Helicobacter Pylori

Infection Clinical Presentation
Dr.Gazmend Bojaj
 History

• In the authors' opinion, no significant differences in the presence

and frequency of symptoms, such as nausea, vomiting, pain,
heartburn, or diarrhea, occur in patients who are infected with H
pylori and patients who are not. No definite evidence demonstrates
a clear relationship between the symptoms of the H pylori -
associated gastritis and abdominal pain or dyspeptic symptoms
from other conditions. Of patients, 30-35% have no symptoms.
• Adults and children differ in immune response to H pylori infection.
This is probably due to a physiologic lower density of neutrophils
and T lymphocytes during childhood, especially in children younger
than 8 years.
• Although H pylori infection is not significantly related to recurrent
abdominal pain, weekly pain is reported more often in children who
are infected with H pylori compared with children who are not
infected.
 Physical

• No specific clinical signs have been

described in patients with H
pylori infection.
• Patients may feel dyspepsia or abdominal
discomfort, such as during gastritis or with
epigastric pain (eg, duodenal ulcers).
• In some cases, patients may feel hungry in
the morning and may have halitosis.
 Causes

• H pylori infection causes atrophic and even metaplastic changes in the

stomach.
• The bacterial adhesion appears to result in tyrosine phosphorylation and is
specific for gastric cells.
• The adhesion of H pylori to the gastric cells causes a direct decrease in
mucosal levels of glutathione, a fundamental molecule in the maintenance
of the cellular redox status and in the molecular regulation of host immune
responses. However, the LPS of H pylori may induce the production of
autoantibodies that are able to worsen atrophy in the corpus mucosa and
cause a concomitant increase in parietal cell antibodies. Such events are
accompanied by a decrease in anti-H pylori immunoglobulin titers. This
process leads to a scenario of severe atrophy without bacterial colonization
combined with high levels of autoantibodies against gastric parietal cells.
• A number of reports show the close association between H pylori infection
and low-grade gastric MALTomas.
• Giannakis and colleagues demonstrated that H pylori may adapt to gastric
stem cells, influencing their biology and contributing to tumorigenesis of the
stomach.[7]
 Differential Diagnoses

• Acute Gastritis
• Atrophic Gastritis
• Chronic Gastritis
• Gastric Cancer
• Gastrinoma
• Gastroesophageal Reflux Disease
• Non-Hodgkin Lymphoma
• Peptic Ulcer Disease
• Stress-Induced Gastritis
 Laboratory Studies
• H pylori fecal antigen test
– This novel rapid test is based on monoclonal antibody immunochromatography of stool samples. The test has been reported to be
very specific (98%) and sensitive (94%).
– The results are positive in the initial stages of infection and can be used to detect eradication after treatment.
– Although the H pylori fecal antigen test is an interesting tool, information about the cost of the test is pending.
• Carbon 13 urea breath test
– The carbon 13 urea breath test (UBT) is based on the detection of the products created when urea is split by the organism.
– Patients are asked to drink urea (usually with a beverage) labeled with a carbon isotope (carbon 13 or carbon 14). After a certain
duration, the concentration of the labeled carbon is measured in the breath. The concentration is high only when urease is present
in the stomach. Because the human stomach does not produce urease, such a reaction is possible only with H pylori infection.
– The breath test is expensive but is becoming increasingly more available.
– Other problems include false-negative results due to infection with coccoid forms of H pylori that do not produce as much urease
or intake of antibiotics, bismuth, histamine 2 (H2) blockers, or proton pump inhibitors.
• H pylori serology
– The serology test has a high (>90%) specificity and sensitivity. It is currently based on the quantitation of immunoglobulin G
antibodies against H pylori by the means of an enzyme-linked immunosorbent assay.
– It is useful for detecting a newly infected patient, but it is not a good test for follow-up of treated patients because the results do not
indicate present infection with H pylori. The antibody titer may remain elevated for a long time after H pylori eradication. The
number of false-positive results is age related and increases with age.
• Antibiogram
– In geographic areas with a high resistance rate against metronidazole and clarithromycin, culture for antibiotic susceptibility testing
(antibiogram) seems to be useful.[3, 4]
– Alternatively, metronidazole and clarithromycin should not be recommended as first-line drugs in such areas.
 Imaging Studies

• Imaging studies are not helpful in the

diagnosis of H pylori infection. Otherwise,
they may be useful in patients with
complicated disease (eg, ulcer disease,
gastric cancer, MALToma).
 Laboratory Studies
• H pylori fecal antigen test
– This novel rapid test is based on monoclonal antibody immunochromatography of stool samples. The test has been reported to be
very specific (98%) and sensitive (94%).
– The results are positive in the initial stages of infection and can be used to detect eradication after treatment.
– Although the H pylori fecal antigen test is an interesting tool, information about the cost of the test is pending.
• Carbon 13 urea breath test
– The carbon 13 urea breath test (UBT) is based on the detection of the products created when urea is split by the organism.
– Patients are asked to drink urea (usually with a beverage) labeled with a carbon isotope (carbon 13 or carbon 14). After a certain
duration, the concentration of the labeled carbon is measured in the breath. The concentration is high only when urease is present
in the stomach. Because the human stomach does not produce urease, such a reaction is possible only with H pylori infection.
– The breath test is expensive but is becoming increasingly more available.
– Other problems include false-negative results due to infection with coccoid forms of H pylori that do not produce as much urease
or intake of antibiotics, bismuth, histamine 2 (H2) blockers, or proton pump inhibitors.
• H pylori serology
– The serology test has a high (>90%) specificity and sensitivity. It is currently based on the quantitation of immunoglobulin G
antibodies against H pylori by the means of an enzyme-linked immunosorbent assay.
– It is useful for detecting a newly infected patient, but it is not a good test for follow-up of treated patients because the results do not
indicate present infection with H pylori. The antibody titer may remain elevated for a long time after H pylori eradication. The
number of false-positive results is age related and increases with age.
• Antibiogram
– In geographic areas with a high resistance rate against metronidazole and clarithromycin, culture for antibiotic susceptibility testing
(antibiogram) seems to be useful.[3, 4]
– Alternatively, metronidazole and clarithromycin should not be recommended as first-line drugs in such areas.
 Other Tests
• Esophagogastroduodenoscopy
– An esophagogastroduodenoscopy (EGD) is often necessary in
patients with symptoms of peptic ulcer disease in order to view
the condition of the mucosal lining of the stomach and
duodenum and to obtain biopsy specimens from the gastric
antrum.
– An echography associated with an EGD is mandatory in patients
with biopsy results that are positive for gastric MALTomas in
order to allow a more precise staging of the disease.
• Peptic ulcer disease and gastric cancer may manifest
with the same symptoms, and the only way to
differentiate them is to view the lesion and to perform a
histologic examination of the biopsy specimens.
 Imaging Studies

• Imaging studies are not helpful in the

diagnosis of H pylori infection. Otherwise,
they may be useful in patients with
complicated disease (eg, ulcer disease,
gastric cancer, MALToma).
 Procedures

• Patients with new peptic ulcer disease

should have a UBT, they should be tested
for antibody titers, or they may require an
investigation for stool antigens.
• In patients with prior peptic ulcer disease,
an EGD with biopsy and histological
studies may be performed. Also, a UBT is
helpful in these patients.
 Staging

• Although a staging system for the H pylori infection does

not exist, some steps in the disease process are well
described.
• The first step is chronic gastritis, followed after a time by
the second step, atrophic gastritis. The third step is
intestinal metaplasia, which may evolve into dysplasia.
The last step is gastric adenocarcinoma.
• This process is very slow and may stop at any step
because gastric cancers undoubtedly require several
other factors to develop, not only an H pylori infection.
As reported above, ultrasound and EGD should be
considered in patients with gastric MALTomas in order to
allow a more precise staging of the disease.
 Questions?
• Common Questions
• What is the treatment of peptic ulcer cause
d by 
Helicobacter pylori?
• Does everyone with H. pylori get ulcers?
• Why is the blood test for H.
pylori antibodies not recommended?
 1.  What is the treatment of peptic ulcer caused
by Helicobacter pylori?

• Treatment usually involves a combination

of antibiotics and drugs to reduce the
amount of stomach acid produced, such
as proton pump inhibitors and histamine
receptor blockers, as well as a bismuth
preparation, such as Pepto-Bismol®,
taken for several weeks.
 2.  Does everyone with H.
pylori get ulcers?
• No, many people have evidence of
infection but have no symptoms of
ulcerative disease. The reason why some
people with H. pylori infections develop 
peptic ulcers and others do not is not yet
understood.
 1.  What is the treatment of peptic ulcer caused
by Helicobacter pylori?

• Treatment usually involves a combination

of antibiotics and drugs to reduce the
amount of stomach acid produced, such
as proton pump inhibitors and histamine
receptor blockers, as well as a bismuth
preparation, such as Pepto-Bismol®,
taken for several weeks.
 3.Why is the blood test for H. pylori antibodies not
recommended?

• The American Gastroenterology Association, the

American College of Gastroenterologists, the Infectious
Diseases Society of America and the American Society
for Microbiology do not recommend the antibody blood
test for routine use in diagnosing an H. pylori infection or
evaluating its treatment as the test cannot distinguish
between a present and previous infection.
• However, some health practitioners still use this test. If
the blood test is negative, then it is unlikely that the
person has had an H. pylori infection.
• If it is positive, then the presence of a current H.
pylori infection should be confirmed with a stool antigen
or breath test.
 References
• Jump up^ Chan, FK; To, KF; Wu, JC; Yung, MY; Leung, WK; Kwok, T; Hui, Y; Chan, HL; Chan, CS; Hui, E; Woo,
J; Sung, JJ (5 January 2002). "Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-
term treatment with non-steroidal anti-inflammatory drugs: a randomised trial.". Lancet 359 (9300): 9–13. doi:
10.1016/s0140-6736(02)07272-0.PMID 11809180.
• Jump up^ Sonnenberg, A (June 2007). "Time trends of ulcer mortality in Europe.". Gastroenterology 132 (7):
2320–7. doi:10.1053/j.gastro.2007.03.108. PMID 17570207.
• Jump up^ Gatta, L; Vakil, N; Vaira, D; Scarpignato, C (7 August 2013). "Global eradication rates for Helicobacter
pylori infection: systematic review and meta-analysis of sequential therapy.". BMJ (Clinical research ed.) 347:
f4587. doi:10.1136/bmj.f4587. PMID 23926315.
• Jump up^ Malfertheiner, P.; Megraud, F.; O'Morain, C. A.; Atherton, J.; Axon, A. T. R.; Bazzoli, F.; Gensini, G. F.;
Gisbert, J. P.; Graham, D. Y.; Rokkas, T.; El-Omar, E. M.; Kuipers, E. J. (5 April 2012). "Management of
Helicobacter pylori infection--the Maastricht IV/ Florence Consensus Report". Gut 61 (5): 646–664. doi:
10.1136/gutjnl-2012-302084. PMID 22491499.
• Jump up^ Molina-Infante, J; Romano, M; Fernandez-Bermejo, M; Federico, A; Gravina, AG; Pozzati, L; Garcia-
Abadia, E; Vinagre-Rodriguez, G; Martinez-Alcala, C; Hernandez-Alonso, M; Miranda, A; Iovene, MR; Pazos-
Pacheco, C; Gisbert, JP (July 2013). "Optimized nonbismuth quadruple therapies cure most patients with
Helicobacter pylori infection in populations with high rates of antibiotic resistance.". Gastroenterology 145 (1):
121–128.e1. doi:10.1053/j.gastro.2013.03.050. PMID 23562754.
• Jump up^ Malfertheiner, P; Megraud, F; O'Morain, C; Bazzoli, F; El-Omar, E; Graham, D; Hunt, R; Rokkas, T;
Vakil, N; Kuipers, EJ (June 2007). 
"Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report."
. Gut 56 (6): 772–81. doi:10.1136/gut.2006.101634. PMC 1954853. PMID 17170018.
• Jump up^ Malfertheiner, P; Megraud, F; O'Morain, CA; Atherton, J; Axon, AT; Bazzoli, F; Gensini, GF; Gisbert,
JP; Graham, DY; Rokkas, T; El-Omar, EM; Kuipers, EJ; European Helicobacter Study, Group (May 2012).
"Management of Helicobacter pylori infection--the Maastricht IV/ Florence Consensus Report.". Gut 61 (5): 646–
64. doi:10.1136/gutjnl-2012-302084.PMID 22491499.
• Jump up^ B, Yaşar; H, Abut (2010). "Efficacy of probiotics in Helicobacter pylori eradication therapy.". Turk J
Gastroenterol 21 (3): 212–217.
• Jump up^ Borody, Thomas J.; P. Cole; S. Noonan; A. Morgan; J. Lenne; L. Hyland; S. Brandl; E. G. Borody; L. L.
George (October 16, 1989). "Recurrence of duodenal ulcer and Campylobacter pylori infection after
eradication". Medical Journal of Australia 151 (8): 431–435. PMID 2687668.
• ^ Jump up to:a b Mirbagheri, Seyed Amir; Mehrdad Hasibi; Mehdi Abouzari; Armin Rashidi (August 14, 2006). 
"Triple, standard quadruple and ampicillin–sulbactam-based quadruple therapies for H pylori eradication: A comp
arative three-armed randomized clinical trial"
. World Journal of Gastroenterology 12 (30): 4888–4891. PMID 16937475. Retrieved 2006-09-30.
Thank you?
 References
• Jump up^ Chan, FK; To, KF; Wu, JC; Yung, MY; Leung, WK; Kwok, T; Hui, Y; Chan, HL; Chan, CS; Hui, E; Woo,
J; Sung, JJ (5 January 2002). "Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-
term treatment with non-steroidal anti-inflammatory drugs: a randomised trial.".  Lancet 359 (9300): 9–13. doi:
10.1016/s0140-6736(02)07272-0.PMID 11809180.
• Jump up^ Sonnenberg, A (June 2007). "Time trends of ulcer mortality in Europe.". Gastroenterology 132 (7): 2320–
7. doi:10.1053/j.gastro.2007.03.108. PMID 17570207.
• Jump up^ Gatta, L; Vakil, N; Vaira, D; Scarpignato, C (7 August 2013). "Global eradication rates for Helicobacter
pylori infection: systematic review and meta-analysis of sequential therapy.".  BMJ (Clinical research ed.) 347:
f4587. doi:10.1136/bmj.f4587. PMID 23926315.
• Jump up^ Malfertheiner, P.; Megraud, F.; O'Morain, C. A.; Atherton, J.; Axon, A. T. R.; Bazzoli, F.; Gensini, G. F.;
Gisbert, J. P.; Graham, D. Y.; Rokkas, T.; El-Omar, E. M.; Kuipers, E. J. (5 April 2012). "Management of
Helicobacter pylori infection--the Maastricht IV/ Florence Consensus Report".  Gut 61 (5): 646–664. doi:
10.1136/gutjnl-2012-302084. PMID 22491499.
• Jump up^ Molina-Infante, J; Romano, M; Fernandez-Bermejo, M; Federico, A; Gravina, AG; Pozzati, L; Garcia-
Abadia, E; Vinagre-Rodriguez, G; Martinez-Alcala, C; Hernandez-Alonso, M; Miranda, A; Iovene, MR; Pazos-
Pacheco, C; Gisbert, JP (July 2013). "Optimized nonbismuth quadruple therapies cure most patients with
Helicobacter pylori infection in populations with high rates of antibiotic resistance.".  Gastroenterology 145 (1): 121–
128.e1. doi:10.1053/j.gastro.2013.03.050. PMID 23562754.
• Jump up^ Malfertheiner, P; Megraud, F; O'Morain, C; Bazzoli, F; El-Omar, E; Graham, D; Hunt, R; Rokkas, T;
Vakil, N; Kuipers, EJ (June 2007). 
"Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report."
. Gut 56 (6): 772–81. doi:10.1136/gut.2006.101634. PMC 1954853. PMID 17170018.
• Jump up^ Malfertheiner, P; Megraud, F; O'Morain, CA; Atherton, J; Axon, AT; Bazzoli, F; Gensini, GF; Gisbert, JP;
Graham, DY; Rokkas, T; El-Omar, EM; Kuipers, EJ; European Helicobacter Study, Group (May 2012).
"Management of Helicobacter pylori infection--the Maastricht IV/ Florence Consensus Report.".  Gut 61 (5): 646–
64. doi:10.1136/gutjnl-2012-302084.PMID 22491499.
• Jump up^ B, Yaşar; H, Abut (2010). "Efficacy of probiotics in Helicobacter pylori eradication therapy.".  Turk J
Gastroenterol 21 (3): 212–217.
• Jump up^ Borody, Thomas J.; P. Cole; S. Noonan; A. Morgan; J. Lenne; L. Hyland; S. Brandl; E. G. Borody; L. L.
George (October 16, 1989). "Recurrence of duodenal ulcer and Campylobacter pylori infection after
eradication". Medical Journal of Australia 151 (8): 431–435. PMID 2687668.
• ^ Jump up to:a b Mirbagheri, Seyed Amir; Mehrdad Hasibi; Mehdi Abouzari; Armin Rashidi (August 14,
2006). "Triple, standard quadruple and ampicillin–sulbactam-based quadruple therapies for H pylori eradication: A
comparative three-armed randomized clinical trial". World Journal of Gastroenterology 12 (30): 4888–
4891. PMID 16937475. Retrieved 2006-09-30.