TY - JOUR
T1 - Relevance of CagA positivity to clinical course of Helicobacter pylori infection in children
AU - Yahav, J.
AU - Fradkin, A.
AU - Weisselberg, B.
AU - Diver-Haver, A.
AU - Shmuely, H.
AU - Jonas, A.
PY - 2000
Y1 - 2000
N2 - A potential virulence determinant of Helicobacter pylori is the cagA gene product. To determine the relevance of the expression of CagA to the clinical picture and outcome of H. pylori infection in children, we examined 104 consecutive children diagnosed with H. pylori infection. Serum samples were collected to test for the presence of immunoglobulin G (IgG) anti-CagA antibodies. Forty-five patients (43%) had antibodies to the CagA protein (group I), and 59 did not (group II). Seropositive patients had a longer prediagnostic history of abdominal pain (P = 0.02), more severe abdominal pain (defined as ulcer pain) (P = 0.05), a higher prevalence of duodenal ulcer (38 versus 7%; P < 0.01), more active chronic gastritis (82 versus 32%; P < 0.001), and a higher titer of serum IgG anti-H. pylori antibodies (P < 0.001). Ninety percent of the patients were monitored for 27 ± 18 months. On multivariate analysis, CagA-negative patients had a 3.8-fold-higher chance of achieving a disease-free state than CagA-positive patients (95% confidence interval, 1.5- to 9.5-fold). We conclude that infection with CagA-producing strains of H. pylori is a risk factor for severe clinical disease and ongoing infection.
AB - A potential virulence determinant of Helicobacter pylori is the cagA gene product. To determine the relevance of the expression of CagA to the clinical picture and outcome of H. pylori infection in children, we examined 104 consecutive children diagnosed with H. pylori infection. Serum samples were collected to test for the presence of immunoglobulin G (IgG) anti-CagA antibodies. Forty-five patients (43%) had antibodies to the CagA protein (group I), and 59 did not (group II). Seropositive patients had a longer prediagnostic history of abdominal pain (P = 0.02), more severe abdominal pain (defined as ulcer pain) (P = 0.05), a higher prevalence of duodenal ulcer (38 versus 7%; P < 0.01), more active chronic gastritis (82 versus 32%; P < 0.001), and a higher titer of serum IgG anti-H. pylori antibodies (P < 0.001). Ninety percent of the patients were monitored for 27 ± 18 months. On multivariate analysis, CagA-negative patients had a 3.8-fold-higher chance of achieving a disease-free state than CagA-positive patients (95% confidence interval, 1.5- to 9.5-fold). We conclude that infection with CagA-producing strains of H. pylori is a risk factor for severe clinical disease and ongoing infection.
UR - http://www.scopus.com/inward/record.url?scp=0033778611&partnerID=8YFLogxK
U2 - 10.1128/jcm.38.10.3534-3537.2000
DO - 10.1128/jcm.38.10.3534-3537.2000
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AN - SCOPUS:0033778611
VL - 38
SP - 3534
EP - 3537
JO - Journal of Clinical Microbiology
JF - Journal of Clinical Microbiology
SN - 0095-1137
IS - 10
ER -