Comparative analysis of the Helicobacter pylori status in patients with gastric Malt-type lymphoma and their respective spouses[1]*

Summary

Helicobacter pylori is of major importance for the development and progression of gastric MALT-type lymphoma. In case of localized low grade lymphoma successfully treated by Helicobacter pylori eradication reinfection by the bacterium may involve the risk of lymphoma reoccurence.

Aims: To assess the frequency and type of Helicobacter pylori infection among patients with gastric MALT-type lymphoma and their respective spouses as potential sources of person to person spread of the infection.

Subjects: 35 patients with gastric MALT-type lymphoma and their cohabiting spouses.

Methods: We investigated serum IgG titers in response to the infection by Helicobacter pylori and to its virulence factors CagA and VacA by enzyme linked immunosorbent assay (ELISA) and by Western blot.

Results: Seropositivity of Helicobacter pylori, Cag A and Vac A was found to be 100/89/69 % and 97/86/66 % in patients and respective partners, respectively. The seroprevalence rates of the latter group by far exceed those of the German population.

Conclusion: These data provide evidence for a high Helicobacter pylori infection rate in both patients with gastric MALT-type lymphoma and their respective spouses. Considering the latter as a potential source of reinfection with the risk of lymphoma reoccurence for the successfully treated patient with gastric MALT-type lymphoma careful follow-up seems highly reasonable to decide on the necessity of a future test-and-treat strategy of this population.

Helicobacter-pylori-Status bei Patienten mit MALT-Lymphomen des Magens und ihren Lebenspartnern

Helicobacter pylori ist von entscheidender Bedeutung für die Entstehung und Progression von MALT-Lymphomen des Magens. Im Falle lokalisierter Lymphome niedriger Malignität beinhaltet eine Reinfektion nach erfolgreicher Eradikation und Lymphom­regression das Risiko eines Rezidivs. Wir untersuchten daher die Häufigkeit und den Typ der Helicobacter-pylori-Infektion bei 35 Patienten mit gastralen MALT-Lymphomen und ihren Partnern, die eine potenzielle Quelle für eine direkte Übertragung dar­stellen.

Methode: Serum-IgG-Titer für Helicobacter pylori und die Virulenzfaktoren CagA und VacA wurden mittels ELISA und Western blot analysiert.

Ergebnisse: Eine Seropositivität für Helicobacter pylori, CagA und VacA fand sich bei 100/89/69 % der Patienten und bei 97/86/66 % ihrer Partner. Die Seroprävalenzraten der Partner übersteigen damit bei weitem die Infektionsraten in der deutschen Bevölkerung.

Schlussfolgerung: Sowohl bei Patienten mit MALT-Lymphomen des Magens als auch bei ihren Partnern besteht eine hohe Infektionsrate mit Helicobacter pylori. Angesichts einer potenziellen Reinfektion mit dem Risiko eines Lymphomrezidivs sind sorgfältige Kontrolluntersuchungen nötig, um zukünftig über die Notwendigkeit einer „Teste-und-behandle-Strategie” der Partner von Lymphompatienten zu entscheiden.

Helicobacter pylori - Cag A - Vac A; - MALT lymphoma - Spouses

Helicobacter pylori - CagA - VacA - MALT-Lymphom - Partner

References

• 1 Doglioni C, Wotherspoon A C, Moschini A, De B oni M, Isaacson P G. High incidence of primary gastric lymphoma in north-eastern Italy.  Lancet. 1992;  339 834-5
• 2 Parsonnet J, Hansen S, Rodriguez L  et al. Helicobacter pylori infection and gastric lymphoma.  N Engl J Med. 1994;  330 1267-71
• 3 Wotherspoon A C, Ortiz-Hidalgo C, Falzon M R, Isaacson P G. Helicobacter pylori-associated gastritis and primary B-cell gastric lymphoma.  Lancet. 1991;  338 1175-6
• 4 Greiner A, Marx A, Heesemann J  et al. Idiotype identity in a MALT-type lymphoma and B cells in Helicobacter pylori associated gastritis.  Lab Invest. 1994;  70 572-8
• 5 Hussell T, Isaacson P G, Crabtree J E, Spencer J. Helicobacter pylori specific tumour infiltrating T cells provide contact dependent help for the growth of malignant B cells in low grade gastric lymphoma of mucosa associated lymphoid tissue.  J Pathol. 1996;  178 122-7
• 6 Enno A, ORourke J, Lee A, Dixon M F. MALToma-like lesions in the stomach resulting from longstanding Helicobacter infection in the mouse.  Am J Gastroenterol. 1994;  89 1357
• 7 Wotherspoon A C, Doglioni C, Diss T C et al. Regression of primary low-grade B-cell gastric lymphoma of mucosa associated lymphoid tissue type after eradication of Helicobacter pylori.  Lancet. 1993;  342 575-7
• 8 Bayerdörffer E, Neubauer A, Rudolph B  et al. Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pylori infection.  Lancet. 1995;  345 1591-4
• 9 Fischbach W. Clinical management of primary gastric lymphoma.  Onkologie. 1999;  22 25-9
• 10 Georgopoulos S D, Mentis A F, Spiliadis C A et al. Helicobacter pylori infection in spouses of patients with duodenal ulcers and comparison of ribosomal RNA gene patterns.  Gut. 1996;  39 634-8
• 11 Parente F, Maconi G, Sangaletti O  et al. Prevalence of Helicobacter pylori infection and related gastroduodenal lesions in spouses of Helicobacter pylori positive patients with duodenal ulcer.  Gut. 1996;  39 629-33
• 12 Fischbach W, Kolve M E, Dragosics B  et al. Histology and stage stratified therapy offers promising results in primary gastric non-Hodgkin’s lymphoma: Experiences of the German-Austrian prospective multicenter trial.  Gastroenterology. 1998;  114 A595
• 13 Eck M, Schmaußer B, Haas R  et al. MALT-type lymphoma of the stomach is associated with Helicobacter pylori strains expressing the CagA protein.  Gastroenterology. 1997;  112 1482-6
• 14 Musshoff K. Klinische Stadieneinteilung der Nicht-Hodgkin-Lymphome.  Strahlentherapie. 1977;  153 218-21
• 15 Alam K, Cutler A, Schubert T. Prevalence of Helicobacter pylori in spouses of infected patients.  Gastroenterology. 1993;  104 A31
• 16 Bamford K B, Bickley J, Collins J SA et al. Helicobacter pylori: Comparison of DNA fingerprints provides evidence for intrafamiliar infection.  Gut. 1993;  34 1348-50
• 17 Perez-Perez G I, Witkin S S, Decker M D, Blaser M J. Seroprevalence of Helicobacter pylori infection in couples.  J Clin Microbiol. 1991;  29 642-4
• 18 Schutze K, Hentschel E, Dragosics B, Hirschl A M. Helicobacter pylori reinfection with identical organisms: Transmission by the patients’ spouses.  Gut. 1995;  36 831-2
• 19 Vincent P, Gottrand F, Pernes P  et al. High prevalence of Helicobacter pylori infection in cohabiting children. Epidemiology of a cluster, with special emphasis on molecular typing.  Gut. 1994;  35 313-6
• 20 Wang J T, Sheu J C, Lin J T, Wang T H, Wu M S. Direct DNA amplification and restriction pattern analysis of Helicobacter pylori in patients with duodenal ulcer and their families.  J Infect Dis. 1993;  168 1544-8
• 21 De J ong D, van D ijk WC, van d er Hulst RWM. CagA+ H. pylori strains and gastric lymphoma.  Gastroenterology. 1997;  113 2022
• 22 Bouzourene H, Haefliger T, Delacretaz F, Saraga E. The role of Helicobacter pylori in primary gastric MALT lymphoma.  Histopathology. 1999;  34 118-23
• 23 Karat D, O’Hanlon D M, Hayes N  et al. Prospective study of Helicobacter pylori infection in gastric lymphoma.  Br J Surg. 1995;  82 1369-70
• 24 Miettinen A, Karttunen T J, Alavaikko M. Lymphocytic gastritis and Helicobacter pylori infection in gastric lymphoma.  Gut. 1995;  37 471-6
• 25 Nakamura S, Yao T, Aoyagi K  et al. Helicobacter pylori and primary gastric lymphoma: A histopathologic and immunohistochemical analysis of 237 patients.  Cancer. 1997;  79 3-11
• 26 Xu W S, Ho F C, Chan A C, Srivastava G. Pathogenesis of gastric lymphoma: The enigma in Hong Kong.  Ann Oncol. 1997;  2 (Suppl) 41-4
• 27 Eck M, Greiner A, Schmaußer B  et al. Evaluation of Helicobacter pylori in gastric MALT-type lymphoma: Differences between histologic and serologic diagnosis.  Mod Pathol. 1999;  12 1148-51
• 28 Labenz J, Jung-Stilling, Hollenz M, Stolte M. Prospective Helicobacter pylori (H. pylori) screening of patients consulting a general practitioner.  Gastroenterology. 1999;  116 A226
• 29 EUROGAST S tudy Group. Epidemiology of, and risk factors for, Helicobacter pylori infection among 3194 asymptomatic subjects in 17 populations.  Gut. 1993;  34 1672-6

Fußnoten

1 These data have been presented at the Digestive Disease Week, Orlando, Florida 1999 and published as abstract (Gastroenterology 1999; 116: A403)

Address for correspondence