Acute Lymphoblastic Leukemia - question about hematological investigations

[BlondeCookie]

Hi. I'm studying some blood pathology review and am a little stumped about Acute Lymphoblastic Leukemia (ALL). According to my review book, the common hematological findings of ALL reveal the following:

• leukocytosis
• anemia
• neutropenia
• thrombocytopenia

The leukocytosis bit, I understand since there is neoplastic proliferation of leukemic cells in ALL. However, anemia, neutropenia, and thrombocytopenia all come from a common myeloid[/d] stem cell, not a common lymphoid stem cell. So, in order to get the latter 3 clinical disorders, wouldn't a person have to have Acute Myeloblastic Leukemia (AML) and not Acute Lymphoblastic Leukemia (ALL)?

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[QuinnB]

AML would be marked by an excess of cells in the myeloid line (granulocytes, thrombocytes, rbcs) and ALL is marked by excess lymphocytes. You determine what it is by 1) what cell type is in excess (lymphoblastic vs. myeloblastic) 2) what level of maturity (acute vs chronic)

Having ALL means you have a huge excess of precursor lymphocytes that are defective and b/c you have the excess of lymphocytes, I believe, you get crowding and in conjunction w/ various cytokines you get a decrease in myeloblast proliferation which means you get infections (defective lymphocytes, low polys), bleeding (thrombocytopenia) and pretty bad anemia (low rbcs) which I think is the classic presentation for a kid w/ ALL (I don't think it is common in adults).

 

[UCLAstudent]

QuinnB is right. The proliferating clonal lymphoblasts essentially hijack the entire bone marrow by crowding the out myeloid precursors and impairing normal hematopoeisis. Thus, you see excessive lymphocytes with corresponding anemia, neutropenia, and thrombocytopenia.

 

[BlondeCookie]

Yes, you guys are absolutely correct. I also made a stupid mistake by misreading the review book. The clinical features of ALL & AML are similar. So, to correct my earlier error....
The hematological investigations for both ALL & AML are:

• Anemia
• Leukocytosis
• Neutropenia
• Thrombocytopenia

Thanks for helping me understand that one of the mechanisms for similar hematology is due to the overcrowding of abnormal precursor leukocytic cells. So, whether the precursor cells are lymphoblastic or myeloblastic, it doesn't matter since overcrowding of the abnormal cells will negatively affect the growth and differentiation of the other marrow cells. I think I've got this correct. Yes?

Also, does the fact that ALL & AML are both acute have anything to do with it? I mean, acute-type leukemias are supposedly characterized by more immature blast cells while chronic-type leukemias are characterized by more mature blast cells. So, does being an 'acute' leukemia have anything to do with ALL & AML sharing similar clinical and hematological features?

 

[QuinnB]

Hi blonde cookie,

In AML you can have an excess of either rbcs, thrombocytes, monocytes, neutrophils, etc...whereas all of the others may be decreased. What ever happens to be elevated will you allow you to classify the particular dz process in one of the 0-7 classifications of the French, American and British (FAB) classification for AML. For instance, an elevated number of immature megakaryoblasts may be indicative of the "M7" variety of AML. Another example is an elevated promyelocyte level (or early polys) may be indicative of the M3 variety - important for boards b/c this condition has an excellent response to retinoic acids which are readily available for treatment.

So whatever the dz is, is determined by what is elevated. Consequently all of the other cell lines (not always true, but mostly) will be decreased 2/2 to overcrowding.

 

[BlondeCookie]

Hi blonde cookie,

In AML you can have an excess of either rbcs, thrombocytes, monocytes, neutrophils, etc...whereas all of the others may be decreased. What ever happens to be elevated will you allow you to classify the particular dz process in one of the 0-7 classifications of the French, American and British (FAB) classification for AML. For instance, an elevated number of immature megakaryoblasts may be indicative of the "M7" variety of AML. Another example is an elevated promyelocyte level (or early polys) may be indicative of the M3 variety - important for boards b/c this condition has an excellent response to retinoic acids which are readily available for treatment.

So whatever the dz is, is determined by what is elevated. Consequently all of the other cell lines (not always true, but mostly) will be decreased 2/2 to overcrowding.

Thanks very much for clearing that up. It's easy to understand if you look at the disease as causing secondary overcrowding issues as you said. Thanks again. Please let this be on the USMLE now that I get it!