Impaired Gallbladder Motility Research Articles

Ayurvedic Management of Cholelithiasis (Pittashmari) – A CaseStudy

Gallstone formation, or cholelithiasis, is caused by a number of factors, including supersaturation of bile with cholesterol, accelerated nucleation of cholesterol monohydrate in bile, bile stasis, or delayed gallbladder emptying due to impaired gallbladder motility. After carefully rewriting Ayurvedic scriptures, we find that, because of its resemblance in location and function, the bile secreted from the gallbladder can be compared to the Accha Pitta stated in Ayurveda. We report that a case of cholelithiasis (Pittashmari) in a 31-year-old female patient had been complaining of severe abdominal pain, distension of the abdomen, and vomiting. Oral medications such as Arogyavardhini vati, tablet Trikatu, Kashaya of Trivrit, Katuki, Sanaya, Arghvad, and Daruharidra were administered to the patient for 3 months. A significant response was observed over clinical symptoms and USG reports. Ayurvedic remedies were used to treat the patient for 3 months. This case study demonstrates the efficacy of Ayurvedic treatment for cholelithiasis (Pittashmari). The study reached the conclusion that Ayurvedic therapy was significantly effective in the treatment of cholelithiasis (Pittashmari).

Gallstone Disease and Its Correlation With Thyroid Disorders: A Narrative Review.

Over the years, several studies have revealed an important link between thyroid disorders and gallstone disease. According to these studies, hypothyroidism and hyperthyroidism are associated with cholesterol gallstone disease. This association between thyroid hormone disorders and cholesterol gallstone disease is due to the importance of thyroid hormones on cholesterol synthesis, bile functioning and content, and gallbladder motility. Several genes and receptors have been found on the thyroid gland, liver, and gallbladder to verify this association. These genes affect thyroid hormone secretion, lipid metabolism, and bile secretion. Defects in these various gene expression and protein functions lead to bile duct diseases. Other causes that lead to cholesterol gallstone disease are supersaturation of the bile with cholesterol and impaired gallbladder motility, which leads to bile stasis. This article has discussed these factors in detail while highlighting the association between thyroid hormones and cholesterol gallstone disease.

Research progress on the immune microenvironment of the gallbladder in patients with cholesterol gallstones.

Cholesterol gallstones are very common in hepatobiliary surgery and have been studied to a certain extent by doctors worldwide for decades. However, the mechanism of cholesterol gallstone formation is not fully understood, so there is currently no completely effective drug for the treatment and prevention of cholesterol gallstones. The formation and development of cholesterol gallstones are caused by a variety of genetic and environmental factors, among which genetic susceptibility, intestinal microflora disorders, impaired gallbladder motility, and immune disorders are important in the pathogenesis of cholesterol gallstones. This review focuses on recent advances in these mechanisms. We also discuss some new targets that may be effective in the treatment and prevention of cholesterol gallstones, which may be hot areas in the future.

Фенотипическая трансформация гладких миоцитов стенки желчного пузыря при развитии некалькулезного холецистита

The aim of the study was to analyse ultrastructural changes in the smooth muscle tissue of different gallbladder sections during the development of experimental acalculous cholecystitis. Materials and methods. The research was performed on 20 guinea pigs. The duration of the experiment ranged from 4 to 15 days. Each experimental and control group included 5 animals. A standard model of chronic acalculous cholecystitis was used, in which ligation of the proximal part of the common bile duct is accompanied by inflammation and impaired gallbladder motility. Results. In guinea pigs with cholecystitis, on day 15 of the experiment using electron microscopic examination we revealed cells in the smooth muscle tissue that retain a well-structured contractile apparatus, represented by separate thin bundles of myofilaments, and a developed synthetic apparatus. The ultrastructural organization of this type of cells is quite characteristic of myofibroblasts. Studying the modulation of gallbladder smooth muscle cells in an experiment, we need to take into account that in the conditions of inflammation and impaired gallbladder motility, during the restructuring of the intercellular matrix, myofibroblasts can appear, causing the development of sclerotic processes in the organ wall due to their ability to express high levels of collagen and glycosaminoglycans, as well as numerous other extracellular matrix molecules and fibrogenic cytokines. The research showed that adenomyomatous hyperplasia of the gallbladder wall is accompanied by proliferation of myofibroblasts and smooth muscle cells. Thus, impaired stromal-epithelial interactions can be assumed to underlie the pathology in adenomyomatous hyperplasia of the gallbladder.

A Case Study on the management of Pittashmari w.s.r. to Gall Bladder Stone

Introduction: Ankylosing Spondylitis (AS) is a sero negative chronic inflammatory arthritis of Gall stone disease is a worldwide medical problem, but the incidence rates show substantial geographical variation, Cholelithiasis (gallstone formation) results from a combination of several factors, including super saturation of bile with cholesterol, accelerated nucleation of cholesterol monohydrate in bile, and bile stasis or delayed gallbladder emptying due to impaired gallbladder motility. In India it is more common in women in north, north-east and east as compared to other zones in the country. The disease Gall Stone has not been described directly in Ayurvedic classics. The word Ashmari in Ayurveda stands for stone which is described only in the context of Bastigata Ashmari (urinary calculi). After analyzing the Ayurvedic texts it was found that the bile secreted from gall bladder can be correlated with Accha Pitta mentioned in Ayurveda due to the similarity in location and function. The pathogenesis of the disease occurs due to the abnormal formation of Kapha during the process of digestion and its vitiation due to Vata. Once gallstones become symptomatic, definitive surgical intervention with cholecystectomy is usually indicated (typically, laparoscopic cholecystectomy is first-line therapy at centers with experience in this procedure). The present article deals with “Management of Pittashmari - A Case Study”

Impaired Gallbladder Motility and Increased Gallbladder Wall Thickness in Patients with Nonalcoholic Fatty Liver Disease.

Background/AimsNonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide. Along with the increase in the incidence of NAFLD and associated obesity, an increase in gallbladder disease (GD) has been noted. This has led to the identification of a new disease entity called fatty GD. There is a gap in the literature on the dynamics of gallbladder function in patients with NAFLD.MethodsAn observational case-control study, a total of 50 patients with biopsy proven NAFLD without gallbladder stone/sludge and 38 healthy comparison subjects were enrolled. Fasting, postprandial gallbladder volumes (PGV), gallbladder ejection fraction (GEF), and fasting gallbladder wall thickness (FGWT) were measured by real-time 2-dimensional ultrasonography.ResultsFasting gallbladder wall thickness, fasting gallbladder volumes and PGV were significantly higher in patients with NAFLD than control subjects (P < 0.001, P = 0.006, and P < 0.001, respectively). Gallbladder ejection fraction was significantly lower in the NAFLD group than the controls (P = 0.008). The presence of NAFLD was an independent predictor for GEF, PGV, and FGWT. Also, steatosis grade was an independent predictor for GEF, and GEF was significantly lower in the nonalcoholic steatohepatitis (NASH) subgroup than the controls.ConclusionsGallbladder dysfunction and increase in gallbladder wall thickness exists in asymptomatic (without stone/sludge and related symptoms) patients with NAFLD and are useful in identifying fatty GD. Measurement of these variables in NAFLD patients may be useful in identifying those at higher risk for GD.

The Concept of Cholelithiasis as Per Ayurvedic Text

Cholelithiasis (gallstone formation) results from a combination of several factors, including super saturation of bile with cholesterol, accelerated nucleation of cholesterol monohydrate in bile, and bile stasis or delayed gallbladder emptying due to impaired gallbladder motility. In India it is more common in women in north, north-east and east as compared to other zones in the country. The disease Gall Stone has not been described directly in Ayurvedic classics. The word Ashmari in Ayurveda stands for stone which is described only in the context of Bastigat Ashmari (urinary calculi). After analyzing the Ayurvedic texts it was found that the bile secreted from gall bladder can be correlated with Accha Pitta mentioned in Ayurveda due to the similarity in location and function. The pathogenesis of the disease occurs due to the abnormal formation of Kapha during the process of digestion and its vitiation due to Vata. The present article deals with description of formation of gall stone from the Ayurvedic perspective. Along with this the specific remedy for gall stone according to Ayurveda is also described.

Autonomic neuropathy and gallbladder motility in patients with liver cirrhosis.

Impaired gallbladder motility has been suggested as a contributor to increased incidence of gallstones in patients with liver cirrhosis. The purpose of this study was to determine gallbladder function and its relation with autonomic neuropathy in liver cirrhosis. Gallbladder function was measured using ultrasonography in 48 patients with liver cirrhosis and in 31 controls. Autonomic neuropathy tests were applied in patients with liver cirrhosis. Patients with liver cirrhosis were analyzed in subgroups according to the severity of disease using the Child-Pugh classification. Fasting gallbladder volume was 16.2 mL (range: 2.1 mL-71.9 mL) in patients and 17.6 mL (range: 4.9 mL-76.6 mL) in controls. There were no differences in fasting gallbladder volume among the study groups (p>0.05). Gallbladder ejection fraction was significantly higher in patients compared with controls (84% vs. 65%) (p<0.001). No correlation was found between gallbladder ejection fraction and autonomic neuropathy (p>0.05). Our results indicate that liver cirrhosis does not impair gallbladder emptying, and that there is no association between gallbladder motility and autonomic neuropathy. Further investigations are required to explain increased gallbladder motility in liver cirrhosis.

The role of interstitial Cajal-like cells in the formation of cholesterol stones in guinea pig gallbladder.

To investigate the effect of interstitial Cajal-like cells (ICLCs) on contraction of gallbladder muscle strips; and to analyze the changes of ICLCs during cholesterol gallstone formation in guinea pig. The cholesterol gallstone animal model was made by feeding guinea pig with high cholesterol diet (HCD). In vitro isolated gallbladder muscle strips were prepared. Gallbladder motility was assessed by the contraction frequency and amplitude of slow wave in response to CCK-8. The alteration in ICLC density was estimated by using immunohistochemistry. The expression of c-kit and stem cell factor (SCF) were determined. The amplitude and frequency of slow wave was significantly lower in gallbladder muscle strips with the impaired ICLCs. And it is correlated with the decreased contractile response to CCK-8. In HCD guinea pig, the ICLC density and bile flow in response to CCK-8 were remarkably decreased. The results indicated that gallbladder ICLCs can create slow wave potential, and also get involved in the regulation of CCK-8 induced gallbladder smooth muscle motility. In the process of cholesterol gallstone formation, ICLC density clearly decreased. This further impaired gallbladder motility. The decrease in ICLC density may result from decreased expression of c-kit and SCF during cholesterol gallstone formation.

Impaired cholecystokinin-induced gallbladder emptying incriminated in spontaneous "black" pigment gallstone formation in germfree Swiss Webster mice.

"Black" pigment gallstones form in sterile gallbladder bile in the presence of excess bilirubin conjugates ("hyperbilirubinbilia") from ineffective erythropoiesis, hemolysis, or induced enterohepatic cycling (EHC) of unconjugated bilirubin. Impaired gallbladder motility is a less well-studied risk factor. We evaluated the spontaneous occurrence of gallstones in adult germfree (GF) and conventionally housed specific pathogen-free (SPF) Swiss Webster (SW) mice. GF SW mice were more likely to have gallstones than SPF SW mice, with 75% and 23% prevalence, respectively. In GF SW mice, gallstones were observed predominately in heavier, older females. Gallbladders of GF SW mice were markedly enlarged, contained sterile black gallstones composed of calcium bilirubinate and <1% cholesterol, and had low-grade inflammation, edema, and epithelial hyperplasia. Hemograms were normal, but serum cholesterol was elevated in GF compared with SPF SW mice, and serum glucose levels were positively related to increasing age. Aged GF and SPF SW mice had deficits in gallbladder smooth muscle activity. In response to cholecystokinin (CCK), gallbladders of fasted GF SW mice showed impaired emptying (females: 29%; males: 1% emptying), whereas SPF SW females and males emptied 89% and 53% of volume, respectively. Bilirubin secretion rates of GF SW mice were not greater than SPF SW mice, repudiating an induced EHC. Gallstones likely developed in GF SW mice because of gallbladder hypomotility, enabled by features of GF physiology, including decreased intestinal CCK concentration and delayed intestinal transit, as well as an apparent genetic predisposition of the SW stock. GF SW mice may provide a valuable model to study gallbladder stasis as a cause of black pigment gallstones.

Impaired gallbladder motility in adults with newly detected type 2 diabetes and lack of reversibility after achieving euglycemia.

The effects of hyperglycemia and normoglycemia on gallbladder emptying have not been studied in detail. This prospective case-control study was designed to investigate the gallbladder ejection fraction in patients with newly detected diabetes and to assess the impact of restoring normoglycemia on gallbladder ejection fraction in such patients. (99m)Tc-mebrofenin scintigraphy was performed in 22 patients with newly detected type 2 diabetes for measurement of gallbladder ejection fraction. The scintigraphy was performed at the time of first presentation and again 6 months after control of diabetes (glycated hemoglobin [A1C] <7%). Also, gallbladder ejection fraction was measured in 20 age- and sex-matched controls without diabetes. Gallbladder ejection fraction was lower in patients with newly detected diabetes compared with controls (31.4%±5.9% vs. 70.7%±4.3%, p<0.001). Gallbladder ejection fraction did not improve after the treatment of diabetes mellitus (21.3%±5.7%, p=0.395). Gallbladder ejection fraction was markedly reduced in patients with newly detected diabetes compared to controls without diabetes. Control of diabetes and normalization of A1C did not reverse the motility defect.

Castanea sativa Mill. Extract Contracts Gallbladder and Relaxes Sphincter of Oddi in Guinea Pig: A Natural Approach to Biliary Tract Motility Disorders

Impaired gallbladder motility is a contributing factor to gallstone formation. Since many drugs delaying intestinal motility inhibit gallbladder emptying, the aim of the present study was to evaluate the effect on gallbladder and sphincter of Oddi motility of a Natural Chestnut Wood Extract (NEC) that reduces intestinal motility. In order to evaluate the effect of the extract in normal- and high-risk gallstone conditions, the investigation was performed using tissues from animals fed normal and lithogenic diet. Fifty guinea pigs were administered either control or lithogenic diet. The spontaneous motility of the gallbladder and sphincter of Oddi were recorded on isolated gallbladder tissues; thereafter, the effect of NEC on motility was tested and compared with carbachol (CCh), potassium chloride (KCl), noradrenaline (NA), and A71623. Compared to controls, the lithogenic diet induced an irregular and disordered motor pattern in both the gallbladder and sphincter of Oddi. NEC increased gallbladder and decreased sphincter of Oddi spontaneous motility independently of cholinergic, adrenergic, and CCK-1 receptor-mediated pathways both in controls and in lithogenic diet-fed animals, although the effect was lower in the latter group. The effect was reversible and mediated by calcium channels. The natural extract of chestnut increasing gallbladder contraction and inducing the relaxation of the sphincter of Oddi can be of benefit in pathological conditions associated with increased transit time at risk of gallstones.

Gastrointestinal peptides, gastrointestinal motility, and anorexia of aging in frail elderly persons

The mechanisms involved in anorexia in frail elderly people remain unclear. The objective of this study was to establish whether fasting and postprandial levels of gastrointestinal peptides, gastrointestinal motility, and hunger are modified by age and frailty. Three groups of subjects were studied: (a) frail elderly (>70 years) persons, (b) non-frail elderly (>70 years) persons, and (c) healthy adults (aged 25-65 years). After an overnight fast, participants ingested a 400 Kcal liquid meal and appetite, hormonal, and gastrointestinal responses were monitored during early (0-60 min) and late (60-240 min) postprandial periods. Frail persons showed poor nutritional status, sarcopenia, and almost absence of hunger during fasting and postprandial periods. Older persons presented higher levels of glucose and insulin during fasting, enhanced postprandial CCK release in early postprandial period and postprandial hyperglycemia and hyperinsulinemia, but similar ghrelin levels than younger adults. Ultrasound scan showed that the fasting antral area was higher and antral compliance lower in old persons. The paracetamol absorption test showed enhanced postprandial gastric emptying in the frail. Non-gallbladder contractors showed no CCK peak in younger and non-frail groups, but the same high CCK peak as contractors in the frail. Frailty was associated with anorexia, risk of malnutrition, and sarcopenia. Frail persons showed impaired gastric motility (larger antral area at rest, impaired antral compliance, and enhanced postprandial emptying), impaired gallbladder motility, and fasting and/or postprandial alterations in CCK, glucose, and insulin release. Further studies are needed to determine if these factors may contribute to anorexia of aging in frail persons.

Changes of interstitial Cajal-like cells and gallbladder motility during the formation of cholesterol stones in guinea pig gallbladder

Objective To analyze the changes of interstitial Cajal-like cells (ICLCs) and gallbladder motility during the process of gallbladder cholesterol stone formation in the guinea pig model.Methods 100 guinea pigs were divided into two groups of 50 each.The animals in the experimental group were fed on a high cholesterol diet (cholesterol 2％),while those in the control group fed on a normal diet.The guinea pigs were sacrificed at the 8th week.The morphological and distribution characteristics of ICLCs were observed by using immunohistochemistry.Ultrastructure of ICLCs was observed under a transmission electron microscope.Gallbaldder motility was assessed by cholecystokinin (CCK)-8 stimulation test in vivo.Results The average positive area of ICLCs was decreased obviously in the experimental group as compared with the control group [(18.37 ± 0.64) ％ vs (2.47 ± 0.28) ％,t =21.122,P ＜ 0.01].The area under the time-flow curve of the gallbladder juice was decreased significantly in the experimental group as compared with the control group [(31.58 ± 2.26) μl vs (15.02 ± 1.98) μl,t =8.586,P ＜ 0.01].Conclusion Decreased number of ICLCs and impaired gallbladder motility are present in guinea pigs fed on a lithogenous diet,and this may have a role in the pathogenesis of cholesterol gallstone formation. Key words: Cholesterol gallstones; Gallbladder; Interstitial cells; Cholecystokinin

Gallbladder and gastric motility in obese newborns, pre‐adolescents and adults

Impaired gallbladder and gastric motility have been associated with obesity in adults. The timing of appearance of this dysfunction, however, is unclear. Lean and obese subjects from three different age groups were studied noninvasively: 50 newborns (1-12 months old, six obese), 18 pre-adolescents (7-8 years old, seven obese), and 99 adults (22-80 years old, 32 obese) classified according to standard normal tables and body mass index. Changes of fasting/postprandial gallbladder and gastric motility were assessed simultaneously by functional ultrasonography in response to milk (newborns and pre-adolescents) and to a liquid test meal (adults). In newborns, fasting and postprandial gallbladder volumes and gastric emptying were similar between obese and lean subjects. In pre-adolescents, obese subjects had a larger fasting gallbladder volume, with slower postprandial gastric emptying than lean subjects. In obese adults, the most evident dysfunction emerged, with larger fasting and postprandial residual gallbladder volume, and slower postprandial gastric emptying than lean subjects. Obese subjects display abnormal gallbladder and gastric motility patterns, which first appear in pre-adolescents and deteriorate in adults. Such abnormalities are absent in obese newborns. Functional ultrasonography can detect altered cholecysto-gastric motility at the earliest stage. Our findings suggest an age-related decline of motility, probably secondary to excessive fat and insulin-resistance.

Impaired gallbladder motility and the effect of metformin therapy in patients with polycystic ovary syndrome

Impaired gallbladder (GB) emptying is a well-documented contributor to gallstone formation. The aim of this study was to evaluate GB motility in patients with polycystic ovary syndrome (PCOS). The study population consisted of 36 PCOS patients and 20 healthy controls. GB volume was calculated using the ellipsoid formula (π/6 × L × D × W) after three-dimensional measurements were made by ultrasound [length (L), width (W) and depth (D)]. Following the determination of fasting GB volume (V0), patients were given a standard liquid meal. GB volume measurement was then repeated after 10, 20, 30, 40, 50, 60, 75 and 90 min. Gallbladder ejection fraction (GBEF) was calculated after each measurement. PCOS patients were re-evaluated after a 12-week course of metformin therapy at a dose of 1000 mg/day. Mean baseline GB volume (V0) was significantly higher in the patient group compared to the control group (27·2 ± 12·5 cm(3) vs 13·3 ± 7·0 cm(3) , P < 0·001). While baseline GBEF values were similar between groups, increases in GBEF were significantly lower in the PCOS group starting from 20 min after consumption of a standard test meal. A 12-week course of metformin therapy resulted in significant improvements in GB volume and GBEF values with a reversal of metabolic and hormonal abnormalities. For the first time in the literature, we managed to demonstrate impaired GB motility in patients with PCOS. Metformin therapy not only improves the metabolic and hormonal imbalances associated with PCOS but also has a positive influence on GB motility.

Gall bladder contractility in children with beta-thalassaemia

We studied gall bladder contractility in 61 children with beta-thalassaemia who were asymptomatic for gall bladder disease and 51 sex- and age-matched controls in Cairo, Egypt, using, andreal-time ultrasonography. Multiple gall bladder stones were present in 18.0% of thalassaemia patients and sludge in 6.6%. There were statistically significant differences between thalassaemia patients controls in gall bladder fasting volume, residual volume, emptying time and contraction index. There was significant positive correlation between fasting and residual volumes and age, weight and height, and between fasting volume and body mass index and serum ferritin level. Contraction index was negatively correlated with serum total bilirubin. Impaired gall bladder motility was evident in patients with beta-thalassaemia and it may be related to disease duration, serum ferritin and total serum bilirubin level.

Patients with iron deficiency anemia have an increased prevalence of gallstones

We determined the frequency of gallstones (GS) in iron deficiency anemia (IDA) patients and evaluated factors that could affect GS formation-like lipid levels and gallbladder (GB) motilities of the patients. One hundred and eleven IDA patients (88 females, 23 males; median age, 42) and 81 healthy controls (68 females, 13 males; median age, 42) were included into our study. The clinical findings of all IDA patients were recorded down; biochemical values and body mass index (BMI) were determined; and abdominal ultrasonography was performed. In addition, GB emptying was monitored by ultrasound at 30-min intervals for 2 h after a mixed meal in randomly chosen, age-matched 25 IDA patients and 26 controls. Fasting volume (FV), residual volume (RV), and ejection fraction (EF) for all GBs were determined. The frequency of GS plus cholecystectomy was significantly higher in IDA patients (15 cases, 13.5%) than in the control group (five cases, 6.2%, p = 0.048). IDA patients with GS plus cholecystectomy were older than those without GS plus cholecystectomy (p < 0.001). FV and EF did not differ between IDA and control groups (p > 0.05). On the other hand, RV was significantly higher in IDA group than in controls (p = 0.035). The frequency of GS in IDA patients was significantly higher than in controls. The increased prevalence of GS in IDA might be explained with impaired GB motility.

A putative role of ribonuclear inclusions and MBNL1 in the impairment of gallbladder smooth muscle contractility with cholelithiasis in myotonic dystrophy type 1

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystemic disorder caused by expansion of unstable trinucleotide (CTG) repeats at 3′ untranslated region of the DMPK gene on chromosome 19q13.3. Mutant transcripts are retained in muscle nuclei as ribonuclear inclusions and interact with RNA-binding proteins, such as muscleblind-like protein 1 (MBNL1), leading to a reduction in their activity. The reduced MBNL1 activity has been associated to skeletal and cardiac muscle dysfunction. However, other organs and systems may be involved. It has been reported that 25–50% of DM1 patients have abdominal symptoms due to cholelithiasis or gallstones. Since impaired gallbladder motility plays an important role in gallstones formation, we have analyzed by FISH combined with MBNL1-immunofluorescence, the gallbladder obtained from a woman affected by DM1 who required a cholecystectomy at the age of 30. Gallbladders obtained from two no-DM1 subjects have been used as controls. Ribonuclear inclusions and MBNL1 foci accumulate and colocalize in nuclei of DM1 gallbladder smooth muscle cells. On the contrary, no ribonuclear inclusions are detectable in cell nuclei of control gallbladders and MBNL1 is uniformly distributed in smooth muscle cell nuclei. These results suggest that nuclear accumulation of MBNL1 and ribonuclear inclusions may have a direct adverse effect on gallbladder smooth muscle contractility and thus contribute to gallstones formation in DM1 patients.

Increased Prevalence of Gallstone Disease and Impaired Gallbladder Motility in Patients with Barrett’s Esophagus

The prevalence of gallstones in patients with Barrett's esophagus (BE) and their gallbladder motility relative to that of healthy volunteers and GERD patients without BE were investigated. Of the 707 patients reviewed, 203 (125 males and 78 females) had BE. The prevalence of gallstones was significantly higher in the patients with BE than in those without BE (34 vs. 20%, respectively). The gallbladder functions of 22 patients with GERD, 27 patients with BE and 21 healthy volunteers were assessed by ultrasonography before and after a test meal. The patients with BE had significantly higher fasting volume and residual volume, but lower ejection volume, ejection fraction and ejection rate values than those of the healthy controls. None of the ultrasonographic parameters of patients without BE were significantly different from those of the controls. Patients with BE have a more complex gastrointestinal motility disorder that involves the gallbladder, and this makes this subset of patients with GERD more prone to gallstone disease.