Baylor University Medical Center Proceedings July 2017 - 346

Pseudothrombotic microangiopathy and vitamin B12 deficiency
in pernicious anemia
Kaleb Veit, DO

Vitamin B12 deficiency may present as pseudothrombotic microangiopathy. Pseudothrombotic microangiopathy is anemia, thrombocytopenia,
and schistocytosis caused by vitamin B12 deficiency. Pseudothrombotic
microangiopathy may be mistaken for microangiopathic hemolytic
anemia, confounding appropriate treatment. Evaluation of lactate dehydrogenase, reticulocyte count, bilirubin, and platelet count are most
helpful in differentiating pseudothrombotic microangiopathy from a true
microangiopathic hemolytic anemia. A case of pseudothrombotic microangiopathy due to severe vitamin B12 deficiency is presented.

itamin B12 deﬁciency may present with hemolytic anemia, thrombocytopenia, and schistocytosis, mimicking
a microangiopathic hemolytic anemia. This is known
as pseudothrombotic microangiopathy. Diﬀerentiating
between pseudothrombotic microangiopathy and a true microangiopathic hemolytic anemia is of paramount importance, as
the treatments are markedly diﬀerent. A true microangiopathic
hemolytic anemia such as thrombotic thrombocytopenic purpura (TTP) may be treated with intensive care unit admission
and plasmapheresis, while pseudothrombotic microangiopathy
may be treated with outpatient vitamin B12 supplementation.
CASE REPORT
A 36-year-old black man presented to an urban emergency
department with a chief complaint of fatigue and poor exercise tolerance. His symptoms had been present for the past
2 years and were progressively worsening. His hemoglobin was
7.9 g/dL. There were no signs of active hemorrhage, fecal occult
blood testing was negative, and he was hemodynamically stable.
Laboratory studies (Table 1) revealed a concurrent leukopenia and a platelet count in the low normal range. Erythrocyte
indices showed macrocytosis, and corrected reticulocyte count
reﬂected an inadequate reticulocyte response for the degree
of anemia present. Iron studies were consistent with anemia
of chronic inﬂammation. Vitamin B12 was determined to be
markedly low, with an associated elevation in methylmalonic
acid. Lactate dehydrogenase was profoundly elevated and haptoglobin was diminished, suggesting hemolysis. Renal function
was normal and electrolytes were unremarkable. A peripheral
smear (Figure 1) revealed moderate to severe macrocytic anemia
346

Table 1. Laboratory findings in the patient described
Test

Result

Leukocytes (/mL)

3300

Hemoglobin (g/dL)

7.9

Platelets (/μL)

157,000

Mean corpuscular volume (fL)

104.4

Corrected reticulocyte count

1.6%

Ferritin (ng/mL)

380

Iron (μg/dL)

Total iron binding capacity (μg/dL)

222

Iron saturation

39%

Vitamin B12 (pg/mL)

111

Folate (ng/mL)

>24

Homocysteine (μM/L)

181.3

Methylmalonic acid (mM/L)

19.69

Lactate dehydrogenase (U/L)

3988

Haptoglobin (mg/dL)

<30

Aspartate aminotransferase (U/L)

130

Alanine aminotransferase (U/L)

Bilirubin (mg/dL)

1.2

Direct antiglobulin test

Negative

with red cell fragmentation and schistocytes, as well as rare
hypersegmented neutrophils. Prominent anisopoikilocytosis
with teardrop cells, elliptocytes, macroovalocytes, and target
cells was also identiﬁed.
Neurologic examination, including mental status, cognition,
reﬂexes, vibration, and proprioception, was normal. A bone
marrow biopsy was performed, revealing macrocytic anemia,
neutropenia, and mild marrow hypercellularity with trilineage
dysplasia and a shift towards immaturity. Erythroid precursors
From the Department of Internal Medicine, the University of Oklahoma School of
Community Medicine, Tulsa, Oklahoma.
Corresponding author: Kaleb Veit, DO, Department of Internal Medicine,
University of Oklahoma School of Community Medicine, 4502 East 41st Street,
Tulsa, OK 74135 (e-mail: kaleb-veit@ouhsc.edu).
Proc (Bayl Univ Med Cent) 2017;30(3):346-347

Table of Contents for the Digital Edition of Baylor University Medical Center Proceedings July 2017