Second Asia–Pacific Consensus Guidelines for Helicobacter pylori infection
Journal Articles
Overview
Research
Identity
Additional Document Info
View All
Overview
abstract
AbstractThe Asia–Pacific Consensus Conference was convened to review and synthesize the most current information on Helicobacter pylori management so as to update the previously published regional guidelines. The group recognized that in addition to long‐established indications, such as peptic ulcer disease, early mucosa‐associated lymphoid tissue (MALT) type lymphoma and family history of gastric cancer, H. pylori eradication was also indicated for H. pylori infected patients with functional dyspepsia, in those receiving long‐term maintenance proton pump inhibitor (PPI) for gastroesophageal reflux disease, and in cases of unexplained iron deficiency anemia or idiopathic thrombocytopenic purpura. In addition, a population ‘test and treat’ strategy for H. pylori infection in communities with high incidence of gastric cancer was considered to be an effective strategy for gastric cancer prevention. It was recommended that H. pylori infection should be tested for and eradicated prior to long‐term aspirin or non‐steroidal anti‐inflammatory drug therapy in patients at high risk for ulcers and ulcer‐related complications. In Asia, the currently recommended first‐line therapy for H. pylori infection is PPI‐based triple therapy with amoxicillin/metronidazole and clarithromycin for 7 days, while bismuth‐based quadruple therapy is an effective alternative. There appears to be an increasing rate of resistance to clarithromycin and metronidazole in parts of Asia, leading to reduced efficacy of PPI‐based triple therapy. There are insufficient data to recommend sequential therapy as an alternative first‐line therapy in Asia. Salvage therapies that can be used include: (i) standard triple therapy that has not been previously used; (ii) bismuth‐based quadruple therapy; (iii) levofloxacin‐based triple therapy; and (iv) rifabutin‐based triple therapy. Both CYP2C19 genetic polymorphisms and cigarette smoking can influence future H. pylori eradication rates.
