title: Clinical use of proton-pump inhibitors but not H2-blockers or antacid/alginates raises the serum levels of amidated gastrin-17, pepsinogen I and pepsinogen II in a random adult population.
abstract: OBJECTIVE
  Proton-pump inhibitors (PPIs), H(2) receptor antagonists (H(2)RAs) and antacids/alginates reduce intragastric acidity and may thus influence normal gastric physiology. The purpose of this study was to examine the effect of these compounds on serum levels of amidated gastrin-17 (G-17) and pepsinogens (PGI & PGII) in a large, random, adult Swedish population sample with uninfected stomach mucosa.
  
  
  METHODS
  The initial sample subjects (n=1000, mean age 50 years, range 20-80 years) completed a questionnaire on the use of acid inhibitory drugs 1 week and/or 3 months before study entry. All subjects (n=590) with normal gastric mucosa as delineated by serum biomarkers were included. Among them, serum levels of PGI, PGII and G-17 were compared between those who used acid inhibitory drugs and those who did not.
  
  
  RESULTS
  The serum levels of G-17 or pepsinogens in the subjects who reported use of H(2)RAs (n=18) or antacid/alginates (n=66) during the previous 3 months did not differ from those in non-users (n=471). However, the median levels of G-17 and pepsinogens were significantly (p<0.001) higher among the PPI users (n=35) than among non-users: the levels were approximately doubled. The ratio of PGI/PGII was, however, similar between PPI users and non-users, or those using antacids/alginates or H(2)RAs. Among subjects using PPIs, the serum levels of pepsinogens correlated positively (p<0.01) with the serum levels of G-17.
  
  
  CONCLUSIONS
  PPIs but not antacids/alginates or H(2)RAs markedly increase the fasting levels of serum amidated G-17 and pepsinogens among ordinary patients in everyday clinical practice.
authors.affiliation: Centre for Family Medicine, Karolinska Institutet, Stockholm, Sweden. lars.agreus@ki.se
authors.forename: Lars
authors.initials: L
authors.lastname: Agréus
authors.forename: Tom
authors.initials: T
authors.lastname: Storskrubb
authors.forename: Pertti
authors.initials: P
authors.lastname: Aro
authors.forename: Jukka
authors.initials: J
authors.lastname: Ronkainen
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Talley
authors.forename: Pentti
authors.initials: P
authors.lastname: Sipponen
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000473:pathology; D005755:Gastrins / Q000097:blood* / Q000378:metabolism; D006635:Histamine H2 Antagonists / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D020115:Pepsinogen C / Q000097:blood; D010435:Pepsinogens / Q000097:blood* / Q000378:metabolism; D011336:Probability; D054328:Proton Pump Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D018570:Risk Assessment; D018709:Statistics, Nonparametric; D011795:Surveys and Questionnaires; D055815:Young Adult
chemical_list: D015415:Biomarkers; D005755:Gastrins; D006635:Histamine H2 Antagonists; D010435:Pepsinogens; D054328:Proton Pump Inhibitors; C013550:gastrin 17; D020115:Pepsinogen C; D020116:Pepsinogen A