The Prevalence of Reactive Thrombocytosis and Thromboembolic Events in Arab Population with Iron Deficiency Anemia (a retrospective study)

INTRODUCTION

Iron deficiency is the most prevalent nutritional deficiency worldwide. Iron deficiency anemia (IDA) is the most common type of anemia, its prevalence is 1 out of 5 of the population. IDA is a well-known cause of reactive thrombocytosis which is mostly asymptomatic. Only few observational studies and case reports have described thromboembolic events in the context of this reactive thrombocytosis in the absence of other hypercoagulable states

OBJECTIVES

To assess the frequency of thromboembolic events in Arab patients with reactive thrombocytosis secondary to iron deficiency anemia (IDA).

METHODS

We retrospectively reviewed thromboembolic events in iron-deficient patients with reactive thrombocytosis. Our study sample included female patients who received iron replacement for IDA between April 2018 and March 2020 at Hamad Medical Corporation, Doha, Qatar. We excluded pregnant, non-Arab patients and patients under 18 or over 65 years of age. Reactive thrombocytosis was defined as thrombocyte count of more than or equal to 450 x 10⁹ /L in the presence of iron deficiency anemia and ferritin level less than 30µg/l.

RESULTS

Out of 1567 patients (mean age =50 +/- 8.66 years) with the diagnosis of IDA, 292 (18.63%) had thrombocytosis. They had a mean platelet count = 534 +/- 121 x 10⁹ /L). None of them had any symptom or sign of thromboembolic events.

Discussion

Thrombocytosis can be categorized into primary causes such as primary bone marrow disorders and myeloproliferative neoplasms, and secondary causes including infection, inflammation or drug-induced. Iron deficiency anemia leads to reactive thrombocytosis in a mechanism that is yet to be fully understood.

The clinical impact of increased platelet counts is not well recognized in literature, and it has not been studied in the Arab population. Although reactive thrombocytosis has been generally considered benign, few case reports described thromboembolic events in patients with IDA reactive thrombocytosis.

Few cases in the literature described thromboembolic events in reactive thrombocytosis with IDA. H. Z. Batur Caglayan et al published a case report of a 41-year-old Turkish female patient who presented with transient ischemic attack (TIA) due to intraluminal carotid artery thrombus, which was attributed to IDA-associated thrombocytosis. Another case series by P T Akins et al described three women with severe IDA and thrombocytosis secondary to menorrhagia who developed carotid artery thrombi.

The mechanism by which low iron can affect thrombocyte count is still unknown. One study in mice and humans demonstrated that iron deficiency caused reduced megakaryocyte proliferation but increased ploidy independent of thrombopoietin. However, another study failed to identify the exact mechanism by which iron deficiency leads to increased platelet count.

CONCLUSION

Our study did not find any thromboembolic incident in a large number of patients with reactive thrombocytosis secondary to IDA diagnosed over two years in our Arab population.