Twenty seven cases of elevated heterotopic gastric fundic mucosa of the duodenal bulb were studied. They were distributed from 20 to 83 years in age and male to female ratio was 16 to 11. Eight cases had solitary lesion, and nineteen cases had multiple lesions. Most of them existed on the anterior wall or posterior wall of the bulb. Biopsy specimens obtained from the lesions showed gastric glands containing chief and parietal cells with gastric type surface epithelium. Duodenal ulcer or ulcer scar existed in only three cases apart from the lesions. Endoscopic follow-up studies performed in twelve cases from 2 to 61 months (mean 21.6 months) showed no change in appearance of the lesions. In order to evaluate the differences between heterotopic gastric fundic mucosa and gastric type epithelium, 95 cases (116 lesions) with resected duodenal ulcer, 63 cases with duodenitis, 64 cases with duodenal polyp and 30 cases of endoscopically normal duodenal mucosa were histologically investigated. Gastric type epithelium was observed in 83.6%, 58.7%, 51.8%, 3.3%, respectively, and no gastric fundic glands were detected in any cases. From these results it was concluded that heterotopic gastric mucosa should be clearly distinguished from gastric type epithelium which is thought to be metaplastic change, and the erm "heterotopic gastric mucosa" should be used only in the lesions containing gastric fundic glands.
We have developed a RIA of human hemoglobin A0 for the purpose of clinical application as a new fecal blood test. A RIA for human hemoglobin A0 was developed using solid-phase assay. This RIA was specific for human hemoglobin A0, and could measure hemoglobin concentration of more than 1ng/ml. Sensitivity of this RIA was 1000 folds than that in Guaiac method. Twelve of 51 cases without GI diseaes showed positive Guaiac test, whereas only 2 cases were positive in hemoglobin A0 RIA (more than 10ng/ml). Five of 19 cases with olon polyp showed positive Guaiac test, while 6 of 19 cases with colon polyp showed increased hemoglobin A0 levels. Seven of 11 cases with colon cancer showed positive Guaiac test, while 9 of 11 cases with colon cancer showed increased hemoglobin A0 levels. We conclude that immunological fecal blood test using homoglobin A0 RIA may be a more useful tool for the diagnosis of lower GI diseases like colon cancer than Guaiac test.
The efficacy of low residue diet (LRD; Clinimeal®) on Crohn's disease was studied. The patients consisted of 11 with active Crohn's disease for primary therapy and 23 with inactive Crohn's disease for maintenance therapy. Eight weeks after primary therapy, significant improvement was noted in Crohn's desease activity index and labolatory data such as inflammatory and nutritional index. In addition, radiographic findings revealed healing or improvement of active lesions such as longitudinal ulcer, cobblestone appearance, and aphthoid ulcer in 21 of 22 small intestinal lesions and in 8 of 9 colonic lesions. In maitenance therapy by oral intake at home, patients treated with a larger amount of LRD had lower relapsing and hosipitalization rates. These reuslts suggest that LRD is effective for primary and maintenance therapy of Crohn's disease.
The mucosal hexosamine content was studied, which is an indicator of mucosal glycoproteins, in the biopsied materials by endoscopy in 36 gastric ulcer cases and 58 outpatients free of gastric lesions as control cases. In control cases, the biopsied materials were taken from three points; from the lesser curvature of the antrum, the lesser curvature of the gastric angle and the posterior wall of the upper corpus. In gastric ulcer cases, the biopsied materials were taken from four points; from the same three points as the control cases and from the edge of ulcer. The Neuhaus's method was employed for measurement of the mucosal hexosamine content. In control group, the mucosal hexosamine content was significantly higher in the lesser curvature of the antrum than that in the posterior wall of the upper corpus. With advancing age of subjects, the mucosal hexosamine content became significantly decreased in the antrum and at the gastric angle, while unchanged in the upper corpus. In addition, the mucosal hexosamine content was significantly decreased in the antrum and at the gastric angle, with advance of the glandular atrophy in the pyloric gland area. In gastric ulcer group, the mucosal hexosamine contents of the upper corpus and the antrum were lower at the active stage, higher at the healing stage and lower at the scarring stage of ulcer as well as that of the edge of ulcer. Furthermore, in any case of gastric ulcer, the mucosal hexosamine contents showed significantly lower compared with that in control group.
Changes in metabolism of mucus in rat gastric mucosa following oral administration of acetic acid-glycerin solution were investigated. Hexosamine content reduced remarkablly 3hrs after administration and showed a recovery to normal level on 2nd day of administration. Both glucosamine synthetase and glucosaminidase activities also showed significant decreases 3hrs after administration. Glucosamine synthetase activity then showed a gradual increase and reached a plateau after 12hrs of administration. Thereafter, a gradual decrease in glucosamine synthetase activity was observed. On the other hand, the activity of glucosaminidase progressively elevated until 7th day of administration. These results indicate that the recovery of glucosamine synthesizing system precedes the accumulation of hexosamine and suggest that the content of hexosamine in gastric mucosal lesions following administration of acetic acid-glycerin mixture may be regulated by both glucosamine synthetase and glucosaminidase. The results presented in this study also indicate that the model for gastric mucosal lesions used in the present study is a useful experimental tool to investigate the regulatory mechanism for gastric glycoprotein metabolism during formation and recovery of gastric mucosal lesions.
We studied changes in the concentrations of the immunoreactive thyrotropin-releasing hormone (IR-TRH) in the hypothalamus, stomach and gastric juice under water-immersion stress in rats. Male Sprague-Dawley rats, restrained in water for 0.5, 1, 2, 4, 6 and 8 hours, were decapitated and the IR-TRH concentrations in the tissues and gastric juice were measured by a specific radioimmunoassay. The ulcer index of the rat stomach became higher, as the time of water-immersion stres became longer. The IR-TRH concentrations in the hypothalamus of rats restrained for 0.5, 1 and 2 hours were significantly lower than pre-stress levels. However, IR-TRH concentrations in the hypothalamus of rats stressed for 4 to 8 hours returned to normal levels. In the rat adenostomach, the concentrations of IR-TRH were significantly lower in the all restrained groups, whereas IR-TRH concentrations in gastric juice were significantly higher after 1 hour or more water immersion stress. These findings suggest that TRH is released from hypothalamus in the central nervous system (CNS) and from gastric tissue to gastric juice in the stomach under water-immersion stress in rats. We suggest that TRH may be related to the pathogenesis of stress ulcers in the CNS and stomach.
The effect of epidermal growth factor (EGF) on pepsinogen secretion stimulated by carbachol, CCK-8, forskolin and db-cAMP were evaluated using an organ culture of rabbit gastric mucosa. The 10-8 and 10-7M EGF significantly reduced pepsinogen secretion induced by 10-5M forskolin and 10-3M db-cAMP which resulted in an increase of intracellular cAMP of chief cells. However, there was no effect of EGF on pepsinogen secretion stimulated by 10-4M carbachol and 10-8M CCK-8 which produced pepsinogen secretion due to a mobilization of intracellular calcium ion of chief cells. We conclude that EGF possesses an inhibitory effects on pepsinogen secretion which is mediated by intracellular cAMP of chief cells in the rabbit stomach.
Cellular localization of prostaglandin E2 (PGE2) producing cells, which play an important role in the gastric mucosal protecting system, were investigated by the immunoperoxidase technique in rat gastric mucosa. Gastric mucosa was perfused and fixed with 0.5% glutaraldehyde-8% paraformaldehyde followed by post fixation with periodate-lysine-2% paraformaldehyde, and stained for prostaglandin E2 by avidin-biotin-peroxidase method. Positive stainings for prostaglandin E2 were observed on the luminal surface of the surface epithelial cells, and in the cytoplasm of the parietal cells in the deeper layers of the mucosa. These specific stainigs, however, were abolished by preabsorption of anti-prostaglandin E2 antiserum with purified prostaglandin E2. Furthermore, positive stainings in the parietal cells were markedly diminished by the pretreatment of animals by indomethacin. These results strongly suggest that mainly parietal cells synthesize prostaglandin E2 in rat gastric mucosa, and play an important role in the gastric mucosal defence.
In the present study, we have investigated the incidence of osteopenia in patients with liver cirrhosis and the clinical characteristics of cirrhotic patients accompanying osteopenia. Osteopenia was found only 21.2% by Microdensitometry (MD) method but was 61.5% when determined by Jikei method. Three of 28 patients with liver cirrhosis presenting normal pattern by MD method had vertebral compression fractures. In a addition, results obtained with Jikei method is nearly the same as those of Singh index. These present observations suggest that roentgengraphic examination of the trabecular bones such as vertebrae is necessary for the diagnosis of osteopenia in liver cirrhosis. The number of patients with osteopenia was significantly high in patients with decompensated liver cirrhosis, decreased serum cholinesterase activity and increased serum γ-globulin level compared with compensated cirrhotic patients. These observations indicate that the incidence of osteopenia in liver cirrhosis had gradually increased with progression of liver damage. In addition, alcohol intake and secondary hyperparathyroidism may have significantly influenced osteopenia in liver cirrhosis.
Serum HBV-DNA was examined in 33 patients with acute hepatitis B (AVH), 15 asymptomatic HBV carriers (ASC), 40 chronic hepatitis B (CH), and the results were analyzed in relation to other HBV markers and clinical features. Serum HBV-DNA was positive in 9 (27.3%) of 33 patients with AVH, who needed longer duration for normalization of GPT as compared with cases negative for HBV-DNA. In ASC, appearance of serum HBV-DNA well correlated with the HBeAg/anti-HBe status. Serum HBV-DNA was detected in all cases of 30 patients with CH positive for HBeAg and in 6 of 10 patients with CH positive for anti-HBe. Serum HBV-DNA was the best parameter to reflect the exacerbation of chronic hepatitis B. Although serum HBV-DNA did not correlate with HBsAg in the liver, good correlation was found between serum HBV-DNA and HBsAg in the liver. These results suggested that serum HBV-DNA was useful as a parameter of prolongation of acute hepatitis B and, at the same time, it could serve as the most sensitive parameter reflecting exacerbation of hepatitis associated with HBV replication in patients with CH.