Anti-H.

pylori drugs
-shrey bhatia

found that it was present in patients with chronic gastritis and gastric ulcers . In 1982 Barry Marshall and Robin Warren.HELICOBACTER PYLORI Previously named Campylobacter pyloridis. is a Gram-negative. microaerophilic bacterium found in the stomach.

catalase. Microaerophilic.MORPHOLOGY Scanning spirochaete). It produces oxidase. 3. micrograph of H. and urease. helix-shaped (curved rod.5 pylori micrometres. It is capable of forming biofilms and can convert from spiral to a coccoid form . requires oxygen. About 3 micrometres long. It contains a hydrogenase which can be used hydrogen to obtain energy by oxidizing molecular (H2) produced by bacteria intestinal 5. 6. 4. notelectron 2. 1. diameter-0.

pylori survives the acidic pH of the stomach lumen • Uses its microenvironment.pylori INFECTION • H. pylori senses the pH gradient within the mucus layer by flagella to burrow into the mucus of stomach to reach its chemotaxis . close to the stomach's epithelial cell layer • H.PATHOPHYSIOLOGY OF H.

. The ammonia is converted to ammonium by accepting a proton (H+). which neutralizes gastric acid. pylori produces large amounts of the enzyme urease. surface. • Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia.CONTINUED • It swims towards the more neutral pH environment of epithelial cell • H.

pylori results in chronic gastritis • The inflammatory response to the bacteria induces G cells in the antrum to secrete the hormone gastrin. • Gastrin stimulates the parietal cells to secrete even more acid • The number of parietal cells to also increase. and ulceration may eventually result .CONTINUED • Colonization of the stomach by H. • The increased acid load damages the duodenum. further escalating the amount of acid secreted.

producing labelled carbon dioxide that can be detected in the breath) urea.or 13C-labelled metabolizes.LABORATORY DIAGNOSIS • Blood antibody test • Stool antigen test • Carbon urea breath test (in which the patient drinks 14C. which the bacterium .

pylori hydrolyzes urea to ammonia. • Microbial culture. and is placed into a medium containing urea and an indicator such as phenol red.continued Rapid urease test: A biopsy of mucosa is taken from the antrum. • Urine ELISA • . and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE) • Histological examination. The urease produced by H. which raises the pH of the medium.

which adds a Second line treatment ‘tripple theray’ done for bismuth colloid . require alternative strategies.pylori and allow the ulcer to heal one standard dose of proton pump inhibitor and two antibiotics 7-14days This is called First line treatment consists of Individuals harbouring antibiotic-resistant bacteria.TREATMENT The normal procedure is to eradicate H. such as a ‘quadruple therapy’.

lansoprazole 30 mg/day. qid = 4 times daily 14 days 14 days 10 days * Standard PPI doses: esomeprazole 40 mg/day. omeraprazole 20 mg/day. rabeprazole 20 mg/day . omeraprazole 20 mg/day.FIRST AND SECOND LINE THERAPIES bd*/clarithromycin 14First and second PPI standard dosemg bd/metronidazole 500 mg bd 500 mg days line therapies 7 days PPI standard dose bd*/clarithromycin 500 bd/amoxicillin 1000 mg 120 14 days PPI standard dose bd*/colloidal bismuth subcitrate bd mg qid**/tetracycline 500 mg qid**#/metronidazole 400 mg qid 10 days 5 days ofPPI standard dose bd*/clarithromycin 500 mg PPI standard dose bd*/amoxicillin 1000 mg bd bd/metronidazole 500 mg bd followed by 5 days of PPI standard dose bd*/clarithromycin 500 mg bd/ tinidazole 500 mg bd Third line (‘rescue/salvage’) therapies dose bd*/colloidal bismuth subcitrate 120 PPI standard 14 days PPI standard dose bd*/bismuth subcitrate 120 mg qid**/furazolidone 200 mg bd**/tetracycline qid mg qid/tetracycline 500 mg qid/metronidazole 500 mg 500 mg qid**# 14 days PPI standard dose bd*/amoxicillin 1000 mg bd/rifabutin 150 mg bd/ciprofloxacin1000 mg bd 5 days of PPI standard dose bd*/amoxicillin 500 mg bd * Standard PPI doses: esomeprazole 40 mg/day. rabeprazole 20 mg/day 5 days of PPI standard dose bd*/clarithromycin 500 mg ** Available from supplier once TGA-SAS approval is obtained (see Table 5) # Tetracycline cannot be replaced with doxycycline because of different pharmacokinetics bd/ tinidazole 500 mg bd bd = twice daily. followed by pantoprazole 40 mg/day. pantoprazole 40 mg/day. lansoprazole 30 mg/day.

pantoprazole 40 mg/day. rabeprazole 20 mg/day .THIRD LINE THERAPIES 14 days 14 days PPI standard dose bd*/bismuth subcitrate 120 mg qid/furazolidone 200 mg bd/tetracycline 500 mg qid PPI standard dose bd*/amoxicillin 1000 mg bd/rifabutin 150 mg bd/ciprofloxacin 500 mg bd * Standard PPI doses: esomeprazole 40 mg/day. omeraprazole 20 mg/day. lansoprazole 30 mg/day.

bismuth subcitrate potassium . bismuth subsalicylate. ppi should be continued once daily for 4-6 weeks to ensure complete ulcer healing Amoxicillin could be replaced with metronidazole for people who are allergic to penicillin Bismuth compounds have direct Examples- antimicrobial activity against H.pylori.After complition of triple therapy.

nausea. and altered taste GI upset. and headache Tends to be dose related. diarrhoea. diarrhoea. photosensitivity Darkening of the tongue and stool. a metallic taste. vomiting . headache.SIDE EFFECTS OF TREATMENT PPIs Headache and diarrhoea Clarithromycin Amoxicillin Metronidazole Gastrointestinal (GI) upset. and GI upset Nausea. vomiting. nausea. dyspepsia. Rash. diarrhoea. a disulfiram-like reaction with alcohol consumption Tetracycline Bismuth subcitrate Furazolidone Rifabutin GI upset. and malaise in up to a third of patients Red discoloration of urine while using the drug.

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