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Phospholipase A2 levels in acute chest syndrome of sickle cell disease.

Abstract

Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non-SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100-fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS.

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  • Authors+Show Affiliations

    ,

    Department of Hematology/Oncology, Children's Hospital Oakland, CA 94609 USA.

    , , , ,

    Source

    Blood 87:6 1996 Mar 15 pg 2573-8

    MeSH

    Acute Disease
    Adolescent
    Adult
    Anemia, Sickle Cell
    Child
    Child, Preschool
    Embolism, Fat
    Fatty Acids, Nonesterified
    Female
    Humans
    Infant
    Inflammation
    Ischemia
    Lung Diseases
    Male
    Phospholipases A
    Phospholipases A2
    Pneumonia
    Pulmonary Embolism

    Pub Type(s)

    Comparative Study
    Journal Article
    Research Support, U.S. Gov't, P.H.S.

    Language

    eng

    PubMed ID

    8630425

    Citation

    Styles, L A., et al. "Phospholipase A2 Levels in Acute Chest Syndrome of Sickle Cell Disease." Blood, vol. 87, no. 6, 1996, pp. 2573-8.
    Styles LA, Schalkwijk CG, Aarsman AJ, et al. Phospholipase A2 levels in acute chest syndrome of sickle cell disease. Blood. 1996;87(6):2573-8.
    Styles, L. A., Schalkwijk, C. G., Aarsman, A. J., Vichinsky, E. P., Lubin, B. H., & Kuypers, F. A. (1996). Phospholipase A2 levels in acute chest syndrome of sickle cell disease. Blood, 87(6), pp. 2573-8.
    Styles LA, et al. Phospholipase A2 Levels in Acute Chest Syndrome of Sickle Cell Disease. Blood. 1996 Mar 15;87(6):2573-8. PubMed PMID: 8630425.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Phospholipase A2 levels in acute chest syndrome of sickle cell disease. AU - Styles,L A, AU - Schalkwijk,C G, AU - Aarsman,A J, AU - Vichinsky,E P, AU - Lubin,B H, AU - Kuypers,F A, PY - 1996/3/15/pubmed PY - 1996/3/15/medline PY - 1996/3/15/entrez SP - 2573 EP - 8 JF - Blood JO - Blood VL - 87 IS - 6 N2 - Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non-SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100-fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS. SN - 0006-4971 UR - https://www.unboundmedicine.com/medline/citation/8630425/Phospholipase_A2_levels_in_acute_chest_syndrome_of_sickle_cell_disease_ L2 - http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=8630425 DB - PRIME DP - Unbound Medicine ER -