Thrombocytosis can be primary or secondary and can cause venous pro-thrombotic states like cerebral venous thrombosis due to quantitative platelet alterations. Untreated iron deficiency anemia is postulated to cause secondary (reactive) thrombocytosis due to proliferation of common progenitor cells.  

Work-up including JAK2 kinase mutation for primary thrombocytosis, bone marrow biopsy and BCR-ABL mutation for myeloproliferative disorders, Hb electrophoresis and for hypercoagulable states are all negative. Her thrombocytosis was deemed secondary to iron deficiency anemia and platelet count has normalized to 445,000 with correction of iron deficiency anemia (Hb/Hct 10.1/33.2) at 1 year. Repeat MR at 4 months showed resolution of meningeal enhancement and improvement in venous filling via SSS. Apixaban was stopped at 1 year and she remains on iron supplementation with hematology follow-up.

Thrombocytosis needs to be recognized as a risk factor for cerebral venous thrombosis and extensive work-up for both its primary and secondary causes like anemia and infection/inflammation has to be undertaken. This is imperative especially in our case since iron deficiency anemia is a common hematologic disorder that can be readily treated.