The Mexican consensus on the diagnosis, treatment, and prevention of NSAID-induced gastropathy and enteropathy. / Consenso mexicano sobre diagnóstico, prevención y tratamiento de la gastropatía y enteropatía por antiinflamatorios no esteroideos.

More than 30 million persons worldwide take nonsteroidal anti-inflammatory drugs (NSAIDs) on a daily basis, and annual consumption is increasing. In addition to their analgesic and anti-inflammatory properties, NSAIDs also produce well-known gastrointestinal adverse events. There is no consensus in Mexico on the diagnosis, treatment, and prevention of NSAID-induced gastropathy and enteropathy, and so the Asociación Mexicana de Gastroenterología brought together a group of experts to establish useful recommendations for the medical community. Thirty-three recommendations were formulated in the present consensus, highlighting the fact that the risk for NSAID-induced gastrointestinal toxicity varies according to the drug employed and its pharmacokinetics, which should be taken into account at the time of prescription. The risk factors for gastroduodenal complications due to NSAIDs are: a history of peptic ulcer, age above 65 years, high doses of NSAIDs, Helicobacter pylori infection, and the presence of severe comorbidities. The symptoms and gastroduodenal damage induced by NSAIDs vary, ranging from an asymptomatic course to the presentation of iron-deficiency anemia, bleeding, stricture, and perforation. Capsule endoscopy and enteroscopy are direct diagnostic methods in NSAID enteropathy. Regarding prevention, the minimum dose of an NSAID needed to achieve the desired effect, administered for the shortest period of time, is the recommendation. Finally, proton pump inhibitors are the gold standard for the prophylaxis and treatment of gastroduodenal effects, but they are not useful in enteropathy.

[Prophylaxis for stress ulcer bleeding in the intensive care unit]. / Profilaxis para sangrado por ulceras de estrés en la unidad de cuidados intensivos.

BACKGROUND: The critically ill patient can develop gastric erosions and, on occasion, stress ulcers with severe gastrointestinal bleeding that can be fatal. AIMS: The purpose of this review was to provide current information on the pathophysiology, risk factors, and prophylaxis of digestive tract bleeding from stress ulcers in the intensive care unit. METHODS: We identified articles through a PubMed search, covering the years 1970 to 2013. The most relevant articles were selected using the search phrases "stress ulcer", "stress ulcer bleeding prophylaxis", and "stress-related mucosal bleeding" in combination with "intensive care unit". RESULTS: The incidence of clinically significant bleeding has decreased dramatically since 1980. The most important risk factors are respiratory failure and coagulopathy. Proton pump inhibitors (PPIs) or H2 receptor antagonists (H2RAs) are used in stress ulcer bleeding prophylaxis. Both drugs have been shown to be superior to placebo in reducing the risk for gastrointestinal bleeding and PPIs are at least as effective as H2RAs. Early enteral feeding has been shown to reduce the risk for stress ulcer bleeding, albeit in retrospective studies. CONCLUSIONS: Admittance to the intensive care unit in itself does not justify prophylaxis. PPIs are at least as effective as H2RAs. We should individualize the treatment of each patient in the intensive care unit, determining risk and evaluating the need to begin prophylaxis.

[Budd-Chiari syndrome associated with systemic aspergillosis. Case report and literature review.]. / Síndrome de Budd-Chiari asociado a aspergilosis sistémica; informe de un caso y revisión de la literatura.

Budd-Chiari syndrome is a very rare disease related to hepatic vein obstruction. Vascular invasion by fungus is seldom seen and reported. After thorough research of the literature only three cases have been reported. We reported a case of a diabetic patient who showed an acute and aggressive disease, characterized by sepsis, acute hepatic failure and death. Postmortem examination showed disseminated aspergillosis, massive hepatic necrosis, hepatic vein thrombosis and venous occlusion by the fungus.