title: '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.
  
  
  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 between the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 +/- 58.4 microg/L) were significantly lower than those in Group B (sPGI 159.5 +/- 80.6 microg/L; P < 0.0001) as well as sPGII (12.5 microg/L = 6.24 versus 20.6 +/- 58 microg/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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Dept. of Clinical Science, University of Parma, Parma, Italy. francesco.dimario@unipr.it
authors.forename: F
authors.initials: F
authors.lastname: Di Mario
authors.forename: A M
authors.initials: AM
authors.lastname: Moussa
authors.forename: P
authors.initials: P
authors.lastname: Caruana
authors.forename: R
authors.initials: R
authors.lastname: Merli
authors.forename: L G
authors.initials: LG
authors.lastname: Cavallaro
authors.forename: G M
authors.initials: GM
authors.lastname: Cavestro
authors.forename: N
authors.initials: N
authors.lastname: Dal Bò
authors.forename: V
authors.initials: V
authors.lastname: Iori
authors.forename: A
authors.initials: A
authors.lastname: Pilotto
authors.forename: G
authors.initials: G
authors.lastname: Leandro
authors.forename: A
authors.initials: A
authors.lastname: Franzè
authors.forename: M
authors.initials: M
authors.lastname: Rugge
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000276:immunology; D001426:Bacterial Proteins / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D004415:Dyspepsia / Q000382:microbiology; D005192:Family Health; D005260:Female; D005755:Gastrins / Q000097:blood; D005757:Gastritis, Atrophic / Q000150:complications / Q000382:microbiology; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D020115:Pepsinogen C / Q000097:blood; D013274:Stomach Neoplasms / Q000175:diagnosis* / Q000235:genetics* / Q000382:microbiology
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; D005755:Gastrins; D007074:Immunoglobulin G; C080866:cagA protein, Helicobacter pylori; C013550:gastrin 17; D020115:Pepsinogen C; D020116:Pepsinogen A