Helicobacter therapy

PPI treatment leads to dose-dependent inhibition of H. pylori in the stomach [11, 12]. The explanation for this effect comes from in vitro observations. At high pH values, in the presence of urea and a weak buffer, urease activity produces very high periplasmatic pH values which are bactericidal [13-16]. The detailed explanation of this mechanism is given in the chapter dealing with interactions between PPIs and H. pylori in vitro. This inhibition is, in our view, the major explanation of the adjuvant effect of PPIs during anti-i/. pylori therapy. Other effects, such as a PPI-induced increase of antibiotic secretion by the gastric epithelium [17] and a diminished inactivation of antibiotics by lowered gastric acid [18], may play a less important role. The suppressive effect of PPIs on H. pylori is the basis for anti-Helicobacter therapies with a PPI plus one or, preferably, two antibiotics [19, 20]. 

Reliance on conventional antiulcer drug therapy as an alternative to Helicobacter pylori (HP) eradication is discouraged because it is associated with a higher incidence of ulcer recurrence and side effects. 

Helicobacter pylori treatment regimens are presented in Table 15-3. Eradication therapy with a PPI-based three-drug regimen should be considered for all patients who test positive for HP and have an active ulcer or a documented history of either an ulcer or ulcer-related complication. Different antibiotics should be used if a second course of HP eradication therapy is required. 

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... 

Losec (omeprazole) Duodenal ulcer Gastro-oesophageal reflux Helicobacter infections 5.7 1.9 1989 - UK and US Once daily, except when used as part of combination therapy... 

Furuta T, Shirai N, Takashima M et al. Effect of genotypic differences in CYP2C19 on cure rates for Helicobacter pylori infection by triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin. Clin Pharmacol Ther 2001 69[3] 158—168. 

Gisbert JP, Pajares JM Helicobacter pylori rescue regimen when proton pump inhibitor-based triple therapies fail. Aliment Pharmacol Ther 2002 16 1047-1057. 

Gisbert JP, Calvet X, Bujanda L, Marcos S, Gisbert JL, Pajares JM Rescue therapy with rifabutin after multiple Helicobacter pylori treatment failures. Helicobacter 2003 8 90-94. 

Wong WM, Gu Q, Lam SK, Fung FM, Lai KC, Hu WH, Yee YK, Chan CK, Xia HH, Yuen MF, Wong BC Randomized controlled study of rabeprazole, levofloxacin and rifabutin triple therapy vs. quadruple therapy as second-line treatment for Helicobacter pylori infection. Aliment Pharmacol Ther 2003 17 553-560. 

Perri F, Festa V, Clemente R, Quitadamo M, Andriulli A Rifabutin-based rescue therapy for Helicobacter pylori infected patients after failure of standard regimens. Aliment Pharmacol Ther 2000 14 311—316. 

Zullo A, Hassan C, Campo S, Morini S Evolving therapy for Helicobacter pylori infection. Exp Opin Ther Patents 2004 14 1453-1464. 

G, Gasbarrini A Effect of Lactobacillus GG supplementation on antibiotic-associated gastrointestinal side effects during Helicobacter pylori eradication therapy A pilot study. Digestion 2001 63 1-7. 

Aging is one of the major risk factors for developing gastric ulcers because of an increased incidence of Helicobacter pylori infections and a widely spread use of non-steroidal anti-inflammatory drugs (NSAID). Co-morbidity, with the need for prophylactic medication with antiplatelet therapy, warfarin and other anticoagulants, also increases the risk of gastrointestinal bleeding and ulcerations (Murakami et al. 1968). 

Schwab, M., Schaeffeler, E., Klotz, U., and Treiber, G. (2004) CYP2C19 polymorphism is a major predictor of treatment faUure in white patients by use of lansoprazole-based quadruple therapy for eradication of Helicobacter pylori. Clin. Pharmacol. Ther. 76, 201-209. 

The therapy prescribed is a 1-week triple therapy regimen consisting of amoxicillin, clarithromycin and omeprazole against Helicobacter pylori infection. 

Clarithromycin is a macrolide that has a longer half-life than erythromycin so is administered twice daily. Clarithromycin is more active against Grampositive organisms than erythromycin. Clarithromycin may be used in combination with amoxicillin, for example, as part of triple therapy used for the eradication of Helicobacter pylori. 

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. 

Healed duodenal ulcer, gastroesophageal reflux disease PO 15 mg/day Helicobacter pylori infection PO (Triple drug therapy) 30mgql2hfor 1 OH 4 days. PO (Dual drug therapy) 30 mg q8h for 14 days. 

Helicobacter pylori duodenal ulcer PO 20 mg once daily or 40 mg/day as a single or in 2 divided doses in combination therapy with antibiotics. Dose varies with regimen used. 

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]. 

Jafri NS et al Meta-analysis Sequential therapy appears superior to standard therapy for Helicobacter pylori infection in patients naive to treatment. Ann Intern Med 2008 148 923. [PMID 18490667]... 

Finally, it is universally accepted at present that Helicobacter pylori infection has a definitive ethiological role in peptic ulcer disease, and that erradication therapy is warranted in these clinical scenarios. The majority of therapeutic trials have included the application of triple therapy with proton pump inhibitors or ranitidine bismuth citrate, clarithromycin and either amoxycillin or metronidazol and is to date the treatment of choice. However, recent studies have reported antibiotic resistance which can be one reason for failure of treatment of Helicobacter pylori infection [101-103], and new treatment strategies are therefore Wellcome. Flavonoids, in addition to their gastroprotective activity previously commented, have been also shown to inhibit Helicobacter pylori growth in vitro. In this way, Beil et al. [50]... 

For the eradication of Helicobacter pylori in peptic ulceration, omeprazole may be combined with antibacterials in dual or triple therapy. Effective triple therapy regimens include omeprazole 20 mg twice daily combined with amoxycillin 500 mg and metronidazole 400 mg, both three times daily clarithromycin 500 mg and metronidazole 40 mg (or tinidazole 500 mg) both twice daily or with amoxycillin 1 g and clarithromycin 500 mg both twice daily. These regimens are given for 1 week. Dual therapy regimens, such as omeprazole 40 mg daily with either amoxycillin 750 mg to 1 g twice daily or clarithromycin 500 mg three times daily, are less effective and must be given for 2 weeks. Omeprazole alone may be continued for a further 4r-8 weeks [1]. 

P.S. Phule, et al., Are weak treatment for Helicobacter pylori infects A randomized study of quadruple therapy versus triple therapy. J. Antimicrob. Chemother. 36 1085-1088, 1995. 

Petersen U, et al. Verwendung von 7-( 1-Aminomethyl-2-oxa-7-aza-bicy-clo[3.3.0]oct-7-yl)-chinoloncarbonsaure-und -naphthyridoncarbonsaure-Deriva-ten zur Therapie von Helicobacter pylori-Infektionen und den damit assoziierten gastroduodenalen Erkrankungen. 1996. Bayer AG DE 19 652 219. 

Helicobacter pylori infection 20 mg p.o. b.i.d. in conjunction with triple therapy... 

Azuma T, Ito S, Suto H, et al. (2000) Pharmacokinetics of clarithromycin in Helicobacter pylori eradication therapy in patients with liver cirrhosis. Aliment Pharmacol Ther 14 (Suppl 1) 216-222. 

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