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Megaloblastic Anemia

November 2, 2007

RBC precursors of megaloblastic anemia

abnormally large and have nuclei that appear much less mature than would be expected from the development of the cytoplasm (nuclear-cytoplasmic asynchrony).

Drugs causing Megaloblastic Anemia:



P–>Phenytoin (Fenytoin–>Folate deficiency)

L–>Liver Disease (speaking of the MC drug Alcohol, think of Liver as well)


The MC drug is Ethanol. This is easy to remember. You cannot buy drugs like Methotrexate, AZT or Phenytoin OTC, but you can cause yourself liver disease and megaloblastic anemia using the ethanol=alcohol, because it is so easy to buy it. Alcohol is not OTC drug, alcohol is OTS drug, which means On The Shelf drug. Everybody can buy alcohol, and that is why ethanol is the MCC of Megaloblastic Anemia and many other disease. The second MC killer in US right after cigarettes smoking.

Image source: wikipedia

6 Comments leave one →
  1. Christine permalink
    December 29, 2007 9:48 pm

    Could you please explain the acronyms MC and MCC? Also OTS usually means off-the-self. Is that correct?

    Thanks, that is an amazing blog!

  2. December 31, 2007 3:37 am

    Thank you for the good words about my blog.
    MC means Most Common.
    MCC means Most Common Cause.
    OTC means Over The Counter, in other words you don’t need a doctor’s prescription to buy a particular drug.
    For other acronyms you can use this website
    You can find a link to it on my blog as well.

  3. Francis permalink
    January 15, 2008 9:28 pm

    Why AZT give Megaloblastic Anemia?

  4. January 17, 2008 8:57 am

    The effect of azidothymidine (Zidovudine, AZT) on pyrimidine (thymidine, deoxyuridine, and thymidine triphosphate) incorporation into DNA in folate- and/or vitamin B12-deficient and normal human bone marrow cells was studied to Investigate whether such vitamin deficiency affects susceptibility to AZT-induced hematologic toxicity. Bone marrow cells from 12 patients were studied: 5 had folate and/or vitamin B12 deficiency; 7 controls included 5 with anemia related to chronic disease and 2 with iron deficiency.
    At 0.2 M AZT (3 hr, 37°C), the approximate pharmacologic serum trough level, pyrimidine incorporation into DNA was suppressed by 12 to 19% in folate- and/or vitamin B12-deficient cells and by 16 to 23% in normal cells. At 2.0 M AZT (3 hr, 37°C), the approximate pharmacologic serum peak level, this was suppressed by 15 to 40% in folate- and/or vitamin B12-deficient cells and by 32 to 47% in controls. Deoxyuridine incorporation into DNA was inhibited signlficantly greater than thymidine at 2.0 M AZT (3 hr, 37°C) in both groups. Inhibition of deoxyuridine incorporation was not reversed with methyltetrahydrofolate or vitamin B12. There tended to be less striking suppression by AZT of deoxyuridine incorporation into DNA in bone marrow cells from vitamin B12-deficient patients, which was made more striking by adding vitamin B12. This suggests that some of what passes for AZT damage to bone marrow cells may in fact be coincident deficiency of vitamin B12.
    AZT Inhibition of DNA synthesis in 3 hr bone marrow cultures is relatively consistent in a varlety of hematologic disorders. As approximately two-thirds of AIDS patients appear to be in negative balance with respect to folate and/or vitamin B12, the fact that AZT-induced inhibition of pyrimidine incorporation into DNA is occurring in cells which may be megaloblastic, i. e., In a state of Impaired DNA synthesis, suggests that these cells may be more susceptible to AZT toxicity. The data also support the notion that AZT inhibition results predominantly from termination of DNA chain elongation.
    Whether folate or vitamin B12 supplementation may partially overcome apparent AZT inhibition of DNA synthesis (hematologic toxicity) and whether the benefit of such therapy exceeds the risk will require further study.

  5. bilal permalink
    August 19, 2008 3:47 pm

    well you are right


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