Abstract
background: NAFLD patients had higher anti IgG H pylori and might be a clue that H
pylori infection had a strong link the pathogenesis of early stage NAFLD mostly had
simple steatosis. H pylori infection had a role in pathogenesis of IR and NAFLD. H
pylori is strong inducer of pro inflammatory cytokine (IL6, IL8, TNF- α).Serum
triglyceride was higher in H pylori positive group and NASH. Recent study have investigated
weather H pylori induce insulin resistance mediated through fetuin which decrease in patients
with sero positive Hpylori IgG patients.
and
Patient and method: Fifty six patients were collecting randomly as a case of fatty liver by
ultrasound In Imam AL- Hussain Medical City in Karbala .Obese, DM, alcoholic patients,
renal
hepatic
diseases
were
exclude
from
study.
Fasting blood sample was taken and sent for IgG antibody H pylori, lipid profile, liver
function test including ALT and AST.
this
Result: The mean age of patients was 45+10 and majority (65%) was females.
(67)% of patients who were fatty liver had Hpylori sero positive IgG (p value<0.05).
(66)% of patients who were fatty liver had normal liver function ALT mean±SD(31±7) and
only 34% had increased liver function, ALT mean SD±(110±13)with p value<0.01.
(71)% of patients who were fatty liver and H pylori sero positive IgG had normal liver
function mostly ALT mean±SD (29±10) in comparism with 29% who had increase liver
function mostly ALT mean ±SD(98±18) p value <0.01.
(83)% of fatty liver patients had hyperlipidaemia mean±SD (290±20), (395±22) respectively
p value<0.01.
(75)% of fatty liver patients with H pylori sero positive IgG had hyperlipidaemia mean±SD
(279±15),(320±20) respectively p value <0.01.
Conclusion This study shown significant correlation between chronic H pylori infection and
NAFLD .The pathogenic mediator include fetuin-A, TNF-α and adiponectin and on long term
IR.
pylori infection had a strong link the pathogenesis of early stage NAFLD mostly had
simple steatosis. H pylori infection had a role in pathogenesis of IR and NAFLD. H
pylori is strong inducer of pro inflammatory cytokine (IL6, IL8, TNF- α).Serum
triglyceride was higher in H pylori positive group and NASH. Recent study have investigated
weather H pylori induce insulin resistance mediated through fetuin which decrease in patients
with sero positive Hpylori IgG patients.
and
Patient and method: Fifty six patients were collecting randomly as a case of fatty liver by
ultrasound In Imam AL- Hussain Medical City in Karbala .Obese, DM, alcoholic patients,
renal
hepatic
diseases
were
exclude
from
study.
Fasting blood sample was taken and sent for IgG antibody H pylori, lipid profile, liver
function test including ALT and AST.
this
Result: The mean age of patients was 45+10 and majority (65%) was females.
(67)% of patients who were fatty liver had Hpylori sero positive IgG (p value<0.05).
(66)% of patients who were fatty liver had normal liver function ALT mean±SD(31±7) and
only 34% had increased liver function, ALT mean SD±(110±13)with p value<0.01.
(71)% of patients who were fatty liver and H pylori sero positive IgG had normal liver
function mostly ALT mean±SD (29±10) in comparism with 29% who had increase liver
function mostly ALT mean ±SD(98±18) p value <0.01.
(83)% of fatty liver patients had hyperlipidaemia mean±SD (290±20), (395±22) respectively
p value<0.01.
(75)% of fatty liver patients with H pylori sero positive IgG had hyperlipidaemia mean±SD
(279±15),(320±20) respectively p value <0.01.
Conclusion This study shown significant correlation between chronic H pylori infection and
NAFLD .The pathogenic mediator include fetuin-A, TNF-α and adiponectin and on long term
IR.