Despite access to colonoscopy and a shared electronic health record system, colonoscopy completion after an abnormal FIT is inadequate within this safety-net system. Inadequate follow-up is in part explained by inappropriate screening, but there is an absence of clear documentation and systematic workflow within both primary care and GI specialty care addressing abnormal FIT results.
Neuronal apoptosis following ischemia can be mediated by a caspase-dependent pathway, which involves the mitochondrial release of cytochrome c that initiates a cascade of caspase activation. In addition, there is a caspase-independent pathway, which is mediated by the release of apoptosisinducing factor (AIF). Using caspase-inhibitor gene therapy, we investigated the roles of caspases on the mitochondrial release of cyt c and the release of AIF. Specifically, we used herpes simplex virus-1 amplicon vectors to ectopically express a viral caspase inhibitor (crmA or p35) in mixed cortical cultures exposed to oxygen/glucose deprivation. Overexpression of either crmA or p35 (but not the caspase-3 inhibitor DEVD) inhibited the release of AIF; this suggests that there can be crosstalk between the caspase-dependent and the ostensibly caspase-independent pathway. In addition, both crmA overexpression and DEVD inhibited cyt c release, suggesting a positive feedback loop involving activated caspases stimulating cyt c release.
Objectives
Secretin stimulation testing (SST) is used to evaluate patients with hypergastrinemia in the diagnosis of Zollinger-Ellison syndrome (ZES). Case series have documented false-positive SST in patients with achlorhydria. This study reviews our experience with SST in hypo- and achlorhydric patients.
Methods
We examined 27 patients with hypo- or achlorhydria based on a predefined basal acid output (BAO) measurement of <5.0mEq/hour who also underwent SST for diagnosis of ZES. We report the frequency of false positive SST results in this setting.
Results
330 patients underwent gastric analysis of which 27 had BAO<5.0mEq/hour and SST conducted. The mean fasting gastrin level was 247±304pg/mL and the mean BAO measurement was 1.6±1.8mEq/hour. Twenty patients were off and 7 were on anti-secretory therapy at time of testing. Four patients had false-positive SSTs; three with gastric atrophy (BAO=0mEq/hr) and one with drug-induced hypochlorhydria (BAO=0.5mEq/hr). These false-positive test results were confirmed by structural and functional imaging studies.
Conclusions
We have identified a 14.8% false-positive rate in SST in patients with hypo- or achlorhydria. Growing literature has identified severe consequences associated with discontinuing anti-secretory treatment for testing; therefore, SST will require interpretation in the setting of gastric acid suppression and needs to be interpreted in this context.
In a retrospective analysis of patients in a diverse safety-net population who underwent OC-Light FIT for CRC screening, we found that approximately 3% of patients with a positive result from a FIT to have CRC and approximately 21% to have advanced adenoma.
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