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Of peptic ulcer disease

Bismuth subsahcylate [14882-18-9] Pepto-Bismol, is a basic salt of varying composition, corresponding approximately to i9-H0CgH4C02(Bi0). Like a number of other insoluble bismuth preparations, it is not currentiy approved in the United States for the treatment of peptic ulcer disease but is under active investigation for this purpose (180). It does appear to be effective for the rehef of mild diarrhea and for the prevention of travelers diarrhea (181). The ready availabiUty of this dmg, however, may lead to its ovemse and result in toxic effects caused by both the saUcylate and bismuth components. It has been suggested that bismuth subsahcylate is somewhat effective in the symptomatic treatment of isosporiasis, a disease caused by the intracellular parasite Isospora belli (182). [Pg.135]

TABLE 15-1. Characteristics of Common Causes of Peptic Ulcer Disease... [Pg.270]

The analgesic effects of NSAIDs are attributed to inhibition of the COX-2 enzyme, whereas the negative GI effects are due to inhibition of COX-1.28 Patients taking oral anticoagulants, those with a history of peptic ulcer disease, or others at high risk for GI complications may be considered candidates for a COX-2 inhibitor or a combination of a nonselective NSAID with a gastroprotective agent such as a proton pump inhibitor (PPI). Because most PPIs are available by prescription only, such patients should be referred to a physician. [Pg.904]

There are certain histologic subtypes of diffuse, aggressive NHL that respond less well to treatment with conventional regimens such as CHOP. Burkitt s lymphoma, lymphoblastic lymphoma, mantel cell lymphoma, and primary CNS lymphoma are examples of disease that benefit from more intensive therapy. Regimens such as hyper-CVAD, which alternate cycles of hyperfractionated cyclophosphamide, doxorubicin, vincristine, and dexamethasone with high-dose cytarabine and methotrexate, often are substituted for CHOP. Intrathecal therapy with methotrexate is indicated with documented CNS infiltration of tumor or involvement of the sinuses. The recent appreciation of the etiology of Helicobacter pylori in the etiology of peptic ulcer disease and the association between colonization and mucosal-associated lymphoma (MALT) has spurred... [Pg.1381]

Although the risk of GI complications is relatively small with short-term therapy, coadministration with a proton pump inhibitor should be considered in elderly patients and others at increased GI risk. NSAIDs should be used with caution in individuals with a history of peptic ulcer disease, heart failure, uncontrolled hypertension, renal insufficiency, coronary artery disease, or if they are receiving anticoagulants concurrently. [Pg.18]

Q23 Characteristic symptoms of peptic ulcer disease include all EXCEPT ... [Pg.224]

Localised upper abdominal pain is the most common symptom of peptic ulcer disease. The pain is relieved by antacids, proton pump inhibitors and H2 antagonists. The pain may or may not be relieved by food and is often v/orse during the night. Peptic ulceration may be accompanied by occasional vomiting, anorexia and weight loss. Diffuse abdominal pain is not a characteristic symptom of peptic ulcer disease. [Pg.247]

Helicobacter pylori infections are now also accepted as the primary cause of peptic ulcer disease (PUD). In the US, approximately four to five million people suffer from PUD, and the economic consequences of the disease are responsible for as much as 3 to 4 billion in annual health care costs. The situation is even more serious in many developing countries, where HP infections, PUD and gastric cancer are major causes of morbidity. [Pg.476]

Gl effects - Do not use ketorolac in active peptic ulcer disease, recent Gl bleeding or perforation, a history of peptic ulcer disease, or Gl bleeding. [Pg.937]

The goals of medical treatment of peptic ulcer disease are to relieve symptoms, heal the ulcer and to prevent recurrence. For the first two the therapeutic tactics are aimed at reducing aggressive factors, in the first place gastric acid, and to promote or introduce defensive or cytoprotective factors. For... [Pg.377]

For prevention of peptic ulcer disease avoiding ulcerogenic medication such as NSAIDs, including aspirin, is probably the most important strategy. Reducing gastric acidity is also the main approach for the treatment of reflux esophagitis. [Pg.377]

SoU AH. Consensus conference. Medical treatment of peptic ulcer disease. Practice guidehnes. Practice Parameters Committee of the American College of Gastroenterology. JAMA 1996 275(8) 622-9. [Pg.386]

Misoprostol (Cytotec) is a prostaglandin Ej analogue that is being evaluated as a cervical ripening agent. It also is used in the treatment and prevention of peptic ulcer disease (see Chapter 40). Clinical trials show that misoprostol is an effective agent for both cervical ripening and labor induction. It appears to be as effective as dinoprostone and is much less expensive. [Pg.719]

COX-2 specific inhibition good choice for patients with inflammatory conditions who are at high risk of gastrointestinal adverse effects (e.g., older than 60 years history of peptic ulcer disease prolonged, high-dose NSAID therapy concurrent use of corticosteroids or anticoagulants)... [Pg.232]

G. L. Garay, J. M. Muchowski (1985). Agents for the treatment of peptic ulcer disease. Annu. [Pg.305]

Bismuth compounds have been used in the treatment of peptic ulcer disease. They function by selective binding to the ulcer, coating it and shielding it from the effects of gastric acid. Bismuth may also have activity against bacteria such as Helicobacter pylori, shown to be a causative factor in peptic ulcer disease of the stomach. Bismuth has been administered as bismuth subsalicylate (8.95) or tripotassium dicitrato bismuthate. [Pg.533]

The high incidence of peptic ulcer disease created great interest in the therapeutic potential of these H2-receptor antagonists when first discovered. Even though they are not the most efficacious agents available, their ability to reduce gastric acid secretion with very low toxicity has made them extremely popular and they have become OTC items. These drugs are discussed in more detail in Chapter 62. [Pg.355]

The author commented that 50-75% of gastrocolic fistulas are related to benign gastric ulcers secondary to the use of NSAIDs. The use of aspirin plus prednisone, as in this patient, increases the risk of complication of peptic ulcer disease two- to fourfold. [Pg.21]

Lehmann F, Hildebrand P, Beghnger C. New molecular targets for treatment of peptic ulcer disease. Drugs. 2003 63 1785-1797. [Pg.399]

Circunstantial evidence directly implicating dopamine in the pathogenesis of duodenal ulcer in man is the unusual incidence of peptic ulcer disease in dopamine-deficient disorders. From purely descriptive clinical and epidemiologic studies we know that patients with Parkinson s disease, before the introduction of dopamine therapy, had an excess of ulcer disease (72). One report even comments on the curiosity that after initiation of L-DOPA administration the ulcer symptoms have virtually disappeared (72 ). On the other hand, less clearly, schizophrenia which is associated with dopamine excess and/or receptor hyperactivity is accompanied by virtual lack, or decreased prevalence, of peptic ulcer (73-76). Schizophrenia associated with ulcer disease has been viewed as a reportable curiosity in medical literature (75). At present, possibly because of the widespread therapeutic application of neuroleptics, the lack of peptic ulcer disease in schizophrenics is less striking than in the past. On the other hand, we recently observed in our autopsy series perforated duodenal ulcers in two schizophrenic patients who had been on large doses of haloperidol therapy (Szabo, unpublished observation). Thus, even in man, dopamine may indeed be implicated in the pathogenesis of duodenal ulcer disease. [Pg.193]

Muscarinic receptor stimulation increases gastrointestinal motility and secretory activity (see p. 29). Cholinergic antagonists, such as hyoscyamine, are used as adjuncts in the management of peptic ulcer disease and Zollinger-Ellison syndrome, particularly in patients... [Pg.250]

Cimetidine closely resembled metiamide but did not exhibit the granulocytopenia side effect. It was marketed as Tagamet at the end of 1976, as the pioneer drug which revolutionized the medical treatment of peptic ulcer disease [4]. Indeed, in many countries it became the best-selling prescription medicine and was the first of the block-busler products (billion dollar annual sales). [Pg.72]

The discovery and development of cimetidine and ranitidine provided a revolution in the medical treatment and management of peptic ulcer disease. Subsequently, many pharmaceutical companies became involved in research programs to discover additional compounds as H2-receptor histamine antagonists. As a result, a very wide range of chemical structures now exists for this class of drug (for a review, see Cooper et al. [19]). Many of these compounds have been investigated in human studies, but only the above-mentioned five drugs - cimetidine, ranitidine, nizatidine, famotidine, and roxatidine - are marketed as medicines. [Pg.78]

As stated above, cimetidine revolutionized the medical treatment of peptic ulcer disease, and other products which followed continued the same type of treatment. Thus, H2-receptor histamine antagonists in general were given daily for 4—6 weeks... [Pg.78]


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See also in sourсe #XX -- [ Pg.643 ]




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