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Pravastatin dissolves gallstones in patients with hypercholesterolemia by reducing the cholesterol saturation index (CSI) of bile. There are few reports on effect of pravastatin on bile lipids, CSI and nucleation time (NT) in patients with gallstones and normal plasma lipid levels, or on the effect of pravastatin on gallbladder motility. Therefore we studied the effect of pravastatin on bile lipids, CSI, NT, and gallbladder motility in persons with normal cholesterol levels. We included 10 patients (ages 32 +/- 8 years; 6 men) with symptomatic gallstones and normal plasma lipid profiles. Estimation of bile lipids, CSI, and NT in duodenal bile and gallbladder motility were done using standard methods. Subsequently each patient was given 40 mg pravastatin daily for 1 month. At completion of pravastatin therapy, bile lipids and gallbladder motility studies were repeated. After pravastatin therapy, we found no significant reduction in bile cholesterol (11.2 +/- 3.2 vs. 10.4 +/- 2.8 mmol/l), bile acids (114.6 +/- 7.4 vs. 133 +/- 16 mmol/l), phospholipids (23 +/- 3.5 vs. 24 +/- 6.2 mmol/l), CSI (1.28 +/- 0.4 vs. 1.22 +/- 0.3), and nucleation time (7 +/- 3 vs. 7 +/- 3 days). In addition, there was no significant change in gallbladder fasting volume (26 +/- 3 vs. 26.6 +/- 3 ml), residual volume (14.6 +/- 1.1 vs. 15.08 +/- 1.4 ml), ejection fraction (44% vs. 43%), and rate constant of gallbladder emptying (0.018/min vs. 0.022/min). One-month therapy with pravastatin does not alter bile lipids, CSI, NT, and gallbladder contractility in persons with normal levels of cholesterol.

In experimental animals, sphincterotomy facilitates passage of solids from the gallbladder and inhibits gallstone formation apparently by improvement in gallbladder emptying. In humans, however, gallbladder emptying has not been studied following endoscopic sphincterotomy (ES) in patients with gallstones. We therefore prospectively studied resting and cerulin-stimulated gallbladder volumes by real time ultrasonography in 15 patients of choledocholithiasis with gallbladder in situ (eight with and seven without gallbladder calculi) before and after (after bile duct clearance) ES. ES significantly lowered resting gallbladder volume (21.2 +/- 10.6 vs 11.1 +/- 5.0; P < 0.0001) and cerulin-stimulated residual gallbladder volume (10.8 +/- 5.6 vs 4.4 +/- 2.1; P < 0.0001). ES also significantly increased the gallbladder ejection fraction (47.3 +/- 12.1% vs 58.8 +/- 11.1%; P < 0.0001). The rate constant for gallbladder emptying after cerulin infusion also increased significantly after ES (-0.022/min vs -0.031/ min; P < 0.0001). Significant improvement in gallbladder motility was observed in both groups of patients with and without gallbladder calculi. ES significantly improves gallbladder motility in humans.

Patients with gallstone disease have impaired gallbladder motility. Prostaglandins are thought to be important mediators of gallbladder hypomotility. We assessed the effect of aspirin, a prostaglandin inhibitor on gallbladder resting volume and ejection fraction according to a double-blind study protocol in 20 healthy volunteers and 30 patients with gallstone disease. Healthy volunteers had a higher ejection fraction compared to patients with gallstone disease (73.9 +/- 0.9% vs 60.4 +/- 1.0%, P < 0.05). Aspirin in a dose of 350 mg/day for two weeks did not alter gallbladder motility in the healthy volunteers. Thirty patients with gallstone disease were randomized into three treatment groups: group I (placebo), group II (aspirin 350 mg/day), and group III (aspirin 1400 mg/day). After two weeks of treatment, gallbladder ejection fraction was improved in group II (74.0 +/- 1.7% vs 62.0 +/- 1.7%, P < 0.01) and group III (69.8 +/- 3.8% vs 61.2 +/- 1.3%, P < 0.01) but not in group I (60.4 +/- 2.6% vs 59.0 +/- 1.9%, P = NS). The higher dose of aspirin did not induce a greater increase in gallbladder emptying. It is concluded that impaired gallbladder motility in patients with gallstone disease is corrected by short-term oral aspirin even in low dosage. This may be clinically useful in secondary prophylaxis after nonsurgical therapy for gallstone disease.

A case of traumatic pseudo-aneurysm of the superficial temporal artery documented on Computed tomography (CT) and angiography is described in a 55-years-old female, who was treated by surgical excision. Computed tomographic appearance of this lesion is illustrated. This represents, to our knowledge, the first CT demonstration of traumatic aneurysm of superficial temporal artery within a large subgaleal haematoma.