BACKGROUND: Infection by Helicobacter pylori (Hp) has been linked to extradigestive pathologies including ischemic cerebral disease. The aim of our study was to assess the relationship between chronic Hp infection and ischemic stroke risk factors. MATERIAL/ METHODS: 80 patients (pts) aged 60-75 years with ischemic stroke confirmed by CT scans (group I) and 80 age- and gender-matched healthy controls (group II) were included into trial. Atherosclerotic plaques from 20 Hp positive pts were obtained at carotid endarterectomy for Hp DNA assessment by PCR. In all groups following parameters were determined; 1) the prevalence of Hp infection using (13)C-Urea Breath Test (UBT), 2) plasma anti-Hp and anti-CagA IgG and interleukin-8 (IL-8), and 3) plasma lipids and fibrinogen. Hp positive pts and controls received one-week anti-Hp therapy and after six months total cholesterol, low-density lipoprotein (LDL)-cholesterol, fibrinogen and IL-8 levels were re-examined. RESULTS: Hp infection was detected by UBT in 83.75% of stroke pts but only in 65% of controls. CagA seropositivity was also significantly higher in stroke pts (57.5%) than in controls (33.75%). Plasma levels of cholesterol, LDL-cholesterol and fibrinogen as well as IL-8 were significantly higher in Hp positive subjects, especially in pts with ischemic stroke. Six months following successful anti-Hp therapy, the plasma levels of total cholesterol, LDL-cholesterol, fibrinogen and IL-8 were significantly lower than those in Hp positive stroke pts and controls. CONCLUSIONS: Hp infection represents risk factor of ischemic stoke via an interaction of Hp cytotoxins or cytokines with atherosclerotic plaques in carotic arteries.
BACKGROUND:Infection by Helicobacter pylori (Hp) has been linked to extradigestive pathologies including ischemic cerebral disease. The aim of our study was to assess the relationship between chronic Hp infection and ischemic stroke risk factors. MATERIAL/ METHODS: 80 patients (pts) aged 60-75 years with ischemic stroke confirmed by CT scans (group I) and 80 age- and gender-matched healthy controls (group II) were included into trial. Atherosclerotic plaques from 20 Hp positive pts were obtained at carotid endarterectomy for Hp DNA assessment by PCR. In all groups following parameters were determined; 1) the prevalence of Hp infection using (13)C-Urea Breath Test (UBT), 2) plasma anti-Hp and anti-CagA IgG and interleukin-8 (IL-8), and 3) plasma lipids and fibrinogen. Hp positive pts and controls received one-week anti-Hp therapy and after six months total cholesterol, low-density lipoprotein (LDL)-cholesterol, fibrinogen and IL-8 levels were re-examined. RESULTS:Hp infection was detected by UBT in 83.75% of strokepts but only in 65% of controls. CagA seropositivity was also significantly higher in strokepts (57.5%) than in controls (33.75%). Plasma levels of cholesterol, LDL-cholesterol and fibrinogen as well as IL-8 were significantly higher in Hp positive subjects, especially in pts with ischemic stroke. Six months following successful anti-Hp therapy, the plasma levels of total cholesterol, LDL-cholesterol, fibrinogen and IL-8 were significantly lower than those in Hp positive strokepts and controls. CONCLUSIONS:Hp infection represents risk factor of ischemic stoke via an interaction of Hp cytotoxins or cytokines with atherosclerotic plaques in carotic arteries.