Natural history of irritable bowel syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73897/1/j.1365-2036.2004.01929.x.pd

Opportunities for preventing esophageal adenocarcinoma

VetenskapsrådetCancerfondenAccepte

Association of Diet Quality With Metabolic (Dysfunction) associated Fatty Liver Disease in Veterans in Primary Care

BACKGROUND: Diet is associated with metabolic (dysfunction)-associated fatty liver disease (MAFLD), but the dietary composition associated with MAFLD risk has not been well-examined. AIM: The purpose of this study was to assess the association of two healthy eating indices with the presence and severity of MAFLD in a sample of Veterans in a primary care setting. METHODS: This was a single center cross-sectional study using a random stratified sample of Veterans enrolled in primary care. Participants underwent a Fibroscan and completed an interviewer-administered Diet History Questionnaire II from which we calculated the Healthy Eating Index-2015 and Alternate Mediterranean Diet Score. We used multivariable logistic regression models to assess associations of dietary quality with MAFLD. RESULTS: We analyzed data from 187 participants, 53.5% of whom were female. On average, participants were 50.2 years of age (SD, 12.3 years) with an average BMI of 31.7 kg/m DISCUSSION: We found that the Alternate Mediterranean Diet Score was significantly associated with lower MAFLD risk in Veterans; however, the association was mediated by BMI and total energy intake. A Mediterranean-style diet could potentially help reduce the risk of MAFLD, particularly if it helps control total energy intake and weight

Association between laparoscopic antireflux surgery and recurrence of gastroesophageal reflux

IMPORTANCE: Cohort studies, mainly based on questionnaires and interviews, have reported high rates of reflux recurrence after antireflux surgery, which may have contributed to a decline in its use. Reflux recurrence after laparoscopic antireflux surgery has not been assessed in a long-term population-based study of unselected patients. OBJECTIVES: To determine the risk of reflux recurrence after laparoscopic antireflux surgery and to identify risk factors for recurrence. DESIGN AND SETTING: Nationwide population-based retrospective cohort study in Sweden between January 1, 2005, and December 31, 2014, based on all Swedish health care and including 2655 patients who underwent laparoscopic antireflux surgery according to the Swedish Patient Registry. Their records were linked to the Swedish Causes of Death Registry and Prescribed Drug Registry. EXPOSURES: Primary laparoscopic antireflux surgery due to gastroesophageal reflux disease in adults (>18 years). MAIN OUTCOMES AND MEASURES: The outcomewas recurrence of reflux, defined as use of antireflux medication (proton pump inhibitors or histamine2 receptor antagonists for >6 months) or secondary antireflux surgery. Multivariable Cox regression was used to assess risk factors for reflux recurrence. RESULTS: Among all 2655 patients who underwent antireflux surgery (median age, 51.0 years; interquartile range, 40.0-61.0 years; 1354 men [51.0%]) and were followed up for a median of 5.6 years, 470 patients (17.7%) had reflux recurrence; 393 (83.6%) received long-term antireflux medication and 77 (16.4%) underwent secondary antireflux surgery. Risk factors for reflux recurrence included female sex (hazard ratio [HR], 1.57 [95%CI, 1.29-1.90]; 286 of 1301 women [22.0%] and 184 of 1354 men [13.6%] had recurrence of reflux), older age (HR, 1.41 [95%CI, 1.10-1.81] for age 61 years compared with 45 years; recurrence among 156 of 715 patients and 133 of 989 patients, respectively), and comorbidity (HR, 1.36 [95%CI, 1.13-1.65] for Charlson comorbidity index score 1 compared with 0; recurrence among 180 of 804 patients and 290 of 1851 patients, respectively). Hospital volume of antireflux surgery was not associated with risk of reflux recurrence (HR, 1.09 [95%CI, 0.77-1.53] for hospital volume 24 surgeries compared with 76 surgeries; recurrence among 38 of 266 patients [14.3%] and 271 of 1526 patients [17.8%], respectively). CONCLUSIONS AND RELEVANCE: Among patients who underwent primary laparoscopic antireflux surgery, 17.7%experienced recurrent gastroesophageal reflux requiring long-term medication use or secondary antireflux surgery. Risk factors for recurrence were older age, female sex, and comorbidity. Laparoscopic antireflux surgery was associated with a relatively high rate of recurrent gastroesophageal reflux disease requiring treatment, diminishing some of the benefits of the operation.Swedish Research Council, D0547801Publishe

HCV Genotype 3 Is Associated With an Increased Risk of Cirrhosis and Hepatocellular Cancer in a National Sample of U.S. Veterans With HCV

Data show that viral genotype 1 may increase the risk of cirrhosis and hepatocellular carcinoma (HCC) compared to genotype 2 in patients with chronic hepatitis C virus (HCV) infection. However, the effect of HCV genotype 3 on cirrhosis and HCC risk is uncertain. We identified patients with active HCV infection, confirmed by positive polymerase chain reaction (PCR) and a known HCV genotype, from the VA HCV Clinical Case Registry between 2000 and 2009. We examined the effect of HCV genotype on the risk of cirrhosis and HCC in a Cox proportional hazards model adjusting for patients' age, period of service (World War I/II, Vietnam era, post-Vietnam era), race, gender, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment receipt. Of the 110,484 patients with active HCV viremia, 88,348 (79.9%) had genotype 1, 13,077 (11.8%) genotype 2, 8,337 (7.5%) genotype 3, and 1,082 (0.9%) patients had genotype 4 infection. Despite being younger, patients with genotype 3 had a higher risk of developing cirrhosis (unadjusted hazard ratio [HR] 5 1.40, 95% confidence interval [CI] 5 1.32-1.50) and HCC (unadjusted HR 5 1.66, 95% CI 5 1.48-1.85) than HCV genotype 1 patients. After adjustment for prespecified demographic, clinical, and antiviral treatment factors, the risk of cirrhosis and HCC was 31% (adjusted HR 5 1.31, 95% CI 5 1.22-1.39) and 80% (adjusted HR 5 1.80, 95% CI 5 1.61-2.03) higher in patients with genotype 3 compared to genotype 1 infected patients. Conclusion: HCV genotype 3 is associated with a significantly increased risk of developing cirrhosis and HCC compared to HCV genotype 1. This association is independent of patients' age, diabetes, body mass index, or antiviral treatment. (HEPATOLOGY 2014;60:98-105

An Electronic Health Record Model for Predicting Risk of Hepatic Fibrosis in Primary Care Patients

BackgroundOne challenge for primary care providers caring for patients with nonalcoholic fatty liver disease is to identify those at the highest risk for clinically significant liver disease.AimTo derive a risk stratification tool using variables from structured electronic health record (EHR) data for use in populations which are disproportionately affected with obesity and diabetes.MethodsWe used data from 344 participants who underwent Fibroscan examination to measure liver fat and liver stiffness measurement [LSM]. Using two approaches, multivariable logistic regression and random forest classification, we assessed risk factors for any hepatic fibrosis (LSM > 7 kPa) and significant hepatic fibrosis (> 8 kPa). Possible predictors included data from the EHR for age, gender, diabetes, hypertension, FIB-4, body mass index (BMI), LDL, HDL, and triglycerides.ResultsOf 344 patients (56.4% women), 34 had any hepatic fibrosis, and 15 significant hepatic fibrosis. Three variables (BMI, FIB-4, diabetes) were identified from both approaches. When we used variable cut-offs defined by Youden's index, the final model predicting any hepatic fibrosis had an AUC of 0.75 (95% CI 0.67-0.84), NPV of 91.5% and PPV of 40.0%. The final model with variable categories based on standard clinical thresholds (i.e., BMI ≥ 30 kg/m2; FIB-4 ≥ 1.45) had lower discriminatory ability (AUC 0.65), but higher PPV (50.0%) and similar NPV (91.3%). We observed similar findings for predicting significant hepatic fibrosis.ConclusionsOur results demonstrate that standard thresholds for clinical risk factors/biomarkers may need to be modified for greater discriminatory ability among populations with high prevalence of obesity and diabetes

Esophageal adenocarcinoma after obesity surgery in a population-based cohort study

Background: Obesity is strongly associated with esophageal adenocarcinoma (EAC), yet whether weight loss reduces the risk of EAC is unclear. Objectives: To test the hypothesis that the risk of EAC decreases following weight reduction achieved by obesity surgery. Setting: Nationwide register-based cohort study. Methods: This study included a majority of individuals who underwent obesity surgery in Sweden in 1980-2012. The incidence of EAC following obesity surgery was compared to the incidence in the corresponding background population of Sweden by means of calculation of standardized incidence ratios (SIRs) with 95% confidence intervals (CIs). The risk of EAC after obesity surgery was also compared with the risk in non-operated obese individuals by means of multivariable Cox regression, providing hazard ratios (HRs) with 95% CIs, adjusted for potential confounders. Results: Among 34,437 study participants undergoing obesity surgery and 239,775 person- 15" years of follow-up, 8 cases of EAC occurred (SIR 1.6, 95% CI 0.7-3.2). No clear trend of decreased SIRs was seen in relation to increased follow-up time after surgery. The SIR of EACs (n=53) among 123,695 non-operated obese individuals (673,238 person-years) was increased to a similar extent as in the obesity surgery cohort (SIR=1.9, 95% CI 1.4-2.5). Cox regression showed no difference in risk of EAC between operated and non-operated participants (adjusted HR=0.9, 95% CI 0.4-1.9). Conclusions: The risk of EAC might not decrease following obesity surgery, but even larger studies with longer follow-up are needed to establish this association.The Swedish Research Council (SIMSAM), the Swedish Cancer Society, and the Nordic Cancer Union.Accepte

External Validation of a Model Determining Risk of Neoplastic Progression of Barrett\u27s Esophagus in a Cohort of Us Veterans

BACKGROUND AND AIMS: Risk of esophageal adenocarcinoma (EAC) in those with Barrett\u27s esophagus (BE) is 11-fold greater than the general population. It remains unclear which BE patients are at highest risk of progression to EAC. We aimed to validate a predictive model risk-stratifying BE patients. METHODS: We conducted a retrospective cohort study at the Houston Veteran Affairs Medical Center of consecutive patients with a new diagnosis of BE from November 1990 to January 2019. Study follow-up was through February 2020. Patients were excluded if they had no follow-up EGD with esophageal biopsy sampling after the initial BE-diagnosing EGD or evidence of high-grade dysplasia (HGD) or EAC on initial EGD. We performed an external validation study of a risk model containing sex, smoking, BE length, and low-grade dysplasia (LGD) status and assessed discriminatory ability using the area under the receiver operating characteristic curve (AUROC). RESULTS: Among 608 BE patients, 24 progressed to HGD/EAC. The points-based model discriminated well with an AUROC of .72 (95% confidence interval [CI], .63-.82). When categorized into low-, intermediate-, and high-risk groups according to published cutoffs, the AUROC was poor at .57. Restructured into low-risk versus high-risk groups, the AUROC was .72 (95% CI, .64-.80). Excluding baseline LGD did not reduce discriminatory ability (AUROC, .73; 95% CI, .64-.82). CONCLUSIONS: This external validation provides further evidence that the model including sex, LGD status, smoking status, and BE length may help to risk stratify BE patients. A simplified version excluding LGD status and/or reducing the number of risk groups has increased utility in clinical practice without loss of discriminatory ability

Synergistic associations of Pnpla3 I148M Variant, alcohol intake, and Obesity With Risk of Cirrhosis, Hepatocellular Carcinoma, and Mortality

IMPORTANCE: Alcohol drinking and obesity are associated with an increased risk of cirrhosis and hepatocellular carcinoma (HCC), but the risk is not uniform among people with these risk factors. Genetic variants, such as I148M in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene, may play an important role in modulating cirrhosis and HCC risk. OBJECTIVE: to investigate the joint associations of the PNPLA3 I148M variant, alcohol intake, and obesity with the risk of cirrhosis, HCC, and liver disease-related mortality. DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study analyzed 414 209 participants enrolled in the UK Biobank study from March 2006 to December 2010. Participants had no previous diagnosis of cirrhosis and HCC and were followed up through March 2021. EXPOSURES: Self-reported alcohol intake (nonexcessive vs excessive), obesity (body mass index ≥30 [calculated as weight in kilograms divided by height in meters squared]), and PNPLA3 I148M variant status (noncarrier, heterozygous carrier, or homozygous carrier) from initial assessment. MAIN OUTCOMES AND MEASURES: The primary outcomes were incident cirrhosis and HCC cases and liver disease-related death ascertained from inpatient hospitalization records and death registry. The risks were calculated by Cox proportional hazards regression models. RESULTS: A total of 414 209 participants (mean [SD] age, 56.3 [8.09] years; 218 567 women [52.8%]; 389 452 White race and ethnicity [94.0%]) were included. Of these participants, 2398 participants (0.6%) developed cirrhosis (5.07 [95% CI, 4.87-5.28] cases per 100 person-years), 323 (0.1%) developed HCC (0.68 [95% CI, 0.61-0.76] cases per 100 person-years), and 878 (0.2%) died from a liver disease-related cause (1.76 [95% CI, 1.64-1.88] cases per 100 person-years) during a median follow-up of 10.9 years. Synergistic interactions between the PNPLA3 I148M variant, obesity, and alcohol intake were associated with the risk of cirrhosis, HCC, and liver disease-related mortality. The risk of cirrhosis increased supramultiplicatively (adjusted hazard ratio [aHR], 17.52; 95% CI, 12.84-23.90) in individuals with obesity, with excessive drinking, and who were homozygous carriers compared with those with no obesity, with nonexcessive drinking, and who were noncarriers. Supramultiplicative associations between the 3 factors and risks of HCC were found in individuals with 3 risk factors (aHR, 30.13; 95% CI, 16.51-54.98) and liver disease-related mortality (aHR, 21.82; 95% CI, 13.78-34.56). The PNPLA3 I148M variant status significantly differentiated the risk of cirrhosis, HCC, and liver disease-related mortality in persons with excessive drinking and obesity. CONCLUSIONS AND RELEVANCE: This study found synergistic associations of the PNPLA3 I148M variant, excessive alcohol intake, and obesity with increased risk of cirrhosis, HCC, and liver disease-related death in the general population. The PNPLA3 I148M variant status may help refine the risk stratification for liver disease in persons with excessive drinking and obesity who may need early preventive measures