TRAINING and EDUCATION
You Make the Call
Each month in “You Make the Call,” we’ll pick a challenging clinical question
submitted through the Consult-a-Colleague program and post the expert’s
response. But, what would YOU do? We’ll also pose a submitted question
and ask you to send your responses. See how your answer matches up to the
experts in the next print issue.
This month, Stanley Schrier, MD, answers a question about Wilson’s disease.
Clinical Dilemma:
I was asked to see a 41-year-old male with Wilson’s disease. He has resulting cirrhosis and hypersplenism with a
chronic pancytopenia. His leukopenia is worsening with an absolute neutrophil count of 400. His hemoglobin is mildly
decreased by 2 g/dL and is currently at 8.3 g/dL, and his platelet count is stable at 73,000. He is continuing chronic zinc
therapy for his Wilson’s disease. I am concerned that his zinc therapy has resulted in copper depletion as a cause for
his worsened neutropenia, which more typically remains with an ANC of 1700. A vitamin B12 level and folic acid are
normal, his LDH is normal, and his absolute reticulocyte count is 160 (6.4%). I am interested in further thoughts on
evaluation and treatment.
Consult a Colleague
Through ASH
Consult a Colleague is a service for ASH
members that helps facilitate the exchange of information between hematologists and their peers. ASH members
can seek consultation on clinical cases
from qualified experts in 11 categories:
• Anemias
• Hematopoietic cell
transplantation
• Hemoglobinopathies
Experts Make the Call
• Hemostasis/thrombosis
• Lymphomas
Stanley L. Schrier, MD
Professor of Medicine (Hematology), Active Emeritus
Stanford School of Medicine
Stanford, California
• Lymphoproliferative disorders
• Leukemias
• Multiple myeloma & Waldenström
macroglobulinemia
• Myeloproliferative Disorders
• Myelodysplastic Syndromes
• Thrombocytopenias
This case is complicated by cirrhosis and
hypersplenism. The patient is essentially
pancytopenic, likely due to hypersplenism
with an inadequate reticulocyte response
of 160,000/µL. The role of zinc is to block
copper absorption, but have you measured
his recent copper – either urine or blood?
Has his liver copper been adequately
treated with penicillamine? Lastly, has the
patient had a recent marrow to look for
a fuller explanation of his pancytopenia,
reticulocytopenia, or even ringed sideroblasts
possibly caused by copper depletion.
Assigned volunteers (“colleagues”) will
respond to inquiries within two business
days (either by email or phone).
Have a puzzling clinical dilemma?
Submit a question, and read more
about Consult-a-Colleague volunteers at
hematology.org/Clinicians/Consult.aspx
or scan the QR code.
*If you have a request related to a
hematologic disorder not listed here, please
email your recommendation to ashconsult@
hematology.org so it can be considered for
addition in the future.
DISCLAIMER: ASH does not recommend or endorse any specific tests,
physicians, products, procedures, or opinions, and disclaims any
representation, warranty, or guaranty as to the same. Reliance on
any information provided in this article is solely at your own risk.
Next Month’s Clinical Dilemma:
I have a young patient who was diagnosed with IgG lamda multiple myeloma
in 1997. He was induced by vincristine,
doxorubicin, and dexamethasone (VAD)
followed by an auto transplant in 1998.
ASHClinicalNews.org
He relapsed six years later. At this point
(in 2004) he was started on thalidomide
and dexamethasone and intermittently
switched to thalidomide alone. In 2013,
he was switched to lenalidomide; he has
been on 10 mg a day. His labs show no
monoclonal protein. All of his other parameters suggest that he is in complete
remission. How long should he continue
taking lenalidomide? If we decide to discontinue, what will guide us in decision
making?
How would you respond? Email us at
[email protected].
ASH Clinical News
51