Fifteen patients with esophageal carcinoma (superficial, six cases; advanced, nine cases) were treated with 250 MeV proton beam irradiation with or without external x-ray irradiation (12 MV linear accelerator) from October, 1985, to May, 1991. Eleven patients were initially treated with x-ray at doses of 16.2-50.4 (mean 42.5) Gy, followed by proton beam at doses of 30.0-52.9 (mean 37.6) Gy. The other four patients were treated with proton beams alone at total doses of 75.0-88.5 (mean 81.4) Gy. The mean total dose for the 15 patients was 80.4 Gy. As a result, the primary tumor lesions of all 15 patients disappeared and complete responses were obtained. Approximately four to five months later, nine of the 15 patients developed esophageal ulcer formations at the circumferences of their primary lesions. The ulcerations were healed, however, by conservative management. There was no evidence of local recurrence throughout the observations on six cases of superficial carcinoma. Among nine advanced carcinoma patients, three relapsed into esophageal carcinoma. Recurrences were observed eight, 16 and 44 months, respectively, after the treatment. Ten of the 15 patients died, but eight died of other diseases. Three of four cases at autopsy did not show any cancer cells in irradiated primary lesions. Four of the 15 patients lived for over five years. The results suggest that a high dose of irradiation delivered by a well-defined proton field could result in improved local control and long-term survival in esophageal carcinoma without undue risk of injury to primary and adjacent organs.

Aged↗

PubMed1993

Endothelin-1-induced gastric ulcer is attenuated by cetraxate.

We investigated the effect of the anti-ulcer drug cetraxate on the development of the gastric ulcer induced by the submucosal injection of endothelin-1 in the rat gastric body, and its effects on gastric mucosal hemodynamics and tissue oxygenation by Laser doppler flowmetry and tissue spectrophotometry. Endothelin-1 induced gastric ulcer (ulcer length: 11.85 +/- 0.89 mm, mean +/- SEM, n = 4) which was strongly attenuated by cetraxate (ulcer length: 3.27 +/- 0.3 mm, mean +/- SEM, n = 8, p < 0.0001). Cetraxate maintained also tissue oxygenation without causing any significant effect on the endothelin-1-induced changes in gastric mucosal blood flow and volume. These results show that cetraxate exerts its cytoprotective action partly by maintaining mucosal oxygenation.

Animals↗

PubMed1993

Gastric ulcer induced by submucosal injection of ET-1: role of potent vasoconstriction and intraluminal acid.

To investigate whether submucosally applied endothelin-1 (ET-1) can induce gastric ulcer, ET-1 (62.5, 125, 250, and 500 pmol/kg) was injected in the submucosal layer of the rat gastric body. Twenty-four hours later, gastric ulcer (ulcer area: 10.31 +/- 5.13 mm2, mean +/- SE, at 500 pmol/kg, n = 8) was induced. The mucosal damage induced by the two highest doses was present even at 2 wk after their injection. Measurement of the mucosal blood flow at the injected area with three different methods (laser-Doppler flowmetry, hydrogen gas clearance, and reflectance spectrophotometry) revealed that injected ET-1 produced an extremely long-lasting vasoconstriction. Pretreatment with nicardipine, a Ca(2+)-channel blocker (1 mg/kg iv), significantly attenuated the ET-1-induced mucosal damage as well as the decrease in mucosal blood flow. Pretreatment with omeprazole (5-40 mumol/kg) also, significantly attenuated the ET-1-induced mucosal damage. Combined pretreatment with omeprazole (40 mumol/kg) and nicardipine almost abolished the ET-1-induced damage. The present study shows that a novel model for experimental ulcers can be induced by submucosal injection of ET-1.

Acids↗

PubMed1993

Superficial and protruding type of esophageal adenocarcinoma mucocellulare and muconodulare confined mostly to the lamina propria mucosa and partly in the submucosal layer.

We report a case with an adenocarcinoma mucocellulare and muconodulare of the esophagus which is limited to the lamina propria mucosa and the submucosal layer. The patient, a 74-year-old man had the chief complaints of hematemesis and melena. A superficial and protruding (0-I) type of lesion was found at the lower thoracic portion of the esophagus by X-ray and endoscopic examination. The surgically resected esophageal specimen showed 0-I and predominantly subepithelial (Sep) type. The tumor is presumed to have arisen from the cardiac glands in the lamina propria mucosa of the lowermost region of the esophagus.

Adenocarcinoma↗

PubMed1992

Prognosis of early gastric cancer after laser endoscopic therapy.

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Endoscopy, Gastrointestinal↗

PubMed1992

Changes in subcellular structures of parietal cells in the rat gastric gland after omeprazole.

Omeprazole, an inhibitor of gastric acid secretion, was administered to rats at a dosage of 20 mg/kg/day for 14 and 35 days, and subsequent changes in subcellular structures of parietal cells were analyzed using morphometry and immunocytochemistry. Plasma gastrin levels were also examined, showing two times higher levels in the experimental groups than in the non-treated control. The volume and surface densities significantly decreased in tubulovesicles of the cells in the experimental rats. In the long term treatment of omeprazole (35 days), the volume density of microvilli on the membranes of secretory canaliculi in the cells also decreased significantly, whereas that of lysosomes clearly increased. By electron microscopy, many dense bodies of various shapes often appeared in the cytoplasm of parietal cells after the omeprazole treatment. Immunocytochemistry revealed that large granular immunodeposits for cathepsin B increase in the epithelial cells of the gastric glands after omeprazole treatment. These results suggest that omeprazole induces quantitatively significant decreases in both tubulovesicles and canalicular microvilli. The decreases in these membrane structures may possibly be ascribed to the degradation of the membrane in lysosomes; the proton pump on the membranes bound irreversibly with omeprazole is believed destined to be degraded in lysosomes.

Animals↗

PubMed1992

[Concept and differential diagnosis of irritable bowel syndrome].

The exact etiology of irritable bowel syndrome (IBS) is unknown. IBS is probably one of the commonest gastrointestinal disorders, but it has proved to be one of the most difficult conditions to diagnose. A proportion of patients give a strong history of stress-related or stress-evoked symptoms. In the past there has been a paucity of studies of this disorder because of difficulties in patient selection, choice of appropriate marker to be tested and the correlation of findings with the clinical presentation. A clear and precise definition of IBS is of most importance in the understanding of psychopathophysiological markers in this disorders.

Autonomic Nervous System Diseases↗

PubMed1992

Early extramedullary plasmacytoma confined to the lamina propria of the gastric mucosa: case report.

A case of early gastric plasmacytoma in a 51-year-old woman is reported. The demonstration of monotypic IgM-kappa immunoglobulin in biopsy specimens by an immunoperoxidase technique contributed to the histological diagnosis. The patient had non-ulcerative lesions (of approximately 15 x 16 cm) of a superficially spreading type of gastric plasmacytoma. Extensive histological analysis of the resected stomach showed the IgM-kappa monoclonal proliferation of plasmacytic tumor cells to infiltrate merely into the lamina propria of the gastric mucosa and not to extend deeply into the submucosa, proper muscle and serosa of the stomach.

Female↗

PubMed1991

[Drug therapy of peptic ulcers].

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Alkalies↗

PubMed1991

Immunocytochemical localization of cathepsins B, H, and L in the rat gastro-duodenal mucosa.

Cathepsins B, H, and L are representative cysteine proteinases in lysosomes of a large variety of cells. Previous immunochemical studies indicated the presence of these enzymes also in the gastrointestinal wall. Using specific antisera, the cellular and subcellular distribution of cathepsins B, H, and L in rat gastric (oxyntic and pyloric part) and duodenal mucosa was investigated by light and electron microscopical immunocytochemistry. The subtypes of cathepsins were distributed differently in the cellular constituents of the epithelia: Cathepsin B was localized to lysosomes of all cells except goblet cells. Cathepsin H was found predominantly in gastric parietal cells (lysosomes) and in secretion granules of pyloric gastrin and duodenal cholecystokinin cells. Cathepsin L immunoreactivities were weak and restricted to a minority of cells (gastric mucous cells, enterocytes). Interstitial cells of the lamina propria immunoreactive for cathepsins H and L were identified as macrophages. The present findings suggest a dual function of cathepsins in the gastro-duodenal mucosa. They (1) cleave enzymatically proteins and peptides ingested in lysosomes, and (2) they may be involved in the processing of biologically active peptides (enteric hormones) from their precursor proteins.

Animals↗

PubMed1991