Erythropoietin Therapy for Subarachnoid Hemorrhage
Status:
Completed
Trial end date:
2007-03-01
Target enrollment:
Participant gender:
Summary
ABSTRACT:
Delayed ischemic deficits (DID) and strokes caused by low cerebral blood flow (CBF) are major
sources of poor outcome following aneurysmal subarachnoid hemorrhage (SAH). DID are often
accompanied by vasospasm and abnormalities in cerebrovascular autoregulation, an important
reflex involved in the defense against low CBF. Assessment of vasospasm and impaired
autoregulation can be conveniently measured non-invasively by use of transcranial Doppler
(TCD) and the transient hyperaemic response test (THRT). Vasospasm and abnormalities in the
THRT can predict those patients who are at risk of developing DID. In this study, the
investigators wish to explore the neuroprotective and angiogenic effects of systemic
erythropoietin (EPO) therapy on vasospasm and autoregulation following SAH, and examine
whether any improvements translate into reduced incidences of DID and poor outcome. Eighty
patients with SAH will be recruited over one year to receive three doses in the first week of
either intravenous epoetin beta 30000 IU or placebo (0.9% saline) 50 ml/30 min as part of a
randomized, double-blind, placebo-controlled trial. The investigators propose daily TCD
assessment for detecting vasospasm and abnormal autoregulation. Outcome measures will examine
the influence of EPO therapy on the incidence, severity, and duration of vasospasm, abnormal
autoregulation, and DID.
PURPOSE:
This study is a randomized, double-blind, placebo-controlled clinical trial investigating the
potentially beneficial effects of systemic recombinant human erythropoietin therapy (Epoetin
beta, NeoRecormon®, Roche, 30000IU/50 ml/30 min, three times in the first week) on cerebral
autoregulation and incidence of delayed ischemic deficits (DID) following aneurysmal
subarachnoid haemorrhage (SAH).
HYPOTHESIS Systemic recombinant human erythropoietin therapy can be used safely following SAH
to ameliorate vasospasm, improve cerebral autoregulation, reduce DID, and facilitate
neurological recovery.
Phase:
Phase 2
Details
Lead Sponsor:
University of Cambridge
Collaborators:
Hoffmann-La Roche Roche Foundation of Anemia Research (RoFAR, Switzerland)