Thrombocytosis in Iron Deficiency Anemia

Background: Thrombocytosis can be a result of a reactive process such as acute blood loss, infections, iron deficiency anemia (IDA) or a clonal disorder such as Essential Thrombocythemia. The challenge of correctly identifying the etiology of thrombocytosis in an individual patient becomes particularly essential when the clinician is confronted with decisions regarding further workup, follow up as well as preventing future complications such as thrombotic events. Prior data linking iron deficiency anemia and thrombocytosis has been concluded from studies with small sample size, and to a large part, this association is based on anecdotal evidence. Our study examines the association between IDA and platelet counts and to the best of our knowledge is the largest study to do so.

Methods: We performed a retrospective chart review of patients seen at our outpatient clinic from 1^st January to 31^st December 2017. We defined Iron deficiency as serum ferritin <30 mcg/dl, anemia in males as hemoglobin (Hb) <13.1 g/dl, anemia in females as Hb <11.7g/dl and thrombocytosis as platelet count >450,000/ul. Patient demographics, as well as hematological data, were collected and compared between three groups: Iron deficiency anemia, Iron deficiency without anemia, and control. We defined controls as subjects with neither iron deficiency nor anemia. Bivariate analysis using the Chi-square test for categorical variables, and a One-Way ANOVA for continuous variables were used to determine the association between the three groups of interest and the covariates. The relationship between platelet counts and other hematological parameters was evaluated using Pearson's correlation test.

Results: Of the 4896 subjects included in our study, 1225 (25.02%) had iron deficiency anemia, 699 (14.28%) had iron deficiency without anemia, and 2972 (60.70%) were controls. The mean age of the cohort was 55.8 (SD = 18.31) years, and 73.9% of the subjects were females. In the IDA group, the mean hemoglobin was 10.21 (SD = 1.39) g/dl, the mean platelet count was 319.24 (SD = 106.92) k/uL, and 127 (10.37%) subjects had thrombocytosis whereas 1098 (89.63%) had normal platelet counts. When compared to the control group, 32 (1.08%) subjects had thrombocytosis, and 2940 ( 98.92%) had normal platelet counts. The difference in numbers of subjects with thrombocytosis between iron deficiency anemia, iron deficiency without anemia and control group was statistically significant as indicated by P<0.001 on the Chi-Square test. Furthermore, we found an inverse relationship between platelet count and ferritin as well as hemoglobin level with a p < 0.0001 across all groups.

Conclusions: Our study demonstrated a significant association between iron deficiency anemia and thrombocytosis when compared to the control group however at a lower frequency than seen in the previously published studies. Further studies are needed to study causality and to elucidate the mechanism by which iron deficiency anemia leads to thrombocytosis.

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