scholarly journals Intrinsic factor antibodies and intrinsic factor mediated vitamin B-12 absorption in pernicious anaemia.

Gut ◽  
1965 ◽  
Vol 6 (5) ◽  
pp. 436-438 ◽  
Author(s):  
S Ardeman ◽  
I Chanarin
2019 ◽  
Vol 109 (3) ◽  
pp. 674-683
Author(s):  
Ma'atem B Fofou-Caillierez ◽  
Rosa-Maria Guéant-Rodriguez ◽  
Jean-Marc Alberto ◽  
Céline Chéry ◽  
Thomas Josse ◽  
...  

ABSTRACT Background The risk of neural tube defects (NTDs) is influenced by nutritional factors and genetic determinants of one-carbon metabolism. A key pathway of this metabolism is the vitamin B-12– and folate-dependent remethylation of homocysteine, which depends on methionine synthase (MS, encoded by MTR), methionine synthase reductase, and methylenetetrahydrofolate reductase. Methionine, the product of this pathway, is the direct precursor of S-adenosylmethionine (SAM), the universal methyl donor needed for epigenetic mechanisms. Objectives This study aimed to evaluate whether the availability of vitamin B-12 and folate and the expression or activity of the target enzymes of the remethylation pathway are involved in NTD risk. Methods We studied folate and vitamin B-12 concentrations and activity, expression, and gene variants of the 3 enzymes in liver from 14 NTD and 16 non-NTD fetuses. We replicated the main findings in cord blood from pregnancies of 41 NTD fetuses compared with 21 fetuses with polymalformations (metabolic and genetic findings) and 375 control pregnancies (genetic findings). Results The tissue concentration of vitamin B-12 (P = 0.003), but not folate, and the activity (P = 0.001), transcriptional level (P = 0.016), and protein expression (P = 0.003) of MS were decreased and the truncated inactive isoforms of MS were increased in NTD livers. SAM was significantly correlated with MS activity and vitamin B-12. A gene variant in exon 1 of GIF (Gastric Intrinsic Factor gene) was associated with a dramatic decrease of liver vitamin B-12 in 2 cases. We confirmed the decreased vitamin B-12 in cord blood from NTD pregnancies. A gene variant of GIF exon 3 was associated with NTD risk. Conclusions The decreased vitamin B-12 in liver and cord blood and decreased expression and activity of MS in liver point out the impaired remethylation pathway as hallmarks associated with NTD risk. We suggest evaluating vitamin B-12 in the nutritional recommendations for prevention of NTD risk beside folate fortification or supplementation.


1968 ◽  
Vol 13 (12) ◽  
pp. 425-429 ◽  
Author(s):  
R. D. Finney ◽  
R. W. Payne

Levels of plasma radioactivity were measured 8 1/2 hours after an oral dose of 1 μg of 57Co-labelled vitamin B12. The oral test dose was followed after 2 hours by a large parenteral dose (1,000 μg) of non-radioactive vitamin B12. The results of this test have been compared with the results of the urinary excretion (Schilling test) in 14 normal subjects and in 14 patients suffering from pernicious anaemia (in 10 of whom the test was later repeated with added hog intrinsic factor). Very low levels of plasma radioactivity were found in patients suffering from pernicious anaemia (less than 0.21% of the administered dose per litre of plasma); much higher levels of radioactivity (more than 0.95% of administered radioactivity per litre of plasma) were found in normal subjects. Levels of plasma radioactivity approaching but not quite reaching the normal range were found in patients with pernicious anaemia when the test was repeated with the addition of hog intrinsic factor. It is concluded that this test provides a simple, rapid, semi-quantitative method of assessing the absorption of vitamin B12 from the gastro-intestinal tract. In our view, it is likely to supplant the Schilling test for routine use in a busy general hospital.


2021 ◽  
Vol 14 (5) ◽  
pp. e242836
Author(s):  
Masahiro Taniguchi ◽  
Gota Sudo ◽  
Yuzufumi Sekiguchi ◽  
Hiroshi Nakase

A 62-year-old woman was referred to our department for further investigation of anaemia. Blood test showed macrocytic anaemia. Oesophagogastroduodenoscopy (OGD) revealed proximal-predominant gastric atrophy and flat elevated lesion in the gastric body. Several days after OGD, she complained of gait disturbance and was diagnosed with subacute combined degeneration of the spinal cord. Furthermore, laboratory tests showed positive for both anti-parietal cell and anti-intrinsic factor antibodies, as well as increased serum gastrin level and decreased pepsinogen I level, which confirmed the diagnosis of autoimmune gastritis (AIG). Anaemia and neurological symptoms were improved after vitamin B12 supplementation. Subsequently, the patient underwent gastric endoscopic submucosal dissection; histopathological examination revealed gastric adenoma. AIG can cause gastric neoplasms and vitamin B12 deficiency, with the latter resulting in pernicious anaemia and neurological disorders. These diseases are treatable but potentially life-threatening. This case highlights the importance of early diagnosis of AIG and proper management of its comorbidities.


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