Impaired gallbladder motility and delayed orocecal transit contribute to pigment gallstone and biliary sludge formation in beta-thalassemia major adults. (73/734)

AIM: Gallbladder and gastrointestinal motility defects exist in gallstones patients and to a lesser extent in pigment gallstone patients. To investigated the role of gallbladder and gastrointestinal motility disorders in pigment gallstone formation in beta-thalassemia major. METHODS: Twenty-three patients with beta-thalassemia major (16 females; age range 18-37 years) and 70 controls (47 females, age range 18-40 years) were studied for gallbladder and gastric emptying (functional ultrasonography), orocecal transit (OCTT, H(2)-breath test), autonomic dysfunction (sweat-spot, cardiorespiratory reflex tests), bowel habits, gastrointestinal symptoms and quality of life (all with questionnaires). Gallbladder content (ultrasonography) was examined before and during 8-12 mo follow-up. RESULTS: Gallstones and/or biliary sludge were found in 13 (56%) patients. beta-thalassemia major patients had increased fasting (38.0+/-4.8 mL vs 20.3+/-0.7 mL, P = 0.0001) and residual (7.9+/-1.3 mL vs 5.1+/-0.3 mL, P = 0.002) volume and slightly slower emptying (24.9+/-1.7 min vs 20.1+/-0.7 min, P = 0.04) of the gallbladder, together with longer OCTT (132.2+/-7.8 min vs 99.7+/-2.3 min, P = 0.00003) than controls. No differences in gastric emptying and bowel habits were found. Also, patients had higher dyspepsia (score: 6.7+/-1.2 vs 4.9+/-0.2, P = 0.027), greater appetite (P = 0.000004) and lower health perception (P = 0.00002) than controls. Autonomic dysfunction was diagnosed in 52% of patients (positive tests: 76.2% and 66.7% for parasympathetic and sympathetic involvement, respectively). Patients developing sludge during follow-up (38%, 2 with prior stones) had increased fasting and residual gallbladder volume. CONCLUSION: Adult beta-thalassemia major patients have gallbladder dysmotility associated with delayed small intestinal transit and autonomic dysfunction. These abnormalities apparently contribute together with haemolytic hyperbilirubinemia to the pathogenesis of pigment gallstones/sludge in beta-thalassemia major.  (+info)

Expression of tumor necrosis factor and its receptor in gallstone and gallbladder carcinoma tissue. (74/734)

BACKGROUND: Some reports have confirmed that occurrence and development of tumor are related with lots of oncogene, anti-oncogene and cytokine. This study was to detect the expression of TNFmRNA, tumor necrosis factor (TNF) and TNF receptor (TNFR) in the gallbladder mucosa which developed from hyperplasia, dysplasia to carcinoma, and to further discuss the pathogenecity of gallbladder carcinoma. METHODS: The expression of TNFmRNA, TNF and TNFR was detected by in situ hybridization and immunohistochemistry on the surgical specimens of hyperplasia, dysplasia and carcinoma of the gallbladder. RESULTS: The percentage of positive cells expressed TNFmRNA in the gallbladder mucosa was 0%, 20%, and 90%, respectively in hyperplasia, dysplasia and carcinoma (P<0.05). The percentage of positive mononuclear cells (MNCs) expressed TNFmRNA in hyperplasia, dysplasia and carcinoma of gallbladder tissues was 15%, 85%, and 90%, respectively (P<0.05). The number of positive MNC high-power field (Hpf) was 4.85+/-1.50, 6.00+/-2.71, and 9.33+/-3.07, respectively (P<0.05). The number of carcinoma cells and MNCs expressed by TNFmRNA per high-power field was increased with the increase of tumor stage. The number of carcinoma cells/Hpf in stages I-III and IV-V was 9.13+/-4.39 and 7.13+/-2.53 (P<0.05), and that of MNC/Hpf was 14.80+/-4.02 and 11.10+/-2.23 (P<0.01). The number of carcinoma cells and MNCs expressed by TNFmRNA per Hpf was increased with the increase of tumor size. In tumors of more than 2 cm or less than 2 cm in diameter, the number of positive carcinoma cells/Hpf was 14.00+/-4.20 and 8.83+/-4.96, respectively (P<0.05), but that of MNC/Hpf was 10.50+/-2.54 and 7.00+/-2.83 (P<0.05). The pattern of TNF protein expression was similar to that of TNFmRNA, whereas TNF protein expression was more frequent and extensive than TNFmRNA expression. TNFR was expressed in endothelial cells and MNCs of carcinoma, and was negative in mucosal epithelial cells and tumor cells. A positive linear correlation in TNFmRNA expression was observed between tumor cells and MNCs (r=0.687, P<0.01), a correlation in TNFmRNA and TNF protein expression of tumor cells (r=0.847, P<0.001), and a correlation in TNFmRNA and TNF protein expression of MNC in tumor tissue (r=0.643, P<0.01). CONCLUSIONS: TNFmRNA and TNF protein expression is increased during the development of gallbladder mucosa from hyperplasia, dysplasia to carcinoma, and is increased with tumor stage. This finding suggests that TNF is involved in the pathogenesis of gallbladder carcinoma induced by gallstones and the TNF expression in cancer cells may serve as a marker for tumor stage.  (+info)

Laparoscopic cholangiography. Results and indications. (75/734)

One hundred sixty-five operative cholangiograms were attempted in 364 patients who underwent laparoscopic cholecystectomy (45%). Laparoscopic cholangiography was successful in 150 of 165 attempts (91%). Eighty-nine per cent of studies were normal (134/150) and 11% were abnormal (16/150). All 134 patients with normal cholangiograms remained asymptomatic (false-negative rate, 0%). False-positive studies occurred in 3 of 150 (2%) total cholangiograms and 3 of 12 (25%) abnormal cholangiograms consistent with choledocholithiasis. A total of 16 of 364 patients had proven common bile duct stones (4.4%). Eight of the sixteen stones were removed by preoperative endoscopic retrograde cholangiopancreatography/sphincterotomy. Five of sixteen stones were found at cholangiography, four of which were unsuspected (4/150, 2.6%). Retained common duct stones were found in 3 of 214 patients not undergoing cholangiography (1.4%). No complications or deaths occurred that were due to cholangiography. One biliary injury occurred (1/364, 0.3%), in a patient with aberrant anatomy who did not undergo cholangiography. Laparoscopic cholangiography is a safe technique with a success rate greater than 90%. Routine cholangiography is presently recommended for prevention of biliary injury, detection of stones in the cystic and common ducts, and for training purposes, especially during the learning phase of laparoscopic cholecystectomy.  (+info)

Outcome and patient acceptance of outpatient laparoscopic cholecystectomy. (76/734)

OBJECTIVE: The aim of this prospective study was to evaluate patients' experience and the outcome of outpatient laparoscopic cholecystectomy performed by a single upper gastrointestinal surgeon at a district hospital. METHODS: Between November 1999 and May 2003, 100 patients underwent outpatient laparoscopic cholecystectomy. Patients were followed up at 2 weeks as outpatients, and a questionnaire was mailed to all patients to assess their experiences. RESULTS: None of the patients required conversion to open cholecystectomy. One patient required admission to the hospital following drain insertion, and one patient was readmitted for pain control. One patient developed an epigastric port infection that resolved with antibiotics. Sixty-eight of the 100 patients completed the postal questionnaire. Thirty-five patients rated their overall experience as excellent. Twenty-three patients experienced very mild or no pain. All patients' right upper quadrant pain subsided or improved following surgery except one patient who stated that it became worse. Sixty-three patients (92.7%) stated they would recommend outpatient laparoscopic cholecystectomy to a friend or relative. CONCLUSION: Laparoscopic cholecystectomy can be performed safely as an outpatient procedure with a high acceptance and satisfaction rate in select patients.  (+info)

Evaluation of fundus-first laparoscopic cholecystectomy. (77/734)

OBJECTIVES: Laparoscopic cholecystectomy is the gold standard for gallbladder surgery. Cholecystectomy from the fundus to the cystic duct may be advantageous when cystic duct exposure becomes difficult due to adhesions on Calot's triangle. The aim of this study was to compare conventional laparoscopic cholecystectomy with the fundus-first procedure and to evaluate whether the fundus-first technique can prevent conversion in difficult cases. METHODS: The study included 145 patients treated over 18 months. The inclusion criterion was the presence of ultrasound proven gallstones. Patients were excluded from the study if there was evidence of common bile duct stones, a bilioenteric fistula, or carcinoma of the gallbladder. RESULTS: The fundus-first approach was started in 45 patients; all procedures were completed laparoscopically. Conventional laparoscopic cholecystectomy was begun in 100 patients. Twenty-seven of the 100 patients were converted to fundus dissection (adhesions within Calot's triangle). Four of the 27 were further converted to open surgery. One patient had a drop in blood pressure on creation of pneumoperitoneum. Time taken for severely inflammatory and noninflammatory cases was significantly greater (P<0.05) in the fundus-first group. The average hospital stay was 48 hours in both groups. No major complications were observed. CONCLUSION: The rate of conversion in the conventional laparoscopic cholecystectomy group decreased from 18.75% (27/144) to 2.08% (3/144). The fundus-first technique has the potential to decrease conversion in difficult cases.  (+info)

UGT1A1 variation and gallstone formation in sickle cell disease. (78/734)

Pigment gallstones are a common clinical complication of sickle cell (SS) disease. Genetic variation in the promoter of uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) underlies Gilbert syndrome, a chronic form of unconjugated hyperbilirubinemia, and appears to be a risk factor for gallstone formation. We investigated the association between UGT1A1 (TA)(n) genotype, hyperbilirubinemia, and gallstones in a sample of Jamaicans with SS disease. Subjects were from the Jamaican Sickle Cell Cohort Study (cohort sample, n = 209) and the Sickle Cell Clinic at the University of the West Indies, Kingston, Jamaica (clinic sample, n = 357). The UGT1A1 (TA)(n) promoter region was sequenced in 541 SS disease subjects and 111 healthy controls (control sample). Indirect bilirubin levels for (TA)(7)/(TA)(7) and (TA)(7)/(TA)(8) genotypes were elevated compared with (TA)(6)/(TA)(6) (clinic sample, P < 10(-5); cohort sample, P < 10(-3)). The (TA)(7)/(TA)(7) genotype was also associated with symptomatic presentation and gallstones in the clinic sample (odds ratio [OR] = 11.3; P = 7.0 x 10(-4)) but not in the younger cohort sample. These unexpected findings indicate that the temporal evolution of symptomatic gallstones may involve factors other than the bilirubin level. Although further studies of the pathogenesis of gallstones in SS disease are required, the (TA)(7)/(TA)(7) genotype may be a risk factor for symptomatic gallstones in older people with SS disease.  (+info)

Opisthorchiasis-associated biliary stones: light and scanning electron microscopic study. (79/734)

AIM: Biliary stones are frequently encountered in areas endemic for opisthorchiasis in Thailand. The present study was to describe the prevalence and pathogenesis of these stones. METHODS: Gallstones and/or common bile duct stones and bile specimens from 113 consecutive cholecystectomies were included. Bile samples, including sludge and/or microcalculi, were examined for Opisthorchis viverrini eggs, calcium and bilirubin. The stones were also processed for scanning electron microscopic (SEM) study. RESULTS: Of the 113 cases, 82 had pigment stones, while one had cholesterol stones. The other 30 cases had no stones. Most of the stone cases (76%, 63/83) had multiple stones, while the remainder had a single stone. Stones were more frequently observed in females. Bile examination was positive for O. viverrini eggs in 50% of the cases studied. Aggregates of calcium bilirubinate precipitates were observed in all cases with sludge. Deposition of calcium bilirubinate on the eggshell was visualized by special staining. A SEM study demonstrated the presence of the parasite eggs in the stones. Numerous crystals, morphologically consistent with calcium derivatives and cholesterol precipitates, were seen. CONCLUSION: Northeast Thailand has a high prevalence of pigment stones, as observed at the cholecystectomy, and liver fluke infestation seems involved in the pathogenesis of stone formation.  (+info)

Impaired cytoprotective function of muscle in human gallbladders with cholesterol stones. (80/734)

Acute cholecystitis develops in gallbladders (GB) with excessive bile cholesterol (Ch). Increased membrane Ch content affects membrane function and may affect PGE(2) receptors involved in the cytoprotection against acute inflammation. This study was aimed at determining whether the cytoprotective response to PGE(2) is affected by lithogenic bile with Ch. Muscle cells from human GB with cholesterol stones (ChS) or pigment stones (PS) were obtained by enzymatic digestion. PGE(2) levels were measured by radioimmunoassay, and activities of superoxide dismutase (SOD) and catalase were assayed by spectrophotometry. The contraction in response to H(2)O(2) in muscle cells from PS was 14 +/- 0.3%, not different from normal controls, and decreased after the cells were incubated with Ch-rich liposomes (P < 0.05), which increase the Ch content in the plasma membranes. In muscle cells from GB with ChS, H(2)O(2)-induced contraction was only 9.2 +/- 1.3% and increased to 14 +/- 0.2% after Ch-free liposome treatment to remove Ch from the plasma membranes (P < 0.01). H(2)O(2) caused a similar increase in the levels of lipid peroxidation and PGE(2) content in muscle cells from GBs with ChS and PS. However, the activities of SOD and catalase were significantly lower in muscle cells from GBs with ChS compared with those with PS. The binding capacity of PGE(2) receptors was also significantly lower in muscle cells from GBs with ChS compared with those with PS. In conclusion, the cytoprotective response to reactive oxygen species is reduced in muscle cells from GBs with ChS despite a normal increase in the cellular levels of PGE(2). This impaired cytoprotective response may be due to a dysfunction of PGE(2) receptors with decreased binding capacity resulting from excessive Ch levels in the plasma membrane.  (+info)