'Serological Biopsy' in First-Degree Relatives of Patients with Gastric Cancer Affected by Helicobacter pylori Infection

F. Di Mario, A. M. Moussa, P. Caruana, R. Merli, L. G. Cavallaro, G. M. Cavestro, N. Dal Bò, V. Iori, A. Pilotto, G. Leandro, A. Franzè, M. Rugge

Research output: Contribution to journalArticle

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Abstract

Background: Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori-related atrophic gastritis and hypochlorhydria are well-documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a 'Gastropanel' blood test, including sPGI, sPGII, gastrin-17 (G-17) and antibodies anti-H. pylori (IgG-Hp), both functional and morphological features of gastric mucosa in Hp + ve subjects with a family history of gastric cancer. Materials and Methods: Twenty-five Hp + ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first-degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp + ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed. Results: No statistically significant differences were detected zbetween the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 ± 58.4 μg/L) were significantly lower than those in Group B (sPGI 159.5 ± 80.6 μg/L; P <0.0001) as well as sPGII (12. 5 μg/L ± 6.24 versus 20.6 ± 58 μg/L; P <0.006). No statistical difference was found between the two groups in relation to G-17 levels, IgG-Hp titres and antibodies against CagA. Conclusion: First-degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPG1 and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.

Original languageEnglish
Pages (from-to)1223-1227
Number of pages5
JournalScandinavian Journal of Gastroenterology
Volume38
Issue number12
DOIs
Publication statusPublished - Dec 2003

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Helicobacter Infections
Pepsinogen A
Helicobacter pylori
Stomach Neoplasms
Biopsy
Pepsinogen C
Serum
Immunoglobulin G
Achlorhydria
Atrophic Gastritis
Antibodies
Coffee
Hematologic Tests
Gastric Mucosa
Alcohol Drinking
Habits
Anti-Idiotypic Antibodies
Stomach
Smoking
gastrin 17

Keywords

  • Family relatives
  • Gastric cancer
  • H. pylori
  • Serum pepsinogens

ASJC Scopus subject areas

  • Gastroenterology

Cite this

'Serological Biopsy' in First-Degree Relatives of Patients with Gastric Cancer Affected by Helicobacter pylori Infection. / Di Mario, F.; Moussa, A. M.; Caruana, P.; Merli, R.; Cavallaro, L. G.; Cavestro, G. M.; Dal Bò, N.; Iori, V.; Pilotto, A.; Leandro, G.; Franzè, A.; Rugge, M.

In: Scandinavian Journal of Gastroenterology, Vol. 38, No. 12, 12.2003, p. 1223-1227.

Research output: Contribution to journalArticle

Di Mario, F, Moussa, AM, Caruana, P, Merli, R, Cavallaro, LG, Cavestro, GM, Dal Bò, N, Iori, V, Pilotto, A, Leandro, G, Franzè, A & Rugge, M 2003, ''Serological Biopsy' in First-Degree Relatives of Patients with Gastric Cancer Affected by Helicobacter pylori Infection', Scandinavian Journal of Gastroenterology, vol. 38, no. 12, pp. 1223-1227. https://doi.org/10.1080/00365520310007044
Di Mario, F. ; Moussa, A. M. ; Caruana, P. ; Merli, R. ; Cavallaro, L. G. ; Cavestro, G. M. ; Dal Bò, N. ; Iori, V. ; Pilotto, A. ; Leandro, G. ; Franzè, A. ; Rugge, M. / 'Serological Biopsy' in First-Degree Relatives of Patients with Gastric Cancer Affected by Helicobacter pylori Infection. In: Scandinavian Journal of Gastroenterology. 2003 ; Vol. 38, No. 12. pp. 1223-1227.
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abstract = "Background: Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori-related atrophic gastritis and hypochlorhydria are well-documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a 'Gastropanel' blood test, including sPGI, sPGII, gastrin-17 (G-17) and antibodies anti-H. pylori (IgG-Hp), both functional and morphological features of gastric mucosa in Hp + ve subjects with a family history of gastric cancer. Materials and Methods: Twenty-five Hp + ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first-degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp + ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed. Results: No statistically significant differences were detected zbetween the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 ± 58.4 μg/L) were significantly lower than those in Group B (sPGI 159.5 ± 80.6 μg/L; P <0.0001) as well as sPGII (12. 5 μg/L ± 6.24 versus 20.6 ± 58 μg/L; P <0.006). No statistical difference was found between the two groups in relation to G-17 levels, IgG-Hp titres and antibodies against CagA. Conclusion: First-degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPG1 and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.",
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AU - Di Mario, F.

AU - Moussa, A. M.

AU - Caruana, P.

AU - Merli, R.

AU - Cavallaro, L. G.

AU - Cavestro, G. M.

AU - Dal Bò, N.

AU - Iori, V.

AU - Pilotto, A.

AU - Leandro, G.

AU - Franzè, A.

AU - Rugge, M.

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N2 - Background: Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori-related atrophic gastritis and hypochlorhydria are well-documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a 'Gastropanel' blood test, including sPGI, sPGII, gastrin-17 (G-17) and antibodies anti-H. pylori (IgG-Hp), both functional and morphological features of gastric mucosa in Hp + ve subjects with a family history of gastric cancer. Materials and Methods: Twenty-five Hp + ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first-degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp + ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed. Results: No statistically significant differences were detected zbetween the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 ± 58.4 μg/L) were significantly lower than those in Group B (sPGI 159.5 ± 80.6 μg/L; P <0.0001) as well as sPGII (12. 5 μg/L ± 6.24 versus 20.6 ± 58 μg/L; P <0.006). No statistical difference was found between the two groups in relation to G-17 levels, IgG-Hp titres and antibodies against CagA. Conclusion: First-degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPG1 and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.

AB - Background: Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori-related atrophic gastritis and hypochlorhydria are well-documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a 'Gastropanel' blood test, including sPGI, sPGII, gastrin-17 (G-17) and antibodies anti-H. pylori (IgG-Hp), both functional and morphological features of gastric mucosa in Hp + ve subjects with a family history of gastric cancer. Materials and Methods: Twenty-five Hp + ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first-degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp + ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed. Results: No statistically significant differences were detected zbetween the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 ± 58.4 μg/L) were significantly lower than those in Group B (sPGI 159.5 ± 80.6 μg/L; P <0.0001) as well as sPGII (12. 5 μg/L ± 6.24 versus 20.6 ± 58 μg/L; P <0.006). No statistical difference was found between the two groups in relation to G-17 levels, IgG-Hp titres and antibodies against CagA. Conclusion: First-degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPG1 and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.

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