Gastroduodenal damage due to drugs, alcohol and smoking.

In man, convincing data have been obtained in short-term observations that some drugs can cause acute gastroduodenal damage including gastritis and erosions. Useful clinical and epidemiological studies on the relationship between these acute lesions and peptic ulceration, and between the chronic ingestion of these drugs and peptic ulceration or massive upper gastrointestinal haemorrhage are, however, rare. Even for the most widely used and studied greatest offender--acetylsalicylic acid (ASA)--an association with major bleeding or gastric ulceration could only be established for frequent and heavy ASA intake. The percentage of those ASA users who will experience such a serious event each year is about 0.01 to 0.05 per cent. By the use of special (e.g. enteric-coated) ASA formulations and other precautions, this low rate may be further reduced. Although for most of the other non-steroidal anti-inflammatory drugs (NSAIDs), anecdotal reports on putative drug-related major gastric bleeding or peptic ulceration exist, the ulcerogenicity of these drugs has not yet been conclusively proven in controlled studies. Some of the newer NSAIDs seem at normal dosage to be far less damaging than traditional ASA or indomethacin. Glucocorticoids might enhance ulcer risk to a minor extent when administered at high dosage for prolonged periods to susceptible individuals. Chronic moderate alcohol consumption by itself does not seem to increase the liability to peptic ulceration. With highly concentrated alcoholic beverages, gastric bleeding from acute lesions may, however, be occasionally precipitated under certain circumstances, such as when unbuffered ASA is taken concomitantly. Smoking of cigarettes is associated, and perhaps causally related, with an increased incidence of gastric and duodenal ulcerations, impaired ulcer healing, and more frequent ulcer recurrences. Duodenal ulcer patients in particular should be advised to stop smoking.