RESUMEN
OBJECTIVE: Helicobacter pylori (H pylori) represents a potential initiator of cholesterol crystallization and it has been proposed that it is related to gallstone formation. In this study, any possible association between the H pylori identification in the mucosa of gallbladder and cholesterol gallstone formation was evaluated. METHODS: Gallbladders containing pure or mixed cholesterol gallstones (cholelithiasis group, n = 89) and gallbladders without gallstones (control group, n = 42) were submitted to standard histopathological examination for H pylori detection, as well as to nested polymerase chain reaction amplification for H pylori DNA detection. RESULTS: Helicobacter pylori was identified in the gallbladder's epithelium in four patients with cholelithiasis and in two patients in the control group by histology. In all the cases which were found to be H pylori positive by histological examination, H pylori DNA were also detected. No correlation between gallstone formation and H pylori detection in the biliary epithelium was found. A higher incidence of acute inflammation in the cholelithiasis (22.5% vs 9.5%, p = not significant [ns]) and in the H pylori positive groups (33% vs 17.6%, p = ns) were histologically detected. A higher incidence (10% vs 0%), p = ns) of H pylori in gallbladders with gallstones and acute inflammation, compared to gallbladders with acute inflammation but without gallstones, was noticed. CONCLUSION: Helicobacter pylori is detectable in low frequency in the mucosa of the gallbladder and it does not seem to act as a lithogenic component for cholesterol gallstone formation. Its higher incidence in gallbladders with gallstones and acute inflammation, suggests a possible accessory role in a subset of patients with cholelithiasis.
OBJETIVO: Helicobacter pylori (H pylori) representa un iniciador potencial de la cristalización del colesterol, y se ha propuesto que guarda relación con la formación del cálculo biliar. En este estudio, se evaluó cualquier posible asociación entre la identificación de H pylori en la mucosa de la vesícula y la formación del cálculo biliar de colesterol. MÉTODOS: Las vesículas que contienen cálculos biliares de colesterol puros o mixtos (grupo de colelitiasis, n = 89) y vesículas sin cálculos biliares (grupo control, n = 42) fueron sometidos a un examen histopatológico estándar con el fin de detectar el H pylori descubrimiento, así como a la amplificación de la reacción en cadena de polimerasa para la detección de ADN H pilori. RESULTOS: El Helicobacter pylori fue identificado mediante histología en el epitelio de la vesícula en cuatro pacientes con el colelitiasis y en dos pacientes en el grupo de control. En todos los casos que resultaron ser H pylori positivo por el examen histológico, se halló también DNA H pylori. No se halló correlación ninguna entre la formación del cálculo biliar y la detección de H pylori en el epitelio biliar. Se detectó histológicamente una incidencia más alta de inflamación aguda en la colelitiasis (22.5% contra 9.5%, p = no significativo [ns]) y en los grupos H pylori positivos (33% contra 17.6%, p = ns). Se observó una incidencia más alta (10% contra 0%), p = ns) de H pylori en las vesículas con los cálculos biliares e inflamación aguda, en comparación con las vesículas con la inflamación aguda pero sin cálculos biliares. CONCLUSIÓN: Helicobacter pylori es detectable en baja frecuencia en la mucosa de la vesícula y no parece actuar como un componente litogénico en la formación del cálculo biliar de colesterol. Su mayor incidencia en las vesículas con cálculo biliar e inflamación aguda, hace pensar en un posible papel auxiliar en un subconjunto de pacientes con colelitiasis.
Asunto(s)
Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Vesícula Biliar/microbiología , Cálculos Biliares/microbiología , Helicobacter pylori/aislamiento & purificación , Mucosa Intestinal/microbiología , Estudios de Casos y Controles , ADN Bacteriano/análisis , Histocitoquímica , Reacción en Cadena de la PolimerasaRESUMEN
OBJECTIVE: Helicobacter pylori (H pylori) represents a potential initiator of cholesterol crystallization and it has been proposed that it is related to gallstone formation. In this study, any possible association between the H pylori identification in the mucosa of gallbladder and cholesterol gallstone formation was evaluated METHODS: Gallbladders containing pure or mixed cholesterol gallstones (cholelithiasis group, n = 89) and gallbladders without gallstones (control group, n = 42) were submitted to standard histopathological examination for H pylori detection, as well as to nested polymerase chain reaction amplification for H pylori DNA detection. RESULTS: Helicobacter pylori was identified in the gallbladder's epithelium in four patients with cholelithiasis and in two patients in the control group by histology. In all the cases which were found to be H pylori positive by histological examination, H pylori DNA were also detected. No correlation between gallstone formation and H pylori detection in the biliary epithelium was found. A higher incidence of acute inflammation in the cholelithiasis (22.5% vs 9.5%, p = not significant [ns]) and in the H pylori positive groups (33% vs 17.6%, p = ns) were histologically detected. A higher incidence (10% vs 0%), p = ns) of H pylori in gallbladders with gallstones and acute inflammation, compared to gallbladders with acute inflammation but without gallstones, was noticed CONCLUSION: Helicobacter pylori is detectable in low frequency in the mucosa of the gallbladder and it does not seem to act as a lithogenic component for cholesterol gallstone formation. Its higher incidence in gallbladders with gallstones and acute inflammation, suggests a possible accessory role in a subset of patients with cholelithiasis.