No abstract

No abstract

In present-day opinion a humoral disturbance, resulting in chemical changes in the composition of the bile, makes an essential contribution to the pathogenesis of gallstone disease. Other factors play a secondary part, and among them biliary stasis as a predisposing cause is a t present the subject of active interest. Disturbances in gallbladder motility, dyskinesias, are extremely often associated with biliary stasis which, according to the generally accepted opinion, is not per se a primary cause of stone formation. Copher and Illingworth's (7) well known animal experiments show that stone formation cannot be produced either by stasis alone or by a combination of stasis and infection. Caroli (4) has stated that biliary dyskiiiesia is very seldom the cause of gallstone formation. Westphal (15) disagrees with him and points out that one must reckon not only with muscular dysfunction, but also with disturbances in resorption which modify the composition of the bile and promote concrement formation. The conflicting opinions are largely due to different connotations of the term dyskinesia, i. e, whether this term covers only cases of biliary colic or all disturbances in motility with or without attacks. In my opinion disturbed motility in the bile passages is always a form of dyskinesia, and i)b unoperatea cases the dyskinesia can be defimd as a disturbances i n the reciprocal relations between the motility of the gallbladder and that of the sphincter of Oddi.The sluggishlyr emptying gallbladder (SEG) is a very common radiologic finding which frequently receives no attention. Clinically this group includes asymptomat,ic cases (10 per cent according to Feldman (8)), cases with dyspeptic symptoms and with biliary colics. The pathogenesis of these last cases has been explained with the aid of radiomanometry by Caroli, Albot, Mallet-Guy and coworkers (1, 12) on the basis of mechanical defects and spastic conditions in the cystic duct and the sphincter of Oddi. A positive SEG finding with good ability Parkgatan 7 B, Helsingfors. 530613. dcta med. Scandinao. Vol. CXLV. -

No abstract

No abstract