Abordaje diagnóstico y terapéutico de pancreatitis en niños y adolescentes en Latinoamérica / No disponible

OBJETIVO: presentar los resultados de una encuesta aplicada a pediatras gastroenterólogos de Latinoamérica para conocer como realizan el abordaje diagnóstico y terapéutico de pancreatitis. MATERIAL Y MÉTODOS: estudio transversal, encuesta exploratoria, multicéntrica. RESULTADOS: el 73,6 % definió los tres tipos de pancreatitis de acuerdo con el grupo INSPPIRE. La enfermedad biliar, trauma abdominal e ingesta de medicamentos fueron la etiología más frecuente. El 80 % fueron pancreatitis leve. El 73 % utilizo soporte nutricional; la nutrición enteral fue la más empleada. CONCLUSIÓN: es el primer estudio exploratorio que permite tener una estimación del abordaje diagnóstico y terapéutico de la pancreatitis por PG en Latinoamérica

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Diagnostic and therapeutic approach to pancreatitis in children and adolescents in Latin America.

OBJECTIVE: to present the results of a survey applied to Latin American pediatric gastroenterologists (PGs) to learn how they perform the diagnostic and therapeutic approach to pancreatitis. MATERIAL AND METHODS: a descriptive, exploratory, multicenter study and survey was conducted. RESULTS: 73.6 % defined the three types of pancreatitis according to the INSPPIRE group. Biliary disease, abdominal trauma, and medication intake were the most frequent causes. 80 % of cases were considered mild pancreatitis. 73 % of the PGs utilized nutritional support, with enteral nutrition predominating. CONCLUSION: this is the first exploratory study to describe the diagnostic and therapeutic approach of PGs to pancreatitis in Latin America.

Toll-like receptors and cytokines are upregulated during Helicobacter pylori infection in children.

BACKGROUND AND AIM: Helicobacter pylori infection is mainly acquired during childhood, and establishes a chronic infection that may lead to peptic ulcer or gastric cancer during adulthood. Toll-like receptors (TLRs) are expressed by distinct cell types throughout the gastrointestinal tract, and play an important role in regulation of the innate immune response. Few works have addressed TLRs expression in gastric epithelia of adults, and scarce studies have done it in children. The aim of this work was to analyze the expression of TLR2, TLR4, TLR5, TLR9, and IL-8, IL-10 and TNF-α in the gastric mucosa of children with and without H. pylori infection. METHODS: Gastric biopsies were collected by endoscopy from 50 children with recurrent abdominal pain, 25 with H. pylori infection and 25 without infection. In the gastric biopsies the expression of TLRs and cytokines was studied by immunohistochemistry, and the degree of mucosal inflammation was determined using the Sydney system. RESULTS: We found that H. pylori infection was associated with a significant increased expression of TLRs 2, 4, 5 and 9, although expression varied between surface epithelia and glands. Epithelial cells expressing IL-8, IL-10 and TNF-α were increased in gastric mucosa of children with H. pylori infection. CONCLUSION: This study shows the gastric epithelia of children respond to H. pylori infection by increasing the expression of TLR2, TLR4, TLR5, TLR9 and the cytokines IL-8, IL-10 and TNF-α.

A primary Helicobacter pylori infection does not protect against reinfection in children after eradication therapy.

BACKGROUND: Helicobacter pylori infection is one of the most common chronic infections in the world, and is acquired mainly during childhood. It is not clear to which extent a primary infection protects the child from reinfection. Our aim was to determine the possible protection conferred by a primary infection against H. pylori reinfection in children. METHODS: A follow-up study with 120 children distributed in two cohorts; the first included 80 children without previous H. pylori infection (primo-infection cohort); the second included 40 infected children successfully eradicated (reinfection cohort). Cohorts were monitored during 2 years with urea-breath-test (UBT) at 3, 6, 9, 12, 18 and 24 months for the acquisition of H. pylori infection. We compared the rate of reinfection in eradicated children with the rate of infection in children without previous infection. H. pylori infection during the follow-up was analyzed and compared between cohorts using chi2 and survival curves. A questionnaire was performed for the evaluation of possible risk factors for infection in both cohorts. RESULTS: No significant differences in rates of primo-infection or reinfection were found; 17 (21.2%) primo-infections and 10 (25%) reinfections were documented. Most of the primo-infections (14/17) occurred in the first year of follow-up. In contrast, reinfection episodes occurred more frequently during the second year (6/10). In both cohorts, most infections were transient. Risk factors were similar for both, primo and reinfection cohorts. CONCLUSION: A primary infection does not protect from reinfection in the population of children studied.

High rates of recurrence and of transient reinfections of Helicobacter pylori in a population with high prevalence of infection.

OBJECTIVES: Little is known concerning the magnitude of reinfection versus recrudescence of Helicobacter pylori (H. pylori) infection after eradication treatment. The aims of this study were to determine the magnitude of H. pylori reinfection versus recrudescence, and to identify possible risk factors for reinfection. METHODS: Children and adults with upper GI symptoms treated at the Centro Médico Nacional Siglo XXI (Instituto Mexicano del Seguro Social, in Mexico City, Mexico) were studied. H. pylori infection was diagnosed with urea breath test (UBT), histology, and culture. Infected patients received triple therapy, and those who became UBT negative 4-6 wk after treatment were considered as eradicated and were included in the study. A cohort of 141 patients in whom the disease was eradicated was monitored for recurrence with UBT at 3, 6, 9, 12, 18, and 24 months. H. pylori was isolated from gastric biopsy samples before treatment and at recurrence and isolates compared by genotyping. RESULTS: During this period, 32 (22.7%) cases of recurrence were documented the majority occurring during yr 1. In nine of the 32 (28.1%) cases, recurrence was eradicated spontaneously, suggesting these were transient reinfections. Recurrence rates were significantly higher in the subjects 41-60 yr of age than in younger or older subjects. H. pylori isolates from 12 recurrence cases were genotyped; nine (75%) were classified as true reinfection and three as recrudescence. CONCLUSIONS: In our population, recurrence rate is high in adults and transient reinfection is common. In several cases, reinfection occurred by multiple strains, which suggests that soon after eradication, patients are exposed to multiple sources of reinfection.

Efficacy and safety of oral pantoprazole 20 mg given once daily for reflux esophagitis in children.

OBJECTIVES: To investigate the efficacy and safety of oral pantoprazole, 20 mg (0.5 to 1.0 mg/kg/day) once daily for 28 days, in pediatric patients with reflux esophagitis. METHODS: Patients in this study (n = 15; 6 to 13 years old, 9 boys) had reflux esophagitis grade Ic or II (Vandenplas classification). The efficacy of pantoprazole to reduce esophageal acid exposure time (pH < 4), reduce the number and duration of reflux episodes, and to increase the percentage of time with gastric pH > 3 was assessed by continuous 24-hour pH monitoring. The intensity of 5 common symptoms of esophagitis was scored before and after treatment on a 4-point scale. Esophagitis was assessed at baseline and after treatment by visual inspection and by the histology of biopsies from the distal third of the esophagus. RESULTS: Before treatment, the median percentage of time with intra-esophageal pH <4 was 9.3%. After 28 days of therapy with pantoprazole, this value decreased to 2.7% (P = 0.0006). The median percentage of time with intragastric pH > 3 increased from 21% at baseline to 39% on day 28 of therapy (P = 0.005). After 28 days of treatment, all patients experienced at least partial relief from reflux symptoms. Endoscopically confirmed healing of esophagitis was seen in 47% of children (Savary-Miller classification). Histologic evidence of healing was not observed. Median serum gastrin levels were slightly elevated over baseline levels (from 74 pg/ml to 93 pg/ml). In one patient there was a transient elevation of serum GOT and GPT during treatment. CONCLUSIONS: Oral pantoprazole 20 mg daily provided gastric acid control in 15 pediatric patients with reflux esophagitis with partial clinical improvement of symptoms after 28 days of treatment. Pantoprazole was safe and well tolerated.

Difenilhidantoinato sódico como probable causa de pancreatitis / Sodium diphenylhydantoinate as a probable cause of pancreatitis

Introducción: la pancreatitis inducida por medicamentos es más común en niños que en adultos. Una gran variedad de medicamentos ha sido asociada con pancreatitis. Entre los fármacos neuropsiquiátricos sólo el ácido valproico, la carbamacepina, la clozapina y ergotamina, han sido reportadas como causales de pancreatitis. El difenilhidantoinato sódico es un medicamento utilizado en forma común para el tratamiento de la epilepsia. Éste ha sido asociado a pancreatitis en dos ocasiones previas.Reporte del caso: adolescente masculino que inició con hemorragia en cerebelo secundaria a malformación arteriovenosa. Durante su evolución presentó varias complicaciones: neumonía, dos infecciones de vías urinarias, hemorragia gastrointestinal e hipertensión arterial. Dieciocho días después de su ingreso presentó crisis convulsivas mismas que se manejaron con difenilhidantoinato sódico. Al siguiente día comenzó con síntomas pancreáticos y se confirmó pancreatitis por enzimas elevadas y TAC con edema pancreático. Se descartaron otras causas de pancreatitis. Las enzimas pancreáticas persistieron elevadas hasta que el medicamento fue suspendido, y han persistido normales a 18 meses de seguimiento.Conclusiones: en este caso se han cumplido tres de los cuatro criterios para atribuir la causalidad de pancreatitis a algún medicamento. Consideramos que el tratamiento anticomicial fue la causa directa de la pancreatitis, porque esta entidad tuvo relación temporal directa con el inicio y suspensión del tratamiento