Healing of erosive esophagitis with sucralfate and cimetidine: influence of pretreatment esophageal sphincter pressure and serum pepsinogen I levels

Article Abstract:

The strong acids and powerful digestive enzymes of the stomach are normally kept from flowing up into the esophagus by the action of the esophageal sphincter, a muscle that closes the entrance to the stomach. However, many people suffer heartburn, which results from irritation of the esophagus by stomach acid. If the gastroesophageal reflux, or the movement of stomach acid into the lower esophagus, is chronic, it may result in erosive lesions similar to stomach ulcers. The same drugs used to treat stomach ulcers have been recruited for the treatment of erosive esophagitis. Unfortunately, these drugs are not as effective in the treatment of erosive esophagitis; complete healing is rarely achieved in more than half the cases. A study was conducted to compare cimetidine and sucralfate in treating patients with erosive esophagitis. These anti-ulcer drugs work by different mechanisms. Cimetidine significantly reduces the amount of stomach acid. Sucralfate, on the other hand, has little effect on the stomach acid, but strengthens the protective mucus barrier that separates delicate living tissues from the effects of the strong acid. After eight weeks of treatment, 48 percent of the sucralfate group enjoyed complete healing; the 55 percent healing rate among the patients treated with cimetidine was not significantly different. An additional 19 percent of the sucralfate group and 20 percent of the cimetidine group, while not achieving complete healing, enjoyed significant improvement. One might assume that these results indicate that sucralfate and cimetidine are equally effective. However, physiological measurements revealed differences among the patients treated successfully with each drug. Patients who did not respond to cimetidine tended to have lower pressure of the esophageal sphincter. Patients with low levels of pepsinogen-I (PG-I), indicative of acid-secreting cells in the stomach, tended to do better on sucralfate, while those with high PG-I tended to do better with cimetidine. These results indicate that the two treatments may be appropriate for different subpopulations of patients with erosive esophagitis. If more is learned about these differences, it may be possible to tailor treatment for erosive esophagitis to the individual patient. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Heartburn, Esophagogastric junction, Pepsinogen

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Incidence of pneumonia in mechanically ventilated patients treated with sucralfate or cimetidine as prophylaxis for stress bleeding: bacterial colonization of the stomach

Article Abstract:

Many hospitalized patients acquire infections as a result of their hospital stay. Among these nosocomial, or hospital-acquired, infections, pneumonia is the one most likely to result in death. The risk of developing nosocomial pneumonia is especially high in patients who are mechanically ventilated. In at least some cases, there is reason to believe that the stomach provides the source of bacteria which ultimately cause the pneumonia. Any condition that reduces the amount of stomach acid in a hospitalized patient provides a more suitable environment for the growth of bacteria. Small amounts of bacteria-laden stomach juice work their way up the esophagus and are eventually aspirated into the respiratory tract, seeding the airways with germs. One method of reducing stomach acid is prophylactic (preventive) treatment for stress ulcers. Drugs such as cimetidine reduce the secretion of stomach acid and are sometimes used to prevent peptic ulcer formation in hospitalized patients. Since the anti-ulcer drug sucralfate has been shown to be at least as effective as cimetidine in the prevention of ulcers with only a slight effect on stomach acidity, a study was conducted to determine if the use of sucralfate might reduce the risk of nosocomial pneumonia in patients on mechanical ventilation. Forty-nine patients were assigned to receive sucralfate while on artificial respiration and 55 were assigned to receive cimetidine. Pneumonia affected 45.5 percent of the cimetidine group and 26.5 percent of the sucralfate group. This difference did not quite achieve statistical significance, however. Mortality due to pneumonia is high among patients on artificial respiration, and in the present study 25.5 percent of the patients treated with cimetidine died, as did 18.4 percent of the patients treated with sucralfate. No other patient characteristics could be identified to account for the differences, and these results may therefore be interpreted as highly suggestive that sucralfate reduces the incidence of pneumonia among hospitalized patients on mechanical ventilation, compared with cimetidine. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Prevention, Artificial respiration, Mechanical ventilation, Pneumonia, Nosocomial infections, Cross infection

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Sucralfate therapy and reflux esophagitis: an overview

Article Abstract:

Reflux esophagitis results from the contact of stomach acid with the lower portion of the esophagus. If this contact persists, the acid and digestive enzymes of the gastric juice can produce erosive lesions in the esophagus. Since stomach ulcers and duodenal ulcers also arise from acid-induced damage to delicate tissues, it seems reasonable to use the same types of drugs for the treatment of erosive esophagitis. However, drugs that produce excellent results for patients with stomach and duodenal ulcers have not proved particularly effective in the treatment of erosive esophagitis. The H2-blocker class of drugs, which includes cimetidine and ranitidine, decreases the secretion of stomach acid. Studies of these anti-ulcer agents have demonstrated healing in only half the patients with erosive esophagitis, in contrast with 20 percent healing with placebo treatment. Some studies have found no benefit at all with H2 blockers when compared with placebo. Sucralfate is another medication used in the treatment of peptic ulcers. Unlike the H2 blockers, sucralfate has little effect on the secretion of stomach acid. Sucralfate tends to stick to ulcers and augment the natural protective mucus barrier between the delicate tissues and the erosive acid. Unfortunately, although sucralfate is quite effective in the treatment of peptic ulcers, it has proved to be no more effective than the H2 blockers in the treatment of erosive esophagitis. However, the mode of action of sucralfate suggests that some improvement in effectiveness may be possible. Sucralfate relies upon the presence of acid for its activation. While acid is always present surrounding stomach and duodenal ulcers, it is present only transiently in the esophagus. If sucralfate is administered when acid is present, it is much more likely to be activated and stick to the erosive lesion. It may, therefore, be possible to greatly improve the effectiveness of sucralfate by timing the dose to coincide with the reflux of stomach acid into the esophagus. (Consumer Summary produced by Reliance Medical Information, Inc.)

Dosage and administration

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