The role of magnification endoscopy in the early diagnosis of gastric signet ring cell carcinoma.

We present the case of a 67-year-old woman referred to our outpatient clinic presenting dyspepsia. Gastroscopy was performed, showing antral gastritis. Random biopsies were taken, being positive for poorly differentiated Lauren's diffuse gastric adenocarcinoma. Narrow-band imaging gastroscopy was performed, combining random and targeted biopsies, with negative results. The study was completed with echoendoscopy and thoraco-abdominal-pelvic CT scan, showing no relevant pathological findings. Control endoscopic was performed after 12 months, showing no macroscopic lesions. Random biopsies were repeated, being positive for diffuse gastric adenocarcinoma. Gastroscopy with conventional chromoendoscopy was performed, showing a completely flat area of approximately 2cm of diameter in the body-antrum junction, in the greater curvature; it was well delimited and no indigo carmine staining was observed (Figure 1). Electronic magnification was performed, showing disruption of the crypt pattern and aberrant neovessels (Figures 2 and 3). Targeted biopsies were taken, being positive for poorly differentiated gastric adenocarcinoma. The case was discussed in a multidisciplinary session and subtotal gastrectomy was performed. Magnification endoscopy offers a better performance diagnosing early gastric cancer than white light endoscopy. [1] It allows the identification of patterns that can predict malignancy, such as distortion of the mucosal glandular pattern or aberrant proliferation of neovessels. [2] Once the diagnosis has been established, assessing the depth of invasion has great clinical relevance, as it guides therapeutic decisions. Works such as that of Zhou et al. [3] underline the usefulness of linear echoendoscopy in this process.

[Comparison of esophageal stenoses produced by endoscopic sclerotherapy versus variceal ligation]. / Comparación de las estenosis esofágicas producidas por escleroterapia o ligadura de varices.

INTRODUCTION: Variceal ligation (VL) eradicates esophageal varices faster than endoscopic sclerotherapy (ES) with a lower rebleeding rate and fewer secondary effects. However, most studies have evaluated the short-term effects of these treatments and some late complications may be overlooked. PATIENTS AND METHODS: To determine the incidence and the characteristics of stenosis, we included 253 cirrhotic patients treated endoscopically for variceal bleeding from 1988 to 2004 in our hospital. ES was carried out with ethanolamine 5% and polidocanol 1.5%. ES and VL were carried out every 15 days until varices were eradicated and then at 3-, 6- and 12-month intervals; if varices reappeared, the initial treatment was repeated. Stenosis was considered mild when esophageal size was more than 10 mm and severe when the endoscope could not be passed through the stricture. RESULTS: We found stenosis in seven out of 105 (6.7%) ES-treated patients and in 10 out of 148 (6.7%) VL-treated patients. The clinical characteristics of the patients and the previous number of endoscopic sessions were similar in both groups. Four out of seven ES patients developed stenosis during the first eradication process (mean: 11 months, 1-60), but this early stenosis was observed in one out of 10 VL patients (mean: 20 months, 1-72). Stenosis was severe in three out of seven ES patients (43%) but in only two out of ten VL patients (20%) (NS). CONCLUSIONS: The incidence of esophageal stenosis was similar after treatment of esophageal varices with ES and VL, although VL had a tendency to produce later stenosis.

Comparación de las estenosis esofágicas producidas por escleroterapia o ligadura de varices / Comparison of esophageal stenoses produced by endoscopic sclerotherapy versus variceal ligation

Introducción: La ligadura de varices (LV) erradica las varices esofágicas más rápidamente que la escleroterapia (ES), con menos tasa de recidiva hemorrágica y de complicaciones. Sin embargo, la mayoría de los estudios son a corto plazo y algunas complicaciones tardías pueden pasar desapercibidas. Pacientes y métodos: Analizamos la base de datos de 253 pacientes cirróticos, tratados endoscópicamente tras una hemorragia por varices esofágicas desde 1988 hasta 2004 en nuestro hospital, en busca de incidencia y características de estenosis esofágicas. La esclerosis se realizó con etanolamina al 5% intravariz, y polidocanol al 1,5% perivariz. Las sesiones de tratamiento endoscópico se realizaron cada 15 días hasta la erradicación y, posteriormente, a los 3, 6 y 12 meses, repitiendo el mismo tratamiento inicial si reaparecían las varices. La estenosis se consideró leve cuando tenía una luz superior a 10 mm y grave si no permitía el paso del endoscopio. Resultados: Encontramos 7 estenosis en 105 pacientes tratados con esclerosis (6,7%) y en 10 de 148 tratados con ligadura (6,7%). Las características clínicas de los pacientes y el número previo de sesiones endoscópicas fueron similares en ambos grupos. Cuatro de los 7 pacientes del grupo ES presentaron la estenosis durante el primer proceso de erradicación (media 11, meses; rango, 1-60), pero el desarrollo temprano de estenosis sólo se observó en uno de 10 pacientes del grupo LV (media, 20 meses; rango, 1-72). La estenosis fue grave en 3 de 7 (43%) pacientes del grupo ES, pero sólo en 2 de 10 (20%) pacientes del grupo LV (sin diferencias significativas). Conclusiones: La incidencia de estenosis fue similar tras el tratamiento endoscópico de las varices esofágicas con ES y LV, aunque se observó una tendencia al desarrollo de estenosis mas tardío tras LV

Introduction: Variceal ligation (VL) eradicates esophageal varices faster than endoscopic sclerotherapy (ES) with a lower rebleeding rate and fewer secondary effects. However, most studies have evaluated the short-term effects of these treatments and some late complications may be overlooked. Patients and methods: To determine the incidence and the characteristics of stenosis, we included 253 cirrhotic patients treated endoscopically for variceal bleeding from 1988 to 2004 in our hospital. ES was carried out with ethanolamine 5% and polidocanol 1.5%. ES and VL were carried out every 15 days until varices were eradicated and then at 3-, 6- and 12-month intervals; if varices reappeared, the initial treatment was repeated. Stenosis was considered mild when esophageal size was more than 10 mm and severe when the endoscope could not be passed through the stricture. Results: We found stenosis in seven out of 105 (6.7%) ES-treated patients and in 10 out of 148 (6.7%) VL-treated patients. The clinical characteristics of the patients and the previous number of endoscopic sessions were similar in both groups. Four out of seven ES patients developed stenosis during the first eradication process (mean: 11 months, 1-60), but this early stenosis was observed in one out of 10 VL patients (mean: 20 months, 1-72). Stenosis was severe in three out of seven ES patients (43%) but in only two out of ten VL patients (20%) (NS). Conclusions: The incidence of esophageal stenosis was similar after treatment of esophageal varices with ES and VL, although VL had a tendency to produce later stenosis