Reactive thrombocytosis was observed in approximately one-third of patients with iron deficiency anemia (IDA), and these patients had an estimated 2-fold increase in thrombotic risk relative to patients with IDA and no thrombocytosis, according to the results of a large retrospective study published in the American Journal of Hematology.
Due to standing uncertainty in the field, Andrew B. Song, MD, of the division of hematology at Massachusetts General Hospital, Harvard Medical School, in Boston, and associates sought to define the rate of thrombocytosis in IDA using a large institutional patient data registry, the Partners Research Patient Data Registry, which contains comprehensive electronic health record data for over 6 million patients. They identified patients with IDA with and without thrombocytosis and the number of thrombotic events over a span of 40 years (1979-2019).
Overall, 36,327 cases of IDA were identified and 15,022 of those had thrombocytosis.
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After quality control and detailed manual chart review, the rate of thrombocytosis in patients with IDA was estimated to be 32.6%. The rate of thrombosis was 7.8% in patients with IDA and 15.8% in patients with IDA and thrombocytosis.
The investigators also assessed the relationship between hematologic parameters and thrombocytosis. Hemoglobin was negatively correlated with platelet count at IDA diagnosis (r = -0.1734; P =.0484) and at the time of peak thrombocytosis (r = -0.3785; P <.0001). Hemoglobin had a strong negative correlation with platelet mass index (calculated as platelet count multiplied by mean platelet volume) at the time of peak
thrombocytosis (r = -0.6888; P <.0001). Platelet mass index at the time of peak thrombocytosis was significantly higher than at baseline (4892 vs 2836; P <.0001).
A multivariable regression model yielded a significant predictive relationship between decreasing hemoglobin and increasing platelet count at the time of peak thrombocytosis (P <.0001).
The limitations of the study included its retrospective and observational nature as well as potential sampling bias. Because a laboratory-based definition of iron deficiency has not been established, the authors used a ferritin cutoff in this study.
The authors noted that the rate of thrombosis was high in their study and attributed this to the inclusion of data from both outpatients and inpatients, who are more likely to experience a thromboembolic event. They also indicated that strict inclusion and exclusion criteria were used to ensure that thrombocytosis could clearly be attributed to IDA and not other confounding conditions, such as inflammation.
“To our knowledge, this study is the first to directly assess the thrombotic risk associated with reactive thrombocytosis in [IDA],” wrote the authors. “While our findings require confirmation in additional studies, given the global burden of unrecognized and undertreated [IDA], our findings emphasize the importance of prompt identification and effective treatment of this common hematologic disorder.”
Reference
Song AB, Kuter DJ, Al‐Samkari H. Characterization of the rate, predictors, and thrombotic complications of thrombocytosis in iron deficiency anemia [published online July 3, 2020]. Am J Hematol. doi: 10.1002/ajh.25925
