Mucosal miR-3677 is over-expressed in cirrhotic patients with gastric antral vascular ectasia (GAVE).

INTRODUCTION: Gastric antral vascular ectasia (GAVE) is a rare vasculopathy that associates several diseases, most commonly liver cirrhosis. It usually presents as an occult gastrointestinal bleeding leading to profound iron deficiency anemia. We hypothesized that GAVE is local mucosal pathology dependent on genetic mechanisms, and the purpose of the study was to characterize miRNAs expression in gastric tissue of patients with cirrhosis and GAVE. MATERIALS AND METHODS: Thirteen patients with GAVE and cirrhosis and 35 healthy subjects were recruited. Microarray analysis and comparative microRNA study was done by quantitative polymerase chain reaction (qPCR). The microarray scores were grouped with use of the hierarchical clusterization analysis and miRNA target prediction was done with TargetScan 6.2 algorithm and Gene Ontology analysis (DIANA-miRPath). RESULTS: Concentration of miR-3677 in GAVE-affected mucosa was higher by 72% in comparison with GAVE-free mucosa of patients with cirrhosis (33.7 vs. 35.6 PCR cycles; p < .001) and by 45% in comparison with normal mucosa (33.7 vs. 34.9 PCR cycles; p < .05). According to Gene Ontology analysis miR-3677 was related to angiopoietin-like protein 4 (ANGPTL4) gene. CONCLUSION: GAVE in liver cirrhosis is associated with increased expression of miR-3667 that may be linked with ANGPTL4 gene.

Causa inusual d'obstrucció gàstrica en el lactant: membrana antropilòrica / Causa inusual de obstrucción gástrica en el lactante: membrane antropilórica / Unusual cause of gastric outlet obstruction in infants; antral web

Introducció: la membrana antropilòrica (MA) és una alteració congènita de baixa incidència i difícil diagnòstic per la seva semblança clinicoradiològica amb l'estenosi hipertròfica de pílor (EHP). La MA completa o parcial causa una obstrucció del buidament gàstric que provoca vòmits de repetició no biliosos, deshidratació, pèrdua de pes i alcalosi metabòlica hipoclorèmica. La radiografia d'abdomen mostra una dilatació gàstrica greu, i l'ecografia abdominal ens descarta l'EHP. Aleshores cal plantejar altres causes d'obstrucció a la sortida gàstrica en el lactant, com la MA. Cas clínic: es presenta el cas d'un lactant d'1 mes i 5 dies, sense antecedents obstètrics d'interès, que consulta per vòmits no biliosos, estancament ponderal i hipotonia de 24 hores d'evolució. Les exploracions complementàries fetes van ser normals, tret d'un lleu reflux gastroesofàgic, i es va descartar l'EHP per ecografia abdominal. Davant la sospita d'intolerància a proteïnes de llet de vaca es va fer un canvi de fórmula d'inici a fórmula elemental amb persistència de la clínica i instauració progressiva d'alcalosi metabòlica. Amb la sospita de MA, es va fer un segon estudi ecogràfic dirigit que mostrava un petit ressort antropilòric que es va confirmar en la fibrogastroscòpia, i es va diagnosticar una MA parcial. La resecció quirúrgica de la membrana va re-soldre la clínica. Comentaris: davant d'un lactant amb obstrucció gàstrica, i un cop descartada la causa més comú (EHP), cal pensar en la membrana antral com a possible etiologia, ja que si aquesta es confirma, el seu maneig quirúrgic és definitiu amb resolució clínica posterio

Introducción. La membrana antropilórica (MA) es una alteración de baja incidencia y difícil diagnóstico por el parecido clínico-radiológico con la estenosis hipertrófica de píloro (EHP). La MA completa o parcial causa una obstrucción en la salida gástrica produciendo vómitos de repetición no biliosos, deshidratación, pérdida de peso y alcalosis metabólica hipoclorémica. La radiografía de abdomen muestra una dilatación gástrica severa y la ecografía abdominal descarta la EHP. Es entonces cuando hemos de plantear otras causas de obstrucción de la salida gástrica en el lactante, como la MA. Caso clínico. Se presenta el caso de un lactante de 1 mes y 5 días, sin antecedentes obstétricos de interés, que consulta por vómitos no biliosos, estancamiento ponderal e hipotonía de 24 horas de evolución. Las exploraciones complementarias realizadas fueron normales, excepto un leve reflujo gastroesofágico, y se descartó la EHP por ecografía abdominal. Ante la sospecha de intolerancia a proteínas de leche de vaca se realizó un cambio de fórmula de inicio a fórmula elemental, con persistencia de la clínica e instauración progresiva de alcalosis metabólica. Con la sospecha de MA, se realizó un segundo estudio ecográfico dirigido que mostraba un pequeño resorte antropilórico que se confirmaba en la fibrogastroscopia, y se diagnosticó una MA parcial. Con la resección quirúrgica de la membrana se resolvió la clínica. Comentarios. Ante un lactante con obstrucción gástrica, y una vez descartada la causa más común (EHP), se ha de pensar en la membrana antral como posible etiología, ya que si esta se confirma, su manejo quirúrgico es definitivo con la resolución clínica posterior (AU)

Introduction. The antral web (AW) is a disorder of low incidence and difficult diagnosis despite its similar clinical and radiological findings to hypertrophic pyloric stenosis (HPS). Complete or partial AW cause gastric outlet obstruction with persistent non-bilious vomiting, dehydration, weight loss, and hypochloremic metabolic alkalosis. Abdominal radiograph shows severe gastric dilatation; however, the normal abdominal ultrasound ruling out HPS should raise the suspicion of other causes of gastric outlet obstruction, such as AW. Case report. We report a case of a one-month and five days-old infant with no relevant obstetric history, who presented with a 24- hour history of non-bilious vomiting, lack of weight gain and hypotonia. Diagnostic studies suggested mild gastroesophageal reflux, and an abdominal ultrasound ruled out HPS. The diagnosis of intolerance to cow’s milk protein was first considered, and elemental formula was started without improvement. Suspecting AW, a repeat abdominal ultrasound showed a small prepyloric spring. Gastroscopy confirmed the diagnosis of partial AW, and surgical resection of the membrane resulted in resolution of the symptoms. Comments. In the presence of an infant with gastric outlet obstruction syndrome, and after the most common cause (HPS) has been ruled out, the diagnosis of AW should be considered. Surgery is curative (AU)

CD61, CD31, and CD34 improve diagnostic accuracy in gastric antral vascular ectasia and portal hypertensive gastropathy: An immunohistochemical and digital morphometric study.

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are unusual but important causes of gastrointestinal bleeding with characteristic endoscopic appearances and critically different therapies. However, overlapping features and poor endoscopic-histologic correlation make their distinction challenging. We sought to determine whether CD31, CD34 (vascular markers), and CD61 (platelet marker) could aid in their differentiation. Cases included 11 antral specimens with histologic diagnoses of GAVE, 11 histologically diagnosed as PHG, and biopsies of GAVE (15) or PHG (12) suspected on endoscopy but without histologic agreement. Controls consisted of endoscopically and histologically normal antrum. Image analysis of CD31 and CD34-stained sections was performed to determine mucosal microvessel density (MVD). CD61 revealed thrombi in 100% of histologically confirmed cases of GAVE and 60% of cases suspected of GAVE on endoscopy alone; control biopsies were negative. CD61 was also positive in 26% of cases originally signed out as PHG. Review of hematoxylin and eosin slides from these CD61-positive PHG cases showed other features allowing their correct reclassification as GAVE. MVD was significantly higher in GAVE than PHG. MVD in histologically confirmed PHG did not differ significantly from endoscopically suspected PHG. Review of hematoxylin and eosin slides from the latter showed active gastritis obscuring recognition of ectatic vessels. In conclusion, CD61 reliably differentiates GAVE from PHG. MVD analysis can also assist in their distinction. In PHG, the increased vascularity may be subtle in an inflammatory background; vascular markers may serve as adjunct markers for identifying the aberrant vessels.