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1.
Dis Esophagus ; 35(11)2022 Nov 15.
Artículo en Inglés | MEDLINE | ID: mdl-35641160

RESUMEN

The present study aims to compare the effectiveness of surgical and medical therapy in reducing the risk of cancer in Barrett's esophagus in a long-term evaluation. A prospective cohort was designed that compared Barrett's esophagus patients submitted to medical treatment with omeprazole or laparoscopic Nissen fundoplication. The groups were compared using propensity score matching paired by Barrett's esophagus length. A total of 398 patients met inclusion criteria. There were 207 patients in the omeprazole group (Group A) and 191 in the total fundoplication group (Group B). After applying the propensity score matching paired by Barrett's esophagus length, the groups were 180 (Group A) and 190 (Group B). Median follow-up was 80 months. Group B was significantly superior for controlling GERD symptoms. Group B was more efficient than Group A in promoting Barrett's esophagus regression or blocking its progression. Group B was more efficient than Group A in preventing the development of dysplasia and cancer. Logistic regression was performed for the outcomes of adenocarcinoma and dysplasia. Age and body mass index were used as covariates in the logistic regression models. Even after regression analysis, Group B was still superior to Group A to prevent esophageal adenocarcinoma or dysplasia transformation (odds ratio [OR]: 0.51; 95% confidence interval [CI]: 0.27-0.97, for adenocarcinoma or any dysplasia; and OR: 0.26; 95% CI: 0.08-0.81, for adenocarcinoma or high-grade dysplasia). Surgical treatment is superior to medical management, allowing for better symptom control, less need for reflux medication use, higher regression rate of the columnar epithelium and intestinal metaplasia, and lower risk for progression to dysplasia and cancer.


Asunto(s)
Adenocarcinoma , Esófago de Barrett , Neoplasias Esofágicas , Laparoscopía , Humanos , Esófago de Barrett/complicaciones , Esófago de Barrett/tratamiento farmacológico , Esófago de Barrett/cirugía , Fundoplicación , Estudios Prospectivos , Neoplasias Esofágicas/etiología , Neoplasias Esofágicas/prevención & control , Neoplasias Esofágicas/diagnóstico , Adenocarcinoma/etiología , Adenocarcinoma/prevención & control , Adenocarcinoma/cirugía , Omeprazol
2.
Dis Esophagus ; 22(7): 606-10, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-19302218

RESUMEN

Achalasia surgical treatment alters the esophagogastric junction anatomy (cardiomyotomy plus fundoplication or esophagectomy and gastric pull-up), thus favoring a certain degree of gastroesophageal reflux. Gastric secretory and hormonal functioning is not completely known in chagasic patients. The aim of this study was to evaluate the gastric secretory and hormonal response in patients with end-stage chagasic achalasia compared with normal subjects. Gastric secretion and hormonal response were assessed by estimation of gastric acid secretion (GAS) in basal condition and after pentagastrin stimulation, basal serum gastrin, and serum pepsinogen (SP) in basal condition and after betazole hydrochloride (Histalog; Eli Lilly and Company, Indianapolis, IN, USA) stimulation in 27 patients with chagasic achalasia. The results were then compared with those of 24 normal subjects. In the chagasic group, the mean basal and stimulated GAS were significantly lower than in the control group (basal: 1.277 vs. 3.13, P = 0.002; stimulated: 15.9 vs. 35.8, P = 0.0001). Chagasic patients' SG levels showed a significantly higher basal value than the control group (83.3 vs. 36.8, P = 0.0001). There was a significant increase of SP after stimulation compared with the basal levels in both chagasic and control groups. Although the chagasic patients' SP values were higher than the controls, this difference was not statistically significant, either in basal and stimulated conditions (basal: 122.0 vs. 108.9, stimulated 120 min: 177.1 vs. 158.9). In patients with chronic Chagas' disease (ChD), although autonomic denervation does not suppress the strength of the gastric mucosal cells' secretory response to stimulation, it reduces GAS (parietal cell) without, however, affecting SP production (chief cells). On the other hand, the gastrin-producing cells have continuously been stimulated by low GAS.


Asunto(s)
Enfermedad de Chagas/fisiopatología , Acalasia del Esófago/fisiopatología , Ácido Gástrico/metabolismo , Adulto , Anciano , Betazol/farmacología , Enfermedad Crónica , Acalasia del Esófago/parasitología , Acalasia del Esófago/cirugía , Femenino , Determinación de la Acidez Gástrica , Agonistas de los Receptores Histamínicos/farmacología , Humanos , Masculino , Persona de Mediana Edad , Pepsinógeno A/sangre , Adulto Joven
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