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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are two major principles of ulcer therapy. Today, the most widely accepted drugs are those which substantially reduce aggressive factors (i.c. acid and pepsin), namely histamine H2-receptor antagonists, antimuscarinics and antacids. Less frequently applied are mucoprotective agents like colloidal bismuth compounds and sucralfate. Prostaglandins both reduce acid secretion substantially and are believed to enhance mucosal resistance. Their anti-ulcer efficacy, however, is solely explicable by their antisecretory activity. Although mucosa-strengthening agents and H2-receptor blockers have nearly identical healing rates, mucosa-strengthening agents have inconvenient dosage regimens (four times or twice daily) and are probably less effective in relieving pain. The same holds true for antacids. Prostaglandins, antimuscarinics and antacids have dose related side effects. In contrast, H2-receptor blockers are characterized by a clear mechanism of action, convenient dosage regimens, good tolerance and a low incidence of side-effects. H2-receptor antagonists are the most effective anti-ulcer drugs presently available.
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PMID:What are the current possibilities in treating peptic ulcer disease? 297 97

Enprostil, a synthetic analogue of prostaglandin E2, is effective in the treatment of patients with duodenal or gastric ulcers. As demonstrated in pharmacological studies in healthy volunteers and in patients with inactive ulcer disease, gastric acid secretion is suppressed by up to 80% for almost 12 hours after single doses of enprostil. The drug also reduces the secretion of pepsin, another 'aggressive' factor in peptic ulcer disease. Interestingly, in contrast to the H2-receptor antagonists, which either increase or have no effect on serum gastrin concentrations, enprostil inhibits basal and postprandial gastrin release. Although the possible effects of enprostil on 'defensive' factors in peptic ulcer disease-which are thought to protect the mucosa-require much further clarification, some evidence obtained in man indicates that bicarbonate secretion is enhanced by enprostil. Further, data from animal studies suggest that microvascular integrity may be preserved by a direct action of enprostil on the gastric mucosa. In healthy volunteers, the administration of enprostil in antisecretory doses protects the gastric mucosa against of enprostil in antisecretory doses protects the gastric mucosa against aspirin-induced injury. Cumulative rates of ulcer healing observed in patients with duodenal ulcers after 4 weeks' treatment with enprostil 35 micrograms twice daily were about 50 to 80%, which were similar to those seen in comparative trials with usual therapeutic doses of cimetidine or pirenzepine, but less than occurred with ranitidine. Moreover, enprostil has been shown to relieve daytime pain in a similar percentage of patients as do these H2-receptor antagonists, but night-time pain appears to respond less well to therapy with the prostaglandin. As evidenced by a few controlled trials in patients with gastric ulcers, treatment with enprostil 35 micrograms twice daily for 6 weeks provides ulcer healing in parallel with pain relief as effectively as cimetidine and ranitidine in a high percentage of patients (about 80% after 6 weeks). Prophylactic treatment with enprostil after initial ulcer healing has reduced the rate of duodenal ulcer relapse in patients 'at risk', but to a lesser extent than has ranitidine. Gastrointestinal symptoms-abdominal cramping and pain, flatulence, nausea and notably, diarrhoea-are the most frequently reported side effects during therapy with enprostil. Diarrhoea occurs in about 10% of patients, but is rarely of a severity necessitating treatment discontinuation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enprostil. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of peptic ulcer disease. 312 Dec 76

The current therapeutic approach to peptic ulcer disease includes agents that reduce gastric acidity and hence peptic activity, inactivate or adsorb pepsin, create a physical barrier against the effects of acid and pepsin, or enhance mucosal defence. Profound gastric acid reduction may predispose to infection, and it has been suggested that carcinogenesis is possible, although a cause-effect relationship has never been established. The side-effects of therapy are well-described, and may limit the therapeutic approach. Healing rates correlate closely with acid suppression in duodenal ulcer, but not entirely in gastric ulcer. Maintenance therapy lowers the relapse rate, but does not alter the ulcer diathesis. The optimal strategy for long-term management remains unclear, but in the future one should consider outcome measures which include a decrease in pain, improvement in the quality of life, reduction work loss, and a reduction of complications, in addition to ulcer healing. The ideal therapy should be efficacious, safe, and convenient--with no side-effects--and cost-effective. New agents should suppress acid and peptic activity, while enhancing the gastric mucosal defence mechanisms (such as mucosal blood flow, mucus, and bicarbonate secretion) and stimulating gastric cellular regeneration and restitution.
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PMID:The limitations of current therapy in peptic ulcer disease. 330 47

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.
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PMID:The pathophysiology of peptic ulcer disease. 405 22

In duodenal ulcer, acid and pepsin in greater amounts and at higher concentration enter the duodenum and specific treatment should be directed towards correcting this abnormality. Such treatment is provided by the histamine H2-receptor antagonists. We discuss the first U.S. multicenter trial of the new nitrofuran-based antagonist, ranitidine, in which 382 patients were treated for 4 weeks with either ranitidine 150mg b.i.d. (195 pts.) or placebo (187); both groups were allowed to use antacid for pain. Those treated with ranitidine had significantly less pain and used less antacids than the placebo-treated patients; after 2 weeks, 37% vs 19% were healed, and after 4 weeks, 73% vs 45% were healed (p less than 0.01). After 4 weeks, 124 unhealed patients were randomized to ranitidine vs placebo for another 4 weeks. Ranitidine treatment again produced a greater healing rate (p less than 0.01), regardless of prior treatment. The 3 subsets of the data which contained more than 34 patients were analyzed separately. Each showed 1 or more significant deviations (type I and type II errors) from the overall study, which was in all respects similar to the aggregate results of all similar studies overseas. We emphasize the need for studies of adequate size.
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PMID:Lessons from the U.S. multicenter trial of ranitidine treatment for duodenal ulcer. 631 37

Sucralfate, a complex salt of polyaluminum hydroxide with a sulfated disaccharide skeleton, has recently been approved by the Food and Drug Administration for the short-term treatment of duodenal ulcer. The drug is nonsystemic in action and apparently exerts its antiulcer effects by bonding with proteinaceous exudates in the ulcer crater, thereby protecting it from insult. In vitro and clinical studies have shown that the drug is not an antacid but does block the diffusion of acid. Inhibition of pepsin and bile acid activities have also been demonstrated. In double-blind clinical trials where patients used antacids as needed for pain, sucralfate 1 g 4 times a day was significantly more effective than placebo and as effective as cimetidine. No serious adverse effects have been caused by this locally-acting agent.
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PMID:Pharmacology, clinical efficacy, and adverse effects of sucralfate, a nonsystemic agent for peptic ulcer. 692 35

Laser-assisted uvulopalatoplasty (LAUP) is an outpatient mode of treatment for snoring and perhaps for some mild cases of obstructive sleep apnea syndrome. LAUP results in severe throat pain that usually lasts for 8 to 14 days. Sucralfate adheres to proteins at the duodenal ulcer site, forming a protective coating against gastric acid, pepsin, and bile salts, that promotes healing. If a similar protective coating could be created at the area of LAUP trauma, morbidity may be diminished. Twenty-eight patients have undergone LAUP treatment-2 with mild obstructive sleep apnea syndrome and 26 with simple snoring. A block-randomized, single blind clinical study was performed. Sucralfate was administered in 14 patients (group A) every 6 hours for 15 days as a swish and swallow, whereas the other 14 patients (group B) received water for injection with a strawberry flavor as placebo with the same dosing. As a conclusion, sucralfate significantly lowered postoperative pain and the need for analgesic drug use as well as the total number of the days the patients needed to almost reach their normal diet quantity (> or = 80% of normal quantity).
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PMID:Sucralfate alleviating post-laser-assisted uvulopalatoplasty pain. 1117 15

The effects of the five extracts from Herba pogostmonis being gotten rid of volatile oil on gastrointestinal tract were studied. The results showed that the five extracts could increase gastric secretion of acid and activity of pepsin, reduce the incidence of diarrhea induced by Folium sennae and relieve the gripping pain induced by abdominal administration of acetic acid. The extract of ethyl acetate could also inhibit the normal and neostigmine induced mice intestinal propellant movement. The effect of extract of ethyl acetate was consistent with clinical application. The above results indicated that the clinical effect of Herba pogostmonis may be comprehensive action of above five different polar extracts.
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PMID:[Effects of five different polar extracts from Herba pogostemonis being gotten rid of volatile oil on gastrointestinal tract]. 1156 90

The effects of the three extracts (Decoction, oil-free decoction and volatile oil) of Herba Pogostemonis on gastrointestinal tract were studied. The results showed that all the three extracts inhibited the automatic contraction and Ach, BaCl2-induced spasmodic contraction of isolated rabbit intestine, among the three extracts the volatile oil was the most potent. In vivo the decoction and the oil-free decoction could depress gastric evacuation and inhibit the normal and neostigmine-induced intestinal propellent movement in mice, but the volatile oil could not. The decoction and the oil-free decoction also increased gastric secretion of acid and activity of pepsin and amylase. Furthermore, the decoction and the oil-free decoction reduced the incidence of diarrhea induced by senna but volatile oil enhanced cooperatively. All the three extracts relieved the gripping pain induced by abdominal administration of acetic acid, and the effect of decoction was more potent that the others. The above results revealed that the effective components of Herba Pogostemonis may be mainly water-solube.
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PMID:[Effects of herba Pogostemonis on gastrointestinal tract]. 1256 39

Salicylates have been used since antiquity to relieve pain and inflammation. However, it has been only in the last half century that evidence has emerged that aspirin causes reproducible acute and superficial injury to the gastric and duodenal mucosa, and is an important cause of complicated and uncomplicated peptic ulcer. Superficial damage to the mucosa occurs rapidly and reproducibly and acid and pepsin then produce a second wave of deeper injury. Most of the time this heals rapidly, but some focal deeper mucosal lesions (erosions) occur frequently and the point prevalence of frank ulcers in low dose aspirin users is around 10%. It is even more recently that aspirin's unique antiplatelet action has been recognized, with long-lasting inhibition of platelet aggregation due to irreversible inactivation of the cyclooxygenase-1 mediated production of thromboxane. It has now become the mainstay of pharmacological reduction of thrombotic risk in patients with cardiovascular diseases. In addition, evidence is accumulating about the cancer-reducing effects of blocking cyclooxygenase in a number of tissues. For example, recent data indicate that even at a 75-mg/day dose, it may reduce colorectal cancer risk after a lag of a year or so. Because of its widespread use for cardiovascular protection, aspirin is now one of the most frequently prescribed drugs-and gastroenterologists regularly need to deal with its ulcerative complications along the whole length of the gastrointestinal tract. Strategies that can be used to reduce these risks include using the lowest effective aspirin dose and co-prescribing acid suppressants.
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PMID:Aspirin: old drug, new uses and challenges. 2106 58


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