Toxicidad pulmonar aguda grave secundaria al uso de infliximab biosimilar en un paciente con enfermedad de Crohn / Acute severe pulmonary toxicity due to biosimilar infliximab in a Crohn's disease patient

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Prediction of the presence of esophageal varices using spleen stiffness measurement by transient elastography in cirrhotic patients.

BACKGROUND AND STUDY AIMS: Upper gastrointestinal endoscopy (UGE) is currently recommended in cirrhotic patients to detect the presence of esophageal varices (EV). Spleen stiffness measurement (SSM) with FibroScan has been used for this purpose, showing variable sensitivity (S) and specificity (Sp). The aim of this study was to evaluate the capability of SSM to detect the presence and size of EV in cirrhotic patients in comparison to other noninvasive modalities. PATIENTS AND METHODS: Sixty-six patients with cirrhosis who had undergone UGE in the previous 6 months underwent SSM and liver stiffness measurement (LSM) using FibroScan. Biochemical parameters and ultrasonography data were also collected to calculate other noninvasive indexes. RESULTS: Valid spleen stiffness measurements were obtained for 60 of the 66 patients initially included in the study (90.1%). In the multivariate analysis only splenomegaly and SSM were predictive of esophageal varices. SSM was the most accurate diagnostic tool, obtaining an area under the ROC curve of 0.8 for values below 48 KPascals, with S = 87%, Sp = 69%, and 76.7% of successfully diagnosed patients. CONCLUSIONS: SSM with FibroScan was significantly higher for cirrhotic patients with EV. Our study suggests that spleen stiffness may be useful to identify cirrhotic patients at risk of having EV, although further studies are needed.

Evaluation of the efficacy of therapeutic endoscopy in gastrointestinal bleeding secondary to angiodysplasias. / Evaluación de la eficacia terapéutica endoscópica en hemorragia digestiva secundaria a angiodisplasias.

INTRODUCTION: Gastrointestinal angiodysplasias are defined as vascular dilations that communicate capillaries and veins in the walls of the digestive tract. The clinical presentation of these lesions varies from chronic occult bleeding to severe gastrointestinal hemorrhage. AIM: The primary aim of our study was to analyze lesion location, the efficacy of therapeutic endoscopy with argon plasma coagulation, and the factors associated with rebleeding in patients with gastrointestinal angiodysplasias. MATERIAL AND METHODS: A retrospective study of 32,042 endoscopies was carried out within the time frame of January 2012 and December 2013 at our hospital center. Gastrointestinal angiodysplasia was the diagnosis in 331 of the endoscopies. The procedures included upper gastrointestinal endoscopy, colonoscopy, sigmoidoscopy, and enteroscopy. RESULTS: The most frequent location of the angiodysplasias was the cecum (49%), followed by the ascending colon (17%) and the sigmoid colon (16%). They were most frequently found in the duodenum (60%) and gastric body (49%) at upper gastrointestinal endoscopy. Therapeutic endoscopy was performed in 163 cases (49.8%) and the most predominant methods were fulguration with argon (90%) and combination treatment (argon plasma coagulation and injection sclerotherapy) (6.7%). The macroscopic rebleeding rate after therapeutic endoscopy was 7.4%. Patients that had rebleeding presented with a lower hemoglobin concentration, higher mean age, and the presence of multiple angiodysplasias at endoscopy (P<.05). CONCLUSIONS: Therapeutic endoscopy was performed in 49.8% of the patients with angiodysplasias. The macroscopic rebleeding rate after treatment was 7.4%. There were statistically significant differences in the patients with rebleeding in relation to mean age, hemoglobin values, and the presence of multiple angiodysplasias.

Hipertensión pulmonar y cirrosis hepática / Pulmonary hypertension and hepatic cirrosis

La hipertensión pulmonar es un fenómeno relativamente frecuente en los enfermos con cirrosis hepática y puede aparecer por diversos mecanimos. El escenario más característico que une la hipertensión portal y la hipertensión pulmonar es el síndrome portopulmonar. Sin embargo, la circulación hiperdinámica, la colocación de un TIPS o la insuficiencia cardíaca pueden elevar la presión media de la arteria pulmonar sin incremento de las resistencias. Estas situaciones no serán candidatas a tratamiento con vasodilatadores pulmonares y requieren una terapéutica específica. Una correcta valoración de variables hemodinámicas, ecográficas y clínicas permite el diagnóstico diferencial entre cada situación que produce hipertensión pulmonar en los pacientes cirróticos (AU)

Pulmonary hypertension is a relatively common phenomenon in patients with hepatic cirrhosis and can appear through various mechanisms. The most characteristic scenario that binds portal and pulmonary hypertension is portopulmonary syndrome. However, hyperdynamic circulation, TIPS placement and heart failure can raise the mean pulmonary artery pressure without increasing the resistances. These conditions are not candidates for treatment with pulmonary vasodilators and require a specific therapy. A correct assessment of hemodynamic, ultrasound and clinical variables enables the differential diagnosis of each situation that produces pulmonary hypertension in patients with cirrhosis (AU)

Pulmonary hypertension and hepatic cirrhosis. / Hipertensión pulmonar y cirrosis hepática.

Pulmonary hypertension is a relatively common phenomenon in patients with hepatic cirrhosis and can appear through various mechanisms. The most characteristic scenario that binds portal and pulmonary hypertension is portopulmonary syndrome. However, hyperdynamic circulation, TIPS placement and heart failure can raise the mean pulmonary artery pressure without increasing the resistances. These conditions are not candidates for treatment with pulmonary vasodilators and require a specific therapy. A correct assessment of hemodynamic, ultrasound and clinical variables enables the differential diagnosis of each situation that produces pulmonary hypertension in patients with cirrhosis.

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.

Sistema inmunitario inflamatorio en la cirrosis. Relevancia de la translocación bacteriana / No disponible

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Alteraciones pulmonares en los pacientes cirróticos: actualizaciones de un problema conocido / Hepatopulmonary syndrome and old problems revisited

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Disfunción cardíaca en la cirrosis / Cardiac dysfunction in cirrhosis

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Tratamiento de la hipertensión portal / Treatment of portal hypertension

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