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Symptoms to Diagnosis

An unusual cause of bruising

Tahani Atieh, DO and Alan Lichtin, MD
Cleveland Clinic Journal of Medicine August 2019, 86 (8) 535-542; DOI: https://doi.org/10.3949/ccjm.86a.18119
Gregory W. Rutecki
Department of Internal Medicine, Cleveland Clinic; Clinical Instructor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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Tahani Atieh
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  • For correspondence: [email protected]
Alan Lichtin
Department of Hematologic Oncology and Blood Disorders, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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    Figure 1

    A large granular lymphocyte.

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    Figure 2

    The patient’s clinical course: factor VIII inhibitor response to treatment.

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    TABLE 1

    Our patient’s complete blood cell count results

    TestValueaReference range
    White blood cell count8.91 × 109/L3.70–11.00
    Red blood cell count5.16 × 1012/L3.90–5.20
    Hemoglobin14.6 g/dL11.5–15.5
    Hematocrit44.5%36.0%–46.0%
    Platelet count251 × 109/L150–400
    Neutrophils60.6%40%–60%
    Lymphocytes34.1%20%–40%
    Monocytes4.7%2%–8%
    Eosinophils0.4%1%–4%
    Basophils0.2%0.5%–1%
    • ↵a Abnormal results are shown in bold.

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    TABLE 2

    Our patient’s coagulation test results

    TestValueaReference range
    Prothrombin time11.0 seconds8.4–13.0
    International normalized ratio1.00.8–1.2
    Activated partial thromboplastin time46.7 seconds23.0–32.4
    • ↵a Abnormal results are shown in bold.

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    TABLE 3

    Differential diagnoses associated with coagulation assay results

    Prolonged prothrombin time (PT), normal activated partial thromboplastin time (aPTT)
    Factor VII deficiency or factor VII inhibitor
    Liver disease
    Vitamin K deficiency
    Warfarin use
    Disseminated intravascular coagulation
    Normal PT, prolonged aPTT
    Deficiency of intrinsic pathway factors (VIII, IX, XI, XII) or inhibitors of these clotting factors
    von Willebrand disease (if factor VIII is very low) Heparin use
    Lupus anticoagulant (usually associated with thrombosis instead of bleeding)
    Prolonged PT and aPTT
    Deficiency of common pathway factors (II, V, X, or fibrinogen)
    Severe liver disease
    Vitamin K deficiency
    Warfarin use
    Disseminated intravascular coagulation
    Heparin overdose
    Normal PT and aPTT with bleeding
    Platelet dysfunction (acquired or congenital)
    von Willebrand disease (if factor VIII is mildly decreased)
    Scurvy
    Ehlers-Danlos syndrome
    Hereditary hemorrhagic telangiectasia
    Factor XIII deficiency
    Hyperfibrinolysis
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    TABLE 4

    Our patient’s mixing study results

    TestValueaReference range
    Activated partial thromboplastin time (aPTT) screen61.2 seconds24.4–33.4
    Immediate aPTT 1:1 mix33.1 seconds< 33.5
    Incubated aPTT 1:1 mix42.2 seconds< 37.3
    • ↵a Abnormal results are shown in bold.

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    TABLE 5

    Further studies

    TestValueaReference range
    Factor VIII:C assay1%50%–173%
    Bethesada assay5.8 Bethesda units< 0.5
    • ↵a Abnormal results are shown in bold.

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Cleveland Clinic Journal of Medicine: 86 (8)
Cleveland Clinic Journal of Medicine
Vol. 86, Issue 8
1 Aug 2019
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An unusual cause of bruising
Tahani Atieh, Alan Lichtin
Cleveland Clinic Journal of Medicine Aug 2019, 86 (8) 535-542; DOI: 10.3949/ccjm.86a.18119

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An unusual cause of bruising
Tahani Atieh, Alan Lichtin
Cleveland Clinic Journal of Medicine Aug 2019, 86 (8) 535-542; DOI: 10.3949/ccjm.86a.18119
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  • Article
    • EVALUATION FOR AN ISOLATED PROLONGED aPTT
    • FACTOR VIII INHIBITOR EVALUATION
    • TREATMENT OF ACQUIRED HEMOPHILIA A
    • CASE CONTINUED: TREATMENT, LYMPHOCYTOSIS
    • EVALUATING LYMPHOCYTOSIS
    • CASE CONTINUED: LARGE GRANULAR LYMPHOCYTES
    • LGL LEUKEMIA: CLASSIFICATION AND MANAGEMENT
    • LGL LEUKEMIA AND AUTOIMMUNE DISEASE
    • ACQUIRED HEMOPHILIA A AND HEMATOLOGIC MALIGNANCY
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