Agustín Albillos Martínez

Fisiopatología de la translocación y la peritonitis bacteriana espontánea en la cirrosis

The key pathogenic mechanism initiating spontaneous bacterial peritonitis (SBP) is bacterial translocation (BT), a process through which enteric bacteria cross the intestinal barrier and infect the mesenteric lymph nodes, thus entering the blood circulation and ascitic fluid. The high rate of bacterial translocation in cirrhosis is due to injury to the three pilars composing the intestinal mucosal barrier (the balance of intraluminal bacterial flora, the integrity of the intestinal epithelial barrier, and the local immune system). Blood dissemination and microbial growth in ascitic fluid resulting from SBP are a consequence of damage to the immune system in cirrhosis. Hyperproduction of proinflammatory cytokines and other vasoactive substances contributes to the arterial vasodilation and renal failure that frequently complicate the course of SBP. Even in the absence of SBP, translocation of bacteria and bacterial products from the intestinal lumen contribute to systemic inactivation of immune cells in cirrhosis.Resumen El mecanismo patogenico clave que inicia la peritonitis bacteriana espontanea (PBE) es la translocacion bacteriana (TB), proceso por el cual las bacterias entericas cruzan la barrera mucosa intestinal e infectan los ganglios linfaticos mesentericos, y desde donde alcanzan la circulacion sanguinea y, posteriormente, el liquido ascitico. La alta tasa de TB en la cirrosis se debe al dano en los 3 pilares que constituyen la barrera mucosa del intestino: equilibrio de la flora bacteriana intraluminal, integridad de la barrera epitelial intestinal y sistema inmunitario local. La diseminacion sanguinea y el crecimiento de los germenes en el liquido ascitico que se produce en la PBE es consecuencia del dano en el sistema inmunitario que conlleva la cirrosis. La hiperproduccion en el liquido ascitico de citocinas proinflamatorias y otras sustancias con propiedades vasoactivas contribuye a la vasodilatacion arterial y a la insuficiencia renal que, con frecuencia, complica el curso de la PBE. Aun en ausencia de PBE, la translocacion de bacterias y productos bacterianos desde la luz intestinal contribuye a la activacion sistemica de las celulas inmunitarias en la cirrosis.Abstract The key pathogenic mechanism initiating spontaneous bacterial peritonitis (SBP) is bacterial translocation (BT), a process through which enteric bacteria cross the intestinal barrier and infect the mesenteric lymph nodes, thus entering the blood circulation and ascitic fluid. The high rate of bacterial translocation in cirrhosis is due to injury to the three pilars composing the intestinal mucosal barrier (the balance of intraluminal bacterial flora, the integrity of the intestinal epithelial barrier, and the local immune system). Blood dissemination and microbial growth in ascitic fluid resulting from SBP are a consequence of damage to the immune system in cirrhosis. Hyperproduction of proinflammatory cytokines and other vasoactive substances contributes to the arterial vasodilation and renal failure that frequently complicate the course of SBP. Even in the absence of SBP, translocation of bacteria and bacterial products from the intestinal lumen contribute to systemic inactivation of immune cells in cirrhosis.

¿Cuál es el tratamiento de elección en un paciente con cirrosis hepática y varices esofágicas que han sangrado, con objeto de prevenir el resangrado: bloqueadores beta, ligadura endoscópica, o ambas?

El riesgo de resangrado de los pacientes con cirrosis que sobreviven a un episodio de hemorragia por varices es del 60% en un año, y la mortalidad de cada episodio está próxima al 20%. Las terapias más utilizadas para prevenir el resangrado por varices son la endoscópica (inyección de esclerosante [IE], ligadura con bandas) y la farmacológica con bloqueadores beta (BB) adrenérgicos no selectivos (propranolol, nadolol). La ligadura ha sustituido a la IE como tratamiento endoscópico de elección, pues es más efectiva y segura, si bien ambas causan trombosis, fibrosis y, finalmente, obliteración de las varices. La terapia endoscópica no modifica el aumento de la presión portal y del flujo sanguı́neo esplácnico, que son los factores promotores del desarrollo de las varices, por lo que éstas suelen recurrir una vez obliteradas. Los BB causan vasoconstricción esplácnica, reduciendo el flujo sanguı́neo y la presión en el sistema venoso portal. Los datos disponibles indican que la eficacia del tratamiento endoscópico y farmacológico para prevenir el resangrado es similar. Ahora bien, es probable que, al actuar por diferente mecanismo fisiopatológico, la

Limited effectiveness with a 10-day bismuth-containing quadruple therapy (Pylera®) in third-line recue treatment for Helicobacter pylori infection. A real-life multicenter study

Helicobacter pylori antibiotic resistance is an increasing problem worldwide. Pylera® may be an option as salvage therapy.

Enfermedad litiásica biliar

Resumen Entre un 5 y un 15% de la poblacion occidental presenta litiasis biliar. La mayoria de los calculos estan compuestos por colesterol y se forman en el interior de la vesicula, desde donde pueden migrar a la via biliar, causando eventualmente cuadros obstructivos. El diagnostico de la enfermedad litiasica biliar se basa en datos clinicos, analiticos y de imagen. La primera prueba diagnostica a realizar es la ecografia abdominal, muy sensible para el diagnostico de colelitiasis. En la mayoria de las ocasiones la colelitiasis es asintomatica y no requiere ningun tratamiento especifico. Cuando da lugar a sintomas o complicaciones, esta indicada la realizacion de una colecistectomia. Se recomienda la extraccion de cualquier coledocolitiasis diagnosticada, aunque sea asintomatica, dada la gravedad de sus potenciales complicaciones (colangitis y pancreatitis aguda). En esta actualizacion se revisaran las principales complicaciones de la enfermedad litiasica biliar: colecistitis aguda y cronica, ileo biliar, sindrome de Mirizzi, colangitis aguda y pancreatitis aguda biliar.

Resultados de la implementación de un programa multidisciplinar de trasplante de microbiota fecal por colonoscopia para el tratamiento de la infección recurrente por Clostridium difficile

INTRODUCTION Recurrent Clostridium difficile infection (CDI) is common and often difficult to manage. Faecal microbiota transplant (FMT) is an effective therapeutic tool in these cases, although its applicability and effectiveness in Spain is currently unknown. AIM To analyse the technical aspects, safety and effectiveness of the first consolidated FMT programme in Spain. METHODS Retrospective descriptive study of all patients with recurrent CDI treated with FMT performed by colonoscopy in a tertiary centre after the implementation of a multidisciplinary protocol between March 2015 and September 2016. RESULTS A total of 13 FMT were performed in 12 patients (11/12; 91.7% women) with a median age of 84.6 years (range: 38.2-98.2). Recurrence of CDI was the indication for FMT in all cases. Patients had suffered a median of 3 previous episodes of CDI (range: 2-6) and all had failed treatment with fidaxomicin. All procedures were performed by colonoscopy. Effectiveness with one session of FMT was 91.7% (11/12; 95% CI: 64.6 to 98.5%). In the non-responder patient, a second FMT was performed 17 days after the first procedure, with disappearance of symptoms. No side effects related to the endoscopic procedure or the FMT were recorded after a median follow-up of 6.5 months (range: 1-16 months). Two patients died during follow-up due to causes unrelated to FMT. CONCLUSION FMT by colonoscopy is an effective and safe therapeutic alternative in recurrent CDI. It is a simple procedure that should be implemented in more centres in Spain.

Reply “Endoscopic Therapy with 2-Octyl-Cyanoacrylate for the Treatment of Gastric Varices”: Optimizing the Cyanoacrylate Injection in the Treatment of Gastric Varices

We have read with great interest the study published by Kahloon et al. [1] in this journal. All studies about the management of gastric varices (GV) are relevant due to the paucity of data. Apart from the limitations explained by the authors [1], there are some important aspects we would like to notice. First. An important heterogeneity of the patients included in the study (primary prophylaxis, secondary prophylaxis and active bleeders) has been noticed. Moreover, 5 % of them have non-cirrhotic portal hypertension and/or splenic vein thrombosis. It is well known that these patients usually have a preserved liver function compared with decompensated cirrhotic patients (95 % of the study population). This heterogeneous population has different burden of liver disease and certainly different hepatic venous pressure gradient, which may have influenced the results. Some special limitations exist with patients on primary prophylaxis (5 % of study population): (1) Among all study endpoints, only ‘‘complications’’ are applicable to them; (2) there is high controversy in the strategy of primary prophylaxis. A recent study of Sarin et al. [2] evaluated the primary prophylaxis comparing CAI versus beta-blockers versus no treatment. Significant differences were observed favouring CAI versus no treatment in terms of prevention of bleeding and survival. But when compared with propranolol, CAI only showed significant benefits in the prevention of rebleeding. This study has been criticized due to important limitations as highlighted by Tripathi [3]. In fact, the international consensus on portal hypertension (Baveno V) only recommends beta-blockers for primary prophylaxis [4]. (3) Risk factors associated with bleeding from fundic varices were analyzed by Kim et al. [5]. They are all those listed by the authors except for ‘‘the need of anticoagulation,’’ which is not described in the literature. In our opinion, as secondary prophylaxis patients were 78 % of all the study population, in addition to all limitations of the primary prophylaxis group, a more homogeneous study cohort might have yielded more consistent results. Second. A main point is the subtype of GV included in the study. Only GOV1 and GOV2 are reported (Table 2) [1]. IGV2 are rare, but IGV1 are fundic varices, as well as GOV2. Both of them have the same venous origin and drainage and share many aspects of its pathophysiology and management. Thus, both are considered fundic varices as a whole [6]. IGV1 have been left out this study, unless the authors have considered GOV2 as a synonym of all fundic varices. Apart from that, although GOV1 is a subtype of gastric varix [2], it shares many characteristics with esophageal varices [4, 6]. In fact, many guidelines and international consensus recommend a similar management to that of esophageal varices [4, 6]. Therefore, although other historical series included GOV1, they might have excluded them following recent evidence [5, 6]. Third. Although 75 % of procedures were performed with one injection and median number of GV treated in one session were only one, endoscopists have used much more CA (mean dose of 3.4 cc) than recommended (0.5–1 cc) [7–9]. It is unknown how results could be influenced, as the authors do not explain how varix obliteration was confirmed. Despite it is not universally recommended in the management of gastric varices, endoscopy ultrasound can be easily used to check the varix flow [10]. Finally, one on the endpoints was death (19.5 % of study population). Apart from other causes, it included J. Martinez-Gonzalez (&) M. A. Ramos A. A. Martinez Servicio de Gastroenteroloia y Hepatologia, Hospital Universitario Ramón y Cajal, IRYCIS, Universidad de Alcalá, Alcala de Henares, Madrid, Spain e-mail: martinez.gonzalez.javier@gmail.com

Diagnóstico diferencial de la ictericia obstructiva

Obstructive jaundice is a consequence of the slowdown or interruption of biliray flow at any point between the canalicular membrane of the hepatocyte and the duodenum. It is characterized by direct hyperbilirrubinemia and elevation of cholestasis enzymes. The most common etiology is the presence of bile duct stones, periampullary carcinoma, postsurgical strictures, primary sclerosing cholangitis and cholangiocarcinoma. The first diagnostic approach should be abdominal ultrasonography, in order to establish the presence of a dilated biliry duct. The following diagnostic steps will depend on clinical features. Particularly, an endoscopic ultrasonography or a magnetic resonance cholangiopancreatography will be required when abdominal ultrasonography is unable to identify the cause of the obstruction. Endoscopic retrograde cholangiopancreatography should be avoided as an initial diagnostic method, given the risks it entails. If the biliary tree is not accessible through an endoscopic approach, a percutaneous one may be required.

Varón de 55 años con hepatopatía crónica por virus C, ascitis y fiebre

Varon de 55 anos de edad, previamente intervenido en cuatro ocasiones por enfermedad reumatica valvular grave (protesis metalicas mitral y aortica y anuloplasia tricuspidea), que acudio a nuestro hospital con clinica de insuficiencia cardiaca derecha. Como otros antecedentes personales, destacaban: fibrilacion auricular cronica, anemia cronica intensa por microesferocitosis hereditaria que requirio esplenectomia, hepatitis cronica por virus C conocida desde hace 10 anos (genotipo Ib, viremia actual de 200.000 UI/ml y con una biopsia hepatica en cuna realizada 6 meses atras, durante la esplenectomia, que mostraba un minimo infiltrado linfocitico portal y fibrosis I/IV). Se encontraba en tratamiento con diureticos, dicumarinicos, digoxina y hierro. Presentaba a la exploracion fisica, ictericia mucocutanea, aumento de la presion venosa yugular, auscultacion cardiaca arritmica con soplo pansistolico IV/VI en foco mitral y soplo sistolico y retumbo diastolico tricuspideos sugestivos de insuficiencia tricuspidea (IT) grave, crepitantes basales bilaterales, hepatomegalia a 4 traveses de dedo de reborde costal, semiologia de ascitis moderada e importantes edemas en miembros inferiores. En la evaluacion inicial se incluyeron: hemoglobina de 8,2 g/dl, VCM de 79 fl, bilirrubina de 5,5 mg/dl (indirecta 4 mg/dl), GOT 61 U/l, GPT 12 U/l, GGT 153 U/l, LDH 765 U/l, proteinograma normal y haptoglobina 2 mg/dl y actividad de protrombina del 30%. En el frotis de sangre periferica se observaba anisocitosis moderada, y frecuentes esquistocitos y esferocitos, compatible todo ello con anemia hemolitica microangiopatica. El electrocardiograma (ECG) y la radiografia de torax concordaban con la patologia de base. Un ecocardiograma transtoracico referia IT severa, funcion sistolica conservada, dilatacion biauricular e hipertension pulmonar moderada. La ecografia abdominal objetivo ascitis moderada, hepatomegalia y dilatacion de las venas cava y suprahepaticas. El paciente recibio transfusion de concentrados de hematies y fue tratado con reposo y diureticos. En las 24 horas siguientes a su ingreso presento fiebre de 39° sin signos de focalidad infecciosa. Su estado general, sin embargo, se deterioro considerablemente; la radiografia de torax y la orina eran normales. Una nueva analitica mostraba: hemoglobina 10,1 g/dl, leucocitos 24.300 x 103 cel/µl (polimorfonucleares [PMN] 23.100 x 103/µ l), plaquetas 226.000 x 103/µ l, creatinina: 3,04 mg/dl, urea 155 mg/dl, sodio 128 mEq/l, bilirrubina total 10,1 mg/dl, siendo normales los valores de GOT y GPT. A partir de