English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

320 Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 2 ¦ April June 2017 showed left hemiplegia (2/5 in upper and 3/5 in lower limb). Reflex was sluggish in left upper and lower limb with left extensor plantar response. Her complete hemogram showed mild anemia and thrombocytopenia (hemoglobin – 9.6 g/dL; platelet count – 52,000); renal, liver, and thyroid functions were normal. Serum electrolytes were normal. Magnetic resonance imaging of brain showed acute infarct in the right middle cerebral artery (MCA)/anterior cerebral artery and MCA/posterior cerebral artery borderzone territory. Magnetic resonance angiography of neck vessels and circle of Willis showed decreased flow in the right internal carotid artery from its origin. Duplex ultrasonography showed thrombosis of the right femoral vein [Figure 1]. Serological testing for antinuclear antibody, auto‐antibodies profile including anti‐double‐stranded deoxyribonucleic acid, anti‐Ro, and anti‐La antibodies was negative. Serological testing for human immunodeficiency virus, hepatitis B virus (hepatitis B surface antigen), and venereal disease research laboratory was negative. Serum homocysteine, protein C and S, and antithrombin III levels were within normal limits. A hypercoagulability clinical evaluation showed significantly elevated aPLa (immunoglobulin G 24.6; immunoglobulin M 56.4) and positive lupus‐like anticoagulant. She received systemic anticoagulation with heparin followed by transition to oral warfarin. During her stay, she had mild improvement in limb weakness and modified Rankin score (mRs) at the time of discharge was 4/6. At 3‐month follow‐up, her mRs was 2/6, but persistent elevated aPLa levels. Sir, Antiphospholipid antibodies (aPLas) are associated with an increased risk of arterial and venous thromboembolism.[1] These include lupus anticoagulant, anticardiolipin antibodies, and anti‐β2‐glycoprotein‐1 antibodies. Antiphospholipid antibody syndrome (APS) is a prothrombotic condition characterized by the presence of these antibodies in patients with recurrent pregnancy morbidity and/or thromboembolic complications.[2] Some patients with aPLa develop multiorgan failure due to widespread thrombotic events, known as catastrophic APS.[3] The co‐occurrence of cerebral arterial thrombosis and deep vein thrombosis of lower limb in a patient with APS has not been reported. We report a middle‐aged female with the previous history of second‐trimester pregnancy loss presenting with deep vein thrombosis of lower limb with carotid artery thrombosis simultaneously.

Simultaneous Occurrence of Deep Vein Thrombosis and Carotid Artery Thrombosis in Antiphospholipid Antibody Syndrome