EDITORIAL
The Gastric Ulcer Problem Significant changes have occurred in the relative incidence and significance of the various ulcer disease processes. Terminology has proven a problem. Erosive disease of the esophagus, stomach, and duodenum has come into prominence, but apparently has little relationship to true ulcer disease. Gastric carcinoma is no longer the troublesome differential diagnostic problem it was in the past. Its decline in incidence is startling and unexplained. The incidence relationship of duodenal ulcer and gastric ulcer has altered notably. The gastric site is now more frequently encountered and concomitancy is notable. Perfection of panendoscopy, permitting a comprehensive look at the esophagus, stomach, duodenum, and anastomotic sites, has contributed to the observation of multiple concomitant disease entities. Fiberoptic delineation now permits accuracy in assessing these mucosal alterations, bleeding site identification, and endoscopic operative intervention with the potentiality of laser beam application. Mucosal defense alteration by ingestants and by enteric refluxants is prominently considered in causal relationship. Elucidation of the pathogenesis of all ulcerative entities has lagged, depiction of aggressive vs defense forces, emphasized over the years, permitting the assumption of stress as a duodenal ulcer mechanism against mucosal nutritional failure as causal in gastric disease. Knowledge of specific characteristics of the mucosal barrier as a defense mechanism supporting mucosal integrity through cellular secretion metabolism and healthy replication has created a better understanding of the erosive and ulcerative processes involving the gastric mucosa. Stress, long emphasized as a duodenal causal component, also is involved in gastric ulcer and has been demonstrated a contributor to DNA synthesis inhibition and concomitant cell loss of RNA with related diminished cell replication. Additionally, there is the stress lesion of gastric location encountered in the burn patient, in central nervous system disease, and in stressful cardiovascular and surgical experiences. A component of impaired mucosal Digestive Diseases, Vol. 21, No. 2 (February 1976)
flow in related ischemia susceptibility exists. The "experimental ulcer" is a term that has been abused. The lesion produced, varying in site--gastric, duodenal, and enteric--and diverse in character from hemorrhage to erosion to ulceration, and the fact that the acute lesion does not develop into chronic ulcer, definitely leaves a gap in correlation with ulcer disease in humans. Therapeutically, selective perfusion has modified mucosal bleeding. Endoscopy has permitted a trial of cauterization. The potentiality of laser application via the endoscope is under investigation. Dietary approach to u]lcer management has lost prestige. Antacids remaiin our most effective therapeutic agent. The position of the anticholinergics seems uncertain. Coating agents are hypothesized. Protein binding materials protecting the ulcer base are proposed. Pepsin inhibitors have been emphasized. The It2 blocking agents are under evaluation. Radiation therapy has not gained acceptance. We are, therefore, still therapeutically uncertain. Our faculty, each an authority in his own area, will explore many of the factors responsible for gastric ulcer disease and, hopefully, rationalize the present knowledge as to therapeutic approach. The problem: Alteration of gastric mucosa defense factors in experimental and clinical settings has created a variety of gastric mucosal lesions. These focal areas of gastric mucosal damage resulting from such factors as altered mucus formation, impaired cell replication, barrier disintegration, blood flow impediment rendering the mucosa susceptible to hydrogen ion back-diffusion still leave questions incompletely answered as to occurrence, prophylaxis, and management, which we hope will be the stimulus for continued research. Identification of the role of the offenders and protectors against them, inhibitor application, and enhancement of the defense mechanisms may result therefrom to resolve many of our gastric ulcer problems. GORDON Mc HARDY Louisiana State University Medical Center at New Orleans
137
The Gastric Ulcer Problem Significant changes have occurred in the relative incidence and significance of the various ulcer disease processes. Terminology has proven a problem. Erosive disease of the esophagus, stomach, and duodenum has come into prominence, but apparently has little relationship to true ulcer disease. Gastric carcinoma is no longer the troublesome differential diagnostic problem it was in the past. Its decline in incidence is startling and unexplained. The incidence relationship of duodenal ulcer and gastric ulcer has altered notably. The gastric site is now more frequently encountered and concomitancy is notable. Perfection of panendoscopy, permitting a comprehensive look at the esophagus, stomach, duodenum, and anastomotic sites, has contributed to the observation of multiple concomitant disease entities. Fiberoptic delineation now permits accuracy in assessing these mucosal alterations, bleeding site identification, and endoscopic operative intervention with the potentiality of laser beam application. Mucosal defense alteration by ingestants and by enteric refluxants is prominently considered in causal relationship. Elucidation of the pathogenesis of all ulcerative entities has lagged, depiction of aggressive vs defense forces, emphasized over the years, permitting the assumption of stress as a duodenal ulcer mechanism against mucosal nutritional failure as causal in gastric disease. Knowledge of specific characteristics of the mucosal barrier as a defense mechanism supporting mucosal integrity through cellular secretion metabolism and healthy replication has created a better understanding of the erosive and ulcerative processes involving the gastric mucosa. Stress, long emphasized as a duodenal causal component, also is involved in gastric ulcer and has been demonstrated a contributor to DNA synthesis inhibition and concomitant cell loss of RNA with related diminished cell replication. Additionally, there is the stress lesion of gastric location encountered in the burn patient, in central nervous system disease, and in stressful cardiovascular and surgical experiences. A component of impaired mucosal Digestive Diseases, Vol. 21, No. 2 (February 1976)
flow in related ischemia susceptibility exists. The "experimental ulcer" is a term that has been abused. The lesion produced, varying in site--gastric, duodenal, and enteric--and diverse in character from hemorrhage to erosion to ulceration, and the fact that the acute lesion does not develop into chronic ulcer, definitely leaves a gap in correlation with ulcer disease in humans. Therapeutically, selective perfusion has modified mucosal bleeding. Endoscopy has permitted a trial of cauterization. The potentiality of laser application via the endoscope is under investigation. Dietary approach to u]lcer management has lost prestige. Antacids remaiin our most effective therapeutic agent. The position of the anticholinergics seems uncertain. Coating agents are hypothesized. Protein binding materials protecting the ulcer base are proposed. Pepsin inhibitors have been emphasized. The It2 blocking agents are under evaluation. Radiation therapy has not gained acceptance. We are, therefore, still therapeutically uncertain. Our faculty, each an authority in his own area, will explore many of the factors responsible for gastric ulcer disease and, hopefully, rationalize the present knowledge as to therapeutic approach. The problem: Alteration of gastric mucosa defense factors in experimental and clinical settings has created a variety of gastric mucosal lesions. These focal areas of gastric mucosal damage resulting from such factors as altered mucus formation, impaired cell replication, barrier disintegration, blood flow impediment rendering the mucosa susceptible to hydrogen ion back-diffusion still leave questions incompletely answered as to occurrence, prophylaxis, and management, which we hope will be the stimulus for continued research. Identification of the role of the offenders and protectors against them, inhibitor application, and enhancement of the defense mechanisms may result therefrom to resolve many of our gastric ulcer problems. GORDON Mc HARDY Louisiana State University Medical Center at New Orleans
137
