Heme Onc [MACROCYTIC ANEMIA]

Introduction
Macrocytic anemia is a production anemia – reticulocytes will be CBC
reduced despite an anemia. When identified, the reflex test is the
blood smear. In the case of impaired DNA synthesis
(megaloblastic anemia) there’ll be hypersegmented Anemia
neutrophils. If there are none, it’s said to be non-megaloblastic.
Nonmegaloblastic dz has some risk factors (below). MCV
Megaloblastic dz is either B12 deficiency or folate deficiency.
Folate Deficiency Macrocytosis
Folate comes from leafy greens and has small storage forms (3-
6 weeks) in the body. Thus, it often presents with higher acuity Blood Smear
than B12. Look for people who aren’t eating real food - the
chronic alcoholic or the elderly woman on a tea and toast diet. 5+ Lobes PMN Ø Hypersegmentation
There aren’t symptoms other than the anemia itself. A folate level
will diagnose it and folate supplementation is usually sufficient Megaloblastic NonMegaloblastic
for treatment. In equivocal cases where the folic acid levels are
near normal, ancillary testing may be required. Don’t remember
the homocysteine levels – they’re elevated in both Folate B12 and
deficiency and B12 deficiency. Hence, not useful. The ↑ Folate Folate ↓ Folate
methylmalonic acid is unchanged in folate deficiency. Replace
with oral supplementation. B12 Deficiency Folate Deficiency
Equivocal
*Folate supplementation is performed in pregnancy to prevent Folate
B12
neural tube defects in the fetus rather than to protect mom from
anemia. Methyl
Malonic
B12 Deficiency Acid
B12 comes from animal products. It requires both intact
parietal cells and an intact terminal ileum to be absorbed. The ↑ MMA Nrml MMA
body has 3-10 years of stores it takes a long time to develop. The
pathology is either decreased intake (strict vegans) or reduced
absorption (as in those pernicious anemia, Crohn’s disease
involving the terminal ileum, and gastric bypass). It presents first
with a megaloblastic anemia and then, if left untreated, with
subacute combined degeneration of the cord.
Diagnosis is made with a B12 level. If equivocal, an elevated
methyl malonic acid is indicative of B12 deficiency. Don’t use
the homocysteine level to diagnose. The only time a Schilling test
is done is when there’s uncertainty about the etiology; it’s rarely Subacute Combined Degeneration of the cord.
used. If the urine is positive for B12, then there is no problem with
absorption.
Treatment is with B12 supplementation. If there’s impaired
absorption the supplementation must be intramuscular, else oral
is sufficient. Be cautious with Folate administration. Throwing a
lot of Folate at a B12 deficiency can overcome the anemia, but it
won’t prevent neurologic symptoms.
Nonmegaloblastic Dz
This isn’t that interesting; there’s just a list of things that cause it.
It’s important to first rule out a B12/Folate deficiency then look
for: Liver Disease, EtOH, Medications (AZT, 5-FU, ARA-C)
and metabolic conditions (Lesch-Nyhan, Hereditary Orotic
Aciduria).

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