Gallbladder Motility Research Articles

Effect of oral clarithromycin on gall‐bladder motility in normal subjects and those with gall‐stones

Motilin receptor stimulation with erythromycin has been shown to have a prokinetic effect on gall-bladder motility in human beings. To find out whether oral clarithromycin has similar prokinetic activity to erythromycin on fasting and postprandial gall-bladder emptying in normal humans and those with gall-stone disease. In a blinded two-way crossover study clarithromycin 500 mg and a placebo were administered to 10 normal subjects and 10 subjects with gall-stone disease. Gall-bladder volumes were assessed in the fasting and postprandial state. Fasting volumes were significantly less following clarithromycin administration in both normal subjects and subjects with gall-stones compared with placebo (12.1 +/- 1.8 mL vs. 17.8 +/- 2.0 mL, P < 0.05 and 16.7 +/- 2 mL vs. 26.8 +/- 7.2 mL, P < 0.02, mean +/- S.E.M). Postprandial volumes were also significantly less following clarithromycin administration. Ejection fraction significantly increased following clarithromycin in both normal subjects (66 +/- 5.8% vs. 37 +/- 5.9%, P = 0.02) and subjects with gall-stones (45 +/- 3.2 vs. 20 +/- 1.6%, P < 0.02). Clarithromycin enhances both fasting and postprandial gall-bladder contraction in normal humans and also in those with gall-stone disease.

Functional Gallbladder and Sphincter of Oddi Disorders

The functional disorder of the gallbladder (GB) is a motility disorder caused initially either by metabolic abnormalities or by a primary motility alteration. The functional disorders of the sphincter of Oddi (SO) encompass motor abnormalities of either the biliary or the pancreatic SO. Dysfunction of the GB and/or biliary SO produce similar patterns of pain. The pain caused by a dysfunction of the pancreatic SO can be similar to that of acute pancreatitis. The symptom-based diagnostic criteria of motility dysfunction of the GB and biliary SO are episodes of moderate to severe steady pain located in the epigastrium and right upper abdominal quadrant that last at least 30 minutes. GB motility disorder is suspected after gallstones and other structural abnormalities have been excluded. This diagnosis should then be confirmed by a decreased GB ejection fraction induced by cholecystokinin at cholescintigraphy and after disappearance of the recurrent biliary pain after cholecystectomy. Symptoms of biliary SO dysfunction may be accompanied by features of transient biliary obstruction, and those of pancreatic SO dysfunction are associated with elevation of pancreatic enzymes and even pancreatitis. Biliary-type SO dysfunction is more frequently recognized in postcholecystectomy patients. SO manometry is valuable to select patients with sphincter dysfunction; however, because of the high incidence of complications, these patients should be referred to an expert unit for such assessment. Thus invasive tests should be performed only in the presence of compelling clinical evidence and after noninvasive testing has yielded negative findings. The committee recommends that division of the biliary or pancreatic sphincters only be considered when the patient has severe symptoms, meets the required criteria, and other diagnoses are excluded.

May we predict the clinical course of gallstone disease? Usefulness of a gallbladder motility index

May we predict the clinical course of gallstone disease? Usefulness of a gallbladder motility index

701 Evaluation of gallbladder motility in patients with non-alcoholic steatohepatitis using real time ultrasonography

701 Evaluation of gallbladder motility in patients with non-alcoholic steatohepatitis using real time ultrasonography

Effect of Sildenafil Citrate on Postprandial Gallbladder Motility

Sildenafil stimulates the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway through inhibition of type 5 phosphodiesterase. NO-cGMP pathway causes smooth muscle relaxation. The aim of this study is to evaluate the effects of sildenafil on gallbladder motility. Twenty healthy male volunteers (21-35 years old) participated in this randomized, double blind, crossover, and placebo-controlled study. Oral sildenafil (50 mg) or placebo was randomly dispensed to each volunteer on two consecutive days. After the sildenafil or placebo, a special meal with a high fat content was administered. Gallbladder volume was measured using sonography preprandially and at 5, 15, 30, 60, 120 and 180 minutes postprandially. Sildenafil showed an inhibitory effect on gallbladder contraction in healthy volunteers that began at 30 minutes. Gallbladder volumes showed significant differences at 30 minutes following the test meal (approximately 50-60 min after the sildenafil intake), between placebo (15.4 +/- 5.1 mL) and the sildenafil groups (19.3 +/- 6.1 mL) (P < 0.05). In addition, gallbladder volume was significantly higher during the refilling phase in the sildenafil group (P < 0.05 at 180 min). Maximal contraction was achieved at 60 minutes in each group. Sildenafil constituted a significant inhibitory effect on gallbladder discharge in healthy individuals when compared with placebo group. Because of this inhibitory effect, sildenafil consumption for long periods may potentiate risks of gallbladder disorders and gallstone formation resulting from disturbed gallbladder motility.

PI-72Pancreatic exocrine insufficiency: Second-generation antipsychotic drugs and receptor binding profiles

BACKGROUND/AIMS Exocrine acinar cellular enzyme-secretory response and gallbladder motility are regulated by CCK and the muscarinic (M1-5) system. Metabolic consequences due to islet cell dysfunction have been reported with clozapine (C), risperidone (R), olanzapine (O), and quetiapine (Q). We believe a parallel distortion of islet and acinar cell function exists with antipsychotic drug (APD) use. METHODS We examined structural activity relationships, receptor binding (RB) profiles, and pancreatitis (increased amylase/lipase). “Radar” representations exemplifying similarities/differences among the APDs at RB sites were constructed to visualize APD binding profiles. Databases (joplink.net, pancreasweb.com) were evaluated for signals of acinar cell insufficiency. RESULTS Configurational comparisons revealed a 7-atom diazepine ring and a piperazinyl group as constant features (C, O, Q) associated with pancreatic exocrine insufficiency. The rank order of radar binding profiles (Ki values) were C> O> Q> R; a hierarchical drug cluster for classes of M1-5 receptors. Reports of increased amylase/lipase showed a preponderance for these agents, regardless of marketing exposure. CONCLUSIONS Our observations raise mechanistic questions about signal transduction interplay between exocrine and endocrine pancreas and the gallbladder; postprandial emptying is decreased with cholinergic antagonists. Biliary stones are a common cause of pancreatitis, and increased BMI is associated with cholesterol gallstones. Clinical Pharmacology & Therapeutics (2005) 79, P26–P26; doi: 10.1016/j.clpt.2005.12.093

Elevated transaminases during medical treatment of acromegaly: a review of the German pegvisomant surveillance experience and a report of a patient with histologically proven chronic mild active hepatitis

The new GH receptor antagonist pegvisomant is the most effective medical therapy to normalize IGF-I levels in patients with acromegaly. Based on currently available data pegvisomant is well tolerated; however, treatment-induced elevation of transaminases has been reported and led to the necessity for drug discontinuation in some patients in the pivotal studies. The aim of this study was to evaluate and characterize the prevalence of elevated transaminases and to describe in detail the findings in a single case who required drug discontinuation because of elevation of transaminases which emerged during treatment and who underwent liver biopsy. Retrospective safety analyses were carried out on 142 patients with acromegaly receiving pegvisomant treatment in Germany between March 2003 and the end of 2004. Of these patients, 123 were documented in a post-marketing surveillance study, one case of elevated transaminases was reported spontaneously and the other patients were treated in a clinical study. Mean treatment duration with pegvisomant in the ongoing observational study at the end of 2004 was 28.3 +/- 19.9 (S.D.) weeks. Twelve out of the 142 patients had elevated transaminases above three times the upper limit of normal, likely caused by biliary obstruction in five of the patients. All patients but one affected by elevated transaminases had been previously treated with somatostatin analogues. In six out of 142 (4%) of patients, pegvisomant was permanently withdrawn because of elevated transaminases. The same number of patients showed a transient increase of transaminases with either spontaneous remission without dose modification (n = 4) or no re-increase of transaminases after temporary discontinuation and re-exposure (n = 2). The liver biopsy of one patient who was permanently withdrawn showed a chronic mild hepatitis with a mixed portal inflammation including eosinophilic granulocytes. Liver function tests should be regularly followed on pegvisomant treatment. Biliary complications, which may arise from restitution of normal gall bladder motility after cessation of somatostatin analogue treatment, need to be differentiated from pegvisomant-induced abnormalities. The histological pattern of the liver biopsy performed in one of the patients showed a mild chronic active hepatitis. The lack of dose dependency and rather low frequency of elevated transaminases in those cases where a biliary disorder was excluded render this reaction an idiosyncratic drug toxicity.

Pioglitazone increases gallbladder volume in insulin- resistant obese mice

Introduction: Both obesity and diabetes are associated with an increased incidence of gallstones. Recent animal and human data from our laboratory suggest that insulin resistance is associated with increased gallbladder volume and/or impaired gallbladder emptying. Pioglitazone is a thiazolidinedione which has been shown to improve insulin resistance and has been employed to treat nonalcoholic fatty steatohepatitis. However, in a prior study with a high carbohydrate (75%) diet pioglitazone did not improve gallbladder motility in obese insulin-resistant mice. Therefore, we tested the hypothesis that pioglitazone would improve insulin resistance, decrease resting gallbladder volume and improve gallbladder response to neurotransmitters in insulin-resistant obese mice. Methods: Twenty eight-week old obese leptin-deficient (Lepob) female mice were fed a low carbohydrate (25%) diet for four weeks. Half of the animals had pioglitazone 0.03% added to their diet. At 12 weeks, all animals were fasted overnight and underwent cholecystectomy. Gallbladder volume(μl), weight and area were measured, and fresh gallbladders were placed in a muscle bath to assess response to acetylcholine(ACh,10−6M), neuropeptide Y (NPY,10−8,−7,−6M) and cholecystokinin (CCK, 10−10,−9,−8,−7M). Serum glucose(mg/dl) and insulin (ηg/ml) were measured, and the HOMA Index, a measure of insulin resistance, was calculated. Results: Pioglitazone did not alter gallbladder weight, area or response to ACh, NPY or CCK. Results for glucose, insulin, HOMA Index and gallbladder (GB) volume were: Conclusion: These data suggest that in obese insulin-resistant mice, pioglitazone 1) lowers insulin and insulin-resistance, 2) does not alter gallbladder response to neurotransmitters, and 3) increases resting gallbladder volume. Therefore, we conclude that pioglitazone, while improving insulin resistance, paradoxically increases gallbladder volume and, thereby, may increase the propensity for gallstone formation by enhancing gallbladder stasis.

Ursodeoxycholic acid exerts no beneficial effect in patients with symptomatic gallstones awaiting cholecystectomy†‡§

Ursodeoxycholic acid (UDCA) and impaired gallbladder motility purportedly reduce biliary pain and acute cholecystitis in patients with gallstones. However, the effect of UDCA in this setting has not been studied prospectively. This issue is important, as in several countries (including the Netherlands) scheduling problems result in long waiting periods for elective cholecystectomy. We conducted a randomized, double-blind, placebo-controlled trial on effects of UDCA in 177 highly symptomatic patients with gallstones scheduled for cholecystectomy. Patients were stratified for colic number in the preceding year (<3: 32 patients; > or =3: 145 patients). Baseline postprandial gallbladder motility was measured by ultrasound in 126 consenting patients. Twenty-three patients (26%) receiving UDCA and 29 (33%) receiving placebo remained colic-free during the waiting period (89 +/- 4; median [range]: 75[4-365] days) before cholecystectomy (P = .3). Number of colics, non-severe biliary pain, and analgesics intake were comparable. A low number of prior colics was associated with a higher likelihood of remaining colic-free (59% vs. 23%, P < .001), without effects on the risk of complications. In patients evaluated for gallbladder motility, 57% were weak and 43% were strong contractors (minimal gallbladder volume > respectively < or = 6 mL). Likelihood to remain colic-free was comparable in strong and weak contractors (31% vs. 33%). In weak contractors, UDCA decreased likelihood to remain colic-free (21% vs. 47%, P = .02). In the placebo group, 3 preoperative and 2 post-cholecystectomy complications occurred. In contrast, all 4 complications in the UDCA group occurred after cholecystectomy. In conclusion, UDCA does not reduce biliary symptoms in highly symptomatic patients. Early cholecystectomy is warranted in patients with symptomatic gallstones.

Biliary symptoms, gallbladder motility, and cholecystectomy

Biliary symptoms, gallbladder motility, and cholecystectomy

Apical sodium bile acid transporter and ileal lipid binding protein in gallstone carriers

Although a cholesterol supersaturation of gallbladder bile has been identified as the underlying pathophysiologic defect, the molecular pathomechanism of gallstone formation in humans remains poorly understood. A deficiency of the apical sodium bile acid transporter (ASBT) and ileal lipid binding protein (ILBP) in the small intestine may result in bile acid loss into the colon and might promote gallstone formation by reducing the bile acid pool and increasing the amount of hydrophobic bile salts. To test this hypothesis, protein levels and mRNA expression of ASBT and ILBP were assessed in ileal mucosa biopsies of female gallstone carriers and controls. Neither ASBT nor ILBP levels differed significantly between gallstone carriers and controls. However, when study participants were subgrouped by body weight, ASBT and ILBP protein were 48% and 67% lower in normal weight gallstone carriers than in controls (P < 0.05); similar differences were found for mRNA expression levels. The loss of bile transporters in female normal weight gallstone carriers was coupled with a reduction of protein levels of hepatic nuclear factor 1alpha and farnesoid X receptor. In conclusion, in normal weight female gallstone carriers, the decreased expression of ileal bile acid transporters may form a molecular basis for gallstone formation.

Effects of tegaserod on bile composition and hepatic secretion in Richardson ground squirrels on an enriched cholesterol diet

BackgroundTegaserod is effective in treating IBS patients with constipation, and does not alter gallbladder motility in healthy individuals or in patients with IBS. However, it is not known if tegaserod affects the biliary tract in gallstone disease, so to this end the effects of tegaserod on bile composition and hepatic secretion of Richardson ground squirrels maintained on an enriched cholesterol diet were examined.ResultsAnimals were fed either a control (0.03%) or enriched (1%) cholesterol diet for 28 days, and treated s.c. with tegaserod (0.1 mg/kg BID) or vehicle. Bile flow, bile acid, phospholipids and cholesterol secretion were measured with standard methods. Tegaserod treatment or enriched cholesterol diet, alone or combination, did not alter body or liver weights. The enriched cholesterol diet increased cholesterol saturation index (CSI), cholesterol concentrations in gallbladder and hepatic duct bile by ~50% and decreased bile acids in gallbladder bile by 17%. Tegaserod treatment reversed these cholesterol-induced changes. None of the treatments, drug or diet, altered fasting gallbladder volume, bile flow and bile salts or phospholipid secretion in normal diet and cholesterol-fed animals. However, tegaserod treatment prevented the decreases in bile acid pool size and cycling frequency caused by the enriched cholesterol diet, consequent to re-establishing normal bile acid to concentrations in the gall bladder. Tegaserod had no effect on these parameters with normal diet animals.ConclusionTegaserod treatment results in increased enterohepatic cycling and lowers cholesterol saturation in the bile of cholesterol-fed animals. These effects would decrease conditions favorable to cholesterol gallstone formation.

Ciliary Neurotrophic Factor Restores Gallbladder Contractility in Leptin-Resistant Obese Diabetic Mice 1,2

<h3>Background</h3> Obesity and diabetes are major risk factors for cholesterol gallstones, and the majority of obese people are leptin-resistant. Our previous work has shown that both leptin-deficient (Lep^ob) and leptin-resistant (Lep^db) obese diabetic mice have decreased <i>in vitro</i> gallbladder motility. Leptin administration to leptin-deficient (Lep^ob) animals restores gallbladder motility and reverses obesity and hyperinsulinemia. However, additional leptin in leptin-resistant obesity would not be expected to improve obesity-related parameters. Recent studies demonstrate that ciliary neurotrophic factor (CNTF) reduces weight and hyperinsulinemia in leptin-resistant obesity. Our hypothesis is that CNFT would cause weight loss, lower blood sugars, and restore gallbladder contractility in leptin-resistant (Lep^db) mice. <h3>Materials and methods</h3> 20 C57b/6J and 20 Lep^db 8-week-old female mice were injected daily with either intraperitoneal saline or 0.3 μg/g CNTF_Ax15 for 17 days. Gallbladders were mounted in muscle baths and stimulated with acetylcholine, neuropeptide Y, and cholecystokinin. Gallbladder volume, serum glucose, insulin, liver weight, liver fat, and gallbladder responses were measured. Data were analyzed by ANOVA. <h3>Results</h3> Saline treated obese mice had greater body weight and obesity parameters, but decreased gallbladder contractility to neurotransmitters compared to saline treated lean mice. CNTF administration to obese mice decreased body weight and obesity parameters, and restored gallbladder contractility. CNTF treated lean animals had weight loss and decreased gallbladder contraction to acetylcholine and cholecystokinin compared to saline treated lean animals. <h3>Conclusions</h3> Ciliary neurotrophic factor (CNTF) causes 1) weight loss, 2) improvement of diabetes, and 3) alterations in gallbladder motility that is improved in obese mice but decreased in lean mice. We conclude that CNTF may improve gallbladder contractility in leptin-resistant obesity with diabetes.

Effect of vagal denervation on canine gallbladder motility.

There is an increased incidence of gallstones after truncal vagotomy but the mechanism is unknown. Our aim was to study the early effects of vagotomy on fasting and postprandial gallbladder motility. A chronic model was constructed in 10 dogs to correlate gallbladder motility and emptying with interdigestive and postprandial duodenal motility both before and after selective hepatobiliary vagotomy (five dogs) and truncal vagotomy (5 dogs). During each study recordings were made for one complete interdigestive motor complex (IDMC) and for 90 min after a standard meal of (a) gallbladder and duodenal motility, (b) gallbladder emptying (by a dual radioisotope marker technique) and (c) duodenal output of bilirubin. In control studies the gallbladder contracted at the start of phase II of the interdigestive motor complex and ejected 20-25 per cent of its contents into the duodenum; after meals the gallbladder contracted within 5 min and emptied almost 80 per cent of its contents within 90 min. After both selective hepatobiliary vagotomy and also truncal vagotomy there was no significant difference in the pattern of contraction or emptying of the gallbladder either during fasting or postprandially. We conclude that gallbladder motility and emptying are entirely normal in the early period after vagal denervation.

Biliary lipids, water and cholesterol gallstones

Cholesterol supersaturation, hydrophobic bile salts, pronucleating proteins and impaired gall-bladder motility may contribute to gallstone pathogenesis. We here show that both gallstone-susceptible C57L and gallstone-resistant AKR male inbred mice exhibit supersaturated gall-bladder biles during early lithogenesis, whereas bile-salt composition becomes hydrophobic only in susceptible C57L mice. In vitro, cholesterol crystallization occurs depending on relative amounts of lipids; excess cholesterol may exceed solubilizing capacity of mixed bile salt-phospholipid micelles, whereas excess bile salts compared with phospholipids leads to deficient cholesterol-storage capacity in vesicles. In vivo, bile lipid contents are mainly determined at the level of the hepatocyte canalicular membrane, where specific transport proteins enable lipid secretion [ABCG5/G8 (ATP-binding cassette transporter G5/G8) for cholesterol, MDR3 (multi-drug resistant 3) for phospholipid, BSEP (bile salt export pump)]. These transport proteins are regulated by farnesoid X and liver X nuclear receptors. After nascent bile formation, modulation of bile water contents in biliary tract and gall-bladder exerts critical effects on cholesterol crystallization. During progressive bile concentration (particularly in the fasting gall-bladder), cholesterol and, preferentially, phospholipid transfer occurs from cholesterol-unsaturated vesicles to emerging mixed micelles. The remaining unstable cholesterol-enriched vesicles may nucleate crystals. Various aquaporins have recently been discovered throughout the biliary tract, with potential relevance for gallstone formation.

GALL BLADDERMOTILITY IN CHILDREN WITH FUNCTIONAL CONSTIPATION.

Introduction: Evidences have been accumulated that impaired colonic motility in some patients with functional constipation is part of a generalized motility defect. The aim of this study was to investigate gall bladder motility in children with functional constipation. Methods: Eighty-two consecutive patients with chronic functional constipation referred to a pediatric tertiary outpatient clinic and the same number of controls were evaluated in a cross-sectional study. Using real-time ultrasonography and the ellipsoid method, gall bladder volumes were measured: after overnight fast and 60 minutes after the ingestion of a standard fatty meal. Residual volumes and contractility indexes were calculated. Results: Considering values ≥25% as normal values for contractility index, the frequency of abnormal values was superior in constipated children (p < 0.001). Gall bladder dismotility was observed in 21 of 82 (25.6%) patients and in 14 of 82 (17%) age and gender matched controls. Contractility indexes distributions were different between groups, with superior values found in controls (p < 0.05). Conclusion: Contractility indexes for gall bladder emptying in constipated children were different from indexes in healthy children.

Evaluation of gallbladder motility in patients with irritable bowel syndrome.

Abnormalities involving smooth muscle function in different systems of the body have been reported in irritable bowel syndrome (IBS). There are a few studies on gallbladder function in this disorder with conflicting results. To investigate the motility of gallbladder in patients with IBS. Forty-eight patients (15 male and 33 female) with IBS and 48 healthy volunteers (15 male and 33 female) were included into the study. Thirty-four patients (70.8%) had constipation predominant and 14 patients (29.2%) had diarrhoea predominant type of IBS. Fasting and postprandial gallbladder volumes were studied using real time ultrasonography and ejection fraction (EF) of gallbladder was calculated. While fasting gallbladder volume (FGV) was similar between IBS and control groups (18.0 +/- 4.0 ml vs. 17.8 +/- 4.9 ml, p >0.05), postprandial gallbladder volume (PGV) was lower in IBS group than in the control group (5.5 +/- 1.4 ml vs. 6.2 +/- 1.9 ml, p = 0.03). Accordingly, the mean EF of gallbladders was found to be higher in IBS group than in the control group (69.1% vs. 64.1%, p = 0.0001). There were no difference in FGV, PGV and EF of gallbladders between constipation predominant and diarrhoea predominant IBS patients (p >0.05). The results of this study indicated that IBS patients have increased emptying of gallbladder compared to healthy subjects.

Evaluation of gallbladder motility in patients with irritable bowel syndrome.

Abnormalities involving smooth muscle function in different systems of the body have been reported in irritable bowel syndrome (IBS). There are a few studies on gallbladder function in this disorder with conflicting results. To investigate the motility of gallbladder in patients with IBS. Forty-eight patients (15 male and 33 female) with IBS and 48 healthy volunteers (15 male and 33 female) were included into the study. Thirty-four patients (70.8%) had constipation predominant and 14 patients (29.2%) had diarrhoea predominant type of IBS. Fasting and postprandial gallbladder volumes were studied using real time ultrasonography and ejection fraction (EF) of gallbladder was calculated. While fasting gallbladder volume (FGV) was similar between IBS and control groups (18.0 +/- 4.0 ml vs. 17.8 +/- 4.9 ml, p >0.05), postprandial gallbladder volume (PGV) was lower in IBS group than in the control group (5.5 +/- 1.4 ml vs. 6.2 +/- 1.9 ml, p = 0.03). Accordingly, the mean EF of gallbladders was found to be higher in IBS group than in the control group (69.1% vs. 64.1%, p = 0.0001). There were no difference in FGV, PGV and EF of gallbladders between constipation predominant and diarrhoea predominant IBS patients (p >0.05). The results of this study indicated that IBS patients have increased emptying of gallbladder compared to healthy subjects.

Short‐term ursodeoxycholic acid treatment improves gallbladder bile turnover in gallstone patients: a randomized trial

Ursodeoxycholic acid (UDCA) prevents in vitro gallbladder (GB) muscle damage caused by acute cholecystitis and reduces risk of biliary pain and complications in gallstone (GS) patients. These effects could be partially explained by the improved GB bile turnover. To assess the effect of short-term UDCA treatment on GB motility and bile turnover. Ultrasonographic (US) assessment of GB volumes was performed in 16 GS patients, in the postprandial phase, for 90 min with a time sampling of 1 min, before and after 30 days of UDCA (10 mg kg(-1) die(-1)) or placebo, randomly assigned. US data were analysed with statistical tools and with computer fluido-dynamic (CFD) software Fluent(TM) to simulate GB bile flow. After therapy, fasting volume (FV) increased from 21.6 +/- 9 to 28.2 +/- 12 mL (p < 0.001) while the ejection fraction (EF) remained unchanged (44.5 +/- 17% vs 45.1 +/- 20%; p: ns). Volumes before and after treatment were poorly correlated (0.02 < r < 0.35), unlike those in placebo patients (r > 0.6). The average GB volume was increased in 7 out of 10 patients following UDCA (range 7-67%). CFD analysis supports the finding of improved bile flow after treatment. Unlike results of conventional US parameters of GB motility, CFD analysis shows that UDCA improves GB bile turnover in GS patients.

Drugs Affecting Biliary Lipid Secretion and Gallbladder Motility: Their Potential Role in Gallstone Treatment and Prevention

Gallstone disease in the Western world has an estimated prevalence of 10-15% and more than 75% are cholesterol-enriched gallstones. Defective gallbladder motility has been identified as an important pathogenic factor for cholesterol gallstone disease. Various agents may enhance or impair postprandial gallbladder motility, and their effects on interdigestive gallbladder and intestinal motility should also be taken into account. Patients in high-risk situations for gallstone disease, and those chronically treated with drugs inhibiting gallbladder motility (e.g. somatostatin analogues) may benefit from improving gallbladder motility with prokinetic agents. Whether such a strategy can really prevent gallstone formation is still unknown, long-term studies are lacking so far. The efficacy of bile acid therapy with UDCA for gallstone dissolution or for prevention in high risk patients is limited and hampered by high recurrence rates. The efficacy of UDCA in prevention of colics or gallstone related complications in symptomatic patients with gallbladder stones with contraindications for operation or on the waiting list should be explored further, since several retrospective studies showed favourable outcomes with this strategy.