Abstract
The present review concentrates on environmental factors which influence the outcome of peptic ulcer disease by acting from the outside. Endogenous risk factors, such as acid output, pepsin secretion and serum pepsinogen, gastritis and mucosal defense, blood group, and secretor status, are only dealt with when they help to explain the mechanism by which exogenous risk factors affect the upper gastrointestinal mucosa. After outlining the wax and wane of peptic ulcer, it is concluded that these changes resulted from similar temporal patterns of occupational workload in the general population. Cross sectional studies also support the contention of occupational workload being a risk factor in peptic ulcer, explaining several characteristic features of peptic ulcer, such as its sex, race, and social class distribution, increased incidence in immigrant workers, seasonal variation, healing by bed rest, and urban versus rural distribution. Susceptible subjects may react to a rise in occupational workload and acute exposure to stressful life events by increased gastric secretion which, in turn, leads to ulceration and symptoms. Cigarette smoking, intake of aspirin and related drugs, dietary salt, and alcohol abuse represent additional environmental risk factors, which form the etiologic link of the association of peptic ulcer with chronic lung disease, rheumatoid arthritis, hypertensive disease, and liver cirrhosis, respectively.