Intrinsic Factor

Herbert, Victor; Castle, W. E.

doi:10.1056/nejm196405282702209

Cited by 19 publications

(5 citation statements)

References 52 publications

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“…II I93 Gastric airtoimnzunity and inherited characteristics. Among the probands of the study the prevalence of blood group A (48.5 per cent) was slightly higher and that of Lea-positive red cells (14.6 per cent) was lower than the figures quoted for the general population by Ikin, KopeC, Mourant, Parkin and Walby (1952) and by Callender eta!. (1957), but the differences were not statistically significant.…”

Section: Genetic Consideratioilscontrasting

confidence: 54%

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B₁₂ ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

et al. 1968

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A good but not absolute correlation between the presence of the gastric parietal cell antibody and impairment of gastric secretion was observed in the relatives of patients with pernicious anaemia. By analogy, although the majority of relatives without the antibody secreted normal amounts of acid and of intrinsic factor nearly one-fifth secreted unexpectedly small amounts of intrinsic factor.There was a highly significant correlation between the amounts of acid and of intrinsic factor secreted in response to histamine or gastrin and as a rule impairment of secretion affected these substances to the same extent. However, one young relative who did not have gastric or thyroid antibodies was considered to have selective impairment of intrinsic factor secretion.Thirty-eight subjects had direct measurements of intrinsic factor and tests of vitamin BIZ absorption. Twenty-seven of these secreted less than 600 units of intrinsic factor in the hour following stimulation and all but two had malabsorption of radioactive vitamin BIZ. Similarly all but two of the 11 subjects who secreted more than this amount had normal absorption of the vitamin.Twenty-two per cent of the probands of the study had a family history of pernicious anaemia, 18 per cent one of thyroid disease, 20 per cent one of diabetes mellitus and 3.8 per cent had a family history of carcinoma of the stomach.Analysis of the distribution of inherited characteristics showed that there was a slight but not significant excess of blood group A in the patients with pernicious anaemia and that the proportion of patients with Lea-positive red cells was lower than the figure quoted for the general population. Neither in the probands nor in their relatives was there an association between blood group A or the Lea group and the tendency to form circulating antibodies to gastric parietal cells. Moreover, although the proportion of patients with pernicious anaemia who had light-coloured eyes was of the same order as in a previous study from this department, the prevalence of gastric parietal cell antibodies was no higher in such patients than in those with dark eyes, nor was the prevalence of the antibodies significantly increased in patients who gave a history of premature greying.The gastric parietal cell antibody was no more common in the spouses of probands than in matched control subjects. It was further equally common in relatives of probands without the antibody as in relatives of probands with the antibody. Analysis of three families in which both parents had pernicious anaemia and of seven families in which it was possible to study both parents of the proband suggested that the

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Section: Genetic Consideratioilscontrasting

confidence: 54%

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B₁₂ ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

et al. 1968

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“…Nor was there any evidence that antibodies present in the gastrointestinal secretions (Fisher et a\., 1966;Carmel and Herbert, 1967) or elsewhere in the gastrointestinal tract (Ardeman and Clianarin, 1965 ;Baur et al, 1968) had any significant effect on the action of hog intrinsic factor in patients not previously exposed to hog intrinsic factor. Our findings do not exclude the possibility that the gastric mucosa itself may be the site of action of circulating antibodies to intrinsic factor in pernicious anaemia (Herbert, 1965 ;Baur et al, 1968), or the possibility that human intrinsic factor may be neutralized by antibodies after its release from the gastric niucosa (Ardeman and Chanarin, 1965;Fisher et al, 1966;Carmel and Herbert, 1967) although they do suggest that the quantity of antibody available for this purpose in the gastrointestinal tract is probably quite small.…”

Section: Discussionmentioning

confidence: 60%

“…Although specificity of antibodies to human, hog and rat intrinsic factors has been demonstrated in some assay systems (Ramsay and Herbert, 1965), antibody to human intrinsic factor has been shown to cross react with hog intrinsic factor in vitro (Taylor and Morton, 1958) and under certain experimental conditions in vivo (Taylor, 1959 ;Schwartz, 1960).…”

Section: Discussionmentioning

confidence: 99%

Antibody Activity against Hog Intrinsic Factor in Pernicious Anaemia

Ungar

1969

Br J Haematol

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Summary. The sera of 100 adult patients with Addisonian pernicious anaemia not previously exposed to hog intrinsic factor were tested for antibody activity against hog intrinsic factor by the charcoal method: 55 sera containing antibody to human intrinsic factor showed antibody activity against hog intrinsic factor; 45 sera had no demonstrable antibody activity against human or hog intrinsic factor. A high degree of cross reactivity between antibody to human intrinsic factor and hog intrinsic factor was thus demonstrated in vitro. Hog intrinsic factor was equally effective in potentiating vitamin B12 absorption to normal levels in pernicious anaemia patients with and without circulating antibody active against hog intrinsic factor. Antibody to intrinsic factor circulating in the blood was therefore considered to have no effect on hog intrinsic factor in the human gastrointestinal tract. The possibility of a direct effect of circulating antibodies on the production and/or release of endogenous intrinsic factor by the gastric mucosa could not be excluded.

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“…8). Secretion of Castle's intrinsic factor by the stomach is required for the absorption of vitamin B~2 from the ileum [12,13].…”

Section: Absorption Of Ironmentioning

confidence: 99%

Reconstruction of the esophagus by posterior invagination esophagogastrostomy

et al. 1977

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From October 1967 to August 1976 posterior invagination esophagogastrostomy in 1 stage without positional change was performed on 84 patients. Since 1971 this method has been extended to include 32 cases of cancer of the upper and middle thirds of the thoracic esophagus. The anastomosis was constructed in the neck in 27 patients, and in the thoracic cavity in 5 patients (1 supra-aortic, 2 at the level of the aortic arch, and 2 at the level of the inferior margin of the aortic arch). There were no instances of postoperative anastomotic leakage, hemothorax, chylothorax or pyothorax. Six of these patients (18.8%) died of circulatory insufficiency or pulmonary complications within 1 month of operation. Postoperative esophageal stenosis occurred at the site of anastomosis in 4 patients and was relieved by bougienage dilatation or operation under local anesthesia. Of the 32 patients with lesions in the upper and middle thoracic esophagus, 17 survived for 6 months after operation, 6 have lived for at least 3 years, and 4 are still alive after 4 years. Postoperative examinations of autonomic nervous system and cardiopulmonary functions revealed no abnormalities. In the early postoperative period, lipid and Vitamin B12 absorption was markedly disturbed but returned to normal levels by the time of the follow-up studies.Esophageal surgery originated in 1886 when Mikulicz reconstructed the cervical esophagus with a skin flap after resection of an esophageal cancer. In 1913 Torek [1] reported the first successful resection of the thoracic esophagus for carcinoma. Since then,

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Intrinsic Factor

Cited by 19 publications

References 52 publications

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B₁₂ ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B₁₂ ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

Antibody Activity against Hog Intrinsic Factor in Pernicious Anaemia

Reconstruction of the esophagus by posterior invagination esophagogastrostomy

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Intrinsic Factor

Cited by 19 publications

References 52 publications

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B12 ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B12 ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

Antibody Activity against Hog Intrinsic Factor in Pernicious Anaemia

Reconstruction of the esophagus by posterior invagination esophagogastrostomy

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Product

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A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B₁₂ ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY

A Family Study of Pernicious Anaemia: II. INTRINSIC FACTOR SECRETION, VITAMIN B₁₂ ABSORPTION AND GENETIC ASPECTS OF GASTRIC AUTOIMMUNITY