Journal of gastroenterology
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Acute esophageal necrosis, which presents as a black esophagus on endoscopy, is a rare disorder that is poorly described in the medical literature. In this study, we analyze all cases reported to date to define risk factors, clinical presentation, endoscopic features, histologic appearance, treatment, complications, outcome and etiopathogenesis of the disease and to describe a distinct medical syndrome and propose a staging system. ⋯ This study provides a structured approach to identifying risk factors, diagnosis, and pathogenesis of the acute esophageal necrosis. Risk factors include age, male sex, cardiovascular disease, hemodynamic compromise, gastric outlet obstruction, alcohol ingestion, malnutrition, diabetes, renal insufficiency, hypoxemia, hypercoagulable state, and trauma. Mechanism of damage is usually multifactorial secondary to ischemic compromise, acute gastric outlet obstruction, and malnutrition. Overall, acute esophageal necrosis should be viewed as a poor prognostic factor, associated with high mortality from the underlying clinical disease.
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Acute pancreatitis is rarely seen in children, and, in contrast to cases in adults, it is often drug induced. One possible medication is the antiepileptic drug valproic acid (VPA), which is commonly prescribed for generalized and focal epilepsy, migraine, neuropathic pain, and bipolar disorder. The common side effects associated with VPA are typically benign, but less common but more serious adverse effects may occur. These include hepatotoxicity, hyperammonemic encephalopathy, coagulation disorders, and pancreatitis. Since 1979, a few cases of pancreatitis induced by VPA have been published in the medical literature. ⋯ The difference between 90 patients reported worldwide from 1979 to 2005 and the 16 new documented cases from only Germany over 10 years corroborates that the occurrence of this severe side effect is under reported.
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Review
Role of corticotropin-releasing hormone in irritable bowel syndrome and intestinal inflammation.
Corticotropin-releasing hormone (CRH) is a major mediator of stress response in the brain-gut axis. Irritable bowel syndrome (IBS) is presumed to be a disorder of the brain-gut link associated with exaggerated response to stress. We first showed that peripheral administration of CRH aggravated visceral sensorimotor function as well as adrenocorticotropic hormone (ACTH) response in IBS patients. ⋯ In addition, there is evidence of the contrasting roles of CRH-R1 and CRH-R2 in visceral nociception. While CRH-R1 is involved in the pro-nociceptive effects of visceral pain, CRH-R2 mediates an anti-nociceptive response. These findings suggest the major role of CRH in stress-related pathophysiology of IBS and possibly in inflammation of the intestinal mucosa.