nonmegaloblastic macrocytic anemia

[automaton]

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can anyone explain why alcoholism or aplastic anemia results in MACROCYTIC anemia? that is, why are the cells big? what mechanism?

 

[Mumpu]

IIRC this is because RBC maturation is slowed, so they grow larger before leaving the bone marrow.

 

[idq1i]

Aplastic anemia is normocytic, not macrocytic. Low retic count, too.

Alcoholic macrocytic anemia = you drank so much that you fried your stomach -> no more intrinsic factor -> no more cyanocobalmin for you. Also, alcohol can sufficiently impair folate metabolism

 

[Ramoray]

The alcohol is the same reasoning why you have thiamine def. it is mostly dietary and the fact you dont get enough folate. A minor reason is alcohol minorly interferes with methyl folate coming out of store into folate to use which adds to the decrease folate

With aplastic anemia, not all types are macrocytic, but a common cause of aplastic anemia is something like dna methylating agents, which destroy the bone marrow but the cells that are left and to get produced have their DNA messed up so they cant divide but their protiens and cell constiutients that normally double before division are fine so they double up before division but then cell checks dna, its ****ed up, so it doesnt divide.. Same deal as folate/b12 defic. the dna is messed up. Like the above poster said if the aplastic anemia is due to infection or soemthing than it is normocytic

 

[automaton]

maybe you guys are right, and that would explain why these things are or can be macrocytic, but what i don't understand is, if the mechanism of alcohol induced anemia basically comes down to folate deficiency, shouldn't the RBC look the same? with folate/b12 def, it's classified as megaloblastic, whereas alcohol and aplastic are classified as non-megaloblastic. am i just confused about what megaloblastic means? i thought it means new RBC are trying to be made... so non-megaloblastic means the marrow is screwed up and won't make new RBC...

hope that wasn't too confusing...

 

[HiddenTruth]

well ETOH does cause megaloblastic anemia, but it's a little more complex than malnutrition. Both ETOH and oral contraceptives inhibit intestinal reabsorption of the monoglutamate form. When you take in dietary folate, it is in the polyglutamate form, it then gets converted to monoglutamate by intestinal conjugase (which by the way is inhibited by phenytoin). Well ETOH intereferes with absorption of this monoglutamate form. The malnutrition is not really the cause, since beer specifically has tons of folate and goat milk has none 😀

 

[ucbdancn00]

I think an important point to add is as such.

Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde..

It this acetaldehyde that causes several of your "hang over" type sx; nausea, vomiting, flushing, increased malabsorption of B1 (leads to Wernicke-korsakoff) and of course inactivation of folate. This inactivation may refer to the alteration of folate to a form that also can't be absorbed.

this loss of folate will lead to a your megaloblastic anemia. If i'm not mistaken, alcoholic is also considered in the megaloblastic category; since it indirectly causes the anemia, it may be thought of as "non-megaloblastic". Just my 2 cents.

ucb