A Re-Assessment of the Gastric Lesion in Pernicious Anaemia

Magnus, Hugo

doi:10.1136/jcp.11.4.289

Cited by 50 publications

(25 citation statements)

References 25 publications

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“…Similar results have been reported after gastrin stimulation [41]. Total loss of parietal cells is observed in only 40% of patients with gastric atrophy and pernicious anemia [60]. A reduced secretion of intrinsic factor could thus persist; immunological inactivation of intrinsic factor in the gastric juice, then will explain the absolute deficiency in vitamin B12 absorption [79].…”

Section: Intrinsic-factor Secretion [2 3 37 41 87 109]supporting

confidence: 68%

Chronic Gastritis

Lambert¹

1972

Digestion

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Section: Intrinsic-factor Secretion [2 3 37 41 87 109]supporting

confidence: 68%

Chronic Gastritis

Lambert¹

1972

Digestion

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“…Our data obtained in an unselected series should approximate the real prevalence of the phenomenon, at least in our regions. Furthermore, should autoim mune atrophic gastritis be confirmed as a preneoplastic condition [11][12][13], the present data would indicate vitiligo patients as a pop ulation at risk of gastric neoplasia, which therefore need to be monitored.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Autoimmune Atrophic Gastritis in Vitiligo

et al. 1986

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Gastric biopsies, and measurements of fasting serum gastrin levels and titers of antihuman parietal cell antibodies have been performed in 65 unselected patients with vitiligo. Histologic evidence of autoimmune atrophic gastritis has been obtained in 10 cases (15 %), who were all positive for the antibodies and who had elevated gastrin levels. The study of gastric secretion after pentagastrin stimulation, performed in 7 of these patients, showed a markedly reduced acid output. The present study provides definite evidence of the association of autoimmune atrophic gastritis with a proportion of vitiligo cases and suggests the need for surveillance of these patients in terms of gastric neoplasia.

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“…Before the introduction of peroral biopsy, the original observation by Magnus and Ungley (1938) drew attention to the histological distinction between body and antrum in PA. In chronic atrophic gastritis not associated with the lesion of PA this distinction has not been made.…”

Section: Discussionmentioning

confidence: 99%

Gastric morphology and serum gastrin levels in pernicious anaemia.

Lewin¹,

Dowling²,

Wright³

et al. 1976

Gut

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SUMMARY Mucosal biopsies from multiple sites in the stomachs of 21 patients with pernicious anaemia have been examined. The histological changes almost always involved the entire gastric mucosa, including that of the pyloric antrum. Metaplastic changes were almost universal and consisted of intestinal metaplasia in the body and antrum and pyloric metaplasia in the body. The severity of the pyloric metaplasia was such as to make the distinction between body and antrum on biopsy impossible. No relationship was found between serum gastrin activity and the histological appearances of the gastric antrum or body.The past 25 years have witnessed the introduction of techniques whose application has contributed substantially to the investigation of the nature of chronic gastritis. Peroral suction biopsy (Wood et al., 1949;Joske et al., 1955) of the body and fundus of the stomach has provided a solid histological foundation which, in conjunction with measurements of gastric secretion of acid (Bock et al., 1963) and intrinsic factor and the detection of gastric antibodies (te Velde et al., 1966;Fisher et al., 1967), has considerably extended our knowledge of the pathophysiology of the body of the stomach.In contrast, the structure and function of the gastric antrum was until recently little studied. The introduction of the fibreoptic gastroscope made possible multiple biopsying of the gastric mucosa from well-defined sites in the body and pyloric antrum (Seifert and Knoll, 1968;Konturek and Urban, 1969; Ottenjann et al., 1969a, b) Methods PATIENTSEighteen patients (14 women and four men) referred to our clinic at Stanford University Medical Center with established or suspected PA were studied. Diagnosis was established by failure to secrete detectable acid in response to a maximal dose of gastric stimulant (betazole 1-7 mg/kg body weight) and urinary excretion of less than 10% of a 0-5 Kg oral dose of 57Co B12 in a standard Schilling test, which was corrected with added gastric intrinsic factor. Supporting evidence was low serum vitamin B12 activity, low or absent gastric intrinsic factor secretion, and the presence of circulating gastric antibodies.In addition, studies are included of three patients who were referred for suspected PA but in whom the above criteria were not completely fulfilled (Table 1).

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A Re-Assessment of the Gastric Lesion in Pernicious Anaemia

Cited by 50 publications

References 25 publications

Chronic Gastritis

Chronic Gastritis

Prevalence of Autoimmune Atrophic Gastritis in Vitiligo

Gastric morphology and serum gastrin levels in pernicious anaemia.

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