Helicobacter peptic ulcer

This genus, originally grouped with the Campylobacters (section 6.4.16), is now considered a separate genus. Helicobacter pylori is of interest as a cause of peptic ulcer. 

Helicobacter pylori is associated with chronic gastritis, peptic ulceration and possibly involved in the pathogenesis of gastric carcinoma (Correa and Ruiz, 1992 Dixon,... 

Chan FKL, Leung WK. Peptic ulcer disease. Lancet 2002 360 933-941. Howden CW, Hunt RH. Guidelines for the management of Helicobacter pylori infection. Ad hoc committee on practice parameters of the American College of Gastroenterology. Am J Gastroenterol 1998 93 2330-2338. 

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... 

Helicobacter pylori 1.66/1578 (68) Peptic ulcer, gastric cancer, gastric lymphoma (MALT)... 

Peptic ulcer disease (PUD) refers to a group of ulcerative disorders of the upper GI tract that require acid and pepsin for their formation. Ulcers differ from gastritis and erosions in that they extend deeper into the muscularis mucosa. The three common forms of peptic ulcers include Helicobacter pylori (HP)-associated ulcers, nonsteroidal antiinflammatory drug (NSAID)-induced ulcers, and stress-related mucosal damage (also called stress ulcers). 

Pilotto A, Franceschi M, Valerio G et al. (1999) Helicobacter pylori infection in elderly patients with peptic ulcer. Age Ageing 28(4) 412—414... 

Atherton, J. C., Cao, P., Peek, R. M., Jr., Tummuru, M. K., Blaser, M. J., and Cover, T. L. (1995). Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. /. Biol. Chem. 270, 17771-17777. 

Proton pump inhibitors (PPIs), such as omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole, are commonly prescribed to treat symptoms of heartburn, acid reflux, chest pain, dyspepsia, and chronic cough. PPIs inhibit the transfer of protons into the stomach lumen. Pharmacological acid suppression is thus used to treat gastroesophageal reflux disease (GERD) and esophagitis, peptic ulcers, and Helicobacter pylori infection as well as to prevent ulcer development with concurrent nonsteroidal anti-inflammatory drug use. 

Kurata, J. H., and Nogawa, A. N. (1997) Meta-analysis of risk factors for peptic ulcer. Nonsteroidal anti-inflammatory drugs, Helicobacter pylori, and smoking. J. Clin. Gastroenterol. 24, 2-17. 

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. 

Helicobacter infections are of great concern worldwide due to its association with peptic ulcer disease and gastric cancer. Resistance to available antimicrobials is on the rise, not only in the US but also in the developing countries. This increase in resistance has opened the door for research into... 

Goodwin CS. (1997) Helicobacter pylori gastritis, peptic ulcer, and gastric cancer Clinical and molecular aspects. Clin Infect Dis 25 1017-1019. 

Faine F, Fendrick AM. (1998) Helicobacter pylori peptic ulcer disease Bridging the gap between knowledge and treatment. Postgrad Med 103 231-238. 

In the area of a gastric or duodenal peptic ulcer, the mucosa has been attacked by digestive juices to such an extent as to expose the subjacent connective tissue layer (submucosa). This self-digestion occurs when the equilibrium between the corrosive hydrochloric acid and acid-neutralizing mucus, which forms a protective cover on the mucosal surface, is shifted in favor of hydrochloric acid. Mucosal damage can be promoted by Helicobacter pylori bacteria that colonize the gastric mucus. 

III. Eradication of Helicobacter pylori C. This microorganism plays an important role in the pathogenesis of chronic gastritis and peptic ulcer disease. The combination of antibacterial drugs and omeprazole has proven effective. In case of intolerance to amoxicillin (p. 270) or clarithromycin (p. 276), metronidazole (p. 274) can be used as a substitute. Colloidal bismuth compounds are also effective however, the problem of heavy-metal exposure compromises their long-term use. 

Helicobacter pylori H. pylori is found in approximately 100% of chronic active antral gastritis cases, 90% to 95% of duodenal ulcer patients, and 50% to 80% of gastric ulcer patients. The treatment of documented H. pylori infection in patients with confirmed peptic ulcer on first presentation or recurrence has been recommended by the National Institutes for Health in a 1994 Consensus Conference. Once H. py/on eradication has been achieved, reinfection rates are less than 0.5% per year, and ulcer recurrence rates are dramatically reduced. 

Tetracycline - A6 unct ve therapy for peptic ulcers due to Helicobacter pylori (500 mg 4 times/day). 

There is increasing evidence that eradication of Helicobacter pylori with combination therapy of two antibiotics (often amoxicillin with clarithromycin) with a proton pump inhibitor (e.g. pantoprazol) during one week will heal and prevent peptic ulcer disease. 

Answer Peptic ulcer disease is most frequently secondary to either Helicobacter pylori infection or use of NSAIDs. The patient does admit to NSAID use (naproxen), but should also be checked for concomitant H. pylori infection at time of endoscopy or by a serology test. If the patient was found to have H. pylori, an appropriate eradication regimen should be prescribed. The patient should also be counseled to avoid NSAIDs. The patient should be prescribed a proton pump inhibitor for 8 weeks to heal the ulcer. A repeat endoscopy should be done at that time to document ulcer healing and rule out gastric cancer. In addition, the patient should be counseled to stop smoking, which is a risk factor for more severe peptic ulcer disease. 

Mechanism of Action An antinauseant and antiulcer agent that absorbs water and toxins in the large intestine and forms a protective coating in the intestinal mucosa. Also possesses antisecretory and antimicrobial effects. Therapeutic Effect Prevents diarrhea. Helps treat Helicobacter pybri-associated peptic ulcer disease. 

Unlabeled Uses Peptic ulcer disease, active ulcer bleeding (injection), adjunct in treatment of Helicobacter pylori infecfion. 

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. 

Prophylactic and therapeutic administration of Enterosgel to rats with experimental peptic ulcer and ulcerative colitis, significantly decreased the number and surface area of lesions on gastro-intestinal tract (GIT) mucosa and reduced the severity of the syndrome of endogenous intoxication that accompanied these injuries [21, 22]. The first evidence of clinical use of Enterosgel in combined therapy of peptic gastric ulcer and duodenum was reported by S.M. Tkach, who had noted that enterosorp-tion significantly reduced the number of side effects of treatment, and the rate of Helicobacter eradication increased from 83.3 to 93.3% [23]. 

Large doses of glucocorticoids have been associated with the development of peptic ulcer, possibly by suppressing the local immune response against Helicobacter pylori. They also promote fat redistribution in the body, with increase of visceral, facial, nuchal, and supraclavicular fat, and they appear to antagonize the effect of vitamin D on calcium absorption. The glucocorticoids also have important effects on the hematopoietic system. In addition to their effects on leukocytes, they increase the number of platelets and red blood cells. 

Helicobacter pylori is a bacterium that lives in the human stomach and duodenum. The bacterium is generally recognized as one of the etiological agents of peptic ulcer. Therefore, it is generally accepted that ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to anti-secretory drugs, whether on first... 

Gorden, P. Ferguson, J.H. Fauci, A.S. Conference sponsors, Helicobacter pylori in peptic ulcer disease. NIH Consensus Statement 1994 February 7-9, Bethesda National Institutes of Health, 1994.12 (1) pp. 1-23. 

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