Table of Contents

Pernicious anemia

Introduction

Mayo Clinic overview

Normal human gastric juice contains an “intrinsic factor” that, given simultaneously with vitamin B12 causes erythropoiesis (production of red blood cells).

Quoted from nih.gov/health-topics...Some people get pernicious anemia because they don't have enough vitamin B12 in their diets. This cause of pernicious anemia is less common than other causes.

Good food sources of vitamin B12 include:

Strict vegetarians who don't eat any animal or dairy products and don't take a vitamin B12 supplement are at risk for pernicious anemia.

Breastfed infants of strict vegetarian mothers also are at risk for pernicious anemia. These infants can develop anemia within months of being born.

Gastric parietal cells produce two essential biologics: intrinsic factor and HCl acid. Pernicious anemia is a consequence of intrinsic factor loss and neutralizing intrinsic factor antibody that impairs cobalamin absorption. 1)

Aspects in Diagnosis. 2)

Large intakes of folic acid may delay the diagnosis of vitamin B-12 deficiency, which could lead to irreversible neuropathy. 3)

This review discusses the usefulness and limitations of current biomarkers of B12 status in newborn screening, infant and adult diagnostics, the algorithms utilized to diagnose B12 deficiency and unusual findings of vitamin B12 status in various human disorders. 4)

Laboratory findings

Differing presentations

Evidence of infectious cause

Quoted from nih.gov/health-topics...Sometimes pernicious anemia occurs because the body's small intestine can't properly absorb vitamin B12. This may be the result of:

Supplementation with B vitamins

A high level of blood serum homocysteine (known as “homocysteinemia”) is associated with pernicious anemia. Because supplementation of the B vitamins lower levels of homocysteine, one common intervention for altering this risk factor is to supplement patients at risk for cardiovascular disease with folic acid (B9), pyridoxine (B6), and cyanocobalamin (B12). In fact, interventions designed to lower levels of homocysteine with high-dose supplementation of the B vitamins have been equivocal, in some cases, seeming to exacerbate disease.

Marino et al. showed that eradication of Helicobacter pylori associated with gastritis reduced abnormally high levels of homocysteine.7)

Changes in gut bacteria

Methylcobalamin and cyanocobalamin supplementation differ in their effects on gut bacteria 8)

Patient experiences

One patient suggests this video https://www.youtube.com/watch?v=QqjyAeOLyKM which shows potential consequences of undiagnosed abnormally low B12 . Below is the list of tests required and some quotes

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This material by Elissa Leonard 2011

Management

Given that the B vitamins probably interfere with immune response to microbes, MP patients should as far as possible avoid taking supplemental doses of vitamin B12, provided appropriate tests for B12 deficiency are made with no finding of profoundly low B12. 9)

Caution

Myeloneuropathy is caused by inactivation of vitamin B12 by nitrous oxide. This syndrome can also be seen in patients with borderline vitamin B12 deficiency who have recently been anesthetized with nitrous oxide. 10)

===== Notes and comments =====

<DiseaseHierarchy>

GETCONTENT https://www.ncbi.nlm.nih.gov/pubmed/?term=Thornalley https://www.marshallprotocol.com/view_topic.php?id=16203&forum_id=35&highlight=Pernicious+anemia Tobias Dx https://www.marshallprotocol.com/forum35/16203.html

GillyB to wichien Posted: Tue Jun 25th, 2013 16:41 I have many of the symptoms you list as being associated with B12 deficiency, but I wonder if they could be a result of neurological IP rather than a B12 problem. You are getting a lot of B12 injectables and oral supplementation, yet still feeling the symptoms. I eat a significant amount of red meat, and while my doctor has tried to convince me to supplement B12 because she thinks I have pernicious anemia, I have not done so. I think instead these are symptoms of Th1 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens., and they will resolve themselves over time with my progress on the MP. They have increased and decreased over the course of the year, without any other changes in my diet.

  • legacy content

Sallie Q 10.22.2016 removed ref to curemy

Lots of discussion about PA and B12 deficiency here: https://curemyth1.org/view_topic.php?id=2626&forum_id=2

Lots of content here: https://www.curemyth1.org/forum2/2626.html

===== References =====

1)
Toh B. Pathophysiology and laboratory diagnosis of pernicious anemia. Immunol Res. 2017 Feb;65(1):326-330. doi: 10.1007/s12026-016-8841-7.
[PMID: 27538411] [DOI: 10.1007/s12026-016-8841-7]
2)
Tun AM, Thein KZ, Myint ZW, Oo TH. Pernicious Anemia: Fundamental and Practical Aspects in Diagnosis. Cardiovasc Hematol Agents Med Chem. 2017 Nov 8;15(1):17-22. doi: 10.2174/1871525715666170203114632.
[PMID: 28164751] [DOI: 10.2174/1871525715666170203114632]
3) , 9)
Wyckoff KF, Ganji V. Proportion of individuals with low serum vitamin B-12 concentrations without macrocytosis is higher in the post folic acid fortification period than in the pre folic acid fortification period. Am J Clin Nutr. 2007 Oct;86(4):1187-92. doi: 10.1093/ajcn/86.4.1187.
[PMID: 17921401] [DOI: 10.1093/ajcn/86.4.1187]
4)
Hannibal L, Lysne V, Bjørke-Monsen A, Behringer S, Grünert SC, Spiekerkoetter U, Jacobsen DW, Blom HJ. Biomarkers and Algorithms for the Diagnosis of Vitamin B12 Deficiency. Front Mol Biosci. 2016 Jun 27;3:27. doi: 10.3389/fmolb.2016.00027. eCollection 2016.
[PMID: 27446930] [PMCID: 4921487] [DOI: 10.3389/fmolb.2016.00027]
5)
House AA, Eliasziw M, Cattran DC, Churchill DN, Oliver MJ, Fine A, Dresser GK, Spence JD. Effect of B-vitamin therapy on progression of diabetic nephropathy: a randomized controlled trial. JAMA. 2010 Apr 28;303(16):1603-9. doi: 10.1001/jama.2010.490.
[PMID: 20424250] [DOI: 10.1001/jama.2010.490]
6)
Lonn E, Yusuf S, Arnold MJ, Sheridan P, Pogue J, Micks M, McQueen MJ, Probstfield J, Fodor G, Held C, Genest JJ, Heart Outcomes Prevention Evaluation (HOPE) 2 Investigators. Homocysteine lowering with folic acid and B vitamins in vascular disease. N Engl J Med. 2006 Apr 13;354(15):1567-77. doi: 10.1056/NEJMoa060900. Epub 2006 Mar 12.
[PMID: 16531613] [DOI: 10.1056/NEJMoa060900]
7)
Marino MCA, de Oliveira CA, Rocha AMC, Rocha GA, Clementino NCD, Antunes LF, Oliveira RA, Martins AS, Del Puerto HL, D'Almeida V, Galdieri L, Pedroso ERP, Cabral MMDA, Nogueira AMMF, Queiroz DMM. Long-term effect of Helicobacter pylori eradication on plasma homocysteine in elderly patients with cobalamin deficiency. Gut. 2007 Apr;56(4):469-74. doi: 10.1136/gut.2006.095125. Epub 2006 Sep 27.
[PMID: 17005765] [PMCID: 1856853] [DOI: 10.1136/gut.2006.095125]
8)
Xu Y, Xiang S, Ye K, Zheng Y, Feng X, Zhu X, Chen J, Chen Y. Cobalamin (Vitamin B12) Induced a Shift in Microbial Composition and Metabolic Activity in an in vitro Colon Simulation. Front Microbiol. 2018 Nov 16;9:2780. doi: 10.3389/fmicb.2018.02780. eCollection 2018.
[PMID: 30505299] [PMCID: 6250798] [DOI: 10.3389/fmicb.2018.02780]
10)
Pema PJ, Horak HA, Wyatt RH. Myelopathy caused by nitrous oxide toxicity. AJNR Am J Neuroradiol. 1998 May;19(5):894-6.
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