The American journal of gastroenterology
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Am. J. Gastroenterol. · Dec 2010
Editorial CommentEditorial: Neurolysis for pancreatic cancer pain: same song, different verse?
Since Kappis first performed percutaneous neurolysis in 1914, investigators have employed innumerable technical variations in an effort to enhance the efficacy. Similar efforts have been underway by endosonographers since Wiersema performed the first endoscopic ultrasound (EUS)-guided celiac plexus neurolysis in 1996. ⋯ Sakamoto et al. present a new method of EUS-guided neurolysis in an attempt to improve the outcomes. Although their data are promising, we eagerly await rigorously designed studies that may validate their findings.
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Am. J. Gastroenterol. · Dec 2010
Editorial CommentEditorial: Detection of small polyps: much ado about nothing?
Computed tomographic (CT) colonography (CTC) represents an alternative to optical colonoscopy for colorectal cancer screening. However, diminutive polyps (≤ 5 mm) are not routinely reported for CTC. ⋯ Although the study was not randomized, the results highlight the difference between the two screening strategies. Because of incomplete understanding of the natural history of diminutive adenomas, further study is needed to determine the long-term impact of the use of CTC for colorectal cancer screening.
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Non-anesthesiologist-administered propfol (NAAP) sedation for endoscopic procedures remains controversial despite the overwhelming evidence that with proper training and patient selection, NAAP is safe and results in improved time to sedation and recovery when compared with standard sedation with a combination of an opioid and benzodiazepine. Emerging data suggest that NAAP also results in an improved psychomotor recovery. Can our patients return to meaningful tasks such as driving with NAAP after recovery in the endoscopy suite?
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Am. J. Gastroenterol. · Jun 2009
Editorial CommentHyponatremia in hepatic encephalopathy: an accomplice or innocent bystander?
Hyponatremia, a common complication inpatients with advanced liver disease and impaired free water clearance, has been shown to be an important predictor of short-term mortality. Hepatic encephalopathy, also a late complication of end-stage liver disease, has been associated with low-grade cerebral edema as a result of swelling of astrocytes. Guevara et al. hypothesized that hyponatremia and the resultant depletion of organic osmolytes (e.g.,myo-inositol) from brain cells contribute to brain edema, playing an important role in the pathogenesis of hepatic encephalopathy. ⋯ Their magnetic resonance spectroscopy data correlated low brain concentrations of myoinositol with hepatic encephalopathy. As both hyponatremia and encephalopathy occur in patients with advanced liver disease, it has been difficult to implicate hyponatremia independently in the pathogenesis of hepatic encephalopathy. Guevara's data do suggest that hyponatremia is more likely an accomplice than an innocent bystander.
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Am. J. Gastroenterol. · Nov 2008
Editorial CommentClinical guidelines versus universal molecular testing: are we ready to choose an optimal strategy for Lynch syndrome identification?
Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC), is the most common form of inherited colorectal cancer (CRC). Affected individuals need to undergo intensive CRC surveillance, screening for associated cancers, and possibly prophylactic surgery. Clinically-based guidelines have been used as the basis for Lynch syndrome screening in CRC patient populations. ⋯ In this issue of American Journal of Gastroenterology, Julie et al. compare the performance of clinical guidelines with a molecular strategy based on universal microsatellite instability (MSI) testing for identifying CRC patients who have Lynch syndrome. Although there is insufficient evidence to support universal molecular testing for all CRC patients at the current time, the study highlights the need for a systematic approach to identify patients with Lynch syndrome. Physicians and health care systems need to do a better job of identifying patients and families with early-onset of CRC and/or a consistent cancer family history so that they may undergo appropriate molecular evaluation, genetic counseling, and cancer risk management.