I am referred occasional otherwise healthy patients for evaluation of lymphopenia (aka lymphocytopenia).
What to do?
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1. Let's begin with definitions - lymphopenia is usually defined as an absolute lymphocyte count ALC <1000 cells/microL for adults
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2. Epidemiology - lymphopenia has been documented in 1.5-3% of CBCs from both community and hospitalized patients.
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3. Causes/associated conditions - lymphopenia may be found incidentally in someone without obvious underlying cause (most common) or may be associated with a number of diseases/conditions.
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4. Mechanisms - reduced production, increased destruction, increased apoptosis, redistribution of lymphocytes between blood and various lymphoid tissues.
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5. Clinical implications - no evidence (outside of large population studies that do not take into account underlying cause) that lymphopenia associated with increased risk of infection.
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6. History and physical - focus on symptoms/signs associated with underlying cause/associated conditions(s).
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7. Lab tests - generally not needed in an otherwise healthy individual.
8. Treatment - directed towards the underlying cause.
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a. Used to calculate the Hct (Hct = MCV x RBC count)
b. Used by some to predict iron deficiency vs. thalassemia (e.g., Meltzer index)
b. Largely ignored because it says nothing about the size/Hbization of RBCs
2/7
... you could have LOTS of SMALL RBCs or FEWER LARGE RBCs amounting to the same Hct (viscosity) and Hb (oxygen carrying capacity)!
3/7
MCV
a. Ah, now we're talking 😀! MCV is super helpful because it is the first branch point in the ddx of anemia - microcytic vs. normocytic vs. macrocytic. Each has its own specific causes.
1. The clotting cascade in plasma is activated by the addition of a negative charge, which activates the intrinsic pathway (aPTT) or tissue factor, which activates the extrinsic pathway (PT) in presence of Ca2+ and PL.
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2. Once the ingredients are added together, the "stop watch" is started and time to clot formation at 37C is measured (the assays do not discriminate between crosslinked and uncrosslinked fibrin).
3/5
In vivo (the body):
1. The clotting cascade is ALWAYS activated by TF-mediated activation of FVII. TF hides in the subendothelial layer of the blood vessel wall and is expressed on the surface of activated monocytes.
NORMOCYTIC, NORMOCHROMIC IRON DEFICIENCY ANEMIA (IDA)
We tend to think of IDA as being microcytic (more consistently than hypochromic). However, there are certain situations in which the MCV is normal in IDA.
2/6
Examples include:
1. A patient with high-normal baseline MCV whose MCV falls within the normal range in IDA (see first graphic for an example).
2. A patient with baseline macrocytosis, for example from concomitant liver disease, B12 deficiency, MDS or hydroxyurea use.
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3. Rare cases where the MCV simply doesn't budge from baseline despite clear cut evidence of IDA (i.e. anemia +/- low MCHC with low ferritin that responds to iron treatment).
We are used to considering variation in RBC size (increased variation = anisocytosis) by examining a blood smear or evaluating the RDW.
What about variation in RBC Hb concentration ([Hb]) (anisochromia)?
2/7
We can often identify cell-to-cell differences in central pallor on a blood smear.
While we may make mental note of such differences, we rarely incorporate the finding in a summary of the smear. And there is no lab equivalent to the RDW for Hb concentration or "chromia".
3/7
Or is there? If we plot single cell [Hb], we would likely find a normal distribution with a bell shaped curve (I have not seen any such data published). The mean would provide us with the MCHC and the standard deviation with the RDW for [Hb].
Yesterday I posted a poll showing CBC data from a patient with severe iron deficiency anemia and asked: assuming she receives 4 units pRBCs (which of course would be excessive here), does she need iron therapy on top of that?
70% answered YES.
2/6
Each unit of RBC contains about 250 mg Fe. So she will have received about 1000 mg of Fe, not far off from her total needs. However, such is iron is bound up in Hb inside the donor RBCs and is not readily accessible for erythropoiesis.
3/6
I ran through some rough numbers (see graphic):
1. Oral iron will deliver about 20 mg Fe to the bone marrow each day.