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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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We investigated the relationships between intragastric food maldistribution and antral dysmotility in functional dyspepsia, and whether these abnormalities relate to meal-induced symptoms. Intragastric distribution of food throughout gastric emptying was determined in patients (n = 24) and controls (n = 38) after a liquid nutrient meal labeled with (99m)technetium phytate. Antral contractility was also periodically assessed by dynamic scintigraphy and postprandial symptoms were monitored with visual analog scales. Residence of food in the proximal stomach was decreased in 8 (33%) and antral contractility was increased in 9 (37.5%) and decreased in 2 (8%) patients. Proximal and distal stomach motor abnormalities were neither significantly correlated nor associated. Increased antral contractility was significantly correlated (Rs = 0.54; P < .01) with postprandial nausea. We conclude that diminished residence of food in the proximal stomach and disturbed antral contractility occur independently in different subsets of functional dyspepsia patients. Increased antral contractility seems to play a role in postprandial nausea in functional dyspepsia.

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OBJECTIVES: To evaluate the clinical presentation and to assess the usefulness of antroduodenal manometry (ADM) and the results of multidisciplinary team management in 12 neurologically normal adolescents (9 girls) with rumination. STUDY DESIGN: All patients had extensive investigations that ruled out other causes of their chronic symptoms. We performed ADM in all patients. A multidisciplinary approach was used for the nutritional and behavioral rehabilitation of these patients. RESULTS: The median age at presentation was 14 years (range, 9-19 years), and the average duration of symptoms was 17 months. All patients complained of postprandial, effortless regurgitation, and the majority had weight loss and abdominal pain. Results of fasting ADM were normal in all. The postprandial ADM showed brief, simultaneous pressure increases at all recording sites, associated with regurgitation in 8 patients. No emesis was observed in the other 4 children during the study. Treatment included nutritional support in combination with antidepressants and anxiolytics (n = 6), cognitive therapy with biofeedback or relaxation techniques (n = 7), and pain management (n = 2). Resolution or improvement of symptoms was seen in 10 of the 12 patients, and successful transition to oral feedings was achieved in all during the follow-up period, which ranged from 5 to 36 months. CONCLUSIONS: Rumination is a distinct functional gastrointestinal disorder of otherwise healthy children and adolescents, which can be diagnosed on the basis of clinical features. The ADM shows a characteristic pattern and rules out motility disorders that are often confused with rumination. A multidisciplinary team approach is associated with satisfactory recovery in most patients.

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Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P>0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (l6.4 (6.9-54.4) vs 59.3 (29.6-113.8), P<0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.

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A case of antral membrane in a 23 month old child is presented. He developed an extremely rapid clinical course characterized by vomiting, 4 kg weight loss and acute malnutrition. The UGI showed a probable antropyloric obstruction which was confirmed by endoscopy and lately by surgery. It is suggested that in the approach of a patient with vomit it is very important to make an oriented clinical history and always complete the study of the patients with radiological and endoscopic procedures.

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To determine whether motor activity of the stomach and proximal small intestine is a factor in recurrent abdominal pain in adolescents, we prospectively investigated eight patients with recurrent abdominal pain and compared them with seven normal adolescents. All patients underwent a detailed examination to exclude other known organic causes of the pain. The gastroduodenal motor activity during fasting was studied with a semiconductor recording probe. The recordings were analyzed for periodicity, duration, and propagation velocity of the activity front of the migrating motor complex. The amplitude of the antral and duodenal contractions was also determined. The patients with recurrent abdominal pain had more frequent migrating motor complexes, but these were shorter in duration and moved more slowly down the intestine (slower propagation velocities). The patients also had high-pressure duodenal contractions that were associated with abdominal pain during the study period. These studies suggest that altered intestinal motility may be the underlying mechanism of recurrent abdominal pain in some children.

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Chronic intestinal pseudo-obstruction describes a heterogeneous group of disorders characterized by signs and symptoms of intestinal obstruction in the absence of a mechanical lesion. We studied antroduodenal motility in 13 children with pseudo-obstruction. The diagnosis was based on radiographic evidence in all, surgery in 11, and specific pathologic features in four. Antroduodenal motility was abnormal in all 13. Qualitative abnormalities in the patterns of antroduodenal contractions permitted separation into groups: (1) postprandial hypomotility (n = 3), (2) absent migrating motor complexes, with phase 3-like activity at the start of meals (neuropathic variety) (n = 5) (3) very low amplitude or absent contractions (myopathic variety) (n = 2); the remaining patients (n = 3) had other distinctive abnormalities. Cisapride, a new gastrointestinal prokinetic drug, stimulated proximal duodenal contractions in the 30 minutes after a meal in nine of 10 patients tested. These studies indicate that antroduodenal manometry is useful for characterizing intestinal pseudo-obstruction, and cisapride stimulates postprandial duodenal contractions in patients with pseudo-obstruction.

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A series of duodenal ulcer patients was studied to determine the relationship of the integrated postprandial gastrin response with the maximal acid secretory capacity, the ABO blood groups, age of onset of ulcer dyspepsia, and the family history of ulcer dyspepsia of the patients. It was found that: 1. The A, B, AB duodenal ulcer patients had a significantly higher maximal acid gastric secretory capacity (P less than 0.001), significantly earlier age of onset of ulcer dyspepsia (P less than 0.001) and significantly stronger family history of dyspepsia (P less than 0.05) than those patients with O blood group. 2. The integrated gastrin response was significantly higher in "hipersecreting" duodenal ulcer patients (secreted more than 25 mMol/h in response to histamine) than in "normosecreting" duodenal ulcer patients (secreted less than 25 mMol/h) (P less than 0.001) but the values for the latter were not different from normal subjects. 3. There was not statistical significant difference between the mean values of the basal serum gastrim levels of normosecreting duodenal ulcer patients, the hypersecreting duodenal ulcer patients and the normal subjects. 4. A significant positive correlation exists between the maximal acid output and integrated postprandial gastrin response in duodenal ulcer patients. (P less than 0.001). This correlation was negative in the normal subjects (P less than 0.01). 5. This finding supports the existence of a positive relationship between the functioning parietal cell and gastrin cell masses.

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Forty eight patients were evaluated to ascertain a correlation (if any) between gastric acid secretion, fasting and post prandial serum gastrin levels, gastric biopsy (antrum and fundus) and gastric emptying time after a standard test meal. The following conclusions were obtained: a) 57.8% of patients with atrophic gastritis and achlorhydria had evaluated serum gastrin levels; b) most patients with high gastrin levels had normal antrum on biopsy or showed only minimal inflamatory changes, while those with normal gastrin levels disclosed more pronounced histological changes; c) patients with achlorhydria had slower gastric emptying rates, and this was more evident among those with higher gastrin levels (though differences were not statistically significant). Further studies are required for a better understanding of the relationship between gastric emptying rate and gastrin levels in patients with chronic gastritis.

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