Validation of HIV-infected cohort identification using automated clinical data in the Department of Veterans Affairs.

OBJECTIVES: The US Department of Veterans Affairs (VA) is the largest integrated health care provider for HIV-infected patients in the USA. VA data for HIV-specific clinical and quality improvement research are an important resource. We sought to determine the accuracy of using the VA Corporate Data Warehouse (CDW), a fully automated medical records database for all VA users nationally, to identify HIV-infected patients compared with a gold-standard VA HIV Clinical Case Registry (CCR). METHODS: We assessed the test performance characteristics of each of our CDW criteria-based algorithms (presence of one, two or all of the following: diagnostic codes for HIV, positive HIV laboratory tests, and prescription for HIV medication) by calculating their sensitivity (proportion of HIV-positive patients in the CCR accurately detected as HIV-positive by the CDW algorithm) and positive predictive value (PPV; the proportion of patients identified by the CDW algorithm who were classified as HIV-positive from the CCR). RESULTS: We found that using a CDW algorithm requiring two of three HIV diagnostic criteria yielded the highest sensitivity (95.2%) with very little trade-off in PPV (93.5%). CONCLUSIONS: A two diagnostic criteria-based algorithm can be utilized to accurately identify HIV-infected cohorts seen in the nationwide VA health care system.

Acid suppression medications reduce risk of oesophageal adenocarcinoma in Barrett's oesophagus: a nested case-control study in US male veterans.

BACKGROUND: Proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) may reduce the risk of oesophageal adenocarcinoma (OAC) in Barrett's oesophagus; however, current epidemiologic studies are inconclusive. AIM: To evaluate the independent effects of PPIs and H2RAs on risk of OAC in patients with Barrett's oesophagus. METHODS: We conducted a nested case-control study of male veterans diagnosed with Barrett's oesophagus. Cases with incident OAC were matched by incidence density sampling on birth year and Barrett's diagnosis date to controls with Barrett's oesophagus who did not develop OAC. We identified prescription medication usage 1 year prior to Barrett's oesophagus diagnosis to 3 months prior to the OAC diagnosis. Odds ratios (OR) and 95% CI were estimated using conditional logistic regression. RESULTS: Compared with 798 controls, the 300 cases were less likely to use PPIs (90.0% vs 94.5%, P = 0.01) and H2RAs (19.7% vs 25.7%, P = 0.04). In the multivariable model including the use of statins, H2RAs, aspirin and nonsteroidal anti-inflammatory drugs, PPI use was associated with 41% lower risk of OAC (OR 0.59, 95% CI 0.35-0.99). While risk reduction of OAC was stronger for high-dose PPIs (omeprazole daily dose >40 mg, adjusted OR 0.11, 95% 0.04-0.36), we did not find a dose-response relationship with PPI duration (P trend = 0.45). Likewise, H2RA use was independently associated with 30% lower risk of OAC (OR 0.70, 95% CI 0.50-0.99). CONCLUSION: Use of PPIs and H2RAs among patients with Barrett's oesophagus are associated with lower risk of OAC. Further clinical trials are needed to confirm this possible chemopreventive effect.

Proton pump inhibitor and histamine-2 receptor antagonist use and risk of liver cancer in two population-based studies.

BACKGROUND: Proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) are commonly used. PPIs have been shown to promote liver cancer in rats; however, only one study has examined the association in humans. AIMS: To investigate PPIs and H2RAs and risk of primary liver cancer in two large independent study populations. METHODS: We conducted a nested case-control study within the Primary Care Clinical Informatics Unit (PCCIU) database in which up to five controls were matched to cases with primary liver cancer, recorded by General Practitioners. Odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations with prescribed PPIs and H2RAs were calculated using conditional logistic regression. We also conducted a prospective cohort study within the UK Biobank using self-reported medication use and cancer-registry recorded primary liver cancer. Hazard ratios (HRs) and 95% CIs were calculated using Cox regression. RESULTS: In the PCCIU case-control analysis, 434 liver cancer cases were matched to 2103 controls. In the UK Biobank cohort, 182 of 475 768 participants developed liver cancer. In both, ever use of PPIs was associated with increased liver cancer risk (adjusted OR 1.80, 95% CI 1.34, 2.41 and adjusted HR 1.99, 95% CI 1.34, 2.94 respectively). There was little evidence of association with H2RA use (adjusted OR 1.21, 95% CI 0.84, 1.76 and adjusted HR 1.70, 95% CI 0.82, 3.53 respectively). CONCLUSIONS: We found some evidence that PPI use was associated with liver cancer. Whether this association is causal or reflects residual confounding or reverse causation requires additional research.

Metabolic syndrome and the risk of Barrett's oesophagus in white males.

BACKGROUND: Few studies have examined the association between metabolic syndrome and Barrett's oesophagus (BO). Whether metabolic syndrome confers a risk greater than the sum of its components is unknown. AIM: To investigate associations between metabolic syndrome, its components and BO in white males. METHODS: We conducted a case-control study among eligible symptomatic patients scheduled for elective oesophagogastroduodenoscopy and a sample of patients eligible for screening colonoscopy recruited at primary care clinics. Metabolic syndrome was defined as the presence of at least three of: high waist-to-hip ratio (WHR), hypertriglyceridaemia, low high-density lipoprotein cholesterol, hypertension or diabetes. We used multivariate logistic regression to calculate odds ratios (OR) and 95% confidence intervals (95% CI). RESULTS: There were 244 BO cases, 209 colonoscopy and 615 endoscopy controls. Comparing BO cases with all controls, metabolic syndrome was significantly associated with BO (OR = 1.59, 95% CI 1.05-2.40) and there was a dose effect with increasing number of metabolic syndrome components (Ptrend <0.001); when all five components were present, the OR was 2.61 (95% CI 1.14-5.99). We found that among the components, high WHR, hypertension and hypertriglyceridaemia were associated with increased risk of BO. When we compared cases with the control groups separately, metabolic syndrome was associated with BO for comparisons with endoscopy controls (OR = 1.67, 95% CI 1.10-2.55) but not colonoscopy controls (OR = 0.87, 95% CI 0.49-1.54). Associations with individual components also depended on the comparison group. CONCLUSIONS: Metabolic syndrome is associated with an increased risk of Barrett's oesophagus in men undergoing endoscopy. Metabolic syndrome may confer additional risk of Barrett's oesophagus separate from obesity.

The incidence of esophageal adenocarcinoma continues to rise: analysis of period and birth cohort effects on recent trends.

BACKGROUND: During the past four decades, the incidence of esophageal adenocarcinoma (EAC) has increased markedly in Western populations. Recent reports have suggested that the rate of increase has slowed or plateaued. PATIENTS AND METHODS: Using data from cancer registries in Australia, the United States and Sweden, we examined incidence trends for esophageal and gastric cardia tumors between 1984 and 2008 using joinpoint analyses and age-period-cohort models. RESULTS: EAC incidence continues to undergo statistically significant annual increases in Australia and the United States, although the rate of increase has slowed. Among men, incidence increased annually by 2.2% [95% confidence interval (CI) 1.5% to 2.9%] between 1994 and 2008 in Australia and 1.5% (95% CI 0.2% to 2.8%) between 1998 and 2008 in the United States. EAC incidence among men remained unchanged in Sweden between 2001 and 2008 (P = 0.52). EAC incidence among women showed significant linear increases between 1984 and 2008. Age-period-cohort models suggested strong effects for both period and birth cohort on EAC incidence in Australia and the United States, and a strong period effect for Sweden. CONCLUSIONS: EAC incidence continues to increase in Australia and the United States. The continued increases, even among more recent birth cohorts, suggest that EAC incidence will continue to rise during coming decades.

The use of nonsteroidal anti-inflammatory drugs and the risk of Barrett's oesophagus.

BACKGROUND: Epidemiological studies have consistently reported inverse associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and oesophageal adenocarcinoma, but few have investigated associations with the precursor lesion, Barrett's oesophagus. AIM: To investigate the relationship between NSAID use and risk of Barrett's oesophagus. METHODS: We conducted a large population-based case-control study that collected information on patterns of intake for aspirin and non-aspirin NSAIDs during the past 5 years and other exposures from 285 patients with nondysplastic Barrett's oesophagus, 108 patients with dysplastic Barrett's oesophagus, and two separate control groups: 313 endoscopy patients with acute inflammatory changes ('inflammation controls') and 644 population controls. We calculated odds ratios (ORs) and 95% CIs using unconditional logistic regression. RESULTS: Use of aspirin was not associated with nondysplastic Barrett's oesophagus when compared with population (OR=1.01, 95% CI 0.71-1.43) or inflammation controls (OR=1.16, 95% CI 0.80-1.68). Whereas we observed significant risk reductions for use of non-aspirin NSAIDs when nondysplastic Barrett's oesophagus cases were compared with population controls (OR=0.69, 95% CI 0.49-0.97), the effect was weaker and nonsignificant when cases were compared with inflammation controls (OR=0.82, 95% CI 0.57-1.18), and no dose-response effects were present in either analysis. We found no evidence that aspirin or non-aspirin NSAID use conferred risk reductions for dysplastic Barrett's oesophagus, regardless of the control series. We excluded effect modification by known risk factors as an explanation for these null findings. CONCLUSIONS: We found little support for an inverse association between use of NSAIDs and Barrett's oesophagus. The question of whether or not these medications prevent the onset of Barrett's oesophagus remains open.