‘Serological biopsy’ in first‐degree relatives of patients with gastric cancer affected by Helicobacter pylori infection

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 sPGI and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.

• Family relatives
• gastric cancer
• H. pylori
• serum pepsinogens