-stones 

 for remarkably long periods. 



Recent applications of colloidal chemistry' add much to our under- 

 standing of gall-stone formation. Thus, Lichtwitz points out that 

 the colloids of normal bile, all of which are electro-negative, may be 

 precipitated by positive serum colloids coming from the blood when 

 the gall-bladder is inflamed ; hence we get a precipitate of cholesterol, 

 bilirubin and proteins. Wlien the colloids are thus thrown down the 

 solvent power of the bile for the alkali earths it contains is decreased, 

 and so calcium or magnesium are added to the mixture. Cholesterol 

 is in solution in the bile as an emulsion colloid, and when stagnation 

 of the bile leads to absorption or disintegration of the cholates and 

 fats which keep it in solution, the droplets become confluent, and 

 then ciystallization takes place (Schade) with formation of sphero- 

 liths, and eventually a crystalline cholesterol calculus. If cA'en the 

 slightest pressure is brought to bear on the myelin-like masses before 

 they crystallize, however, they will be pressed into scales, and the 

 common laminated structure results ; hence crystalline calculi are 

 single, while multiple gall-stones are laminated, with perhaps partial 

 crystallization between the lamellae. Also when the gall-stones result 

 from inflammation, and there is much serum colloid present, the 

 stones are lamellated because these colloids deposit in that form (e. g., 

 corpora amylaeea and other protein concretions). These considera- 

 tions explain the formation of gall-stones in the gall-bladder from 

 either inflammation, or stagnation without inflammation. 



AschofiP and Bacmeister,*'" however, hold that the usual series of 

 events in the fonnation 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 cholester- 

 olemia, or because of resorption of solvent substances from stagnating 

 bile; these primary cholesterol stones then cause inflammation and 

 occlusion, leading to the formation of the common mixed stones. 

 Bacmeister ascribes more importance to calcium than do most other 

 investigators, while Kuru ^^ states that fibrin is usually present. 



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

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

 stones comes from the wall of the bile tract througli inflammatory 

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



"^a Concerninfj the stnicturo of frail stonos sec Kibhort. VirchowV Aroli.. IHlo 

 (220), 20. 

 nn Zioplor's Beitr., lOOR (44), .'i2S. 

 «7Virc]iow's Arch., 1912 (210), 4.1.'^. 



