Peptic ulceration and its correlation with symptoms.
Studies in which the numbers of healed or unhealed ulcers and their correlation with symptoms are availabel are summarized in Table 1. A review of the data and inspection of the Table show that the correlation of GU or DU healing with symptomatic remission is generally poor. The reasons for this are unknown and reflect the very incomplete understanding of the mechanism of ulcer pain and of the pathways through which the pain is mediated. The pathogenesis of pain in GU or DU may be due to the action of acid and pepsin, or of bile, on the tissues exposed in the ulcer crater, to abnormal motility, to normal motility acting on inflamed tissue, to areas of inflammation surrounding the ulcer crater, or to a combination of these factors. The relative importance of each of these variables in DU or GU, or in individual patients (because the mechanism of pain may not be the same in each patient) is not known. Nor is it known how much the pathogenesis of ulcer pain is the result of local release of histamine, kinins, and prostaglandins. These biogenic factors are known to be associated with inflammation and produce, or enhance, somatic pain. Their importance in peptic ulcer in man needs to be studied. Relief of pain after neutralization or buffering of gastric contents with alkali or food suggests strongly that acid must play an important part in the pathogenesis of the ulcer symptoms. The rapidity with which relief of symptoms occurs points towards the direct involvement of hydrogen ions in at least one type of ulcer symptom. Lowering of intragastric acidity by histamine H2- receptor antagonists or high-dose alkali may contribute to the observed discrepancies between ulcer healing and the remission of pain, by creating an environment in the gastroduodenal lumen which favours symptomatic improvement, even in the presence of an unhealed crater. This idea, however, does not explain why there is a discordance between healing and symptoms in patients receiving placebo, or in those treated with other drugs, such as carbenoxolone sodium. In the absence of endoscopic evidence, the presence or absence of symptoms cannot be assumed to indicate with certainty the presence or the absence of a peptic ulcer.
D002229:Carbenoxolone / Q000627:therapeutic use; D002908:Chronic Disease; D002927:Cimetidine / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D004381:Duodenal Ulcer / Q000175:diagnosis / Q000188:drug therapy; D004386:Duodenum; D004724:Endoscopy; D005773:Gastroscopy; D006801:Humans; D010146:Pain; D010437:Peptic Ulcer / Q000175:diagnosis / Q000188:drug therapy / Q000473:pathology; D012008:Recurrence; D012075:Remission, Spontaneous; D013276:Stomach Ulcer / Q000175:diagnosis / Q000188:drug therapy
D002927:Cimetidine; D002229:Carbenoxolone