Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surface electrogastrograms were recorded in 95 patients. There were 6 groups of patients: chronic superficial gastritis (20), chronic atrophic gastritis (20), duodenal ulcer (20), gastric ulcer (17), gastric cancer (8), and diabetes mellitus (10). Electrogastrographic examination was continuously carried out for 60 minutes both in fasting and postprandial state. (1) During the fasting state, in 72% of the cases, there was a 50% to 100% change in the mean of the amplitude among six 10-minute periods of recording. (2) In 23 cases (25%), there was no amplitude increase in the postprandial electrogastrogram. Feeding caused an increase in amplitude by 30-240 microV over the prefeeding state in 70 cases (75%). (3) The distribution of amplitude in various groups of disease overlapped each other. The difference in amplitude or frequency would not be used as a diagnostic parameter of gastric diseases. (4) Tachygastria of 5-7.3 cycles per minute was observed in 15 of the 95 patients. The longest episode was a wave with 7.3 cycles per minute lasting for 20 minutes. It is difficult to evaluate the clinical significance of the observed tachygastria.
Zhonghua Nei Ke Za Zhi 1991 Jun
PMID:[Electrogastrography: the clinical significance of changes during fasting and postprandial state]. 191 65

Basal and pentagastrin stimulated gastric acid secretions were measured in 20 patients with duodenal ulcer before and after one week of treatment with oral omeprazole 20 mg daily. Omeprazole markedly inhibited gastric acid secretion in all the patients. The mean basal intragastric pH rose from 1.6 to 6.3, and the BAO and MAO were reduced by 86.9% and 83.9% respectively on day 7 of the study. We also conducted a clinical trial in 63 duodenal and 12 gastric ulcer patients. Each patient received 20 mg omeprazole. 98% of the patients were free of pain within first week of the treatment. After 2, 4 and 6 weeks of treatment, the healing rates of duodenal ulcer were 81.3%, 96.8% and 100% respectively, and those of gastric ulcer were 50%, 91.7% and 100% respectively. The drug was well tolerated and no side effect was observed.
Zhonghua Nei Ke Za Zhi 1989 Dec
PMID:[Omeprazole in peptic ulceration: acid inhibition and endoscopic healing]. 263 88

Half gastric emptying time (GET1/2) was measured by using radionuclide gamma-photography with 99mTc-resin solid experiment meal. The results were as follows: 1. GET1/2 in the normal controls (10 cases) was 51.62 +/- 3.69 minutes. 2. GET1/2 in mild chronic atrophic gastritis (CAG) patients was 51.68 +/- 9.20 Min, not significantly different with the normal controls (P > 0.05). GET1/2 in 15 cases with moderate and severe CAG was 70.39 +/- 14.86 Min, which was apparently longer than that in normal controls (P < 0.01). 3. There was no significant difference in GET1/2 between carcinoma of the gastric corpus, fundus and cardia (50.77 +/- 2.73 Min) as well as the normal controls (P > 0.05). GET1/2 of the cancer of gastric antrum was 89.06 +/- 19.55 Min, being longer than that in normal controls (P < 0.01). 4. No obvious difference was observed between the GET1/2 of patients with corpus and fundus peptic ulcer (55.36 +/- 6.80 Min.) and the normal controls (P > 0.05). It was apparently longer in patients with antral peptic ulcer (76.62 +/- 16.96 Min.) than in patients with ulcers of corpus, fundus and normal controls (P < 0.01). 5. GET1/2 in patients with duodenal ulcer (42.49 +/- 6.26 Min.) was apparently shorter than those with gastric ulcer and normal controls. 6. GET1/2 in diabetic patients was 70.01 +/- 29, 46 Min, it was obviously longer in those patients with autonomic nervous dysfunction (84.03 +/- 22.31 Min.) than that those without (34.14 +/- 7.90 Min.).(ABSTRACT TRUNCATED AT 250 WORDS)
Zhonghua Nei Ke Za Zhi 1993 May
PMID:[Gastric emptying time with 99mTc-resin solid experiment meal]. 826 57

Teprenone (Selbex), a gastric mucosal protective drug for treatment of chronic gastritis and gastric ulcer, has recently been used in the People's Republic of China. Teprenone in the treatment of chronic superficial gastritis (CSG): a surveillance study was recently conducted in 4 major hospitals in Beijing. The study included 98 patients (teprenone group 53 patients, Merzulene-S group 45 patients) with endoscopically proven gastritis. The study showed that teprenone may relieve symptoms of CSG in 8 weeks. The effectiveness rate for flatulence was 90.9% and for epigastralgia 87.2%. The improvement rate for the chronic inflammation in histopathology was 39.6% and disappearance rate for the activity of inflammation was 13.9%. It raised significantly the aminohexose level in gastric mucosa (P < 0.05) and increased gastric mucosal blood flow in gastric antrum (P < 0.05). These data suggest that teprenone is a safe and effective gastric mucosal protective drug.
Zhonghua Nei Ke Za Zhi 1996 Jan
PMID:[Teprenone in the treatment of chronic superficial gastritis, a multicentre study]. 927 38

Non-steroidal anti-inflammatory drugs (NSAIDs) are a broad class of non glucocorticoid drugs which are extensively used in anti-inflammatory, analgesic, and antipyretic therapies. However, NSAIDs may cause many side effects, most commonly in gastrointestinal(GI) tract. Cardiovascular system, kidney, liver, central nervous system and hematopoietic system are also involved. NSAID-induced GI side effects not only endanger the patients' health, increase mortality, but also greatly increase the cost of medical care. Therefore, how to reduce GI side effects is of particular concern to clinicians. The Chinese Rheumatism Data Center(CRDC) and Chinese Systemic Lupus Erythematosus Treatment and Research Group(CSTAR) compose a "Recommendation for the prevention and treatment of non-steroidal anti-inflammatory drug-induced gastrointestinal ulcers and its complications" , as following: (1) GI lesions are the most common side effects of NSAIDs. (2) NSAID-induced GI side effects include gastritis, esophagitis, gastric and duodenal ulcers, bleeding, perforation and obstruction. (3) With the application of capsule endoscopy and small intestinal endoscopy, growing attention is being paid to the NASID-induced small intestine mucosa damage, which is mainly erosion and ulcer. (4) Risk factors related to NSAID-induced GI ulcers include: Helicobacter pylori (Hp) infection, age> 65 years, past history of GI ulcers, high doses of NSAIDs, multiple-drug combination therapy, and comorbidities, such as cardiovascular disease and nephropathy.(5) GI and cardiovascular function should be evaluated before using NSAIDs and gastric mucosal protective agents. (6) The risk of GI ulcers and complications caused by selective cyclooxygenase-2 (COX-2) inhibitors is less than that of non-selective COX-2 inhibitors. (7)Hp eradication therapy helps to cure GI ulcers and prevent recurrence when Hp infection is positive in NSAID-induced ulcers. (8) Proton pump inhibitor (PPI) is the first choice for the prevention and treatment of NSAID-induced GI injury. Gastric mucosal protective agents also suggested.(9) H2 receptor antagonist (H2RA) can reduce the risk of NSAID-induced duodenal injury, however, the therapeutic effect of NSAID-induced gastric ulcer remains to be further confirmed. (10) Endoscopic treatment is the first recommendation for NSAID-induced peptic ulcers combined with upper GI bleeding, high-dose PPI effectively prevent rebleeding, reduce the possibility of surgery and mortality rate.
Zhonghua Nei Ke Za Zhi 2017 Jan 01
PMID:[Recommendation for the prevention and treatment of non-steroidal anti-inflammatory drug-induced gastrointestinal ulcers and its complications]. 2805 33