Thrombocytosis in Iron Deficiency Anemia: What the Primary Care Physician Needs To Know.

The prevalence of reactive thrombocytosis in iron deficiency anemia (IDA) as well as it’s duration and need of further work up is not always known by primary care physicians (PCP). The data we know came mainly from papers published back in the 1960’s involving small sample sizes, most of which consisted of pediatric patients. The most widely cited publication is based on Schloesser’s 1965 review of 46 iron deficient anemic adult patients (Hb <11, Serum iron <70ug per 100ml), of which 60.8% exhibited thrombocytosis. Thrombocytopenia (28.3%) among IDA patients was described by Gross in his 1964 publication. Most of the studies failed to address the mechanism linking thrombocytosis and IDA, Endogenous erythropoietin (EPO) levels are high in IDA and were not available in 1960 therefore we decided to examine any statistically significant relationship between platelets counts and EPO levels. The relationship between platelets, hemoglobin (Hb) and ferritin were also evaluated.

A comprehensive chart review of 450 patients with a diagnosis of anemia between 2002 and 2006 was performed. These patients were screened for iron deficiency anemia using the following criteria: Hb ≤ 12 for women and Hb ≤ 14 for men, ferritin ≤ 20. Anemias other than IDA were excluded by identifying patients with concomitant infectious disease, malignancy, pregnancy or with high CRP levels indicative of inflammatory process. Sample size 140 patients. Pre and Post treatment lab data consisting of Hb, Plt, endogenous EPO, Ferritin and Reticulocyte were collected.

Results see (table 1).

31% of our patients (43 / 140) experienced thrombocytosis. We found a statistically significant correlation between Hb levels and plt counts. R = −0,299 .p < 0.05. however a cause effect relationship was not established. We were not able to find a significant relationship between platelets counts and EPO levels or Ferritin levels.

In 65.6 % of our patients thrombocytosis resolved in 28 days or less. (See table 2)

The prevalence of thrombocytosis in our series 31% differs from the previous published data. Extreme thrombocytosis was not frequent in our series, none of our patients presented with thrombocytopenia. To our knowledge this is the largest sample size surveyed for such study. A mechanism to explain thrombocytosis in IDA remains unclear but according to our data is not related to either the iron cellular concentration (ferritin) or endogenous erythropoietin level. We recommend that patients with IDA related thrombocytosis should be followed with a CBC 4 weeks after treatment was started. No other work up for thrombocytosis seems to be necessary in the presence of diagnosed IDA. Persistent or increasing thrombocytosis should be followed closely and underlying bone marrow disorder such as myelodysplastic disorders considered as a differential after 4 weeks of complied treatment.