Profilaxis preprimaria de la hemorragia por varices / No disponible

La formación de colaterales portosistémicas, en especial en launión esofagogástrica, es una de las consecuencias más graves dela hipertensión portal. El aumento de la presión portal es la fuerzamás importante que dirige la formación de varices esofagogástricas,siendo necesario para que esto ocurra que la presión portal(estimada por el gradiente de presión venosa hepática) alcance unvalor mínimo de 10 mmHg. Posteriormente, la hiperemia esplácnicatambién contribuye al desarrollo de las varices. Las colateralesportosistémicas se forman por repermeabilización de vasospreexistentes, remodelado vascular y angiogénesis. El objetivo dela profilaxis preprimaria es evitar o retrasar la formación de varicesesofagogástricas. En modelos experimentales de hipertensiónportal, la administración precoz de vasoconstrictores esplácnicoscomo los beta-bloqueantes, de inhibidores de la síntesis de óxidonítrico o de sustancias anti-angiogénicas, inhibe la formación decolaterales portosistémicas. Sin embargo, los ensayos clínicos conbeta-bloqueantes realizados en pacientes con cirrosis sin varicescon objeto de retrasar su formación no han alcanzado los resultadosesperados

Portosystemic collateral formation, particularly at the gastroesophagealjunction, is a most serious consequence of portal hypertension.Increased portal pressure is the most significant forceunderlying gastroesophageal variceal formation, to which endportal pressure (estimated from the hepatic venous pressure gradient)must reach at least 10 mmHg. Subsequently, splanchnic hyperemiaalso contributes to variceal development. Portoystemiccollaterals result from repermeabilization of pre-extant vessels,vascular remodeling, and angiogenesis. The goal of pre-primaryprophylaxis is preventing or delaying the formation of gastroesophagealvarices. In experimental models of portal hypertension,early administration of splanchnic vasoconstrictors such as betablockers,nitric oxide synthesis inhibitors, or antiangiogenic substancesinhibits portosystemic collateral formation. However, clinicaltrials of beta-blockers in patients with cirrhosis and no varicesto delay variceal formation have failed to yield expected results (AU)

[Pre-primary prophylaxis of variceal bleeding]. / Profilaxis preprimaria de la hemorragia por varices.

Portosystemic collateral formation, particularly at the gastroesophageal junction, is a most serious consequence of portal hypertension. Increased portal pressure is the most significant force underlying gastroesophageal variceal formation, to which end portal pressure (estimated from the hepatic venous pressure gradient) must reach at least 10 mmHg. Subsequently, splanchnic hyperemia also contributes to variceal development. Portoystemic collaterals result from repermeabilization of pre-extant vessels, vascular remodeling, and angiogenesis. The goal of pre-primary prophylaxis is preventing or delaying the formation of gastroesophageal varices. In experimental models of portal hypertension, early administration of splanchnic vasoconstrictors such as beta-blockers, nitric oxide synthesis inhibitors, or antiangiogenic substances inhibits portosystemic collateral formation. However, clinical trials of beta-blockers in patients with cirrhosis and no varices to delay variceal formation have failed to yield expected results.

Intestinal metaplasia: evolution after Helicobacter pylori eradication and influence in the success of eradicating therapy.

INTRODUCTION: intestinal metaplasia associated with Helicobacter pylori infection is a stage of the temporal sequence of histological lesions gradually induced by this microorganism. It is considered a preneoplastic lesion and its regression after eradication is controversial. AIM: to assess the evolution of intestinal metaplasia after eradication and to investigate whether metaplasia is a factor that contributes to successful treatment. MATERIAL AND METHODS: four hundred Helicobacter pylori positive patients were studied. Eradicating therapy was administered and endoscopic biopsies of gastric antrum and body were taken before and after eradication. Among other histological data, the presence of intestinal metaplasia was assessed. RESULTS: of all patients successfully treated, biopsies were taken before and after eradication in 268 of them: 71 (26,5%) had metaplasia before and 50 (18,7%) after eradication. A significant difference was observed in the outcome (p = 0,036) of the first eradicating treatment between the group without initial metaplasia (72,7%) and the group with initial metaplasia (61.2%). DISCUSSION: Helicobacter pylori eradication can revert intestinal metaplasia in some patients. On the other hand, the first treatment could be less successful in patients with intestinal metaplasia.

Prevention of de novo hepatitis B infection in liver allograft recipients with previous hepatitis B infection or hepatitis B vaccination.

OBJECTIVES: To assess de novo hepatitis B virus (HBV) transmission from liver donors with HBV serum markers (HBM) to their recipients and the need for HBV vaccination before liver transplantation. METHODS: A total of 108 orthotopic liver transplantations for nonviral disease and the risk of developing de novo hepatitis B based on HBMs before transplantation have been studied. Of the 108 patients, 94 met the study criteria and were divided into two groups: 27 who had HBMs before transplantation (from past infection or by previous vaccination) and 67 who had no HBM. Development of de novo hepatitis B was determined by analytical, serological, and histological parameters. RESULTS: No case (0%) of de novo hepatitis B was detected in the pretransplantation HBM group, whereas there were 10 cases (14.5%) in the other group (p < 0.005). CONCLUSIONS: The presence of pretransplantation HBM in liver transplant recipients protects these patients against the development of de novo hepatitis B. This is especially important considering that there is a high prevalence of donors with positive hepatitis B core antibody (especially in some countries), and that these donors transmit HBV infection to recipients without HBM in a significant number of cases. Thus, vaccination against HBV in patients who are candidates for liver transplantation is fundamental to avoid cases of de novo hepatitis B.