ROBERTO TESTA
Direttore s.c. Gastroenterologia A.O. Santa Corona – Pietra Ligure
L’Infezione da Helicobacter
Pylori
Manifestazioni Cliniche e
Percorso Diagnostico
L’Infezione da Helicobacter Pylori (Hp) è
tra le più comuni infezioni in tutto il
mondo.
Patologie gastrointestinali correlate all’infezione da Hp:
• Gastrite Cronica
• Ulcera Peptica
• Linfoma MALT
• Adenocarcinoma Gastrico
Figure 48-1 Seroprevalence of Helicobacter pylori as a function of age in developing countries and developed countries. (Data from Graham DY, Adam E,
Reddy GT, et al: Seroepidemiology of Helicobacter pylori infection in India: Comparison of developing and developed countries. Dig Dis Sci 36:1084, 1991.)
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Figure 48-2 Seroprevalence of Helicobacter pylori in the United States as a function of age in asymptomatic African Americans, Hispanics, and whites. (From
Malaty HM, Evans DG, Evans DJJ, Graham DY: Helicobacter pylori in Hispanics: Comparison with blacks and whites of similar age and socioeconomic class.
Gastroenterology 103:813, 1992.)
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Figure 48-4 Seroprevalence of Helicobacter pylori (Hp) in the United States in spouses and children of parents who are seropositive or seronegative for H.
pylori infection. (From Malaty HM, Graham DY, Evans DG, et al: Transmission of Helicobacter pylori infection. Studies in families of healthy individuals. Scand
J Gastroenterol 26:927, 1991.)
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Figure 34.5 Vacuolating cytotoxin, VacA. A. Pathogenic regions of VacA. B. Effects of VacA on the host.
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Figure 34.8 Functional consequences of H. pylori infection.
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Figure 34.7 Common topographic patterns of chronic active gastritis.
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Figure 49-3 Chronic nonspecific gastritides. A and B, Normal mucosal biopsy from the gastric body and antrum, respectively. C, Diffuse antral gastritis. The
glands show an infiltrate of neutrophils, in addition to an increase in inflammatory cells in the lamina propria. This lesion is typically associated with
Helicobacter pylori infection. D, Multifocal atrophic gastritis with intestinal metaplasia. Note several glands lined by goblet cells (arrow). Biopsy is from the
gastric body, and similar changes were present in the antrum. E, Diffuse corporal atrophic gastritis in a man with pernicious anemia. The gland in the lower
left is lined by goblet cells. Nests of enter-ochromaffin-like cells are also visible (arrows).
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Figure 34.9 How antral H. pylori causes duodenal ulcers. H. pylori colonizes duodenal gastric metaplasia and reduces antral
somatostatin activity, resulting in increased gastrin and enhanced acid secretion by parietal cells.
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Figure 35.7 Hormonal changes in duodenal and gastric ulceration. A. In H. pylori-associated antral-predominant gastritis, the illustrated hormonal changes
lead to hypergastrinemia and increased acid production from the uninflamed gastric corpus. The increased acid load on the duodenum may lead to ulceration
(see text for full explanation). B. In pangastritis, the same hormonal changes pertain, but the inflamed corpus produces reduced acid despite the
hypergastrinemia. Such stomachs are at increased risk of gastric ulceration and adenocarcinoma.
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Figure 35.7 Hormonal changes in duodenal and gastric ulceration. A. In H. pylori-associated antral-predominant gastritis, the illustrated hormonal changes
lead to hypergastrinemia and increased acid production from the uninflamed gastric corpus. The increased acid load on the duodenum may lead to ulceration
(see text for full explanation). B. In pangastritis, the same hormonal changes pertain, but the inflamed corpus produces reduced acid despite the
hypergastrinemia. Such stomachs are at increased risk of gastric ulceration and adenocarcinoma.
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Figure 50-3 Pie charts depicting conditions associated with peptic ulcer disease. The percentages shown are rough approximations based on studies from
Western countries. The relative contributions of H. pylori infection and NSAID use to peptic ulcer vary considerably among different populations and, within
populations, vary with age and socioeconomic status. Also, the separation depicted in this figure is somewhat artificial because NSAID use and H. pylori
infection often coexist. ZE, Zollinger-Ellison syndrome.
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Figure 50-7 Range of COX-1 and COX-2 selectivity of NSAIDs. (Modified from Warner TD, Mitchell JA: Cyclooxygenases: New forms, new inhibitors, and
lessons from the clinic. FASEB J 18:790, 2004.) COX, cyclooxy-genase; IC50, concentration of NSAID that inhibits COX by 50%, NSAID, nonsteroidal antiinflammatory drug.
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Figure 7.1 Overlap of gastrointestinal symptoms. Overlap between heartburn, epigastric pain, and early satiety in 3234 subjects from the
general population with upper gastrointestinal symptoms. Figures do not add up to 100% due to rounding errors.
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Figure 34.10 Possible mechanisms linking H. pylori and cancer.
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Figure 34.11 Evolution of premalignant changes into cancer in patients with H. pylori infection.
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Figure 37.1 Host genetic factors contributing to H. pylori-related gastric cancer.
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Sintomi e Segni di Allarme
•
•
•
•
•
•
Ematemesi o Melena
Disfagia
Perdita di Peso
Vomito Persistente
Massa Addominale
Anemia da Possibile Sanguinamento
Gastrointestinale
RACCOMANDAZIONI DIAGNOSTICHE
• La Ricerca di Hp è indicata nei pazienti
con Ulcera Peptica in atto, pregressa
storia di ulcera documentata, linfoma
MALT.
• La Ricerca di Hp dovrebbe essere
eseguita solo se il medico ha
programmato di trattare il paziente nel
caso in cui l’esito dell’esame risultasse
positivo.
Tests Diagnostici di Infezione da Hp
Sensibilità %
Specificità %
• Tests Invasivi
•
•
•
Urease Test
Istologia
Coltura
85-95
90-95
80-95
95-100
95-98
100
85-95
85-95
70-90
95-97
95-97
65-90
• Tests non Invasivi
•
•
•
C13 Urea Breath Test
Hp Antigene Fecale
Hp Anticorpi Sierici
RACCOMANDAZIONI DIAGNOSTICHE
• Nei pazienti che non abbiano ricevuto
un PPI nelle 2 settimane precedenti o
un Antibiotico entro le 4 settimane
precedenti l’Esame Endoscopico, il test
rapido all’ureasi è accurato e poco
costoso.
• Per i pazienti che sono stati trattati con
PPI, la ricerca endoscopica di Hp deve
includere biopsie dall’antro al corpo
gastrico per l’evidenza istologica di Hp.
Figure 34.12 Urease test. Top: positive; bottom: negative.
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Figure 36.1 Biopsy protocol. Schematic representation of the biopsy protocol recommended by the Updated Sydney System when the objective is to map the
severity and extent of gastritis. A minimum of two specimens is obtained from each of the antrum (A1 and A2 - lesser and greater curvature) and the corpus
(B1 and B2 - lesser and greater curvature). In addition, one biopsy specimen from the incisura angularis (IA) is recommended to detect early atrophic and
metaplastic changes, represented in blue.
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RACCOMANDAZIONI DIAGNOSTICHE
• L’Esame Colturale o con PCR è
raccomandato per testare la Sensibilità
antibiotica, ma non è utilizzabile
routinariamente.
• L’Esame Colturale non è sensibile
come il test rapido o l’esame istologico.
Tests non Invasivi per Identificare Hp
Urea Breath Test
• Caratteristiche: Diagnosi di infezione in atto,
rilevata dall’attività ureasica Hp dipendente
nello stomaco.
• Vantaggi: Sensibilità e Specificità >90%,
utilizzabile nei bambini. Utile per la diagnosi
iniziale e per valutare il trattamento.
• Svantaggi: Richiede apparecchiature per
rilevare C13, relativamente costose.
Figure 34.13 Principles and results of C13 urea breath testing. Note the rapid rise in [13C]carbon dioxide following administration of [13C]urea.
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Tests non Invasivi per Identificare Hp
Tests Sierologici
• Caratteristiche: Rileva Anticorpi anti-Hp IgG
nel siero.
• Vantaggi: I tests approvati hanno alta
sensibilità e specificità. Poco costoso. Utile
per screening iniziale.
• Svantaggi: Rileva infezione pregressa, no
infezione in atto. Utilità limitata per valutare
l’eradicazione di Hp (riduzione lenta del titolo
anticorpale).
Tests non Invasivi per Identificare Hp
Tests Fecali
• Caratteristiche: Rileva l’antigene dell’Hp.
• Vantaggi: Rileva l’infezione in atto. Utile per
valutare l’eradicazione. Eccellente specificità
e sensibilità. Poco costoso. Può essere il test
di scelta nei bambini.
• Svantaggi: La raccolta dei campioni di feci
può costituire problema.
RACCOMANDAZIONI
DIAGNOSTICHE
• Per Valutare l’Eradicazione di Hp sia
Urea Breath Test sia Ricerca Hp
Antigene nelle feci devono essere
eseguiti dopo almeno 2 settimane dal
termine della terapia.
Figure 48-5 Proposed natural history of Helicobacter pylori infection in humans.
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