Neurol India Home 

Year : 2014  |  Volume : 62  |  Issue : 6  |  Page : 674--675

Cerebral venous sinus thrombosis with increased factor VIII activity in an adult with iron deficiency anemia

Hiroshi Yokota1, Yuki Ida1, Shinya Sugiura2, Ken Sasaki2, Hiroo Itoh2,  
1 Department of Neurosurgery, Nabari City Hospital, Mie, Japan
2 Department of Cardiology, Nabari City Hospital, Mie, Japan

Correspondence Address:
Hiroshi Yokota
Department of Neurosurgery, Nabari City Hospital, Mie

How to cite this article:
Yokota H, Ida Y, Sugiura S, Sasaki K, Itoh H. Cerebral venous sinus thrombosis with increased factor VIII activity in an adult with iron deficiency anemia.Neurol India 2014;62:674-675

How to cite this URL:
Yokota H, Ida Y, Sugiura S, Sasaki K, Itoh H. Cerebral venous sinus thrombosis with increased factor VIII activity in an adult with iron deficiency anemia. Neurol India [serial online] 2014 [cited 2022 Aug 10 ];62:674-675
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Full Text


Iron deficiency anemia and elevated factor VIII (FVIII) activity are both known to cause cerebral venous sinus thrombosis (CVST). [1],[2] Herein, we report one such case.

A 37-year-old Japanese woman presented with nonfluent aphasia and right-sided weakness. Brain computed tomography (CT) demonstrated a hypodensity area with hemorrhagic transformation in left frontal lobe. Laboratory examinations revealed hypochromic microcytic anemia (hemoglobin 7.7 g/dL, hematocrit 26.7%, mean corpuscular volume 70.1 fL, mean cell hemoglobin 20.2 pg, serum iron 13 μg/dL, unsaturated iron binding capacity 286 μg/dL, and ferritin 3.8 ng/mL), while erythropoietin was increased to 138 mU/mL (normal, 8-36 mU/mL). White blood cell and platelet counts were 11,040/mm 3 and 356,000/mm 3 , respectively. Prothrombin time was 14.1 s and international normalized ratio (INR) was 1.56. C-reactive protein was 2.7 mg/dL. Antiphospholipid antibodies, antinuclear antibody, anti-mitochondria antibody, and lupus anticoagulant were all negative. Thyroid functions, protein C, protein S, and homocysteine plasma levels were all within normal limits. Thoracic and abdominal CT, abdominal ultrasound, and upper gastrointestinal endoscopy results did not reveal the underlying cause of anemia, such as malignancy, ulcers, or gynecologic disorders. She had no recent history of menorrhagia or taking oral contraceptives. D-dimer and thrombin-antithrombin III complex were mildly elevated to 1.7 μg/ml (normal, 0-1.0 μg/ml) and 5.8 ng/ml (normal, 0-3.0 ng/ml), respectively. FVIII activity was increased to 199% (normal, 60-150%), while factor IX and XIII, and antithrombin III were within normal ranges. Mutation of factor V Leiden was not detected. Venous phase of left internal carotid artery angiography revealed disrupted flow in the anterior part of the superior sagittal sinus (SSS) [Figure 1]. Patient was hydrated and intravenous heparin was initiated, which was followed by oral warfarin, iron supplementation. At a 2-month follow-up examination, the patient had no neurological deficits and magnetic resonance venogram showed recanalization of the SSS [Figure 2]. A laboratory examination demonstrated improvement of iron deficiency anemia and FVIII activity was normalized to 104%.

Increased FVIII activity is a prothrombotic factor and levels greater than 150 IU/dL (or 150% of normal) is reported to increase the risk of CVST, [2] while hematological conditions including those associated with anemia, such as iron deficiency anemia, sickle cell disease, and thalassemia, are also known as causes of the condition. [1] Reactive thrombocytosis, erythropoietin-mediated platelet hyperresponsiveness, and hypercoagulability secondary to red cell deformability have been proposed to be involved in the mechanism of development of CVST due to iron deficiency anemia. [1],[3]{Figure 1}{Figure 2}

Although there are no known studies of the causal relationship between iron deficiency anemia, increased FVIII activity, and CVST. Ozsoylu and Gursel found that children with iron deficiency anemia had increased FVIII activity, which was significantly decreased after iron treatment. [4] CVST with iron deficiency anemia is predominantly found in children and infants, [5] while it is rarely reported in adults [Table 1]. In adult cases, treatments generally consist of transfusion, anticoagulant administration, and iron supplementation.{Table 1}

Considering that CVST is a multifactorial disease, [6] increased FVIII activity in iron deficiency anemia might only have been a coincidental finding in the present case. Furthermore, since increased FVIII activity can be observed as an acute response along with inflammation and fever, higher value could be observed if the patient was infected. [7]


1Benedict SL, Bonkowsky JL, Thompson JA, Van Orman CB, Boyer RS, Bale JF Jr, et al. Cerebral sinovenous thrombosis in children: Another reason to treat iron deficiency anemia. J Child Neurol 2004;19:526-31.
2Bugnicourt JM, Roussel B, Tramier B, Lamy C, Godefroy O. Cerebral venous thrombosis and plasma concentrations of factor VIII and von Willebrand factor: A case control study. J Neurol Neurosurg Psychiatry 2007;78:699-701.
3Stolz E, Valdueza JM, Grebe M, Schlachetzki F, Schmitt E, Madlener K, et al. Anemia as a risk factor for cerebral venous thrombosis? An old hypothesis revisited. Results of a prospective study. J Neurol 2007;254:729-34.
4Ozsoylu S, Gursel T. Factor VIII procoagulant activity in iron deficiency anemia. J Pediatr 1980;96:287-8.
5Hartfield DS, Lowry NJ, Keene DL, Yager JY. Iron deficiency: A cause of stroke in infants and children. Pediatr Neurol 1997;16:50-3.
6Bousser MG, Ferro JM. Cerebral venous thrombosis: An update. Lancet Neurol 2007;6:162-70.
7Federman DG, Kirsner RS. An update on hypercoagulable disorders. Arch Intern Med 2001;161:1051-6.