Jon Ahlberg

Prevalence of gallbladder disease in hyperlipoproteinemia

An analysis of the occurrence of gallbladder disease (ie, cholelithiasis, cholecystitis, cholecystectomy) in 210 consecutive patients with primary hyperlipoproteinemia showed that the prevalence of gallbladder disease was 8%, 18%, and 42% in males with type IIa, IIb, and IV hyperlipoproteinemia, and 22%, 48%, and 72% in the corresponding groups of females. The 40–59-year-old patients were compared to three necropsy series from Malmö, Sweden. The occurrence of gallbladder disease was within normal limits in type IIa and abnormally high in type IV hyperlipoproteinemia. There were no differences with regard to age, body weight, glucose intolerance, or ischemic heart disease between type IV patients with and without GBD. It is suggested that certain forms of disturbances of lipoprotein metabolism are associated with an increased risk for development of gallbladder disease.

Occurrence of cholesterol monohydrate crystals in gallbladder and hepatic bile in man: influence of bile acid treatment

Abstract The occurrence of cholesterol monohydrate crystals was examined and related to the degree of cholesterol saturation in gallbladder bile and hepatic bile of gallstone (GS) patients (n= 34), gallstone‐free (GSF) subjects (n= 33) and GS patients treated with chenodeoxycholic acid (CDCA (n= 7) or ursodeoxycholic acid (UDCA) (n= 11) for 3 weeks prior to cholecystectomy. Twenty‐five untreated GS patients (74%) and four UDCA‐treated patients (40%) displayed cholesterol crystals in the gallbladder bile. Only two GSF subjects (6%) and none of the CDCA‐treated patients had crystals. Half of the patients with crystals in the gallbladder bile had crystals also in the hepatic bile. Cholesterol saturation of the gallbladder bile was higher in GS (142 ± 15%, mean ± SEM) than in GSF patients (74 ± 5%). Saturation was also higher in GS patients with crystals (157 ± 20%) than in those without crystals (99 ± 12%). Gallblader bile was unsaturated in all CDCA‐ and UDCA‐treated patients. The results underline the importance of the degree of cholesterol saturation for the formation of cholesterol crystals. The data also give further support to the concept that the mechanism for inducing gallstone dissolution is different for CDCA and UDCA.

Metabolism of androstenedione in liver microsomes of patients with cholesterol gallstone disease.

Abstract The metabolism of [4- 14 C]-androst-4-ene-3,17-dione was studied in the liver microsomal fraction of 20 patients with cholesterol gallstone disease and nine with adenomyoma of the gallbladder wall (controls). The total conversion of androstenedione was 10–15% in both groups of patients. The 5 α -reductase activity was about 30% lower in the patients with cholesterol gallstones ( P β -hydroxylase and 17 β -hydroxysteroid oxidoreductase were observed. The results give no evidence for any generalized impairment of the hepatic microsomal mixed function oxidase in patients with cholesterol gallstone disease. It is speculated that the decreased 5 α -reductase activity is related to the increased hepatic cholesterol content observed in the gallstone patients.

Gallbladder disease and hyperlipoproteinemia

To The Editor: The observations of Ahlberg et al (1) on gallbladder disease in Sweden suggest an association with type IV endogenous hypertriglyceridemia. As the authors state, these results are quite different from those in Scotland (2). This could reflect factors other than differences between countries. Although the prevalence of gallbladder disease in Sweden (3, 4) is much higher than in other Western countries (3, 57), the cholecystectomy rate in gallbladder disease is similar (17.7-20.3%) (3, 7) to figures from Scotland (13.8%) (5) and North America (24.1%) (6). This fact is important in the analysis of the conclusions of Ahlberg et al (1), because as previously mentioned by coauthor Einarsson (8), the apparent association between type IV endogenous hypertriglyceridemia and gallbladder disease was entirely due to the large number of patients who had cholecystectomies. Thus in the second report of the Stockholm study (1) there had been no less than 45 cholecystectomies in the 210 consecutive patients admitted with hyperlipidemia. Only 30 other patients actually had gallstones at the time of admission. A cholecystectomy rate of 60% in gallbladder disease is extremely high even by Swedish criteria. The group of patients studied was therefore unrepresentative of the general population for factors other than hyperlipidemia and simple gallbladder disease. There could be various explanations for this. There is a known chance association of diseases in hospital inpatients (9). Unconscious selection could occur if, for instance, doctors included serum lipid estimation in the assessment of patients with symptoms of gallbladder disease. Only a third of the hyperlipidemia patients had symptomatic heart disease, and the indication for measurement of serum lipids in the others is not clear, but could have related to their cholecystectomy. Current results in Dundee, Scotland, confirm the reported (2) lack of association between gallbladder disease and raised serum triglycerides (Table 1). Consecutive patients attending a lipid clinic were studied, and almost all referrals were ischemic heart disease patients and their relatives. The standardized gallbladder disease prevalence rates are identical with those found in the general population, both in a concurrent necropsy series and in a cholecystography survey of patients referred to the clinic but who were found to have normal serum lipids (2, 7). The cholecystectomy rate in hyperlipidemia patients with gallbladder disease was 12.5% (3 out 24 patients), similar to that observed in the community. Gallbladder d isease is common, and many claimed associations have subsequently been found to be doubtful or spurious (10), eg, those with hy-