ABSTRACT
The patterns of analgesic ingestion in gastric and duodenal ulcer patients were compared with those of matched community controls in order to ascertain differences that may exist between ulcer and nonulcer subjects of comparable age and sex. The differences sought concerned amounts and types of analgesics ingested. The types of analgesics studied were aspirin and acetaminophen, ingested either alone or together. Analgesics such as dextropropoxyphene and codeine were disregarded. It was found that there was a strong positive association between heavy analgesic intake and chronic gastric ulcer with a relative risk of 29.5. The association was most marked in female patients (relative risk = 51.8). The involvement of aspirin-containing and acetaminophen-containing drugs was of similar significance with relative risk of 17.3 and 24.4, respectively. Aspirin alone was the least frequently ingested. The association was only partly related to painful nonulcer health problems and to ulcer pain. No association was found between chronic duodenal ulcer and analgesic intake. The strong association found between gastric ulcer and heavy analgesic intake does not, per se, necessarily indicate a causal relationship.
Subject(s)
Analgesics/therapeutic use , Peptic Ulcer/epidemiology , Acetaminophen/therapeutic use , Aspirin/therapeutic use , Australia , Duodenal Ulcer/epidemiology , Female , Humans , Male , Risk , Stomach Ulcer/epidemiologySubject(s)
Acidosis/metabolism , Carcinoma/metabolism , Gastric Juice/metabolism , Lactates/metabolism , Peptic Ulcer/metabolism , Stomach Neoplasms/metabolism , Fructose/pharmacology , Gastric Acidity Determination , Gastric Juice/drug effects , Glucose/pharmacology , Humans , Secretory Rate , Sodium/analysisSubject(s)
Gastric Juice/enzymology , L-Lactate Dehydrogenase , Preservation, Biological , Refrigeration , HumansABSTRACT
Lactate dehydrogenase (LDH) isoenzymes were demonstrated electrophoretically in human fundic and pyloric gastric mucosae and in gastric carcinoma tissue. Fundic gastric mucosa consistently displayed a pattern with predominance of LD1, LD2, and LD3. Pyloric gastric mucosa and cancer tissue consistently had identical patterns with a predominance of LD2, LD3, and LD4, differing significantly from the LDH isoenzyme pattern of fundic mucosa. The LDH isoenzyme pattern characteristic of fundic mucosa extended very close to the histological junction between body and pyloric gastric mucosa and was not affected by the presence of gastritis in the stomach. These results serve to demonstrate yet another difference between mucosa from the acid-secreting and the pyloric areas of the human stomach.
