Presence Of Cholesterol Crystals Research Articles

Effect of Colectomy on Bile Composition, Cholesterol Crystal Formation, and Gallstones in Patients With Ulcerative Colitis

Bile composition and the presence of cholesterol crystals in bile were studied in bile samples obtained at the time of surgery in patients with ulcerative colitis. Some patients were sampled before colectomy and others at a second operation months to years after a colectomy. Patients in the precolectomy group were found to have bile composition similar to control patients without gallstones, and few had crystals in their bile. In the postcolectomy group, cholesterol concentrations were very high, all biles were supersaturated, and almost all patients had cholesterol crystals in their bile. These findings are similar to those found in persons with cholesterol gallstones. Twenty patients have been followed for at least 3 years after colectomy and to date three have formed cholesterol gallstones.

Cholesterol crystals and IgE-containing immune complexes in rheumatoid pericarditis

A 72-year-old rheumatoid arthritis patient is described presenting with acute dyspnoea and peripheral oedema. A pericardial effusion with signs of tamponade was diagnosed. Examination of the pericardial fluid revealed the presence of cholesterol crystals and IgE-containing immune complexes. The significance of these findings in the differential diagnosis of pericardial disease is discussed.

Comparison of gall bladder bile and endoscopically obtained duodenal bile.

In 10 patients with gall stone disease (eight women, two men; mean (SD) age 47.4 (13) years), bile was obtained by endoscopic aspiration after stimulation of the gall bladder with ceruletid and also by fine needle puncture of the gall bladder under local anaesthetic. The total lipid concentration of the puncture bile samples was mean (SD) 11.9 (4.7) g/dl, significantly higher than the endoscopic bile samples (3.9 (3.3) g/dl, p less than 0.001). Total bile acids, phospholipids, and biliary cholesterol (expressed in mol%) and cholesterol saturation index showed no significant differences between the two types of samples. The glycocholic acid concentration in the endoscopically obtained bile (27.7 (6.6) mol% v 23.3 (5.4) mol%; p less than 0.01) was significantly higher than the puncture bile samples. Puncture bile exhibited a significantly shorter nucleation time (3.5 (3.3) days v 19.6 (11.9) days; p less than 0.001). For determination of the nucleation time, endoscopic bile aspiration after gall bladder stimulation with ceruletid led to adequately concentrated samples in 50% of the study subjects. Cholesterol monohydrate crystal formation in native bile was observed in six samples of puncture bile and in three samples of the endoscopically obtained bile. The presence of cholesterol crystals and the determination of nucleation time in the puncture bile were the best discriminants between cholesterol and pigment gall stones and correlated well with computed tomogram analysis.

Sensitivity and specificity of microscopic examination of gallbladder bile for gallstone recognition and identification

During cholecystectomy, gallbladder bile and gallstones were obtained from 77 patients and gallbladder bile was obtained from 39 patients free of stones (11 patients had biliary stenosis). According to their chemical composition, gallstones were classified as cholesterol (n = 46) or pigment (n = 31) stones. In patients with gallstones (a) cholesterol crystals better helped to identify cholesterol gallstones (sensitivity, 87%; specificity, 97%; positive predictive value, 97%) than did an abnormal cholesterol saturation index of bile (sensitivity, 93%; specificity, 48%; positive predictive value, 73%); (b) the presence of cholesterol crystals was significantly related to the cholesterol content of gallstones and the bile cholesterol saturation index; and (c) bilirubinate crystals, when present alone (without cholesterol crystals), were good predictors of pigment gallstones (sensitivity, 71%; specificity, 93%; positive predictive value, 88%). In the absence of stones, bilirubinate crystals were present in 9 of 28 patients without biliary stenosis (4 with alcoholic cirrhosis and 2 with alcoholic pancreatitis) and 8 of 11 patients with biliary stenosis. In the absence of stones, cholesterol crystals were present in 2 of 28 patients without biliary stenosis and in 4 of 11 patients with biliary stenosis, suggesting that bile stasis can induce cholesterol crystal formation.

Pathogenesis of cholesterol stones in the gallbladder

SummaryThe secretion by the liver of bile saturated with cholesterol is the first stage in the development of cholesterol stones in the gallbladder. Biliary cholesterol is derived mainly from lipoprotein cholesterol, which is transported to the liver by chylomicron remnants, low-density and high-density lipoproteins. Oestrogens stimulate the uptake and catabolism of low-density lipoproteins in the liver.Newly synthetized cholesterol contributes less to biliary excretion. Insulin may increase gallstone formation by increasing the activity of the rate-limiting enzyme in the synthesis of cholesterol in the liver.Cholesterol is virtually insoluble in water and is held in solution in bile by its association with bile salts and phospholipids. An increased cholesterol secretion into bile can predispose to saturation and gallstone formation in obesity, on high-caloric diet, on weightreduction diet, in hypcrtriglyceridaemia, and by the effects of insulin, oestrogens and clofibrate therapy.Plasma low-density lipoprotein cholesterol is positively correlated with bile cholesterol saturation whereas high-density lipoprotein cholesterol shows an inverse relation.A reduced total body pool and biliary secretion of bile salts may also be responsible for gallstone formation. A low bile salt secretion may result from an excessive intestinal loss of bile salts, from an impaired hepatic bile acid synthesis or from a rapid bile salt circulation within the enterohepatic circulation with normal feedback inhibition of synthesis.Supersaturation of bile with cholesterol not only occurs in patients with cholesterol gallstones but is also quite common in normal individuals. Gallstone patients and normal persons can be discriminated by the presence of cholesterol crystals in bile and by a difference of the in vitro nucleation time. The in vitro nucleation time of gallbladder bile of gallstone patients is more rapid than that of controls. A potent nucleating factor may be added to gallbladder bile in patients with cholesterol gallstones or an inhibitor of cholesterol crystal nucleation might be present in bile from normal persons.An impaired gallbladder emptying with stasis of bile may contribute to gallstone formation in patients on total parenteral nutrition, in pregnancy and during oral contraceptive therapy.

Role of gallbladder mucus in the pathogenesis of cholesterol gallstones

Recent observations indicate that the hepatic secretion of lithogenic bile, gallbladder mucus hypersecretion, and gallbladder stasis are all critical factors in the pathogenesis of cholesterol gallstones. Using the prairie dog gallstone model, we investigated the interaction of these factors and the sequence in which they develop. The results of this study indicated that (1) gallbladder bile mucus concentration is elevated before cholesterol precipitation and increases progressively with the formation of cholesterol crystals, (2) cystic duct resistance increases in the presence of cholesterol crystals, and (3) agglomerates of cholesterol crystals, but not fine, sonicated crystals increase cystic duct resistance. We conclude that these alterations trigger a self-perpetuating cycle of mucus hypersecretion, cholesterol crystallization, and gallbladder stasis which culminates in the formation of cholesterol gallstones.

Cholesterol pericarditis associated with rheumatoid arthritis: Treatment by pericardiectomy

A case of constrictive pericarditis occurring with rheumatoid arthritis in which cholesterol clefts were found in the pericardium is reported. The cholesterol pericarditis was probably related to rheumatoid arthritis, and the presence of cholesterol crystals does not necessarily imply a tuberculous cause.

Pericardial effusion of "gold-paint" appearance following myocardial infarction

ALEXANDER¹published a paper in 1919 entitled, "A Pericardial Fluid of 'Gold Paint' Appearance Due to the Presence of Cholestern." His patient had myxedema and the purpose of his short paper was only to point out that cholesterol crystals can occur in pericardial fluid and can impart to such fluid a shimmering, satiny beauty. Within a few years, however, the term "cholesterol pericarditis" had been coined and Alexander was being credited with having described the first case of an unusual but specific form of pericardial disease in which effusion was produced by the presence of cholesterol crystals that had somehow coated the epicardium and the inner aspect of the pericardium; the whole thing being possibly associated in some vague way with a disturbance in lipid metabolism. In recent years a few authors^2,3have risen to challenge the existence of any such entity as "cholesterol pericarditis." The purpose of