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BACKGROUND: Pyloroplasty is an effective surgery for gastroparesis. However, some patients fail to improve after pyloric drainage and may require subsequent gastric electric stimulation. There is a paucity of data on the efficacy of gastric stimulator as an adjunct to failed pyloroplasty. This study aimed to describe our experience with pyloroplasty, determine the efficacy of gastric stimulator for failed pyloroplasty, and compare the final outcomes of those who required pyloroplasty with and without gastric stimulator for gastroparesis. METHODS: Records of patients who underwent primary pyloroplasty for gastroparesis at our institution were reviewed. Patients with poor symptomatic improvement after pyloroplasty underwent subsequent gastric stimulator. Symptoms were assessed using the gastroparesis cardinal symptom index (GCSI) preoperatively and after each surgery. Severe gastroparesis was defined as GCSI total score ≥3. Outcomes were assessed after pyloroplasty in all patients and after stimulator in patients who failed pyloroplasty. Final outcomes were then compared between those who did and did not require adjunct gastric stimulator. RESULTS: The study population consisted of 104 patients (89.4% females) with a mean (SD) age of 42.2 years (11) and body mass index of 26.9 kg/m2 (7). Gastroparesis etiologies were 71.2% idiopathic, 17.3% diabetic, and 11.5% postsurgical. At 18.7 months (12) after pyloroplasty, there was a decrease in the GCSI total score (3.5 [1] to 2.7 [1.2]; P = .0012) and the rate of severe gastroparesis (71.9%-29.3%; P < .0001). Gastric emptying scintigraphy (GES) 4-hour retention decreased (36.5 [24] to 15.3 [18]; P = .0003). Adjunct gastric stimulator was required by 30 patients (28.8%) owing to suboptimal outcomes with no improvement in GCSI (P = .201) or GES (P = .320). These patients were younger (40.5 [10.6] vs 49.6 [15.2] years; P = .0016), with higher baseline GCSI total scores (4.3 [0.7] vs 3.7 [1.1]; P < .001) and more severe gastroparesis (100% vs 55.6%; P < .001). All other preoperative characteristics were similar. At 21.7 months (15) after gastric stimulator, there was improvement in GCSI (4.1 [0.7] to 2.6 [1.1]; P < .0001), severe gastroparesis (100%-33.3%; P < .0001), and GES 4-hour retention (21.2 [22] to 7.6 [10]; P = .054). Before gastric stimulator, those who failed pyloroplasty had significantly worse GCSI (P = .0009) and GES (P = .048). However, after gastric stimulator, GCSI and GES improved and were comparable with those who only required pyloroplasty (P > .05). CONCLUSION: Pyloroplasty improved gastroparesis symptoms and gastric emptying, yet 28% failed, requiring gastric stimulator. Younger patients and those with preoperative GCSI scores ≥3 were more likely to fail. Gastric stimulator improved outcomes after failed pyloroplasty, with comparable final GCSI and GES with those who did not fail.

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BACKGROUND: Studies indicate sleeve gastrectomy (SG) as a factor of aggravation or even emergence of symptoms of gastroesophageal reflux disease. Accelerated gastric emptying is described as a mitigating factor. SG may be potentiated by adding a pyloroplasty, although with the potential risk of resulting in duodenogastric alkaline reflux. The objective was to standardize sleeve gastrectomy with pyloroplasty in rats, analyze the complementation in terms of mortality and weight evolution, and conduct assessments on gastric emptying, intestinal transit, and genesis of possible duodenogastric reflux. METHODS: Ninety-three male Wistar rats were divided into a pilot study (standardization of the surgical technique and the scintigraphic study), and the main study. They were then subdivided into the SHAM group, the sleeve gastrectomy (SG) group, and the sleeve gastrectomy with pyloroplasty (SGP) group. After 3 months, the animals were submitted to two scintigraphic experiments and histological analysis of gastric biopsies. RESULTS: The surgical groups (SG and SGP) lost initially more weight than the SHAM group, and the gastric emptying and intestinal transit in the first were more accelerated. However, no difference was found between the SG and SGP groups. Scintigraphic and histological analyses did not reveal statistical differences among the SG and SGP groups regarding gastroesophageal and duodenogastric refluxes. CONCLUSIONS: Pyloroplasty did not affect weight reduction or increase duodenogastric reflux, after three postoperative months in this animal model of sleeve gastrectomy.

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We report a case of nonfatal junctional epidermolysis bullosa and pyloric atresia in a newborn. We identified a substitution (c.914C>T) for the integrin ß4 gene that has been associated with favorable outcome. A novel mutation (c.2011T>G) of unknown significance was also found in this patient who is now thriving.

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A gastropatia hipertrófica pilórica crônica é o termo que se refere à hipertrofia pilórica sem especificar se a camada mucosa e/ou muscular estão envolvidas. O presente trabalho relata um caso de gastropatia hipertrófica crônica secundária à gastrite linfoplasmocitária em um cão. O diagnóstico foi confirmado através de celiotomia exploratória e análise histopatológica e o tratamento instituído através de piloroplastia, bem como terapia imunosupressora foram fundamentais para a melhora clínica significativa do paciente.

The gastropathy chronic hypertrophic pyloric is a term that refers to hypertrophic pyloric without specifying the mucous layer and / or muscle are involved. This paper reports a case of hypertrophic gastropathy secondary to chronic lymphoplasmacytic gastritis in a dog. The diagnosis was confirmed by exploratory laparotomy and histopathological analysis and the treatment by pyloroplasty, as well as immunosuppressive therapy have been fundamental to the clinical improvement of the patient.

La gastropatía hipertrófica del píloro crónica es un término que se refiere a hipertrofia pilórica sin especificar la capa mucosa y / o músculos que esten involucrados. Se presenta el caso de gastropatía hipertrófica secundaria a gastritis crónica linfoplasmacítica en un perro. El diagnóstico fue confirmado por el análisis exploratorio de laparotomía y histopatológico y el tratamiento por piloroplastia, así como la terapia inmunosupresora han sido fundamental para la mejoría clínica del paciente.

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RACIONAL: O refluxo duodenogástrico tem sido implicado como potencial carcinógeno para o estômago e esôfago e é um dos fatores que podem explicar o desenvolvimento de câncer no coto gástrico. Modelos experimentais de carcinogênese no estômago ressecado ou nas gastrojejunoanastomoses estão bem definidos. OBJETIVOS: Desenvolver um modelo experimental de carcinogênese gástrica através de piloroplastia à Finney, avaliar a influência da ingestão de nitrito de sódio nesse modelo, analisar as concentrações de ácidos biliares e o valor do pH gástrico. MÉTODOS: Foram operados 110 ratos Wistar divididos em quatro grupos: Grupo I (15 ratos) submetidos à laparotomia (grupo Sham); Grupo II (15 ratos) submetidos à laparotomia (Sham) e à ingestão de nitrito de sódio na água de beber; Grupo III (40 ratos) submetidos à piloroplastia à Finney; Grupo IV (40 ratos) submetidos à piloroplastia à Finney e à ingestão de nitrito de sódio na água de beber. Após 50 semanas da operação, os ratos foram sacrificados, coletadas amostras de suco gástrico para análise do pH, dosagem dos ácidos biliares, e realizada análise histológica. RESULTADOS: A mortalidade pós-operatória imediata foi de 9 por cento e, ao longo do experimento, 10 ratos morreram. O grupo controle (I) não apresentou lesões gástricas; o grupo controle com nitrito de sódio (II) desenvolveu papilomas no pré-estômago em 16.6 por cento; os grupos operados com piloroplastia apresentaram adenomas em 10,3 por cento no Grupo III e 14,2 por cento no Grupo IV, e adenocarcinoma em 55,1 por cento, no grupo III e 14,2 por cento no Grupo IV. A implantação de glândulas para dentro da submucosa e muscular, na zona de anastomose (implantação mucosa), não foi critério suficiente para decidir sobre a malignidade das lesões, sendo necessária a presença simultânea de atipias celulares. A concentração de ácidos biliares do suco gástrico foi maior nos Grupos III e IV. A medida do pH gástrico não foi diferente nos grupos estudados. CONCLUSÃO: 1) A piloroplastia à Finney é modelo experimental adequado de carcinogênese gástrica; 2) ela induziu refluxo duodenogástrico; 3) o refluxo duodenogástrico atuou como carcinógeno para o estômago; 4) não houve relação entre o pH gástrico e o desenvolvimento de carcinoma; 5) o nitrito de sódio não atuou como carcinógeno para o estômago dos ratos.

BACKGROUND: The duodenogastric reflux has been implicated as a potential carcinogen for the stomach and esophagus and is one of the factors that may explain the development of gastric stump cancer. Experimental models of carcinogenesis in the stomach stump or in the duodenogastric anastomosis are well defined. AIM: To develop an experimental model of gastric carcinogenesis through the Finney pyloroplasty, evaluate the influence of ingestion of sodium nitrite in this model, analyze the concentrations of bile acids and the pH of the stomach. METHODS: A hundred and ten Wistar rats were operated and divided into four groups: Group I (15 rats) underwent laparotomy (Sham group); Group II (15 rats) underwent laparotomy (Sham) and ingestion of sodium nitrite in drinking water; Group III (40 rats) submitted to the Finney pyloroplasty and Group IV (40 rats) submitted to the Finney pyloroplasty and ingestion of sodium nitrite in drinking water. After 50 weeks of surgery, the rats were sacrificed and samples collected for analysis of gastric pH, dosing of bile acids and histological analysis. RESULTS: The immediate postoperative mortality was 9 percent, and during the experiment, 10 rats died. The control group (I) did not show gastric lesions; the control group with sodium nitrite (II) developed papillomas in the pre-stomach in 16.6 percent; the operated groups with pyloroplasty had adenomas in 10.3 percent in Group III and 14.2 percent in Group IV, and adenocarcinoma in 55.1 percent in group III and 14.2 percent in Group IV. The implementation of glands into the submucosa and muscle in the area of anastomosis (mucosa deployment) was not sufficient criterion for deciding on the malignancy of the lesions, requiring the simultaneous presence of atypical cells. The concentration of bile acids in gastric juice was higher in Groups III and IV. The measurement of gastric pH was not different in both groups. CONCLUSION: 1) The Finney pyloroplasty is suitable experimental model of gastric carcinogenesis; 2) it induced duodenogastric reflux; 3) the duodenogastric reflux served as a carcinogen for the stomach; 4) there was no relationship between pH and the development of gastric carcinoma; 5 ) sodium nitrite did not act as a carcinogen for the stomach of rats.