PMID- 10445536
OWN - NLM
STAT- MEDLINE
DCOM- 19990823
LR  - 20061115
IS  - 0002-9270 (Print)
IS  - 0002-9270 (Linking)
VI  - 94
IP  - 8
DP  - 1999 Aug
TI  - Gastric cellular turnover and the development of atrophy after 31 years of 
      follow-up: a case-control study.
PG  - 2109-14
AB  - OBJECTIVE: Why only some patients colonized with Helicobacter pylori (H. pylori) 
      develop atrophy, a preneoplastic change, is not known. Because gastric mucosal 
      mass is dependent upon a balance between epithelial proliferation and turnover, 
      we hypothesized that atrophy may develop due to increased apoptosis relative to 
      proliferation. METHODS: Gastric epithelial apoptosis was measured by terminal 
      deoxyuridine nucleotide nick end labeling (TUNEL) assay and proliferation by 
      Ki-67 immunohistochemistry in gastric corpus biopsies in a unique cohort of 
      patients followed for 31 yr (1952-1983). Sixteen patients who developed atrophy 
      over this time were selected (cases), with two matched controls, who did not 
      develop atrophy, for each. Apoptosis and proliferation were measured in the 
      corpus biopsies taken in 1952. RESULTS: Cases (N = 16) and controls (N = 32) were 
      well matched for age, sex, initial histology, and severity of H. pylori 
      infection. In the initial (1952) biopsies, 4.3 +/- 1.7 cells (mean +/- SEM) per 
      gland were Ki-67-positive in the cases, compared with 2.1 +/- 0.4 in controls (p 
      = 0.48). 9.2 +/- 2.3 cells per gland were terminal deoxyuridine nucleotide nick 
      end labeling-positive in cases, compared with 6.3 +/- 0.8 in controls (p = 0.29). 
      Proliferation to apoptosis ratios were similar in both groups (cases, 0.38 +/- 
      0.16; controls 0.39 +/- 0.08, p = 0.37). CONCLUSIONS: Patients who later 
      developed atrophy, initially had mildly (but not statistically significant) 
      increased gastric epithelial cell proliferation and apoptosis, compared with 
      those patients who did not develop atrophy, suggesting increased cellular 
      turnover in the atrophy group. However, in these patients with gastritis, the 
      ratio of apoptosis to proliferation was not a determinant of risk for development 
      of atrophy decades later.
FAU - Moss, S F
AU  - Moss SF
AD  - St. Luke's-Roosevelt Hospital/Columbia University, New York, New York 10025, USA.
FAU - Valle, J
AU  - Valle J
FAU - Abdalla, A M
AU  - Abdalla AM
FAU - Wang, S
AU  - Wang S
FAU - Siurala, M
AU  - Siurala M
FAU - Sipponen, P
AU  - Sipponen P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Gastroenterol
JT  - The American journal of gastroenterology
JID - 0421030
RN  - 0 (Ki-67 Antigen)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Apoptosis/*physiology
MH  - Biopsy
MH  - Case-Control Studies
MH  - Cell Division/physiology
MH  - Female
MH  - Follow-Up Studies
MH  - Gastric Mucosa/microbiology/*pathology
MH  - Gastritis, Atrophic/*pathology
MH  - Helicobacter Infections/*pathology
MH  - *Helicobacter pylori
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Ki-67 Antigen/analysis
MH  - Male
MH  - Middle Aged
EDAT- 1999/08/13 00:00
MHDA- 1999/08/13 00:01
CRDT- 1999/08/13 00:00
PHST- 1999/08/13 00:00 [pubmed]
PHST- 1999/08/13 00:01 [medline]
PHST- 1999/08/13 00:00 [entrez]
AID - S0002927099003421 [pii]
AID - 10.1111/j.1572-0241.1999.01286.x [doi]
PST - ppublish
SO  - Am J Gastroenterol. 1999 Aug;94(8):2109-14. doi: 
      10.1111/j.1572-0241.1999.01286.x.