The humoral immune response to Helicobacter pylori infection in children with recurrent abdominal pain.
The systemic humoral immune response to Helicobacter pylori antigens was investigated in 36 children with recurrent abdominal pain (RAP). H. pylori was cultured and Helicobacter-like organisms (HLO) were seen in six children, three of whom had active and two inactive chronic gastritis. None of these children had endoscopic abnormalities. All sex children had increased IgG antibodies to heat-stable H. pylori antigens which were of the IgG1 and IgG3 subclasses. Using six other IgG tests, four of which were commercially available, two to five H. pylori-positive children were found seropositive. Five of six H. pylori-negative children with inactive chronic gastritis and no endoscopic abnormalities had increased IgM antibody levels in addition to increased or borderline increased IgG antibody levels to H. pylori, indicating activity in a chronic H. pylori infection. Five children without H. pylori and with no morphological changes, but with gastritis or duodenitis by endoscopy, had significantly lower IgG and IgA antibody levels compared to other groups. Six of nineteen children without H. pylori, and with no morphological or endoscopic changes had increased IgG and IgM antibody levels to H. pylori. All H. pylori-negative children were seronegative by the four commercial kits. Overall, 12 (33%) of 36 children with RAP were either H. pylori positive by culture and microscopy or had increased IgG antibody levels to H. pylori, which is significantly different from the 10-14% seropositive rate of asymptomatic children. H. pylori may therefore be a cause of RAP in one quarter to one third of the children with RAP in whom other etiologies of RAP are excluded. Further studies on a large number of children are needed for an extended evaluation of the humoral immune response to H. pylori and for further examination of commercial kits which seem to give a high number of false-negative results.
Andersen
L P
LP
Department of Clinical Microbiology, National University, Rigshospitalet, Copenhagen, Denmark.
Wewer
A V
AV
Christiansen
K M
KM
Tvede
M
M
Hansen
J P
JP
Henriksen
F W
FW
Krasilnikoff
P A
PA
D015746:Abdominal Pain / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology*; D000293:Adolescent; D000907:Antibodies, Bacterial / Q000032:analysis / Q000276:immunology*; D000917:Antibody Formation / Q000276:immunology*; D015153:Blotting, Western; D002648:Child; D002675:Child, Preschool; D002908:Chronic Disease; D016099:Endoscopy, Gastrointestinal; D004797:Enzyme-Linked Immunosorbent Assay; D005188:False Negative Reactions; D005260:Female; D005756:Gastritis / Q000139:chemically induced / Q000175:diagnosis / Q000209:etiology; D016481:Helicobacter Infections / Q000150:complications* / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis / Q000276:immunology; D007074:Immunoglobulin G / Q000032:analysis / Q000276:immunology; D007075:Immunoglobulin M / Q000032:analysis / Q000276:immunology; D008297:Male; D012008:Recurrence
D000907:Antibodies, Bacterial; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M