Reader Responses: Does this patient with diabetes and thrombocytosis need a bone marrow biopsy?

Here’s how readers responded to a You Make the Call question about treatment of thrombocytosis in a patient with diabetes and ischemic cardiomyopathy.


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I would recommend an empiric trial of iron.

David Baer, MD
Oakland, CA

I see this as a high-risk patient with advanced cardiovascular disease.  After nonhematopoietic causes are eliminated (iron deficiency, inflammation, etc.) the next question is whether this patient requires treatment.  If it is felt that cytoreduction would improve the prognosis, a bone marrow biopsy is clearly indicated.  Since the level of thrombocytosis correlates poorly with thrombotic complications, I would be willing to observe, use low-dose aspirin, and wait on the biopsy.  The biopsy can be prognostic in terms of the long-term deterioration to leukemia but doesn’t necessarily affect management.  In short, a biopsy is not unreasonable but not necessary because the situation, even though it is high risk by CV criteria, does not require cytoreduction at this rather borderline level of thrombocytosis.

Robert A. Moss, MD
Fountain Valley, CA

There is no need for bone marrow biopsy testing unless the platelet counts continue to rise or other significantly indicative lab abnormalities arise.

Parth Desai, MD
Rockville, MD

I would check the soluble transferrin receptor level and review his peripheral smear, first looking for iron deficiency.

Joel A. Schor, MD
Bluefield, WV

I think the patient first needs his iron deficiency corrected, then see what the effect of that is on the platelet count.

Anastasia Skandali, MD
Athens, Greece

Thrombocytosis is defined as a platelet count greater than 450,000/µL, which is typically considered the upper limit of the normal laboratory reference range. The most common reason for an elevated platelet count is reactive thrombocytosis. The patient presents mild thrombocytosis (504,000 /µL) and, despite normal hemoglobin, he has borderline ferritin (19 ug/L) and iron saturation (21%) levels. Therefore, the patient is a candidate for iron replacement to rule out the possibility of reactive thrombocytosis secondary to iron deficiency.

João Tadeu Damian Souto Filho, MD, PhD
Rio de Janeiro, Brazil

This patient has iron deficiency anemia. The thrombocytosis is likely secondary. I would not have wasted money on so many expensive molecular studies.

Eduardo Edmundo Reynoso, MD
Juárez, Mexico

Yes, perform a bone marrow biopsy.

Joan Zidulka, MD
Montreal, Canada

With low ferritin level of 19 ug/L (normal range for a male is  23-336 ug/L) and low-normal level of iron saturation 21% (normal range is 20-50%), it can be considered iron deficiency without anemia. As we know, thrombocytosis can be seen with iron deficiency as well (especially in this patient with normal JAK2, MPL, and CALR and low serum ferritin). A bone marrow biopsy can be done to confirm the iron deficiency and to rule out possible MPN, which is less likely. The other option is a trial of iron therapy with follow-up evaluation of complete blood count and serum iron study.

Mohammad Reza Sheikholeslami, MD
San Juan Capistrano, CA

A ferritin level of 19 ug/L is pretty low. I would first have the patient take iron supplementation for a while, then consider a bone marrow biopsy only if the platelet count is still high when the ferritin level is at 50-100 ug/L.

Cynthia Martel MD, PhD
Pasadena, CA

I would correct the iron deficiency first as the thrombocytosis is not critical.  I would also work up the source of his iron deficiency.  A bone marrow biopsy would be indicated if the variant allele frequency were higher and the patient were not iron deficient.  I would not delay the iron deficiency work-up by trying to get a bone marrow biopsy first.

Laura Milligan, MSN, FNP, BC
Charleston, SC

The priority is to look at the cause of the iron deficiency anemia and start iron therapy. I suggest reactive thrombocytosis due to chronic bleeding and iron deficiency.

William Caceres, MD
Rio Piedras, Puerto Rico

This patient’s platelet count is marginally increased and could be attributed to borderline iron deficiency, which should be pursued, especially in regard to gastrointestinal blood loss.

I doubt that the thrombocytosis caused the coronary artery disease, especially if we consider it secondary thrombocytosis that very rarely causes thrombotic disorders.

A good look at a peripheral smear would be simple, and it may be helpful to look for large/abnormal platelet morphology.

I would follow his counts every 3 months and at longer intervals if the counts are unchanged, and  would not do a bone marrow biopsy at this time. I would also add primary hyperoxaluria type 1 testing.

Consider starting oral iron to see if the thrombocytosis improves.  Of course if he undergoes a bone marrow biopsy, I expect you will look for iron stores or ring sideroblasts among other morphologic and cytogenetic abnormalities.

Adel Z. Makary, MD
Danville, PA