Pigment Gallstones Research Articles

Multiple Primary Choledocholithiasis in Sickle Cell Disease

Choledocholithiasis can be caused by either primary or secondary bile duct stones. Although patients with sickle cell disease (SCD) are at high risk of development of pigmented gallstones due to chronic hemolysis, primary choledocholithiasis in SCD is very uncommon. The delay in the diagnosis of biliary tract pathology can occur in patients who had a prior cholecystectomy. There is a possible relationship between prior cholecystectomy and the subsequent occurrence of primary common bile duct stones, due to the higher probability of infection of the biliary system. Here, we report an unusual and severe case of multiple primary choledocholithiasis, associated with pancreatitis, in a patient with SCD, fourteen years after cholecystectomy.

An extended chemical analysis of gallstone.

Chemical composition of gall stones is essential for aetiopathogensis of gallstone disease. We have reported quantitative chemical analysis of total cholesterol bilirubin, calcium, iron and inorganic phosphate in 120 gallstones from haryana. To extend this chemical analysis of gall stones by studying more cases and by analyzing more chemical constituents. A quantitative chemical analysis of total cholesterol, total bilirubin, fatty acids, triglycerides, phospholipids, bile acids, soluble proteins, sodium potassium, magnesium, copper, oxalate and chlorides of biliary calculi (52 cholesterol, 76 mixed and 72 pigment) retrieved from surgical operation of 200 patients from Haryana state was carried out. Total cholesterol as the major component and total bilirubin, phospholipids, triglycerides, bile acids, fatty acids (esterified), soluble protein, calcium, magnesium, iron, copper, sodium, potassium, inorganic phosphate, oxalate and chloride as minor components were found in all types of calculi. The cholesterol stones had higher content of total cholesterol, phospholipids, fatty acids (esterified), inorganic phosphate and copper compared to mixed and pigment stones. The mixed stones had higher content of iron and triglycerides than to cholesterol and pigment stones. The pigment stones were richer in total bilirubin, bile acids, calcium, oxalate, magnesium, sodium, potassium, chloride and soluble protein compared to cholesterol and mixed stones. Although total cholesterol was a major component of cholesterol, mixed and pigment gall stone in Haryana, the content of most of the other lipids, cations and anions was different in different gall stones indicating their different mechanism of formation.

Analysis of Indian pigment gallstones

Particle induced X-ray emission and particle induced γ-ray emission spectroscopic techniques have been carried out to analyse the elemental concentrations of human pigment gallstone samples from eastern region (Orissa) and southern region (Chennai) of India. It was observed that 18 minor/trace elements namely Na, Mg, Al, P, S, Cl, K, Ca, Ti, V, Cr, Mn, Fe, Ni, Cu, Zn, Br and Pb were present in the pigment gallstone samples of both the regions. Our study reveals that average concentration of all elements except Ni in south Indian pigment gallstone samples is higher than that of corresponding values in east Indian pigment gallstone samples whereas elements like Al, P, S, Cl and V did not show much variation between these two regions. Fourier transform infra-red analysis was carried out to identify the functional groups and the classification of the pigment type gallstones of both the regions. The thermal behaviour of pigment gallstones was carried out by thermogravimetry-derivative thermogravimetry analysis.

Can pigment gallstones be induced by biliary stricture and prevented by medicine in Guinea pigs

To determine the relationship between biliary stricture and pigment gallstone formation, and the prevention of pigment gallstones with medicine. One hundred and eighteen male guinea pigs were randomly divided into four groups: stricture group (S, n = 30) underwent partial ligation of common bile duct, and fed on regular chow; S plus medicine group (S+M, n = 27) underwent the same operation but fed on medicinal chow (0.3 g chenodeoxycholic acid, 0.5 g glucurolactone, and 0.5 g aspirin were mixed up in 1.2 kg regular chow); medicinal control group (C+M, n = 30) was free of operation, and fed on medicinal chow; and control group (C, n = 31) was free of operation and fed on regular chow. One week later, laparotomy was performed, and the bile of gallbladder was collected, measured, and cultured. Gallstones were identified. Pigment gallstones were induced by biliary stricture in 95% (22/23) of S group. In the S+M group, the incidence of gallstone was reduced to 55% (11/20, vs S group, P < 0.01). The changes of indirect bilirubin and ionized calcium in the bile were consistent with gallstone incidences. Biliary stricture can cause pigment gallstone formation in guinea pigs, and the medicines used can lower the incidence of gallstones. The bilirubin and ionized calcium play important roles in pigment gallstone formation.

The relationship between Oddi's sphincter and bile duct pigment gallstone

To investigate the relationship between anatomic abnormalities and malfunction of Oddi sphincter with formation of bile duct pigment gallstone. One hundred and twenty-three patients with a T tube after cholecystectomy and choledochotomy were divided into reflux group and control group by measuring the amounts of radioactivity of (99m)Tc-DTPA in the bile. Among them 53 were selected randomly to undergo choledochoscopic manometry. Basal pressure of Oddi's sphincter (SOBP), amplitude of Oddi's sphincter (SOCA), frequency of contraction (SOF), duration of contraction (SOD), duodenal pressure (DP), common bile duct pressure (CBDP) were scored and analyzed. The level of plasma motilin and serum gastrin of 45 patients and 12 healthy volunteers were measured by radioimmunoassay. The incidence rates of duodenal descending part diverticulum in patients with bile duct pigment stones, patients without alimentary tract diseases, patients with gallbladder polyps, patients with gallbladder stones were studied by means of barium meal examination. The incidence rates of intraduodenal peri-ampullary diverticulum in patients with primary bile duct pigment stones, patients with bile duct stone and gallbladder stones, patients with bile duct stones originating from the gallbladder, patients with inflammation and stricture of the extremity of bile duct and papilla, patients with cancer of the extremity of bile duct and papilla, patients with post-cholecystectomy syndrome were detected by duodenoscope. Of the patients, 44 were detected with duodenal-biliary reflux (35.8%). SOBP, SOCA and CBDP in the reflux group were much lower than those in control group (P < 0.001). The level of serum gastrin and plasma motilin of the reflux group were much lower than those of control group (P < 0.01). Positive correlation was found between level of motilin and SOBP while level of gastrin was positively correlated with SOBP and CBDP. The incidence of duodenal diverticulum in patients with bile duct pigment stone was 36.62%, which was higher than that of the other 3 groups. The incidence rate of intraduodenal peri-ampullary diverticulum in patients with primary bile duct pigment stone was higher than that of patients with inflammation and stricture of the extremity of bile duct and papilla, patients with cancer of the extremity of bile duct and papilla and patients with bile duct stones originating from the gallbladder. The patients with bile duct pigment stone have apparent duodenal-biliary reflux and infection of the bile duct. The state of structure and function of Oddi's sphincter is correlated significantly with bile duct pigment stone. The anatomic abnormalities and malfunction of Oddi's sphincter played an important role in the formation of bile duct pigment stone.

Biliary bacterial factors determine the path of gallstone formation

Background Bacteria cause pigment gallstones and can act as a nidus for cholesterol gallstone formation. Bacterial factors that facilitate gallstone formation include beta-glucuronidase (bG), phospholipase (PhL), and slime. The current study sought to determine whether bacterial factors influence the path of gallstone formation. Methods A total of 382 gallstones were cultured and/or examined using scanning electron microscopy (SEM). Bacteria were tested for bG and slime production. Gallstone composition was determined using infrared spectrography. Ca-palmitate presence documented bacterial PhL production. Groups were identified based upon bacterial factors present: slime and bGPhL (slime/bGPhL), bGPhL only, and slime only. Influence of bacterial stone-forming factors on gallstone composition and morphology was analyzed. Results Bacteria were present in 75% of pigment, 76% of mixed, and 20% of cholesterol stones. Gallstones with bGPhL producing bacteria contained more pigment (71% vs. 26%, P < .0001). The slime/bGPhL group was associated (79%) with pigment stones, bGPhL was associated (56%) with mixed stones, while slime (or none) only was associated (67%) with cholesterol stones ( P < .031, all comparisons). Conclusions Bacterial properties determined the path of gallstone formation. Bacteria that produced all stone-forming factors promoted pigment stone formation, while those that produced only bGPhL promoted mixed stone formation. Bacteria that only produced slime lacked the ability to generate pigment solids, and consequently were more common in the centers of cholesterol stones. This shows how bacterial characteristics may govern the process of gallstone formation.

Effects of Shengqing Capsules on expression of nuclear factor-κB protein in liver cells of guinea pigs with pigment gallstone

To study the mechanisms of Shengqing Capsules, a compound Chinese herbal medicine for dispersing stagnated liver qi and promoting bile flow, in prevention and treatment of pigment gallstone. Liver cells from guinea pigs with pigment gallstone were primarily cultured in vitro. The serums containing different concentrations of Shengqing Capsules were prepared by serum pharmacological method. The primary cultured hepatocytes with excessive expression of nuclear factor-kappaB (NF-kappaB) were stimulated with lipopolysaccharides (LPS) and the effects of the drug-containing serums on the NF-kappaB expression were detected by Western-blotting. Shengqing Capsules down-regulated the NF-kappaB expression increased by LPS stimulation. The effect is dose-dependent. Shengqing Capsules can down-regulate the NF-kappaB expression increased by LPS stimulation. It may be one of the important mechanisms of this Chinese herbal medicine in prevention and treatment for pigment gallstone formation and the inflammatory reaction in biliary tract.

Effects of choleretics on bile compositions drained from patients with pigment gallstone

To provide evidence for three-level prevention of cholelithiasis by means of observing the effects of some choleretics on bile compositions drained from patients with pigment gallstone. Twenty-seven patients suffering from primary pigment gallstones and having received treatment of choledochostomies plus T-tube or endoscopic nasal bile drainage (ENBD) were divided equally into three groups, and administered respectively with Lidanling (the LDL group), ursodesoxycholic acid (the UDA group) and combination of LDL and UDA (the LDL + UDA group) through oral intake (7 patients in each group). Besides, 6 post-operational patients got no treatment with any drug were allocated in the control group. Bile of all the patients was collected before treatment and on the 1, 3, 5, 7 th day after the treatment started to detect levels of total bile acid (TBA), glycocholic acid (GCA), taurocholic acid (TCA), glycocholic cheno-desoxycholic acid (GCDCA), total bilirubin (TBIL), uncombined bilirubin (UCB), concentration of calcium ion (Ca(2+)) as well as the bacterio-genetic and endogenous beta-glucuronidase activity for comparing. Levels of TBA, GCA, TCA and GCDCA got gradually increased in the UDA group and the LDL + UDA group after treatment (P < 0.05), while those in the LDL group remained unchanged, showing an insignificant difference as compared with those in the control group. In the LDL group and the LDL + UDA group, TBIL gradually increased while UCB gradually decreased in the course of treatment (P < 0.05). Moreover, levels of Ca(2+) and endogenous beta-glucuronidase activity got significantly lowered (P < 0.05). Combined use of LDL and UDA could elevate levels of TBA, GCA, TCA, GCDCA, enhance the excretion of TBIL in patients with pigment gallstone after bile drainage, lower levels of UCB and Ca(2+) and the activity of endogenous beta-glucuronidase in the bile, so as to reduce the possibility of stone formation of bile, and therefore, it could be used to prevent the production of pigment gallstone, especially to prevent post-operative recurrence of stones.

An Animal Model of Black Pigment Gallstones Caused by Nanobacteria

Black pigment gallstones are often founded in gallbladder, but their pathogenesis is unclear. The present study was undertaken to study the role of nanobacteria in pigment gallstone formation in Japanese white rabbits. Nanobacteria were successfully cultured from 3 of 7 cholecystolithiasis patients gallbladder (without acute cholecystitis) bile samples and affirmed by Hoechst 33258 staining and specific immunostaining using monoclonal antibody. Nanobacteria were injected into rabbits' gallbladder. After 2 weeks follow-up, the incidence of black pigment gallstones in rabbits was significantly greater in nanobacteria-injected group (8/10) than that in DMEM-injected group (2/10) and that in hydroxyapatite-injected group (2/10). This study indicates that nanobacteria exists in gallbladder bile of cholelithiasis patients and causes the formation of black pigment gallstones in rabbits. For the first time, we successfully established an animal model of black pigment gallstones caused by nanobacteria. This will be helpful in further delineating the pathogenesis of black pigment gallstones.

Serum adiponectin levels in cholesterol and pigment cholelithiasis

Altered adiponectin levels are associated with metabolic abnormalities. The aim of this study was to explore the role of adiponectin in cholelithiasis. A radioimmunoassay was used to determine serum adiponectin levels in 58 patients with cholesterol gallstones and 47 with pigment gallstones, and 101 healthy controls. The chemical composition of extracted gallstones was determined by Fourier transform infrared spectroscopy. The mean(s.d.) adiponectin level was decreased in patients with cholesterol gallstones (7.6(4.1) microg/ml; P < 0.001) but raised in patients with pigment gallstones (17.9(9.0) microg/ml; P < 0.001) in comparison with healthy controls (11.7(6.5) microg/ml). Decreased adiponectin levels (odds ratio (OR) 0.85 (95 per cent confidence interval (c.i.) 0.76 to 0.96); P = 0.008) and female sex (OR 6.06 (95 per cent c.i. 2.10 to 17.46); P = 0.001) were associated with cholesterol gallstone formation. Increased adiponectin levels (OR 1.11 (95 per cent c.i. 1.01 to 1.22); P = 0.025) and increased age (OR 1.06 (95 per cent c.i. 1.01 to 1.12); P = 0.029) were associated with pigment gallstone formation. Raised serum aspartate aminotransferase concentration was a risk factor for both cholesterol (OR 1.16 (95 per cent c.i. 1.03 to 1.30); P = 0.013) and pigment (OR 1.23 (95 per cent c.i. 1.10 to 1.38); P < 0.001) gallstones. Gallstone formation is associated with altered serum adiponectin levels. Serum adiponectin might serve as a novel marker for cholesterol and pigment cholelithiasis.

Coinheritance of Gilbert syndrome–associated UGT1A1 mutation increases gallstone risk in cystic fibrosis†

The prevalence of "black" pigment gallstones is increased in patients with cystic fibrosis (CF). Bile acid malabsorption with augmented bilirubin uptake from the intestine and the development of "hyperbilirubinbilia" have been proposed as key factors in gallstone formation in CF patients. We have now tested the hypothesis that the coinheritance of the common UGT1A1 promoter mutation associated with Gilbert syndrome is an additional lithogenic risk factor for gallstone formation in CF. Our results show that patients with CF and gallstones are significantly more likely to carry at least one Gilbert UGT1A1 allele compared with stone-free patients (OR 7.3; P = .042) and that these carriers display significantly higher serum levels of unconjugated bilirubin (P = .002). In conclusion, the Gilbert UGT1A1 allele increases the risk of gallstone formation in CF. This genetic association supports the current concept for gallstone formation in CF and suggests that genetic and exogenous sources contributing to hyperbilirubinbilia might be lithogenic in CF patients.

Autoimmune Liver Disease in Three Children with Sickle Cell Disease

Autoimmune Liver Disease in Three Children with Sickle Cell Disease

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.

Hepatic Wilson’s disease: Initial treatment and long-term management

This article is based on the experience of 320 patients with Wilson's disease who were seen between the years 1954 and 2000. These patients were seen at The Boston City Hospital, 1954 thru 1955, University College Hospital, London,1955 thru 1957; Addenbrooke's Hospital, Cambridge, 1967 thru 1987, and The Middlesex Hospital London, 1988 thru 2000. Wilson's disease is not strictly a gastroenterologic disease but a genetically determined metabolic disease that is mediated by a failure of copper excretion through the bile. The mutation carried on chromosome 13q14.3: it involves a copper-carrying ATPase (ATPase 7B); more than 250 mutations are now known. The first organ to be affected is the liver, then many other tissues, principally the brain but also the eyes, the kidneys, the bone marrow, and the osteoskeletal system. It is with the hepatic form of the disease that this article is concerned. The hepatic illness may be acute, subacute or chronic; it may be progressive or, apparently, self-limiting. In 10% of patients hemolysis may also be found which can later lead to the formation of pigment gallstones. The management of liver disease is not considered in this article, which is strictly confined to the therapeutic options available for the elimination of copper and the long-term welfare of the patient. It must be remembered that all close relatives of the patient must be screened for the presymptomatic stage of the disease so, if they are found to be homozygous carriers for the mutation, they can be started on preventive treatment.

Complementary Stimulation of Hepatobiliary Transport and Detoxification Systems by Rifampicin and Ursodeoxycholic Acid in Humans

Rifampicin (RIFA) and ursodeoxycholic acid (UDCA) improve symptoms and biochemical markers of liver injury in cholestatic liver diseases by largely unknown mechanisms. We aimed to study the molecular mechanisms of action of these drugs in humans. Thirty otherwise healthy gallstone patients scheduled for cholestectomy were randomized to RIFA (600 mg/day for 1 week) or UDCA (1 g/day for 3 weeks) or no medication before surgery. Routine biochemistry, lipids, and surrogate markers for P450 activity (4beta-hydroxy cholesterol, 4beta-OH-C) and bile acid synthesis (7alpha-hydroxy-4-cholesten-3-one, C-4) were measured in serum. Bile acids were analyzed in serum, urine, and bile. A wedge liver biopsy specimen was taken to study expression of hepatobiliary ABC transporters as well as detoxification enzymes and regulatory transcription factors. RIFA enhanced bile acid detoxification as well as bilirubin conjugation and excretion as reflected by enhanced expression of CYP3A4, UGT1A1, and MRP2. These molecular effects were paralleled by decreased bilirubin and deoxycholic acid concentrations in serum and decreased lithocholic and deoxycholic acid concentrations in bile. UDCA on the other hand stimulated the expression of BSEP, MDR3, and MRP4. UDCA became the predominant bile acid after UDCA treatment and lowered the biliary cholesterol saturation index. RIFA enhances bile acid detoxification as well as bilirubin conjugation and export systems, whereas UDCA stimulates the expression of transporters for canalicular and basolateral bile acid export as well as the canalicular phospholipid flippase. These independent but complementary effects may justify a combination of both agents for the treatment of cholestatic liver diseases.

The Genetic Background of Cholesterol Gallstone Formation: An Inventory of Human Lithogenic Genes

Family and twin studies as well as animal studies indicate that gallstone disease is, in part, genetically determined. Recently new single gene defects have been identified in specific patients with cholesterol and pigment gallstones. Examples include low phospholipid-associated cholelithiasis due to mutations of the gene encoding the hepatocanalicular phosphatidylcholine transporter, and pigment stones in association with mutations of the ileal bile salt transporter gene. Here we summarize the evidence for common genetic determinants of human gallstone disease in general and provide an inventory of human lithogenic genes. The precise understanding of such genes and their molecular mechanisms will establish new targets for rational drugdesign for this exceptionally prevalent and economically significant digestive disease.

Lung Abscess Due to Retained Gallstones With an Adenocarcinoma

We describe a patient who had a right lower lobe mass containing calcifications consistent with gallstones develop 3(1)/(2) years after laparoscopic cholecystectomy. Thoracotomy revealed a chronic abscess containing pigmented gallstones and an adjacent area of bronchoalveolar adenocarcinoma involving both N1 and N2 lymph nodes.

Cholelithiasis and Cholecystitis

Gallstone disease remains one of the most common medical problems leading to surgical intervention. Every year, approximately 500,000 cholecystectomies are performed in the US. Cholelithiasis affects approximately 10% of the adult population in the United States. It has been well demonstrated that the presence of gallstones increases with age. An estimated 20% of adults over 40 years of age and 30% of those over age 70 have biliary calculi. During the reproductive years, the female-to-male ratio is about 4:1, with the sex discrepancy narrowing in the older population to near equality. The risk factors predisposing to gallstone formation include obesity, diabetes mellitus, estrogen and pregnancy, hemolytic diseases, and cirrhosis. A study of the natural history of cholelithiasis demonstrates that approximately 35% of patients initially diagnosed with having, but not treated for, gallstones later developed complications or recurrent symptoms leading to cholecystectomy. During the last two decades, the general principles of gallstone management have not notably changed. However, methods of treatment have been dramatically altered. Today, laparoscopic cholecystectomy, laparoscopic common bile duct exploration, and endoscopic retrograde management of common bile duct (CBD) stones play important roles in the treatment of gallstones. These technological advances in the management of biliary tract disease are not infrequently accomplished by a multidisciplinary team of physicians, including surgeons trained in laparoscopic techniques, interventional gastroenterologists, and interventional radiologists. With the evolution of laparoscopic cholecystectomy, there has been a global reeducation and retraining program of surgeons. However, the treatment of choice for gallstones remains cholecystectomy. In recognition of the revolutionary advances in the treatment of cholelithiasis, it is the purpose of this collective review to describe recent information on the following topics: types of gallstones, asymptomatic gallstones, symptomatic gallstones, chronic cholecystitis, acute cholecystitis, and other complications of gallstones. Gross and compositional analysis of gallstones allows them to be classified as cholesterol, mixed, and pigment gallstones. When asymptomatic gallstones are detected during the evaluation of a patient, a prophylactic cholecystectomy is normally not indicated because of several factors. Only about 30% of patients with asymptomatic cholelithiasis will warrant surgery during their lifetime, suggesting that cholelithiasis can be a relatively benign condition in some people. However, there are certain factors that predict a more serious course in patients with asymptomatic gallstones and warrant a prophylactic cholecystectomy when they are present. These factors include patients with large (>2.5 cm) gallstones, patients with congenital hemolytic anemia or nonfunctioning gallbladders, or during bariatric surgery or colectomy. Epigastric and right upper quadrant pain occurring 30-60 minutes after meals is frequently associated with gallstone disease. The diagnosis of chronic cholecystitis is made by the presence of biliary colic with evidence of gallstones on an imaging study. Ultrasonography is the diagnostic test of choice, being 90-95% sensitive. The surgical literature suggests that 3-10% of patients undergoing cholecystectomy will have CBD stones. Intraoperative laparoscopic ultrasonography has recently replaced cholangiography as the method of choice for detecting CBD stones. Ultrasonography and radionuclide cholescintigraphy (HIDA scan) are useful in establishing a diagnosis of acute cholecystitis. Laparoscopic cholecystectomy should also be used in the treatment of acute cholecystitis. Laparoscopic cholecystectomy is more likely to be successful when performed within 3 days of the onset of symptoms. It is important to remember that gallstones can lead to a variety of other complications including choledocholithiasis, gallstone ileus, and acute gallstone pancreatitis.

MRI of gallstones with different compositions.

Gallstones are usually recognized on MRI as filling defects of hypointensity. However, they sometimes may appear as hyperintensities on T1-weighted imaging. This study investigated how gallstones appear on MRI and how their appearance influences the detection of gallstones. Gallstones from 24 patients who had MRI performed before the removal of the gallstones were collected for study. The gallstones were classified either as cholesterol gallstone (n = 4) or as pigment gallstone (n = 20) according to their gross appearance and based on analysis by Fourier transform infrared spectroscopy. MRI included three sequences: single-shot fast spin-echo T2-weighted imaging, 3D fast spoiled gradient-echo T1-weighted imaging, and in-phase fast spoiled gradient-echo T1-weighted imaging. The signal intensity and the detection rate of gallstones on MRI were further correlated with the character of the gallstones. On T1-weighted 3D fast spoiled gradient-echo images, most of the pigment gallstones (18/20) were hyperintense and all the cholesterol gallstones (4/4) were hypointense. The mean ratio of the signal intensity of gallstone to bile was (+/- standard deviation) 3.36 +/- 1.88 for pigment gallstone and 0.24 +/- 0.10 for cholesterol gallstone on the 3D fast spoiled gradient-echo sequence (p < 0.001). Combining the 3D fast spoiled gradient-echo and single-shot fast spin-echo sequences achieved the highest gallstone detection rate (96.4%). Based on the differences of signal intensity of gallstones, the 3D fast spoiled gradient-echo T1-weighted imaging was able to diagnose the composition of gallstones. Adding the 3D fast spoiled gradient-echo imaging to the single-shot fast spin-echo T2-weighted sequence can further improve the detection rate of gallstones.

Lipid atherogenic risk markers can be more favourably influenced by the cis-9,trans-11-octadecadienoate isomer than a conjugated linoleic acid mixture or fish oil in hamsters.

The aim of our present study was to compare the efficiency of conjugated linoleic acids (CLA) and fish oil in modulating atherogenic risk markers. Adult male hamsters were given a cholesterol-rich diet (0.6 g/kg) for 8 weeks; the diet was supplemented with 5 g cis-9,trans-11-CLA isomer/kg, 12 g CLA mixture (CLA-mix)/kg, 12 g fish oil/kg or 12 g fish oil+12 g CLA-mix/kg. The plasma cholesterol status was improved only with the cis-9,trans-11-CLA (HDL-cholesterol and HDL-cholesterol:LDL-cholesterol ratio, P<0.05), but was of borderline significance for CLA-mix (HDL-cholesterol:LDL-cholesterol ratio, P=0.06), with an increase (33-40 %) in the liver lipoprotein receptors (scavenger receptor-type I and LDL ApoB/E receptor) and HDL-binding protein 2 (P<0.05). A 100 % pigment gallstones incidence and a slight insulin resistance (homeostatic model assessment index) were observed in the CLA-mix-fed hamsters (P=-0.031). In comparison, fish-oil feeding alone improved merely the scavenger receptor-type I and HDL-binding protein 2 liver status and faeces sterol output. For most of our present observations, the concomitant intake of fish oil and CLA-mix gave dominant effects that were exclusive and specific to one or the other oil. In conclusion, part of the beneficial effects of CLA in the present study can be ascribed to the cis-9,trans-11-isomer, and these did not generally overlap with those of fish oil. In addition, the CLA-mix effects are clearly affected by the marine (n-3) fatty acids.