Helicobacter pylori Infection Is Not Associated With Specific Symptoms
in Nonulcer-Dyspeptic Children
Nicolas Kalach, MD, PhD*; Karine Mention, MD‡; Dominique Guimber, MD‡; Laurent Michaud, MD‡;
Claire Spyckerelle, MD*; and Fréderic Gottrand, MD, PhD‡
ABSTRACT. Objectives. To assess symptoms associ-
ated with Helicobacter pylori infection in children pre-
senting with nonulcer dyspepsia (NUD).
Study Design. A prospective double-blind study was
conducted between March 2001 and April 2002 in chil-
dren at least 6 years old with NUD who had been re-
ferred for upper gastrointestinal endoscopy for epigastric
pain. A standardized questionnaire was administered
blindly by a pediatric gastroenterologist. This question-
naire characterized epigastric pain and associated factors.
Infection was confirmed by positive culture and histo-
logic examination of the gastric mucosa.
Results. From 100 children enrolled, 26 proved in-
fected (12 female, 14 male; mean age: 11.4 ⴞ 2.6 years),
and 74 were noninfected (44 female, 30 male; mean age:
10.4 ⴞ 3.1 years). There were no differences in age or
symptom characteristics between groups except for epi-
gastric pain during meals that was more frequent in
noninfected than in infected children (25.6% vs 3.8%).
Conclusion. There were no specific characteristics of
symptoms in nonulcer-dyspeptic H pylori–infected chil-
dren as compared with noninfected children. Pediatrics
2005;115:17–21; Helicobacter pylori, nonulcer dyspepsia,
recurrent abdominal pain, children.
ABBREVIATIONS. RAP, recurrent abdominal pain; NUD, nonul-
cer dyspepsia; GI, gastrointestinal.
T
he role of Helicobacter pylori in the colonization
of the stomach in adults and children with
chronic gastritis, peptic ulcer, and possibly
gastric carcinomas is now well documented,1 and
eradication of the bacteria is very effective in pre-
venting peptic-ulcer relapses in both adults2 and
children.3
Recurrent abdominal pain (RAP), according to Ap-
ley’s criteria (ie, at least 3 discrete episodes of ab-
dominal pain of sufficient severity to interrupt nor-
mal daily activities or performance, occurring over a
period of ⱖ3 months4), and nonulcer dyspepsia
(NUD), which refers to pain or discomfort centered
From the *Department of Pediatrics, Clinique de Pédiatrie Saint Antoine,
Hôpital Saint Vincent de Paul, Catholic University, Lille, France; and ‡De-
partment of Pediatric Gastroenterology, Hepatology, and Nutrition, Hôpital
Jeanne de Flandre, Faculty of Medicine, Lille, France.
Accepted for publication Jun 14, 2004.
doi:10.1542/peds.2004-0131
No conflict of interest declared.
Reprint requests to (N.K.) Department of Pediatrics, Clinique de Pédiatrie
Saint Antoine, Hôpital Saint Vincent de Paul, Catholic University, Boule-
vard Belfort, BP 387, 59020 Lille, France. E-mail: kalach.nicolas@ghicl.net
PEDIATRICS (ISSN 0031 4005). Copyright © 2005 by the American Acad-
emy of Pediatrics.
Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020
in the upper abdomen,5 are difficult conditions to
define in children, because many have imprecise
symptoms. Moreover, the role and clinical manifes-
tations of H pylori remain unclear in such children.
Vomiting and acute abdominal pain related to ulcer
disease may be associated with H pylori infection,
whereas the role of this bacterium in children with
RAP and NUD is the subject of conflicting reports.
Localized epigastric pain6 and nocturnal awaken-
ing7,8 have been reported occasionally in children
with this infection. However, a high incidence of H
pylori infection in the course of RAP does not prove
a causal relationship between this infection and ab-
dominal pain.9
Recently, a European pediatric consensus recom-
mended a search for H pylori infection using upper-
gastrointestinal (GI) endoscopy with gastric biopsy
in children suffering from upper-digestive symp-
toms suggestive of organic disease without any ad-
ditional clear information on the nature of these
symptoms.10
There have been several proposals to define crite-
ria for functional GI dyspepsia in children mature
enough to provide an accurate history of pain.5 Func-
tional dyspepsia is subdivided into 3 forms: ulcer-
like dyspepsia, characterized by a centered pain in
the upper abdomen (epigastric pain); dysmotility-
like dyspepsia, characterized by unpleasant discom-
fort centered in the upper abdomen or associated
with upper abdominal fullness, early satiety, bloat-
ing, or nausea; and unspecified dyspepsia.5 The use
of refined clinical characteristics of RAP could be of
help in identifying a subgroup of patients with RAP,
in whom H pylori infection might need investigation
and treatment.11 The aim of this study was therefore
to characterize the symptoms in H pylori–infected
children with NUD.
PATIENTS AND METHODS
A prospective, bicentric, double-blind study was conducted
between March 2001 and April 2002 in children with NUD re-
ferred from pediatricians after clinical and biological assessment
for upper-GI endoscopy because of epigastric pain. A standard-
ized questionnaire was administered blindly by a pediatric gas-
troenterologist on the same day of the endoscopy (before the
procedure was done) and therefore before we had any knowledge
of the patient’s H pylori status. Only patients ⱖ6 years old were
enrolled, with the assumption that they were mature enough to
provide an accurate history of their pain characteristics.
A figure showing the localization of the epigastric region was
first shown and explained to all the enrolled children. Epigastric
pain and tenderness were identified by a pediatric gastroenterol-
ogist after careful clinical assessment. Then a questionnaire was
PEDIATRICS Vol. 115 No. 1 January 2005
17
administered that asked the children to describe the characteristics
of their epigastric pain, namely its intensity, using a visual analog
scale (from 0- to 100-mm extreme ends; 0 indicated the absence of
pain, and 100 indicated the highest degree of pain), and frequency
(days per week). Other items included any occurrence of daytime
or nocturnal awakening; epigastric tenderness; relationship of
pain episodes with eating (before, during, or after); nausea, epi-
sodes of vomiting, or weight loss (⬎5% of the last body weight).
The questionnaire also recorded any episodes of hematemesis, any
drugs taken during the last month (antispasmodics or analgesics),
any school absences, and any family history of peptic-ulcer dis-
ease.
The socioeconomic levels of the enrolled children and the num-
bers of people in their household were recorded. The ethnic back-
ground of each child was defined as European (“white”), North
African, Middle Eastern, African, Asian, or Far Eastern, according
to the mother’s place of birth. The mother’s education level was
defined as unschooled, primary plus secondary school (high
school), or tertiary. The father’s socioeconomic level was defined
as unemployed, low, intermediate, or high according to the French
national social classification system.
We excluded children ⬍6 years old; those who had already
suffered gastric H pylori infections; institutionalized encephalo-
pathic children; and children who had received antibiotics, acid-
suppressing medications, or a nonsteroidal antiinflammatory
drug during the month preceding evaluation.
H pylori infection was confirmed by positive culture as de-
scribed12 and by histologic examination (Sydney classification) of
gastric antral and fundic biopsy specimens. Noninfected children
were defined as those who exhibited negative H pylori cultures
and negative histologic findings from their gastric mucosa. Cul-
tures and histologic examinations of biopsy samples were con-
ducted blindly. Informed consent was obtained from the parents
of all the enrolled patients.
All statistical tests were performed by using StatView software
(Abacus, CA). Means, SDs, medians, and extremes were calculated
for all quantitative parameters. Differences between qualitative
parameters were analyzed by using ␹2 tests. A P value of ⬍ .05
was taken as statistically significant.
RESULTS
One hundred children were enrolled: 68 from
Saint Antoine Hospital and 32 from Lille University
Hospital. They included 56 females and 44 males,
with a median age of 11 years (range: 6 –17 years).
There were 26 H pylori–infected children (mean age:
11.4 ⫾ 2.6 years; 12 females and 14 males) and 74
noninfected children (mean age: 10.4 ⫾ 3.1 years; 44
females and 30 males). The distribution of age and
gender did not differ significantly between groups.
There were no differences between centers in the
prevalence of H pylori infection or the distributions of
age, gender ratio, symptom characteristics, educa-
tion outcome, or socioeconomic levels. There were
TABLE 1. Symptom Characteristics in Nonulcer-Dyspeptic H pylori–Infected and Noninfected Children, n ⫽ 100 (Means ⫾ SD)
H pylori–Infected Children
Age, mo
Gender 12 females, 14 males
RAP characteristics
RAP intensity (visual analog scale), value/100
RAP frequency, days per week
Diurnal (daytime) pain
Nocturnal pain (nocturnal awakening)
Epigastric tenderness at palpation
Other localizations of RAP
RAP before meals
RAP during meals
RAP after meals
NS indicates not significant.
* ␹2 test, P ⬍ .05.
18 H PYLORI AND RECURRENT ABDOMINAL PAIN
Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020
no children presenting with ulcer disease during the
study period.
There were no differences for most of the symp-
tom characteristics when comparing infected with
noninfected children. These characteristics included
histories of nausea (12 of 26 [46.1%] vs 35 of 74
[47.2%]), vomiting (10 of 26 [38.1%] vs 27 of 74
[36.1%]), weight loss (1 of 26 [3.8%] vs 6 of 74 [8.1%]),
hematemesis (1 of 26 [3.8%] vs 2 of 74 [2.7%]), no
drugs being taken (10 [38.1%] vs 36 [48.6%]), a pos-
itive family history of peptic-ulcer disease (16 of 26
[61.5%] vs 36 of 74 [48.6%]), or durations of school
absence (2.6 ⫾ 4.2 vs 4.5 ⫾ 10.1 days) (Table 1).
By contrast, H pylori–infected children exhibited
less frequent epigastric pain during meals than non-
infected children (1 of 26 [3.8%] vs 19 of 74 [25.6%]; P
⬍ .01) (Table 1).
As expected, H pylori infection was more frequent
in nonwhite than in white children (15 of 26 [57.6%]
vs 9 of 74 [12.2%]; P ⬍ .0003) and among those with
low educational backgrounds and socioeconomic
levels (26 of 26 [100%] vs 62 of 74 [83.7%] and 19 of
26 [73%] vs 32 of 74 [43.2%], respectively; P ⬍ .05 for
both).
Finally, H pylori–infected children demonstrated
any erosive esophagitis compared with noninfected
children (7 of 74 [9.4%]; P ⫽ not significant), and H
pylori–infected children more frequently demon-
strated nodular gastritis (19 of 26 [73%]) compared
with noninfected children (7 of 74 [9.4%]; P ⬍ .001).
Surprisingly, the noninfected children more fre-
quently exhibited macroscopic aspects of gastritis at
endoscopy (55 of 74 [74.4%]) rather than mild histo-
logic gastritis (Table 2). H pylori–infected children
demonstrated nodular bulbitis and duodenitis (5 of
26 [19.2%]) compared with noninfected children (3 of
74 [4.1%]; P ⫽ not significant).
DISCUSSION
Despite a strict selection of our population, focus-
ing on children with epigastric-like NUD, we could
not detect any specific symptoms in nonulcer-dys-
peptic children infected with H pylori.
It is unknown whether H pylori gastritis causes
symptoms in children lacking gastric or duodenal
ulcers.9,13–15 Two types of studies have sought to
address the association of H pylori infection with
H pylori–Noninfected Children P*
(n ⫽ 26) (n ⫽ 74)
137 ⫾ 32 125 ⫾ 38
44 females, 30 males NS
71 ⫾ 15 66 ⫾ 20 NS
4.1 ⫾ 1.9 4.4 ⫾ 2.3 NS
25 (96.1%) 73 (98.6%) NS
9 (34.6%) 26 (35.1%) NS
15 (57.6%) 42 (56.7%) NS
12 (46.1%) 34 (45.1%) NS
7 (26.9%) 15 (20.2%) NS
1 (3.8%) 19 (25.6%) .01
18 (69.2%) 40 (54%) NS
 TABLE 2. Histological Characteristics of the Enrolled Children According to Sydney Classifica-
tion†, n ⫽ 100
H pylori–Infected Children
(N ⫽ 26), n (%)
Inflammation grade
0 0
1 6 (23)
2 14 (53.8)
3 6 (23)
Activity grade
0 1 (3.8)
1 16 (61.5)
2 9 (34.6)
NS indicates not significant.
* ␹2 test, P ⬍ .05
† None of the enrolled children exhibited either atrophic or dysplasia of gastric mucosa.
RAP and dyspepsia in children and adults.16 The
first approach investigates the possible association
between H pylori infection and RAP; the second ap-
proach studies whether the eradication of H pylori
infection results in the resolution of symptoms.16
Dyspepsia is poorly characterized in children. Hy-
ams et al,17 in a prospective study on subjects with
dyspepsia and dyspepsia subtypes (ulcer-like and
dysmotility-like), showed that H pylori infection was
unusual. They found only 5 cases out of the 127
subjects fulfilling their criteria for dyspepsia and
concluded that most children with dyspepsia do not
have serious disease.17 Similar results were found by
another study, in which organic abnormalities in the
course of RAP were detected in only 45% of children,
and H pylori infection was found in only 1 of 44.18
However, several authors have suggested that night-
time pain associated with nocturnal awakening, fast-
ing pain relieved by food, pain associated with
meals, postprandial pain, bitter taste, and heartburn
are the clinical signs that help to distinguish ulcer-
positive children from those who are ulcer-negative
yet positive for H pylori infection.19
We found here that the noninfected children more
frequently exhibited epigastric pain during meals
than did the infected ones. However, this clinical
feature was not clinically significant in the nonin-
fected group, because only 26% exhibited epigastric
pain during meals and 74% did not. The absence of
specific characteristics of RAP between these 2
groups in our study could be related either to the
difficulty of children in describing their symptoms
precisely or to an inappropriate selection of our pop-
ulation based on their symptoms, which could have
caused a bias toward the reflux-like group. However,
the prevalence of endoscopic esophagitis was very
weak in the studied children and varied from none in
the infected children to only 9.4% in the noninfected
ones. Moreover, considering results, we observed
that calculation of the required statistical power for
the number of enrolled children to demonstrate a
significant difference between both groups did not
show any difference concerning most clinical dys-
peptic manifestations.
On the other hand, in this study we have an ex-
tremely high prevalence of macroscopic gastritis in
the noninfected children. As a matter of fact, our
results in this highly selected population of children
Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020
H pylori–Noninfected Children P*
(N ⫽ 74), n (%)
21 (28.3) .004
46 (62.1) .005
5 (6.7) .0001
2 (2.7) .0003
61 (82.5) .00001
13 (17.5) .0008
0 .001
with epigastric pain are in agreement with the results
of Snyder et al,20 in which primary antral gastritis
was found in ⬃20% of the 4 different age groups of
408 children studied, in contrast with only 4 of 39
children ⬍10 years old with primary antral gastritis
who had evidence of H pylori infection.
The main feature of this study is that we only
selected children with epigastric-like NUD and that
we detailed the characteristics of their abdominal
pain. Thus, this study differs from other published
studies in which the characteristics of RAP were not
fully described12,21 or were limited to an imprecise
definition of RAP.22 Our hypothesis was that the use
of refined clinical characteristics for describing RAP
could be of help in identifying a subgroup of patients
with this condition in whom H pylori infection might
need to be investigated and treated.11 Our study also
used a rigorous double-blind approach, taking into
account the usual factors associated with infection:
socioeconomic level, the number of subjects in the
same household, and ethnic background.
Children with H pylori–associated gastritis are of-
ten asymptomatic, but a small minority of infected
subjects will experience complications of peptic ulcer
and gastric cancers including adenocarcinoma and
lymphoma.23–25 Fiedorek et al26 studied 245 healthy
children for evidence of H pylori colonization and
found that 30% of them were colonized. Blecker et
al24 investigated 466 asymptomatic children for evi-
dence of H pylori infection by using specific serum
containing H pylori antibodies and found the preva-
lence of H pylori infection to increase from 5.4% to
13.4% with increasing age. Moreover, Bode et al,27 in
a large epidemiologic study of healthy children, also
showed that H pylori infection was not a cause of GI
symptoms. In addition, a Dutch study failed to detect
any difference in the prevalence of H pylori antibod-
ies between children with RAP by using Apley’s
criteria and asymptomatic controls.28 Hardikar et al29
conducted a prospective case-control study in chil-
dren with RAP, testing for serum anti–H pylori IgG
antibodies: 5 subjects (5%) and 14 controls (14%) had
raised serum antibody titers, indicating a negative
association between this infection and RAP. Contro-
versially, Chong et al30 found that the incidence of
positive anti–H pylori IgG antibodies was signifi-
cantly higher in children with RAP (17.4%) than in
those without (10.5%).
ARTICLES 19
 Glassman et al21 assessed the presence of abdom-
inal pain and vomiting in children undergoing up-
per-GI endoscopy; no difference was detected be-
tween H pylori–infected children and those without
infection in regard to their clinical manifestations.
Mahony et al31 also found that the presence of epi-
gastric pain did not discriminate between children
with H pylori gastritis and those with a normal mu-
cosa. Another retrospective study reviewed the
symptomatology of 143 children referred for up-
per-GI endoscopy because of RAP for ⱖ6 weeks; H
pylori infection was diagnosed in only 25.2% of chil-
dren, and no statistically significant differences
could be detected between the symptoms experi-
enced by H pylori–infected children as compared
with those not infected.22 Our previous experience is
in agreement with those reports: we found that RAP
was not significantly present in 63% of patients with
H pylori versus 49% of a control group of 74 age-
matched children negative for H pylori.12,32 A meta-
analysis of 45 studies has shown that the reported
prevalence rates of H pylori infection in children un-
dergoing upper endoscopy for RAP are inconsistent
(median: 22%; range: 0-81%), with lower rates in
children meeting Apley’s criteria (median: 6%; range:
0-9%).33 Our study is in agreement with these stud-
ies: we found no significant difference between H
pylori–infected and –noninfected children either in
the intensity and frequency of RAP or in the other
symptoms. These results suggest that there is no
evidence for an association of this infection with RAP
even in a subgroup of children presenting with epi-
gastric-type NUD.33
The evidence supporting an association between H
pylori gastritis and RAP is based on studies in which
the authors have reported an improvement in symp-
toms after treatment.34–42 On the other hand, contro-
versial results were obtained by a Scandinavian
study conducted in nonulcer-dyspeptic H pylori–in-
fected children in which a long-term follow-up study
after treatment with colloidal bismuth subcitrate and
tinidazole did not reveal any symptom relief for
children in whom infection was eradicated.43 Most of
those studies suffered from methodological prob-
lems because they were retrospective, open, nonran-
domized versus placebo trials. Wever et al44 con-
ducted a double-blind treatment study to elucidate
whether symptoms disappeared in children with H
pylori infection and RAP after bacterial eradication.
The eradication rates were 81% (30 of 37) in the
overall group and 74% (17 of 23) in the blind group;
however, no correlation was seen between the erad-
ication of H pylori and the disappearance of RAP
after 3 or 6 months of observation in the total group
or in the blind group of studied children. This study
was thus unable to prove any causal relationship
between RAP and H pylori infection.
Nevertheless, the interpretation of 1-arm treatment
trials, even if well conducted, must be cautious,
given the lack of a comparison group receiving stan-
dard therapy, unbiased investigators, and patients’
subjective symptom scores. In addition, in most pub-
lished studies, large numbers of children have been
20 H PYLORI AND RECURRENT ABDOMINAL PAIN
Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020
lost to follow-up, making the interpretation of long-
term treatment effects difficult.32
This question thus cannot be resolved. An appro-
priate answer will only be achieved through pro-
spective, well-structured, randomized, double-blind,
placebo-controlled therapeutic clinical trials in non-
ulcer-dyspeptic H pylori–infected children in compa-
rable groups matched for age and socioeconomic
class who undergo specific treatment designed to
relieve dyspeptic symptoms. Only such studies will
lead to standardized common guidelines for treat-
ment.
CONCLUSIONS
This study did not reveal any specific characteris-
tics of symptoms in nonulcer-dyspeptic H pylori–
infected children. Our results provide strong evi-
dence for the absence of a direct causal relationship
between epigastric NUD and H pylori infection. Be-
cause H pylori–infected children cannot be differen-
tiated from those who are not infected based on
presenting symptoms, there is no indication to screen
children with RAP and NUD for H pylori infection on
a systematic basis. A better definition of NUD might
thus allow us to define the very small group of
children (probably, as in adults, ⬍5%) who might
benefit from an eradication regimen.
REFERENCES
1. NIH Consensus Conference. Helicobacter pylori in peptic ulcer disease.
NIH Consensus Development Panel on Helicobacter pylori in Peptic
Ulcer Disease. JAMA. 1994;272:65– 69
2. Hentschel E, Brandstaller G, Dragosics B, et al. Effect of ranitidine and
amoxicillin plus metronidazole on the eradication of Helicobacter pylori
and the recurrence of duodenal ulcer. N Engl J Med. 1993;328:308 –312
3. Yeung CK, Fu KH, Yuen KY, et al. Helicobacter pylori and associated
duodenal ulcer. Arch Dis Child. 1990;65:1212–1216
4. Apley J, Naish N. Recurrent abdominal pain: a field survey of 1,000
school children. Arch Dis Child. 1958;33:165–170
5. Rasquin-Weber A, Hyman PE, Cucchiara S, et al. Childhood functional
gastrointestinal disorders. Gut. 1999;45(suppl II):1160 –1168
6. Mahony MJ, Wyatt JI, Littlewood JM. Campylobacter pylori gastritis. Arch
Dis Child. 1988;63:654 – 655
7. Gormally SM, Prakash N, Durnin MT, et al. Association of symptoms
with Helicobacter pylori infection in children. J Pediatr. 1995;126:753–756
8. Goggin N, Rowland M, Imrie C, Walsh D, Clyne M, Drumm B. Effect of
Helicobacter pylori eradication on the natural history of duodenal ulcer
disease. Arch Dis Child. 1998;79:502–505
9. Gormally S, Drumm B. Helicobacter pylori and gastrointestinal symp-
toms. Arch Dis Child. 1994;70:165–166
10. Drumm B, Koletzko S, Oderda G, on behalf of the European Paediatric
Task Force on Helicobacter pylori. Helicobacter pylori infection in children:
a consensus statement. J Pediatr Gastroenterol Nutr. 2000;30:207–213
11. Gottrand F. The role of Helicobacter pylori in abdominal pain in children.
Arch Pédiatr [in French]. 2000;7:197–200
12. Raymond J, Bergeret M, Benhamou PH, Mensah K, Dupont C. A 2-year
study of Helicobacter pylori in children. J Clin Microbiol. 1994;32:461– 463
13. Macarthur C. Is there an infectious etiology to abdominal pain in
children? J Pediatr Gastroenterol Nutr. 2000;30:112
14. Macarthur C. Helicobacter pylori, non-ulcer dyspepsia, and childhood
recurrent abdominal pain. Pediatr Res. 2001;49:140
15. Sherman PM, Macarthur C. Current controversies associated with Hel-
icobacter pylori infection in the pediatric population. Front Biosci. 2001;
6:E187–E192
16. Splawski JB. Helicobacter pylori and nonulcer dyspepsia: is there a rela-
tion? J Pediatr Gastroenterol Nutr. 2002;34:274 –277
17. Hyams JS, Davis P, Sylvester FA, Zeiter DK, Justinich CJ, Lerer T.
Dyspepsia in children and adolescents: a prospective study. J Pediatr
Gastroenterol Nutr. 2000;30:413– 418
18. Stordal K, Nygaard EA, Bentsen B. Organic abnormalities in recurrent
abdominal pain in children. Acta Paediatr. 2001;90:638 – 642
19. Nijevitch AA, Sataev VU, Vakhitov VA, Loguinovskaya VV, Kotsenko
TM. Childhood peptic ulcer in the Ural area of Russia: clinical status
and Helicobacter pylori-associated immune response. J Pediatr Gastroen-
terol Nutr. 2001;33:558 –564
20. Snyder JD, Hardy SC, Thorne GM, Hirsch BZ, Antonioli DA. Primary
antral gastritis in young American children. Low prevalence of Helico-
bacter pylori infection. Dig Dis Sci. 1994;39:1859 –1863
21. Glassman MS, Dallal S, Berezin SH, et al. Helicobacter pylori-related
gastroduodenal disease in children: diagnostic utility of enzyme-linked
immunosorbent assay. Dig Dis Sci. 1990;35:993–997
22. Blecker U, Hauser B, Lanciers S, Keymolen K, Vandenplas Y. Symp-
tomatology of Helicobacter pylori infection in children. Acta Paediatr.
1995;85:1156 –1158
23. Drumm B. Helicobacter pylori in the pediatric patient. Pediatr Clin North
Am. 1993;22:169 –182
24. Blecker U, Hauser B, Lanciers S, Peeters S, Suys B, Vandenplas Y. The
prevalence of Helicobacter pylori-positive serology in asymptomatic chil-
dren. J Pediatr Gastroenterol Nutr. 1993;16:252–256
25. Parsonnet J, Freidman GD, Vandersteen DP, et al. Helicobacter pylori
infection and the risk of gastric carcinoma. N Engl J Med. 1991;325:
1127–1131
26. Fiedorek SC, Malaty HL, Evans DL, et al. Factors influencing the epi-
demiology of Helicobacter pylori in children. Pediatrics. 1991;88:578 –582
27. Bode G, Rothenbacher D, Brenner H, Adler G. Helicobacter pylori and
abdominal symptoms: a population-based study among preschool chil-
dren in southern Germany. Pediatrics. 1998;101:634 – 637
28. Van Der Meer SB, Forget PP, Loffeld RJLF, Stobberingh E, Kuijten RH,
Arends JW. The prevalence of Helicobacter pylori serum antibodies in
children with recurrent abdominal pain. Eur J Pediatr. 1992;151:799 – 801
29. Hardikar W, Feekery C, Smith A, Oberklaid F, Grimwood K. Helicobac-
ter pylori and recurrent abdominal pain in children. J Pediatr Gastroen-
terol Nutr. 1996;22:148 –152
30. Chong SKF, Lou Q, Asnicar MA, et al. Helicobacter pylori infection in
recurrent abdominal pain in childhood: comparison of diagnostic tests
and therapy. Pediatrics. 1995;96:211–215
31. Mahony MJ, Wyatt JI, Littlewood JM. Management and response to
treatment of Helicobacter pylori gastritis. Arch Dis Child. 1992;67:940 –943
32. Kalach N, Benhamou PH, Raymond J, et al. Helicobacter pylori gastric
infections in children [in French]. Presse Med. 1997;26:1688 –1694
33. Macarthur C, Saunders N, Feldman W. Helicobacter pylori, gastroduo-
denal disease, and recurrent abdominal pain in children. JAMA. 1995;
273:729 –734
34. Oderda G, Dell’olio D, Morra I, Ansaldi N. Campylobacter pylori gastritis:
long term results of treatment with amoxycillin. Arch Dis Child. 1989;
64:326 –329
35. De Giacomo C, Fiocca R, Villani L, et al. Helicobacter pylori infection and
chronic gastritis: clinical, serological, and histologic correlations in chil-
dren treated with amoxicillin and colloidal bismuth subcitrate. J Pediatr
Gastroenterol Nutr. 1990;11:310 –316
36. Maaroos HI, Rägo T, Sipponen T, Siurala M. Helicobacter pylori and
gastritis in children with abdominal complaints. Scand J Gastroenterol.
1991;26(suppl 186):95–99
37. Sferlazza C, Tuccari G, Lombardo M, Nibali SC, Pasquale GD, Magazzù
G. Symptoms and Helicobacter pylori infection in children. J Pediatr.
1996;128:588 –589
38. Frank F, Stricker T, Stallmach T, Braegger CP. Helicobacter pylori infec-
tion in recurrent abdominal pain. J Pediatr Gastroenterol Nutr. 2000;31:
424 – 427
39. Shamaly H, Berkowitz D, Rosenthal E, Naveh Y. Efficacy of bismuth-
based triple therapy in children with recurrent abdominal pain and
Helicobacter pylori gastritis. J Pediatr Gastroenterol Nutr. 2000;30:198 –200
40. Shashidhar H, Peters J, Lin CH, Rabah R, Thomas R, Tolia V. A pro-
spective trial of Lansoprazole triple therapy for pediatric Helicobacter
pylori infection. J Pediatr Gastroenterol Nutr. 2000;30:276 –282
41. Ozen H, Dinder G, Akyon Y, Kocak N, Yuce A, Gurakan F. Helicobacter
pylori infection in recurrent abdominal pain in Turkish children. Heli-
cobacter. 2001;6:234 –238
42. Uc A, Chong SK. Treatment of Helicobacter pylori gastritis improves
dyspeptic symptoms in children. J Pediatr Gastroenterol Nutr. 2002;34:
281–285
43. Ashorn M, Ruuska T, Karikoski R, Miettinen A, Maki M. Helicobacter
pylori gastritis in dyspeptic children. A long-term follow-up after treat-
ment with colloidal bismuth subcitrate and tinidazole. Scand J Gastro-
enterol. 1994;29:203–208
44. Wever V, Anderson LP, Paerregaard A, et al. Treatment of Helicobacter
pylori in children with recurrent abdominal pain. Helicobacter. 2001;6:
244 –248

COOL FLAMES

“[Think of] . . . blue flame dancing on your brandy-soaked plum pudding. Now
imagine an even fainter flame, one so insubstantial that you can barely see or feel
it—less a flame, more an unusually lively chemical reaction. This is a cool flame, a
remarkable phenomenon created by gentle oxidation rather than fully fledged
combustion. First identified nearly 2 centuries ago, cool flames were long regarded
as a mere curiosity. But in the last few years they have become one of the hottest
things in combustion research. Engineers are using cool flames to revolutionize
heating systems and boilers, improving fuel efficiency, allowing them to run on a
variety of fuels, and helping clean up their emissions. Cool flames can also be used
as chemical processors to produce hydrogen for use in fuel cells. They are even
coming to the aid of vehicle engines, potentially transforming them into cleaner,
greener machines.”

Griffiths J. New Scientist. June 5, 2004

Noted by JFL, MD

Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020

ARTICLES 21
 Helicobacter pylori Infection Is Not Associated With Specific Symptoms in
Nonulcer-Dyspeptic Children
Nicolas Kalach, Karine Mention, Dominique Guimber, Laurent Michaud, Claire
Spyckerelle and Fréderic Gottrand
Pediatrics 2005;115;17
DOI: 10.1542/peds.2004-0131

Updated Information & including high resolution figures, can be found at:
Services http://pediatrics.aappublications.org/content/115/1/17
References This article cites 44 articles, 11 of which you can access for free at:
http://pediatrics.aappublications.org/content/115/1/17#BIBL
Subspecialty Collections This article, along with others on similar topics, appears in the
following collection(s):
Gastroenterology
http://www.aappublications.org/cgi/collection/gastroenterology_sub
Permissions & Licensing Information about reproducing this article in parts (figures, tables) or
in its entirety can be found online at:
http://www.aappublications.org/site/misc/Permissions.xhtml
Reprints Information about ordering reprints can be found online:
http://www.aappublications.org/site/misc/reprints.xhtml

Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020

 Helicobacter pylori Infection Is Not Associated With Specific Symptoms in
Nonulcer-Dyspeptic Children
Nicolas Kalach, Karine Mention, Dominique Guimber, Laurent Michaud, Claire
Spyckerelle and Fréderic Gottrand
Pediatrics 2005;115;17
DOI: 10.1542/peds.2004-0131

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pediatrics.aappublications.org/content/115/1/17

Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it
has been published continuously since 1948. Pediatrics is owned, published, and trademarked by
the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois,
60007. Copyright © 2005 by the American Academy of Pediatrics. All rights reserved. Print ISSN:
1073-0397.

Downloaded from www.aappublications.org/news at Indonesia:AAP Sponsored on April 5, 2020