Search

Collagenous gastritis (CG) is an uncommon condition known in the pediatric age. It is characterized by the presence of subepithelial collagen bands (> 10 μm) associated with lymphoplasmacytic infiltration of the stomach's lamina propria. Symptoms manifested by patients with CG may be common with many other disorders. It typically manifests with epigastralgia, vomiting, and iron deficiency during pre-adolescence. This condition's pathophysiology remains unclear. In contrast to adults, where association with collagenous colitis and other autoimmune conditions is more common, pediatric involvement is usually confined to the stomach. Drugs of choice include proton pump inhibitors and corticoids. A case is reported of a 12-year-old girl with abdominal pain and ferritin deficiency who was diagnosed with CG based on gastric biopsy and experienced a favorable outcome.

Background: an overexpression of cyclooxygenase-2 (COX-2) has been seen in colon tumors; therefore, COX-2 specific inhibitors may be used as preventive agents. The aim of this study was to investigate the effect of both selective and non-selective COX-2 inhibitors on the incidence of colonic tumors in a model of chemical carcinogenesis in the rat. Design: experimental study with 65 male Sprague-Dawley rats randomly assigned to one of four groups: (a) control (n = 20), with chemical carcinogenesis using 1-2 dimethylhydrazine (1-2 DMH); (b) acetylsalicylic acid (ASA) (n = 15), with chemical carcinogenesis and the addition of ASA at 30 mg/kg; (c) low-dose rofecoxib (n = 15), with chemical carcinogenesis and the addition of rofecoxib at a dose of 1.2 mg/kg; (d) high-dose rofecoxib (n = 15), with carcinogenesis and the addition of rofecoxib at 3 mg/kg. Carcinogenic induction was performed with 1-2 DMH at a weekly dose of 25 mg/kg for 18 weeks. The main parameter evaluated was percentage of neoplastic colonic tissue, which relates tumor surface area to colon surface area. Results: rofecoxib at a dose of 3 mg/kg significantly reduced chemical colon carcinogenesis in rats (p < 0.01). Rofecoxib in lower doses had the same effect on adenomas (p < 0.05) with no effect on adenocarcinomas. Rofecoxib reduced COX-2 expression in tumoral tissue from adenomas and adenocarcinomas (p < 0.01). Conclusions: rofecoxib prevents chemical colon carcinogenesis in the rat, with a reduction of tumoral colonic percentage in adenocarcinomas and tumoral COX-2 expression.Introducción: se ha comprobado a nivel clínico y experimental la existencia de sobreexpresión de la ciclooxigenasa-2 (COX-2) en los tumores de colon, por lo que los inhibidores de dicha enzima podrían tener un efecto preventivo. El objetivo del estudio es investigar el efecto de la inhibición de la ciclooxigenasa en un modelo de carcinogénesis cólica farmacológica en la rata. Material y métodos: estudio experimental en 65 ratas Sprague-Dawley macho, asignadas a uno de los grupos: control (n = 20), con carcinogénesis farmacológica con 1-2 dimetilhidrazina; grupo ácido acetilsalicílico (n = 15), con carcinogénesis y adición de AAS, grupo Inhibidores COX-2 a bajas dosis (n = 15), con carcinogénesis y adición de rofecoxib a dosis de 1,2 mg/kg, y grupo Inhibidores COX-2 a altas dosis (n = 15), con carcinogénesis y rofecoxib a dosis de 3 mg/kg. El principal parámetro evaluado es el porcentaje de tejido cólico neoplásico y la expresión de COX-2 en el colon normal y neoplásico. Resultados: el rofecoxib a dosis altas reduce el porcentaje de colon ocupado por adenocarcinomas inducidos (p < 0,01). El rofecoxib a dosis bajas presentó el mismo efecto sobre los adenomas (p < 0,05), sin efecto sobre los adenocarcinomas. La expresión COX-2 es superior en los adenocarcinomas frente a los adenomas. El rofecoxib redujo la expresión COX-2 respecto al control y AAS (p < 0,01), tanto en los adenomas como en los adenocarcinomas, no mostrando este efecto sobre el colon normal. Conclusiones: el rofecoxib redujo la carcinogénesis cólica inducida en ratas, reduciendo la expresión COX-2 en los tumores y disminuyendo el porcentaje de colon neoplásico.

Aim: to investigate the effect of the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib on the incidence of perianastomotic colonic tumors in a model of chemical carcinogenesis in the rat. Experimental design: experimental study with 45 male Sprague-Dawley rats randomly assigned to one of three groups: control (n = 15) with colocolic anastomosis and chemical carcinogenesis with 1-2 dimethylhydrazine (1-2 DMH); rofecoxib 0.0027% (n = 15) with colonic anastomosis, chemical carcinogenesis and the addition of dietary rofecoxib at doses of 27 parts per million (ppm), and rofecoxib 0.0058% (n = 15) with colonic anastomosis, chemical carcinogenesis and the addition of dietary rofecoxib at doses of 58 ppm. Carcinogenic induction was performed with 1-2 DMH at a weekly dose of 25 mg/kg of weight for 18 weeks, and colonic tumors induced were analyzed in postoperative week 20. The main parameter evaluated was the percentage of colonic neoplastic tissue, which relates tumor surface area to the colon's surface area. Results: rofecoxib at doses of 2.5 mg/kg or 0.0058 ppm significantly reduced chemical colon carcinogenesis in rats, both in the perianastomotic area and the rest of the colon (p < 0.01). In the extra-anastomotic area, rofecoxib at doses of 2.5 mg/kg has significantly greater inhibitory effect than rofecoxib in doses of 1.2 mg/kg or 0.0027 ppm (p < 0.005). Conclusions: rofecoxib causes a reduction in chemical colon carcinogenesis in rats. This effect is sustained in the perianastomotic area, and the investigation of its role in operated colorectal cancer with risk of locoregional recurrence may therefore be of interest.Objetivo: investigar el efecto de un inhibidor selectivo de la ciclooxigenasa-2, rofecoxib, en la incidencia de tumores cólicos perianastomóticos en un modelo de carcinogénesis farmacológica en ratas. Diseño experimental: estudio experimental con 45 ratas Sprague-Dawley macho, asignadas aleatoriamente a uno de los tres grupos: control (n = 15), con anastomosis colo-cólica y carcinogénesis con 1-2 dimetilhidracina; rofecoxib 0,0027% (n = 15), con anastomosis cólica y carcinogénesis farmacológica y adición de rofecoxib en la dieta a dosis de 27 partes por millón, y rofecoxib 0,0058% (n = 15), con anastomosis, carcinogénesis y adición de rofecoxib en la dieta a dosis de 58 ppm. La inducción carcinogénica se realizó con 1-2 DMH a dosis semanal de 25 mg/kg de peso durante 18 semanas y se analizaron los tumores cólicos inducidos en la semana 20 del postoperatorio. El principal parámetro evaluado fue el porcentaje de tejido cólico neoplásico, que relaciona la superficie tumoral con la superficie del colon. Resultados: el rofecoxib a dosis de 0,0058 ppm redujo significativamente la carcinogénesis cólica inducida en ratas, tanto a nivel perianastomótico como en el resto del colon (p < 0,01). A nivel extraanastomótico, el rofecoxib a dosis de 2,5 mg/kg fue significativamente superior en su efecto inhibidor al rofecoxib a dosis de 1,2 mg/kg o 0,0027 ppm (p < 0,005). Conclusiones: el rofecoxib produce una disminución en la carcinogénesis cólica farmacológicamente inducida en ratas. Este efecto se mantiene en el área perianastomótica, por lo que puede ser interesante investigar su implicación en el cáncer colorrectal intervenido con riesgo de recidiva locorregional.

Aim: to investigate the effect of a selective cyclooxigenase-2 (COX-2) inhibitor, rofecoxib, in the prevalence of experimental colon tumors in rats. Experimental design: experimental study with 35 male Sprague-Dawley rats, divided into four groups: a) control group without experimental manipulation (n = 5); b) pharmacological carcinogenesis with 1-2 dimethylhydrazine dihydrocloride (n = 10); c) pharmacological carcinogenesis and addition of acetylsalicylic acid (AAS) (n = 10); and d) carcinogenesis and addition of rofecoxib (n = 10). Carcinogenesis was induced with 1-2 dimethylhydrazine at a weekly dose of 25 mg/kg for 18 weeks. Colon tumors were isolated at 20 weeks. Antiinflammatory agents were given at a dose of AAS 30 mg/kg and rofecoxib at 3 mg/kg. Results: the percentage of colonic tumors was significantly reduced in the rofecoxib group. This result was found for all tumors and for the malignant lesions, adenocarcinomas. Conclusions: rofecoxib, a selective COX-2 inhibitor, reduced the percentage of drug-induced neoplastic glandular tissue in rats.Objetivo: investigar el efecto de un inhibidor selectivo de la ciclooxigenasa-2, rofecoxib, en la incidencia de tumores cólicos a nivel experimental. Diseño experimental: estudio experimental con 35 ratas Sprague-Dawley macho, asignadas aleatoriamente a uno de los cuatro grupos: a) control (n=5), sin manipulación experimental; b) carcinogénesis farmacológica (n=10); c) carcinogénesis farmacológica y ácido acetilsalicílico (n=10), con administración de este fármaco al tiempo de la carcinogénesis farmacológica; y d) carcinogénesis farmacológica y rofecoxib (n=10) con administración de este fármaco junto a la carcinogénesis farmacológica. La inducción carcinogénica se realizó con 1-2 dimetilhidrazina dihidrocloruro a dosis semanal de 25 mg/kg de peso durante 18 semanas. Se analizaron los tumores cólicos inducidos en la semana 20. Los antiinflamatorios se administraron por vía oral a razón de ácido acetilsalicílico 30 mg/kg de peso del animal y rofecoxib 3 mg/kg. Resultados: el porcentaje de tejido tumoral cólico fue inferior en el grupo con rofecoxib respecto al grupo control, tanto considerando todos los tumores conjuntamente como los adenocarcinomas por separado. El ácido aceetilsalicílico no mostró diferencias significativas respeto al grupo control. Conclusiones: el rofecoxib, inhibidor seletivo de la ciclooxigenasa-2, reduce la aparición de tejido glandular neoplásico inducido farmacológicamente en ratas, suponiendo un freno a la carcinogénesis cólica inducida.

Aim: to investigate the influence of different experimental manipulations in a model of colonic experimental carcinogenesis with pharmacological induction in the rat. Experimental design: a total of 90 Sprague-Dawley male rats, divided into three groups, were used: non-surgical (n = 30); surgical with colonic trauma (n = 20), and surgical with colo-colonic anastomosis (n = 40). Carcinogenic induction was carried out with 1-2 dimethylhydrazine dihydrochloride. Colonic adenocarcinomas were identified and the number of tumors, as well as tumoral surface and percentage of tumoral surface was established. One-way ANOVA and Chi-square were employed for the statistical analysis. Results: the number of tumors was greater in the surgical group than in the control group, and tumors preferentially develop-ed around the manipulated colon. Surface and tumoral percentage were greater in the surgical group than in the control group, being also greater in the anastomosis group than in the group with colonic trauma. Within anastomosis groups, a greater tumor surface and percentage was found in the group with titanium than in the group with reabsorbable material. Conclusions: the experimental manipulation of the colon in rats enhances drug-induced colon carcingenesis. The creation of an anastomosis further increases the carcinogenic process compared with simulated anastomosis. This process is also enhanced by the quantity of suture material included in the anastomosis, and by the non-reabsorbable nature of the materials used in the anastomotic line.Objetivo: valorar la influencia de las distintas manipulaciones experimentales en un modelo de carcinogénesis cólica experimental con inducción farmacológica en la rata. Diseño experimental: se emplearon 90 ratas Sprague-Dawley macho, divididas en tres grupos: no quirúrgico (n=30); quirúrgico con traumatismo cólico (n=20), y quirúrgico con anastomosis colocólica (n=40). La inducción carcinogénica se realizó con 1-2 dimetilhidrazina dihidrocloruro. Se identificaron los adenocarcinomas cólicos y se determinaron número de tumores, superficie tumoral y porcentaje de superficie tumoral. El análisis estadístico se realizó con modelos Anova de comparación de medias y con tablas de contingencia Chi cuadrado. Resultados: el número de tumores fue mayor en el grupo quirúrgico que en el control, apareciendo preferentemente alrededor del colon manipulado. La superficie y el porcentaje tumorales fueron mayores en el grupo quirúrgico que en el control, siendo mayores a su vez en el grupo con anastomosis frente al grupo con traumatismo cólico. Dentro de los grupos con anastomosis, presentó mayor superficie y porcentaje tumoral el grupo con adición de titanio frente al grupo con material reabsorbible. Conclusiones: la manipulación experimental del colon de la rata aumenta la carcinogénesis cólica farmacológicamente inducida. La creación de una anastomosis provoca un mayor incremento del proceso carcinogénico que la anastomosis simulada. Este proceso se ve además favorecido por la cantidad de material de sutura incluida en la anastomosis y por la naturaleza irreabsorbible de los materiales implantados en la línea anastomótica.

We report the case of a 39-year-old patient who presented an episode of upper gastrointestinal bleeding due to hemobilia. The imaging tests showed the gallbladder occupied by solid tissue, with a diagnosis of intracholecystic papillary neoplasm after the cholecystectomy. The intracholecystic papillary neoplasm of the gallbladder is a newly established entity and it is considered a subtype of intraductal papillary neoplasm of the bile duct. Its presentation in the form of hemobilia has barely been described in the literature.