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Background Gallstone disease remains a major health issue. There have been significant changes in the management and demographics of patients with these conditions. We aimed to evaluate trends in hospitalization, management, and post-procedural adverse events for patients with gallstone disease. Methods The National Inpatient Sample was used to identify discharges for symptomatic cholelithiasis and cholecystitis between 2005 and 2014. Temporal trends were evaluated by calculating annual percent changes (APCs). Joinpoint regression was used to assess inflection points. Multivariable regression models were used to evaluate associations between urban and rural divisions and mortality, use of interventional procedures, and post-procedural adverse events. Results From 77,394,755 unweighted discharges, there was a decline in discharges for cholelithiasis (APC − 5.5%, 95% confidence intervals, CI, − 7.6 to − 3.4%) and cholecystitis from 2012 to 2014 (APC − 4.5%, 95% CI − 7.2 to − 1.7%). Interventions were more likely at urban hospitals for symptomatic cholelithiasis (odds ratio, OR, 1.49, 95% CI 1.24 to 1.66) and cholecystitis (OR 1.96, 95% CI 1.86 to 2.05). In-hospital mortality significantly decreased annually for patients with cholecystitis (OR 0.92, 95% CI 0.91 to 0.93). In-hospital mortality between rural and urban centers was comparable for symptomatic cholelithiasis (OR 1.27, 95% CI 0.79 to 2.03) and cholecystitis (OR 0.93, 95% CI 0.84 to 1.04). Conclusions Hospitalizations for gallstone disease have decreased since the 2010s. In-hospital mortality between urban and rural centers is similar, but urban hospitals utilize a higher rate of procedural interventions. Future studies should evaluate practice trends and costs across inpatient and ambulatory settings between rural and urban divisions.

Fatty acids are important dietary factors that have been extensively studied for their implication in health and disease. Evidence from epidemiological studies and randomised controlled trials on their role in cardiovascular, inflammatory, and other diseases remains inconsistent. The objective of this study was to assess whether genetically predicted fatty acid concentrations affect the risk of disease across a wide variety of clinical health outcomes. The UK Biobank (UKB) is a large study involving over 500,000 participants aged 40 to 69 years at recruitment from 2006 to 2010. We used summary-level data for 117,143 UKB samples (base dataset), to extract genetic associations of fatty acids, and individual-level data for 322,232 UKB participants (target dataset) to conduct our discovery analysis. We studied potentially causal relationships of circulating fatty acids with 845 clinical diagnoses, using mendelian randomisation (MR) approach, within a phenome-wide association study (PheWAS) framework. Regression models in PheWAS were adjusted for sex, age, and the first 10 genetic principal components. External summary statistics were used for replication. When several fatty acids were associated with a health outcome, multivariable MR and MR-Bayesian method averaging (MR-BMA) was applied to disentangle their causal role. Genetic predisposition to higher docosahexaenoic acid (DHA) was associated with cholelithiasis and cholecystitis (odds ratio per mmol/L: 0.76, 95% confidence interval: 0.66 to 0.87). This was supported in replication analysis (FinnGen study) and by the genetically predicted omega-3 fatty acids analyses. Genetically predicted linoleic acid (LA), omega-6, polyunsaturated fatty acids (PUFAs), and total fatty acids (total FAs) showed positive associations with cardiovascular outcomes with support from replication analysis. Finally, higher genetically predicted levels of DHA (0.83, 0.73 to 0.95) and omega-3 (0.83, 0.75 to 0.92) were found to have a protective effect on obesity, which was supported using body mass index (BMI) in the GIANT consortium as replication analysis. Multivariable MR analysis suggested a direct detrimental effect of LA (1.64, 1.07 to 2.50) and omega-6 fatty acids (1.81, 1.06 to 3.09) on coronary heart disease (CHD). MR-BMA prioritised LA and omega-6 fatty acids as the top risk factors for CHD. Although we present a range of sensitivity analyses to the address MR assumptions, horizontal pleiotropy may still bias the reported associations and further evaluation in clinical trials is needed. Our study suggests potentially protective effects of circulating DHA and omega-3 concentrations on cholelithiasis and cholecystitis and on obesity, highlighting the need to further assess them as prevention treatments in clinical trials. Moreover, our findings do not support the supplementation of unsaturated fatty acids for cardiovascular disease prevention.

Background Gallstone disease (GSD) is associated with a higher risk of gastrointestinal (GI) cancer. However, it is unclear whether the associations are causal. Methods The prospective China Kadoorie Biobank (CKB) recorded 17,598 cases of GI cancer among 510,137 participants without cancer at baseline during 10 years of follow-up. Cox regression was used to estimate hazard ratios (HRs) for specific cancer by GSD status and duration. Mendelian randomisation was conducted to assess the genetic associations of GSD with specific cancer. Results Overall 6% of participants had symptomatic GSD at baseline. Compared with those without GSD, individuals with symptomatic GSD had adjusted HRs of 1.13 (1.01–1.29) for colorectal, 2.01 (1.78–2.26) for liver, 3.70 (2.88–4.87) for gallbladder, 2.31 (1.78–3.07) for biliary tract, and 1.38 (1.18–1.74) for pancreatic cancer. Compared with participants without GSD, the risks of colorectal, liver, gallbladder, biliary tract, and pancreatic cancer were highest during 0 to <5 years following disease diagnosis. There was evidence of genetic associations of GSD with these cancers, with odds ratios per 1-SD genetic score of 1.08 (1.05–1.11) for colorectal, 1.22 (1.19–1.25) for liver, 1.56 (1.49–1.64) for gallbladder, 1.39 (1.31–1.46) for biliary tract, and 1.16 (1.10–1.22) for pancreatic cancer. When meta-analysing the genetic estimates in CKB and UK Biobank, there was evidence of causal associations of GSD with colon cancer, gallbladder and biliary tract cancer (GBTC), and total GI cancer (RR per 1-SD: 1.05 [0.99–1.11], 2.00 [1.91–2.09], and 1.09 [1.05–1.13]). Conclusions GSD was associated with higher risks of several GI cancers, warranting future studies on the underlying mechanisms.

BackgroundObesity and rapid weight loss after bariatric surgery (BS) are independent risk factors for development of cholelithiasis (CL), a prevalent disease in the Chilean population. This study aimed to determine the incidence of CL in obese Chilean patients 12 months after BS and identify risk factors for development of gallstones.MethodsRetrospective study of patients who underwent BS in 2014. Patients with preoperative negative abdominal ultrasound (US) for CL and follow-up for at least than 12 months were included. Patients underwent US at 6 months and 12 months. We analyzed sex, age, hypertension, dyslipidemia, type 2 diabetes mellitus, body mass index (BMI), surgical procedure, percentage of excess BMI loss (%EBMIL) at 6 months, and BMI at 6 months.ResultsOf 279 patients who underwent bariatric surgery during 2014, 66 had previous gallbladder disease and 176 met the inclusion criteria (82.6%), while 54.6% were female. The mean age was 37.8 ± 10.5 years and preoperative BMI was 37.5 kg/m2. BMI and %EBMIL at 6 months were 27.8 ± 3.3 kg/m2 and 77.9 ± 33.6%, respectively. At 12 months after BS, CL was found in 65 patients (36.9%). Hypertension turned out to be protective against occurrence of gallstones at 1 year with an OR 0.241.ConclusionsIncidence of CL was up to one-third of the patients followed up for 12 months after BS. Excessive weight loss and other variables studied did not increase risk. Hypertension seems to be protective against gallstone formation, but this result needs further analysis.

OBJECTIVE: The objective of this study was to assess the risk of acute pancreatitis in patients with type 2 diabetes compared with that in patients without diabetes. We also examined the risk of biliary disease (defined as occurrence of cholelithiasis, acute cholecystitis, or cholecystectomy), which is a major cause of pancreatitis. RESEARCH DESIGN AND METHODS: We conducted a retrospective cohort study using a large, geographically diverse U.S. health care claims database. Eligible patients (greater-than-or-equal18 years) were enrolled for at least 12 continuous months (1999-2005), with no incident events of pancreatitis or biliary disease during that 1 year baseline period. ICD-9 codes and prescription data were used to identify patients with type 2 diabetes; ICD-9 codes were also used to identify cases of pancreatitis and biliary disease. Overall, 337,067 patients with type 2 diabetes were matched on age and sex with 337,067 patients without diabetes. Incidence rates of disease and 95% CI were calculated per 100,000 person-years of exposure. RESULTS: The type 2 diabetic cohort had a 2.83-fold (95% CI 2.61-3.06) greater risk of pancreatitis and 1.91-fold (1.84-1.99) greater risk of biliary disease compared with the nondiabetic cohort. Relative to patients of corresponding age without diabetes, younger type 2 diabetic patients had the highest risk of pancreatitis (<45 years: incidence rate ratio [IRR] 5.26 [95% CI 4.31-6.42]; greater-than-or-equal45 years: 2.44 [2.23-2.66]). CONCLUSIONS: These data suggest that patients with type 2 diabetes may have an increased risk of acute pancreatitis and biliary disease.

The purpose of the present study was to investigate the incidence of cholelithiasis and evaluate the risk factors for cholelithiasis in patients with spinal cord injury (SCI). We analyzed 1,530 SCI patients (1,186 males and 344 females) from the China Rehabilitation Research Center (2010-2019) and compared patients with cholelithiasis (n = 289) and without cholelithiasis. The variables included age, gender, marital status, blood glucose level, motor function, and American Spinal Injury Association (ASIA) Impairment Scale (AIS) score. A total of 1530 patients with SCI, including 1186 males and 344 females, were included in this study. The prevalence of cholelithiasis was 18.89%. Univariate analysis revealed significant differences in age (P < 0.001), marital status (P < 0.001), blood glucose level (P < 0.001), and preserved motor function (P = 0.033). Multivariate analysis revealed the following independent risk factors: age ≥ 50 years (OR=1.637; 95% CI = 1.016-2.639; P = 0.043), being married (OR=1.902; 95% CI = 1.061-3.411; P = 0.031), lack of motor function (OR=1.587; 95% CI = 1.194-2.111; P < 0.001), and hyperglycemia (OR=1.764; 95% CI = 1.164-2.673; P = 0.007). Gender, lipid levels, SCI segment, and AIS grade were not significantly different. Patients with SCI have a higher incidence of gallstones. Multivariate logistic regression analysis revealed that the occurrence of cholelithiasis in patients with SCI is closely related to age, marital status, blood glucose level and motor function preservation. Tailored preventive and therapeutic approaches should be developed for SCI patients, with intensified monitoring and intervention for high-risk patients to significantly improve quality of life.

ObjectiveAlpha-1 antitrypsin deficiency (AATD) is a common, potentially lethal inborn disorder caused by mutations in alpha-1 antitrypsin (AAT). Homozygosity for the ‘Pi*Z’ variant of AAT (Pi*ZZ genotype) causes lung and liver disease, whereas heterozygous ‘Pi*Z’ carriage (Pi*MZ genotype) predisposes to gallstones and liver fibrosis. The clinical significance of the more common ‘Pi*S’ variant remains largely undefined and no robust data exist on the prevalence of liver tumours in AATD.DesignBaseline phenotypes of AATD individuals and non-carriers were analysed in 482 380 participants in the UK Biobank. 1104 participants of a multinational cohort (586 Pi*ZZ, 239 Pi*SZ, 279 non-carriers) underwent a comprehensive clinical assessment. Associations were adjusted for age, sex, body mass index, diabetes and alcohol consumption.ResultsAmong UK Biobank participants, Pi*ZZ individuals displayed the highest liver enzyme values, the highest occurrence of liver fibrosis/cirrhosis (adjusted OR (aOR)=21.7 (8.8–53.7)) and primary liver cancer (aOR=44.5 (10.8–183.6)). Subjects with Pi*MZ genotype had slightly elevated liver enzymes and moderately increased odds for liver fibrosis/cirrhosis (aOR=1.7 (1.2–2.2)) and cholelithiasis (aOR=1.3 (1.2–1.4)). Individuals with homozygous Pi*S mutation (Pi*SS genotype) harboured minimally elevated alanine aminotransferase values, but no other hepatobiliary abnormalities. Pi*SZ participants displayed higher liver enzymes, more frequent liver fibrosis/cirrhosis (aOR=3.1 (1.1–8.2)) and primary liver cancer (aOR=6.6 (1.6–26.9)). The higher fibrosis burden was confirmed in a multinational cohort. Male sex, age ≥50 years, obesity and the presence of diabetes were associated with significant liver fibrosis.ConclusionOur study defines the hepatobiliary phenotype of individuals with the most relevant AATD genotypes including their predisposition to liver tumours, thereby allowing evidence-based advice and individualised hepatological surveillance.

Cholecystectomy has long been regarded as a safe procedure with no deleterious influence on the body. However, recent studies provide clues that link cholecystectomy to a high risk for metabolic syndrome (MetS). In the present review, we describe the epidemiologic evidence that links cholecystectomy to MetS. Various components of MetS are investigated, including visceral obesity, dyslipidemia, elevated blood pressure, impaired fasting glucose, and insulin resistance. The possible mechanisms that associate cholecystectomy with MetS are discussed on the basis of experimental studies.

BackgroundBariatric surgery predisposes patients to cholelithiasis and therefore the need of a subsequent cholecystectomy; however, the incidence of cholecystectomy after bariatric surgery is debated.Aim and MethodsMedical records of 601patients hospitalized for bariatric surgery between January 2010 and July 2018 were reviewed. Our aim was to evaluate the incidence of cholecystectomy following different types of common bariatric procedures. All patients who developed cholelithiasis and a subsequent cholecystectomy were included. Cholelithiasis was diagnosed by clinical criteria and characteristic ultrasound findings.ResultsWe retrospectively evaluated 580 patients with an average follow-up of 12 months (range 6–24 months). Twenty-one patients were excluded because of missing data. Mean age was 48 ± 19 years (78% females). Twenty-nine patients (5%) underwent laparoscopic cholecystectomy (LC) before the bariatric surgery, and 58 patients (10%) performed concomitant LC with the bariatric procedure due to symptomatic gallstone disease (including stones, sludge, and polyps). There were 203 laparoscopic sleeve gastrectomy (SG) (35%), 175 laparoscopic gastric band (LAGB) (30%), 55 Roux-en-Y gastric bypass (RYGB) (9.5%), and 147 (25%) mini gastric bypass (MGB) procedures during the study period. At the follow-up period, 36 patients (6.2%) developed symptomatic cholelithiasis, while the most common clinical presentation was biliary colic. There was a significant difference between the type of the bariatric procedure and the incidence of symptomatic cholelithiasis after the operation. The incidence of symptomatic gallstone formation in patients who underwent RYGB was 14.5%. This was significantly higher comparing to 4.4% following SG, 4.1% following LAGB, and 7.5% following MGB (p = 0.04). We did not find any predictive risk factors including smoking; BMI at surgery; change in BMI; comorbidities such as diabetes, hyperlipidemia, hypertension, and COPD for gallstone formation; or a subsequent cholecystectomy. Interestingly we found that previous bariatric surgery was a risk factor for gallstone formation and cholecystectomy, 13/82 patients (15.8%) compared to 23/492 patients (4.6%) among those without previous bariatric operation (p < 0.001)].ConclusionOur data demonstrate that patients with previous bariatric surgery or patients planned for RYGB are at high risk to develop postoperative symptomatic gallbladder disease. Concomitant cholecystectomy during the bariatric procedure or alternatively UDCA treatment for at least for 6 months to avoid the high incidence of postoperative symptomatic gallstones should be considered in those asymptomatic patients.

The pathogenesis of pancreatitis involves diverse environmental risk factors, some of which have not yet been clearly elucidated. This study systematically investigated the causal effects of genetically predicted modifiable risk factors on pancreatitis using the Mendelian randomization (MR) approach. Genetic variants associated with 30 exposure factors were obtained from genome-wide association studies. Summary-level statistical data for acute pancreatitis (AP), chronic pancreatitis (CP), alcohol-induced AP (AAP) and alcohol-induced CP (ACP) were obtained from FinnGen consortia. Univariable and multivariable MR analyses were performed to identify causal risk factors for pancreatitis. Genetic predisposition to smoking (OR = 1.314, = 0.021), cholelithiasis (OR = 1.365, = 1.307E-19) and inflammatory bowel disease (IBD) (OR = 1.063, = 0.008) as well as higher triglycerides (OR = 1.189, = 0.016), body mass index (BMI) (OR = 1.335, = 3.077E-04), whole body fat mass (OR = 1.291, = 0.004) and waist circumference (OR = 1.466, = 0.011) were associated with increased risk of AP. The effect of obesity traits on AP was attenuated after correcting for cholelithiasis. Genetically-driven smoking (OR = 1.595, = 0.005), alcohol consumption (OR = 3.142, = 0.020), cholelithiasis (OR = 1.180, = 0.001), autoimmune diseases (OR = 1.123, = 0.008), IBD (OR = 1.066, = 0.042), type 2 diabetes (OR = 1.121, = 0.029), and higher serum calcium (OR = 1.933, = 0.018), triglycerides (OR = 1.222, = 0.021) and waist-to-hip ratio (OR = 1.632, = 0.023) increased the risk of CP. Cholelithiasis, triglycerides and the waist-to-hip ratio remained significant predictors in the multivariable MR. Genetically predicted alcohol drinking was associated with increased risk of AAP (OR = 15.045, = 0.001) and ACP (OR = 6.042, = 0.014). After adjustment of alcohol drinking, genetic liability to IBD had a similar significant causal effect on AAP (OR = 1.137, = 0.049), while testosterone (OR = 0.270, = 0.002) a triglyceride (OR = 1.610, = 0.001) and hip circumference (OR = 0.648, = 0.040) were significantly associated with ACP. Genetically predicted higher education and household income levels could lower the risk of pancreatitis. This MR study provides evidence of complex causal associations between modifiable risk factors and pancreatitis. These findings provide new insights into potential therapeutic and prevention strategies.