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Stuart Jon Spechler, MD; Lori Fischbach, PhD; Mark Feldman, MD

JAMA. 2000;283:1264-1266.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Helicobacter Pylori organisms have been infecting human stomachs for centuries. Antigens of these microaerophilic, gram-negative bacteria have been found in stool samples of ancient mummies.¹ Today, it appears that more than half of the world's population is infected with H pylori.² These organisms are adapted for survival in the stomach in which infection causes a chronic gastritis that persists for decades.

H pylori infection is strongly associated with peptic ulcer disease, and is widely accepted as a risk factor for gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma.³ Antibiotic therapy aimed at eradicating H pylori is recommended for infected patients who have verified peptic ulcerations of the stomach or duodenum, or who have gastric MALT lymphomas.⁴ Nevertheless, it has been estimated that less than 20% of individuals who are chronically infected with H pylori ever develop a peptic ulcer . . . [Full Text of this Article]

Genetic Variability and Virulence

Clinical and Epidemiological Aspects of CagA Positivity

Current Recommendations and Directions for Future Research

Author Affilations: Department of Veterans Affairs Medical Center, Dallas (Drs Spechler and Feldman), University of Texas Southwestern Medical Center (Drs Spechler, Fischbach, and Feldman), School of Public Health (Dr Fischbach); and the University of Texas Health Science Center, Houston (Dr Fischbach).

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