Carey M C
Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Am J Surg. 1993 Apr;165(4):410-9. doi: 10.1016/s0002-9610(05)80932-8.
Gallstones form as a result of many disorders. Unphysiologic supersaturation, generally from hypersecretion of cholesterol, is essential for the formation of cholesterol gallstones. The other common abnormalities of the hepatobiliary system in gallstone patients are accelerated nucleation, gallbladder hypomotility, and the accumulation of mucin gel. An attempt is made here to relate hypersecretion of cholesterol and biliary supersaturation to the molecular basis of the associated phenomena. Supersaturation of bile with calcium hydrogen bilirubinate, the acid calcium salt of unconjugated bilirubin, is essential for pigment gallstone formation, but its magnitude remains undefined in model systems. Nucleation and the precipitation of calcium hydrogen bilirubinate with the polymerization of the pigment in the gallbladder, together with the deposition of the inorganic salts, calcium carbonate and phosphate, result in black pigment gallstone formation. On the basis of ex vivo muscle studies, gallbladder hypomotility is unlikely in patients with black pigment stones but is invariably present in patients with cholesterol stones. Pigment supersaturation in the gallbladder is the result of hepatic hypersecretion of bilirubin conjugates in hemolytic disorders and possibly enterohepatic cycling of unconjugated bilirubin in nonhemolytic states. Less common is bile salt hyposecretion from impaired synthesis in constitutional disorders and cirrhosis, and uncompensated interruption of the enterohepatic circulation in ileal dysfunction syndromes. Bile salt deficiency causes incomplete solubilization of unconjugated bilirubin and impaired binding of calcium ions. Stasis and anaerobic bacterial infection are responsible for brown pigment stones, which usually form in the bile ducts. In addition to the precipitation of calcium hydrogen bilirubinate that remains unpolymerized, there is also the deposition of the calcium salts of saturated fatty acids and free bile acids, both of which are the result of bacterial enzymatic hydrolysis of biliary lipids.
胆结石是由多种病症导致的。通常由于胆固醇分泌过多引起的非生理性过饱和，是胆固醇结石形成的必要条件。胆结石患者肝胆系统的其他常见异常包括成核加速、胆囊运动功能减退以及粘蛋白凝胶的积聚。本文旨在探讨胆固醇分泌过多和胆汁过饱和与相关现象分子基础之间的关系。胆汁与胆红素酸式钙盐（未结合胆红素的酸式钙盐）过饱和，是色素结石形成的必要条件，但其在模型系统中的程度仍不明确。胆红素酸式钙盐的成核和沉淀，以及色素在胆囊中的聚合，再加上无机盐（碳酸钙和磷酸钙）的沉积，导致黑色色素结石的形成。基于离体肌肉研究，黑色色素结石患者不太可能出现胆囊运动功能减退，但胆固醇结石患者则总是存在这种情况。胆囊中色素过饱和是溶血性疾病中肝脏胆红素结合物分泌过多以及非溶血性状态下未结合胆红素可能发生肠肝循环的结果。较少见的情况是，先天性疾病和肝硬化时合成受损导致胆汁盐分泌减少，以及回肠功能障碍综合征中肠肝循环未得到代偿性中断。胆汁盐缺乏会导致未结合胆红素溶解不完全以及钙离子结合受损。胆汁淤积和厌氧菌感染会导致棕色色素结石形成，这种结石通常在胆管中形成。除了未聚合的胆红素酸式钙盐沉淀外，还会有饱和脂肪酸钙盐和游离胆汁酸的沉积，这两者都是胆汁脂质细菌酶解的结果。
