Talk:Megaloblastic anemia

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Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 00:50, 18 January 2022 (UTC)

Wiki Education Foundation-supported course assignment

This article is currently the subject of a Wiki Education Foundation-supported course assignment, between 14 September 2020 and 29 April 2022. Further details are available on the course page. Student editor(s): Jjoyees.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 03:48, 17 January 2022 (UTC)

Second paragraph

Am I the first one to 'discuss' this page? Anyway, I am wondering about the second paragraph:

"The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of vitamin B12 and/or folic acid. Vitamin B12 deficiency alone will not cause the syndrome in the presence of sufficient folate, for the mechanism is loss of B12 dependent folate recycling, followed by folate-deficiency loss of nucleic acid synthesis (specifically thymine), leading to defects in DNA synthesis. Folic acid supplementation in the absence of vitamin B12 prevents this type of anemia (although other vitamin B12-specific pathologies continue)"

There is no reference, and I have yet to find one. Can someone expand on the concept of folate-replete B12 deficient states? 110.33.174.187 (talk) 06:21, 29 May 2011 (UTC)

I agree with this reader. The second paragraph has no reference and is furthermore confusing. How can Vitamin B12 deficiency alone not cause the syndrome, yet other vitamin B12-specific pathologies continue? This is a contradiction. From my research, either deficiency can lead to megaloblastic anemia [1][2][3]. I am going to delete this second paragraph (after the first sentence) for now. I am not sure about this folate masking phenomenon, but if we include it in the article we should be more specific about it. Ylok (talk) 22:16, 7 September 2018 (UTC)

Answer

The folate fortification wars: [4]. The supplemental-folate-masking of B12 deficiency by correcting MCV issue: [5] [6]

That said, there is at least one case of a person claimed to be on high folate supplementation that nevertheless had both macrocytosis AND megaloblastosis by bone marrow exam, so there is a report in which hematological signs are not completely eradicated by oral folate supplementation alone in a PA case, even though there is no good mechanism why they should not have been (why would elevated homocysteine levels make a person macrocytic and megaloblastic? Mechanistically these are both due to the methylene-TH4 trap). Here is the case-report of megaloblastosis in a person taking folate pills due to sickle cell anemia: [7]. I cannot find another one in the literature. This same article has a long list of references suggesting harm from folic acid alone in pernicious anemia patients by means of hiding the hematological symptoms: [8]. For example, here is a similar case from 1987 in which the authors claimed PA symptoms in a patient with sickle cell trait WAS masked by folate: [9]. Here is an article claiming that more than 1 mg a day of folate must be taken before masking of low B12 symptoms becomes a concern, so perhaps the patient above wasn't taking her folate pills (a high folate level can be attained without supplementation in low-B12 states, due to the altered folate metabolism). [10]. Wintrobe (2008 edition of the text) is a bit equivocal on the issue. Anyway, if you search on this, be sure to include the word "mask" or "masking" along with B12 and folate, to get the arguments about why supplementation with one partly corrects problems with the other, including (again supposedly) the anemia and other DNA synthesis problems. SBHarris 20:23, 29 May 2011 (UTC)

Drug-induced forms

NEJM doi:10.1056/NEJMra1508861 JFW | T@lk 09:10, 22 October 2015 (UTC)

This journal article is behind a paywall, without an abstract. Does it have anything in it that isn't in, say, Harrison's Medicine? Dhtwiki (talk) 03:41, 23 October 2015 (UTC)