PubMed · 6927181
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H Jinich. [Cholestasis].. https://pubmed.ncbi.nlm.nih.gov/6927181/
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Laparoscopic cholecystotomy (LCT) with subsequent extraction of gallstones and primary closure of the gallbladder has been introduced as an alternative therapy for patients with cholecystolithiasis and preserved gallbladder function. However, stone recurrence has to be considered as a major drawback that might be related to lithogenic factors of gallbladder bile or the composition of gallbladder stones. Therefore, these were studied in relation to stone recurrence within an observation period of 1 to 5 years (median, 3.6 years) in 50 patients after LCT. The concentrations of total and individual bile acids, phospholipids, cholesterol, total lipids, mucin, protein, and the cholesterol saturation indices in gallbladder bile were not significantly different between 10 patients with and 40 patients without stone recurrence. However, the crystal observation time was significantly (P < .02) shorter (range, 1-2 days; median, 1.5) in the bile of patients with stone recurrence compared to those without (range, 1-21 days, median 3.5). Moreover, all 10 stone recurrences were observed in the 28 patients with a crystal observation time in the bile of less than or equal to 2 days (approximate annual risk: 12%-15%), and no recurrences were observed in the 22 patients with a crystal observation time greater than 2 days (P < .0001) or in patients with pigment stones. The rapid formation of cholesterol monohydrate crystals in bile seems to be the major risk factor for recurrent stones after LCT. These are most likely cholesterol stones and, therefore, are amenable to oral bile-acid prevention or treatment.
Litholytic bile acid ursodeoxycholic acid (UDCA) reduces biliary cholesterol secretion and alters cholesterol metabolism by mechanisms that are not fully understood. To evaluate cholesterol metabolism during UDCA treatment, we studied serum and biliary lipids and cholesterol precursor sterols (lanosterol and other dimethyl and monomethyl sterols, lathosterols, and desmosterol), indicators of cholesterol synthesis, and plant sterols campesterol and sitosterol, indicators of cholesterol absorption, before and during administration of UDCA, 9 mg/kg/d, for 26 weeks in eight patients with radiolucent gallstones. During UDCA administration, serum lipid concentrations were unchanged, but the biliary concentration and molar percentage of cholesterol were markedly decreased. The proportions of the cholesterol precursor sterols to cholesterol were significantly interrelated between serum and bile before and especially during UDCA administration. Lanosterol and lathosterol levels, especially in bile, were significantly decreased by 43% and 34%, suggesting that UDCA may inhibit cholesterol synthesis. Levels of the other methylated precursor sterols were increased in serum and bile. The esterification percentages of all sterols were unchanged. The plant sterol-to-cholesterol ratios increased significantly in serum and bile, and there was an inverse correlation between the increment of serum plant sterols and decreased biliary molar percentage of cholesterol. In conclusion, UDCA may inhibit cholesterol synthesis possibly at the squalene synthase or 4alpha-demethylase steps, resulting in decreased biliary secretion of cholesterol. Reduced biliary sterol secretion probably increased serum plant sterol levels, indicating that under these conditions they no longer reflect the intestinal efficiency of cholesterol absorption.
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