526983
research-article2014
CPJXXX10.1177/0009922814526983Clinical PediatricsZaidi and Berman
Brief Report
Crossing the Thrombotic Threshold: Deep Vein Thrombosis in Henoch– Schönlein Purpura
Clinical Pediatrics 2014, Vol. 53(14) 1396–1398 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814526983 cpj.sagepub.com
Ahmar U. Zaidi, MD1 and Brian Berman, MD1 Case Report
Table 1. Initial Laboratory Values.
A 10-year-old male with a past medical history of attention deficit hyperactivity disorder presented with a 1-day history of acute left calf pain. Four weeks prior to admission, evanescent nonpruritic, nonerythematous nickelsize lower extremity nodules were noted following a transient nonspecific viral illness. Five days prior to development of calf pain, he was diagnosis with Henoch–Schönlein purpura (HSP) when he developed scattered nonthrombocytopenic lower extremity petechiae and mild abdominal discomfort. No specific therapy was prescribed. On the day of admission, he had been sitting stationary at a sporting event for 3 hours prior to the sudden onset of left calf pain, progressing to limp and swelling. There was no history of trauma. Family history was significant for the patient’s mother experiencing 5 first trimester spontaneous abortions. She subsequently received heparin treatment during a future successful pregnancy. Further details of her evaluation were not available, although she recalled being told that she “might have a lupus anticoagulant.” On arrival at the emergency department, laboratory studies where performed (Table 1), and lower extremity venous Doppler study demonstrated acute deep vein thrombosis of the left peroneal vein. Enoxaparin sodium therapy was initiated (1 mg/kg q12hr SQ) and he was admitted for further management. Petechial rash and extremity symptoms and signs readily improved over the next several days. An extensive evaluation initiated for hypercoagulability was completed. Studies are listed in Table 2. Genetic studies for factor V Leiden and prothrombin gene mutation were unremarkable; the patient was found to be doubly heterozygous for MTHFR C677T and MTHFR A1298C (with normal homocysteine level). Enoxaparin was discontinued after 3 months when a repeat Doppler study demonstrated complete resolution of thrombosis. At 2-month follow-up, factor VIII remained mildly elevated at 154%; lipoprotein A was elevated at 85.8 mg/dL. At 9-month follow-up, the child remained well.
Erythrocyte sedimentation rate C-reactive protein Complete blood count WBC Hemoglobin Hematocrit MCV Platelets Neutrophils Lymphocytes Monocytes Eosinophils Antinuclear antibody screen Creatine kinase Basic metabolic panel Sodium Potassium Chloride Carbon dioxide Glucose BUN Creatinine Calcium D-dimer Urinalysis Lipid panel
29 mm/h (0-15) 0.5 mg/dL (0.0-0.8) 8.1 billion/L (5-14) 12.4 g/dL (11.0-15.1) 36.9% (32.2% to 44.4%) 85 fL (78-91) 324 billion/L (150-450) 5.2 billion/L (1.8-8.0) 1.8 billion/L (1.5-6.5) 0.8 billion/L (0.2-0.6) 0.3 billion/L (0.2-0.4) Negative 89 U/L (40-230) 137 mmol/L 3.5 mmol/L 103 mmol/L 25 mmol/L 105 mg/dL 16 mg/dL 0.33 mg/dL 9 mg/dL 1920 ng/mL (0-499) Negative Normal
Abbreviations: WBC, white blood cell; MCV, mean corpuscular volume; BUN, blood urea nitrogen.
Discussion HSP is a well-characterized, multisystem, self-limited small vessel vasculitis mainly affecting children. The 1
Oakland University William Beaumont School of Medicine, Royal Oak, MI, USA Corresponding Author: Ahmar U. Zaidi, Department of Pediatrics, Oakland University William Beaumont School of Medicine, Beaumont Children’s Hospital, 3601 W. 13 Mile Rd, Royal Oak, MI 48073, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at GEORGETOWN UNIV MED CTR on May 24, 2015
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Zaidi and Berman Table 2. Assessment of Hypercoagulability. Fibrinogen DRVVT Anticardiolipin antibodies IgA IgG IgM Beta-2 glycoprotein antibodies IgG IgM Protein C Protein S Antithrombin Factor VIII activity Homocysteine Lipoprotein A
355 mg/dL (175-375 mg/dL) 40 seconds (0-52 seconds)
research-article2014
CPJXXX10.1177/0009922814526983Clinical PediatricsZaidi and Berman
Brief Report
Crossing the Thrombotic Threshold: Deep Vein Thrombosis in Henoch– Schönlein Purpura
Clinical Pediatrics 2014, Vol. 53(14) 1396–1398 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814526983 cpj.sagepub.com
Ahmar U. Zaidi, MD1 and Brian Berman, MD1 Case Report
Table 1. Initial Laboratory Values.
A 10-year-old male with a past medical history of attention deficit hyperactivity disorder presented with a 1-day history of acute left calf pain. Four weeks prior to admission, evanescent nonpruritic, nonerythematous nickelsize lower extremity nodules were noted following a transient nonspecific viral illness. Five days prior to development of calf pain, he was diagnosis with Henoch–Schönlein purpura (HSP) when he developed scattered nonthrombocytopenic lower extremity petechiae and mild abdominal discomfort. No specific therapy was prescribed. On the day of admission, he had been sitting stationary at a sporting event for 3 hours prior to the sudden onset of left calf pain, progressing to limp and swelling. There was no history of trauma. Family history was significant for the patient’s mother experiencing 5 first trimester spontaneous abortions. She subsequently received heparin treatment during a future successful pregnancy. Further details of her evaluation were not available, although she recalled being told that she “might have a lupus anticoagulant.” On arrival at the emergency department, laboratory studies where performed (Table 1), and lower extremity venous Doppler study demonstrated acute deep vein thrombosis of the left peroneal vein. Enoxaparin sodium therapy was initiated (1 mg/kg q12hr SQ) and he was admitted for further management. Petechial rash and extremity symptoms and signs readily improved over the next several days. An extensive evaluation initiated for hypercoagulability was completed. Studies are listed in Table 2. Genetic studies for factor V Leiden and prothrombin gene mutation were unremarkable; the patient was found to be doubly heterozygous for MTHFR C677T and MTHFR A1298C (with normal homocysteine level). Enoxaparin was discontinued after 3 months when a repeat Doppler study demonstrated complete resolution of thrombosis. At 2-month follow-up, factor VIII remained mildly elevated at 154%; lipoprotein A was elevated at 85.8 mg/dL. At 9-month follow-up, the child remained well.
Erythrocyte sedimentation rate C-reactive protein Complete blood count WBC Hemoglobin Hematocrit MCV Platelets Neutrophils Lymphocytes Monocytes Eosinophils Antinuclear antibody screen Creatine kinase Basic metabolic panel Sodium Potassium Chloride Carbon dioxide Glucose BUN Creatinine Calcium D-dimer Urinalysis Lipid panel
29 mm/h (0-15) 0.5 mg/dL (0.0-0.8) 8.1 billion/L (5-14) 12.4 g/dL (11.0-15.1) 36.9% (32.2% to 44.4%) 85 fL (78-91) 324 billion/L (150-450) 5.2 billion/L (1.8-8.0) 1.8 billion/L (1.5-6.5) 0.8 billion/L (0.2-0.6) 0.3 billion/L (0.2-0.4) Negative 89 U/L (40-230) 137 mmol/L 3.5 mmol/L 103 mmol/L 25 mmol/L 105 mg/dL 16 mg/dL 0.33 mg/dL 9 mg/dL 1920 ng/mL (0-499) Negative Normal
Abbreviations: WBC, white blood cell; MCV, mean corpuscular volume; BUN, blood urea nitrogen.
Discussion HSP is a well-characterized, multisystem, self-limited small vessel vasculitis mainly affecting children. The 1
Oakland University William Beaumont School of Medicine, Royal Oak, MI, USA Corresponding Author: Ahmar U. Zaidi, Department of Pediatrics, Oakland University William Beaumont School of Medicine, Beaumont Children’s Hospital, 3601 W. 13 Mile Rd, Royal Oak, MI 48073, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at GEORGETOWN UNIV MED CTR on May 24, 2015
1397
Zaidi and Berman Table 2. Assessment of Hypercoagulability. Fibrinogen DRVVT Anticardiolipin antibodies IgA IgG IgM Beta-2 glycoprotein antibodies IgG IgM Protein C Protein S Antithrombin Factor VIII activity Homocysteine Lipoprotein A
355 mg/dL (175-375 mg/dL) 40 seconds (0-52 seconds)
