Pathogenesis H pylori invade the epithelial cell surface to a certain degree ToXins and LP s may damage the mucosal cells NH3 produced by the urease activity may also damage the cells
Pathogenesis H pylori invade the epithelial cell surface to a certain degree Toxins and LPS may damage the mucosal cells NH3 produced by the urease activity may also damage the cells
Epidemiology 9%:0% 40% 0% SO% 80% 80% 20%
Epidemiology
Epidemiology e Prevalence related to socioeconomic level during childhood Infection occurs in childhood, persists for decades e Prevalence among adults -20%0-100% e Source- stomach of humans e Mode of transmission? Fecal-oral? oral-oral? Vomiting and aerosols e Incidence of HP colonization is declining in developed countries
Epidemiology Prevalence related to socioeconomic level during childhood. Infection occurs in childhood, persists for decades Prevalence among adults – 20%-100% Source – stomach of humans Mode of transmission? Fecal-oral? Oral-oral? Vomiting and aerosols ? Incidence of HP colonization is declining in developed countries
Epidemiology Under age 30 <20% At age 60 40-60% sIn developing countries >80% in adults e Acute epidemics of gastritis suggest a common source for H pylori
Epidemiology Under age 30 <20% At age 60 40-60% In developing countries >80% in adults Acute epidemics of gastritis suggest a common source for H pylori
Clnical features Acute acquisition-nausea, vomiting abdominal pain last for 1w, later-gastyftis e Persistent colonization -after acquisition persist for years. Asymptomatic ● Duodenal ulcer more than 90% with DU-carry HP antimicrobial therapy response, eradication of HP-less recurrences
Clinical features Acute acquisition - nausea, vomiting, abdominal pain last for 1w, later – gastritis. Persistent colonization - after acquisition, persist for years. Asymptomatic. Duodenal ulcer - more than 90% with DU - carry HP. - antimicrobial therapy response, eradication of HP - less recurrences