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Blood, Vol. 92 No. 7 (October 1), 1998:
pp. 2551-2555
Plasma Endothelin-1, Cytokine, and Prostaglandin E2
Levels in Sickle Cell Disease and Acute Vaso-Occlusive Sickle Crisis
Evangeline Graido-Gonzalez,
James C. Doherty,
Eric W. Bergreen,
Gregory Organ,
Margaret Telfer, and
Marvin A. McMillen
From the Department of Internal Medicine, the Department of Surgery,
and the Division of Hematology, Michael Reese Hospital and University
of Illinois College of Medicine at Chicago, Chicago, IL.
The relative contributions of microvascular inflammation and
vasomotor dysregulation to the development of acute vaso-occlusive crisis in sickle cell disease have been intensely studied. The present
observational study was designed to examine the levels of circulating
proinflammatory cytokines, anti-inflammatory cytokines, and vasoactive
mediators during and after acute painful crisis. In symptomatic sickle
cell patients, plasma levels of endothelin-1 and prostaglandin
E2 were elevated during crises compared with healthy
African-American controls. These levels had decreased, but not
normalized, when patients were seen 1 to 3 weeks after discharge from
hospital. Other mediators (tumor necrosis factor  [TNF],
interleukin-1 [IL-1], IL-6, IL-8, and IL-10) were neither
elevated in asymptomatic sickle cell disease nor in acute vaso-occlusive crisis. As a potent long-acting mediator of
vasoconstriction and inflammation, endothelin-1 may play a key role in
the cycle of ischemia and inflammation that initiates and sustains pain of crisis. The downregulatory effects of prostaglandin E2
on immune cell function may contribute to the increased susceptibility
to infection observed in patients with sickle cell disease.
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