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Pentti Sipponen

Publications and source records attributed to Pentti Sipponen.

21 records · Page 2Linked to original sources
PubMed2002

Delayed rise in incidence of gastric cancer in females results in unique sex ratio (M/F) pattern: etiologic hypothesis.

BACKGROUND: The age-standardized and cumulative incidence rates of gastric cancer (GCA) are twice as high in males as in females. METHODS: Based on age-group-specific (5-year age groups) annual incidence data of GCA among males and females published by 18 cancer registries worldwide, and on a consecutive series of 938 GCAs from Finland, we explored how the male predominance of GCA has changed over the decades and how this male predominance may possibly vary worldwide between populations with high and low gastric cancer incidence. RESULTS: It appeared that the age-group-specific male-to-female (M/F) ratio of the annual GCA incidence is not constant but increases with age, reaches a peak at age around 60, and decreases thereafter. This special form of the M/F curve is not seen in other gastrointestinal (GI) cancer types (colon, rectum, pancreas). This "low-high-low" form of the M/F curve is related to a 10- to 15-year delay in the appearance and onset of GCA of the intestinal type in females compared with males. The age-group-specific M/F ratio rises as the GCA of the intestinal subtype prevails in males and is rare in females before age 60 and starts to decrease after age 60 as the GCA of the intestinal subtype begins to be common also in females. This special form of the M/F curve is globally consistent and similar in countries or populations of high and low GCA incidence. The data from the Finnish Cancer Registry indicate that the age group-specific M/F curve of the annual GCA incidence has, in addition, remained unchanged over the decades (from the 1950s) in spite of a decrease in the annual GCA incidence of more than 70%. In order to examine the role of gastritis-related diseases as a cause of the sex difference in GCA, 1700 consecutive endoscopied outpatients were studied in Finland. In this series, the age-group-specific prevalences of Helicobacter pylori gastritis, atrophic gastritis, or intestinal metaplasia were proportionally as common in males as in females in all age groups except for the youngest one (20-49 years), in which H. pylori nonatrophic gastritis was slightly more common in males than in females. CONCLUSION: The male predominance of GCA is a global phenomenon, and is similar in populations with high and low GCA incidence, and this predominance is related to a 10- to 15-year delay in the appearance and onset of GCA of the intestinal subtype in females compared with males. It is suggested that sex hormones (estrogens) protect women against GCA, and that GCA begins to be as prevalent in females as in males only after the menopausal age. Another possibility is that a later acquisition of H. pylori gastritis in females than in males causes the relative delay in the appearance and onset of new GCA cases in females compared with males.

Adult↗
PubMed2002

Diagnosis of atrophic gastritis from a serum sample.

On the basis of the levels of serum pepsinogen I (S-PGI) and gastrin-17 (S-G-17) as well as Helicobacter pylori - antibodies assayed from a blood sample it is possible to establish with high sensitivity and specificity whether the patient has gastritis, whether the gastritis is atrophic or not and in which part of the stomach the atrophic changes are located. The test enables the identification of patients whose risk of gastric cancer, of the consequences of vitamin B12 deficiency (e.g. elevated levels of homocysteine) or of peptic ulcer is considerably increased and who can then undergo gastroscopy. It also facilitates the diagnosis of non-atrophic Helicobacter gastritis enabling treatment before endoscopy.

Finland↗
PubMed2001

Cyclooxygenase-2 and Bcl-2 expression in the stomach mucosa of Wistar rats exposed to Helicobacter pylori, N'-methyl- N'-nitro- N-nitrosoguanidine and bile.

Cyclooxygenase-2 (COX-2) and Bcl-2 have been implicated in upper gastrointestinal tract carcinomas, but the underlying mechanisms are not known. In the present study we assessed the correlation of COX-2 and Bcl-2 to known cell kinetics in the glandular stomach mucosa of 104 Wistar rats given combinations of Helicobacter pylori, MNNG ( N'-methyl- N'-nitro- N-nitrosoguanidine) and bile. COX-2 expression, Bcl-2 and cell proliferation (Ki-67) in antral and corpus mucosa were determined immunohistochemically. Apoptotic cells were detected using terminal uridine deoxynucleotidyl nick end labelling technique. Expression of COX-2 was found in the lower portion of glandular corpus epithelium, and Bcl-2 positivity was mainly seen in the proliferative zone of both antrum and corpus mucosa. COX-2 expression in histologically normal-appearing corpus mucosa was associated with cell proliferation, atrophy and intestinal metaplasia in antrum and with Bcl-2 expression in corpus mucosa. No correlation was found between apoptosis and Bcl-2 expression. MNNG but not H. pylori significantly increased COX-2 in corpus mucosa. H. pylori, however, promoted the COX-2 expression in corpus when bile was added and Bcl-2 expression in antrum. Abnormal expression of both COX-2 and Bcl-2 seem to be involved in H. pylori-induced gastric carcinogenesis by altering the gastric cell kinetics.

Animals↗