Parietal-Cell Antibodies in Patients With Duodenal Ulcer and Gastric Cancer

Kravetz, Robert E.; Noorden, Susan Van; Spiro, Howard M.

doi:10.1016/s0140-6736(67)91299-8

Cited by 26 publications

(5 citation statements)

References 4 publications

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“…These findings, however, confirm those of Kravetz, Van Noorden, and Spiro (1967) and of te Velde (1967) who found no increased prevalence of parietal cell antibody in gastric carcinoma. In addition the present study has demonstrated that the prevalence of intrinsic factor antibody is not increased in gastric carcinoma.…”

Section: Discussionsupporting

confidence: 88%

The prevalence and significance of circulating antibodies to gastric intrinsic factor and parietal cells in gastric carcinoma

Ungar¹,

Strickland²,

Francis³

1971

Gut

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SUMMARYThe prevalence of circulating antibodies to gastric intrinsic factor and parietal cells was examined in 60 patients with histologically proven gastric carcinoma and was found not to differ from the prevalence of these antibodies in control subjects of similar age and sex distribution.Amongst the 60 patients with gastric carcinoma seven were thought to have actual or potential pernicious anaemia.The absence of an increased prevalence of antigastric antibodies in gastric carcinoma indicates that gastritis itself, whether autoimmune or not, is the likely common denominator underlying the predisposition to gastric carcinoma in both pernicious anaemia and chronic atrophic gastritis.The studies of Kaplan and Rigler (1945) and Mosbech and Videbaek (1950) established that pernicious anaemia is associated with an incidence of gastric carcinoma approximately three times greater than that expected for the population at large.On the basis of a study of 35 patients with gastric carcinoma Shearman, Finlayson, Wilson, and Samson (1966) suggested that the extent of this association may have been underestimated. We have investigated this possibility by estimating serum vitamin B12 levels and the prevalence of circulating antibodies to gastric intrinsic factor and parietal cells in 60 patients with histologically proven gastric carcinoma. The prevalence of antigastric antibodies is compared with that in control subjects of similar age and sex distribution. Patients and MethodsThe 60 patients with gastric carcinoma comprised 37 men and 23 women. Blood samples were requested from patients with a diagnosis on admission or subsequently of gastric carcinoma admitted to the Royal Melbourne Hospital over a period of three years. Only those in whom a gastric carcinoma was histologically proven at operation or necropsy were included in this series. The age and sex distribution of the patients is shown in Tables I and II.

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Section: Discussionsupporting

confidence: 88%

The prevalence and significance of circulating antibodies to gastric intrinsic factor and parietal cells in gastric carcinoma

Ungar¹,

Strickland²,

Francis³

1971

Gut

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show abstract

“…MacFadyen, Goldberg, Dagg, and Anderson (1965) found a significant history of bleeding only among those iron-deficient patients with both achlorhydria and antibodies who did not have relatives with antibodies. The equally low incidence of parietal-cell antibodies in patients who had had partial gastrectomy for duodenal ulcer and in others with gastric carcinoma has also suggested that antibodies may be a reaction to gastritis, but that few patients are able to produce them (Kravetz, van Noorden, and Spiro, 1967).…”

Section: Discussionmentioning

confidence: 99%

Gastric secretory response to iron therapy.

Stone¹

1968

Gut

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“…[21][22][23] The presence of PCA was not associated with the risk of noncardia gastric cancer in our study, which is in line with the results of Kravetz and coworkers. 24 Interactions between IgA and IgG antibodies and PG I Study of the interaction between IgA and IgG antibodies showed that one prerequisite for an elevated risk of noncardia gastric cancer at negative PG I levels was that both IgA and IgG antibodies were elevated. The number of subjects who only had an IgA response was too small to allow any risk analysis, however; among those with only an IgG response, helicobacter infection was not significantly associated with noncardia gastric cancer risk.…”

Section: Pepsinogen I (Pgi) and Pcamentioning

confidence: 99%

Helicobacter pylori IgA and IgG antibodies, serum pepsinogen I and the risk of gastric cancer: Changes in the risk with extended follow‐up period

Knekt

Teppo

Aromaa

et al. 2006

Intl Journal of Cancer

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The prediction of Helicobacter pylori antibodies immunoglobulin A (IgA) and immunoglobulin G (IgG) and serum pepsinogen I (PG I) on gastric cancer occurrence was studied in a nested case-control study, based on 225 incident cancer cases and 435 matched controls from a Finnish cohort followed from 1966-1991. The odds ratio of noncardia gastric cancer between infected and noninfected persons was 3.12 (95% confidence interval (CI) 5 1.97-4.95) for elevated IgA and 2.88 (CI: 1.63-5.07) for elevated IgG antibodies. The odds ratio between low and high PG I was 2.24 (CI: 1.43-3.49). The strength of association was significant for IgA antibodies during the total follow-up, but for IgG antibodies this was only true for follow-up periods of 15 years or more. IgA antibodies were significantly associated with all registered histological subtypes apart from intestinal type adenocarcinoma. The highest gastric cancer risk was found among individuals with simultaneously elevated IgA and IgG antibodies and low PG I with an odds ratio of 10.9 (CI: 4.31-27.7) in comparison with those who were negative for both antibodies and had normal PG I. Elevated IgA and IgG antibodies and low PG I were not associated with cancers of the gastric cardia. The findings support the hypothesis that H. pylori infection is a cause of noncardia gastric cancer. Although elevated H. pylori IgA and IgG antibodies and low PG I independently could predict the occurrence of noncardia gastric cancer, their power to do so varied with the stage and length of the follow-up period and it increased when they were applied in combination. ' 2006 Wiley-Liss, Inc.Key words: gastric cancer; H. pylori; IgA antibodies; IgG antibodies; pepsinogen I Chronic infection with Helicobacter pylori leads to chronic gastritis, which may progress to atrophy, intestinal metaplasia and finally to noncardia gastric cancer. 1,2 This hypothesis is in line with results from prospective serologic studies that have shown higher incidence of noncardia gastric cancer in subjects with H. pylori infection, verified by specific IgG antibodies, than in noninfected ones. 3 Practically, all helicobacter-infected subjects have immunoglobulin G (IgG) antibodies, whereas immunoglobulin A (IgA) antibodies are found in approximately two-thirds of infected subjects. 4 Of infected individuals, 2-3% show an elevated IgA antibody level alone. 4 In a 13-year gastric cancer follow-up of the Finnish Mobile Clinic Health Examination cohort, we demonstrated an elevated risk of the disease in persons with H. pylori antibodies of the IgA class and in those with a low serum pepsinogen I (PG I) level. Unexpectedly, however, H. pylori antibodies of the IgG class were not significantly related to the risk of gastric cancer in this cohort characterized by high prevalence of helicobacter infection also in control subjects. 5 We have now conducted a new study for a follow-up period that has been extended up to 24 years within the same study population, to clarify whether the impact of high IgA and IgG antibodies and l...

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Parietal-Cell Antibodies in Patients With Duodenal Ulcer and Gastric Cancer

Cited by 26 publications

References 4 publications

The prevalence and significance of circulating antibodies to gastric intrinsic factor and parietal cells in gastric carcinoma

The prevalence and significance of circulating antibodies to gastric intrinsic factor and parietal cells in gastric carcinoma

Gastric secretory response to iron therapy.

Helicobacter pylori IgA and IgG antibodies, serum pepsinogen I and the risk of gastric cancer: Changes in the risk with extended follow‐up period

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