ArticleJournal of epidemiology2002
Long-term effect of smoking on serum pepsinogen values.
Article in Journal of epidemiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Gastric mucosal status in populations with a low prevalence of Helicobacter pylori in Indonesia.PloS one · 2017Article
- Accuracy and cut-off values of pepsinogens I, II and gastrin 17 for diagnosis of gastric fundic atrophy: influence of gastritis.PloS one · 2011Article
- Cytochrome p450 2E1 polymorphisms and the risk of gastric cardia cancer.World journal of gastroenterology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe serum pepsinogen I to II ratio (PG I/II) is related to the risk of stomach cancer. Smoking is an established risk factor for stomach cancer. The effect of smoking on the change in PG I/II over a 7-year span was investigated.
methodsData were from 1889 male subjects who underwent phlebotomy in both 1989 and 1996. The subjects were classified into smoking and non-smoking groups: those who continued smoking, and those who never smoked during the span. The subjects were stratified by Helicobacter pylori status (negative or positive) and age (20-29 or 30-56 years in 1989), and the change in PG I/II was compared between the smoking and the non-smoking groups.
resultsPG I/II increased less (age adjusted mean +/- standard error of the difference was 0.209 +/- 0.069, p < 0.001) and less frequently in the smoking group (65.8% versus 58.9%, p = 0.002), but these differences were not clear among H. pylori-positive subjects.
conclusionsThe less frequent increase (i.e. a more frequent decline) in PG I/II may be a long-term effect of smoking, although the effect is not clear under H. pylori infection. The decline may be one of the mechanisms through which smoking elevates the risk of stomach cancer.
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Registered trials
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