Vascular endothelial growth factor (VEGF) is increased in serum, but not in cerebrospinal fluid in HIV associated CNS diseases
- 1Department of Neurology, Heinrich Heine-University, Düsseldorf, Germany
- 2Department of Neurology, Ludwig-Maximilians University, Munich, Germany
- 3Max von Pettenkofer Institute for Hygiene and Medical Microbiology, Ludwig-Maximilians University, Munich, Germany
- Correspondence to: B Sporer Department of Neurology, Ludwig-Maximilians-University, Marchioninistr. 15, 81377 Munich, Germany; BSPORERnefo.med.uni-muenchen.de
- Received 4 April 2003
- Accepted 9 July 2003
- Revised 2 July 2003
Abstract
Vascular endothelial growth factor (VEGF) is a potent angiogenic and mitogenic peptide, which also induces several mediators that may play a role in HIV induced CNS damage. VEGF levels were determined in cerebrospinal fluid (CSF) and serum samples from patients with (n = 8) and without (n = 19) directly HIV associated CNS disorders and HIV negative control patients (n = 18). VEGF serum but not CSF levels were significantly increased in HIV infected patients with (381.1 (78.9) pg/ml) HIV associated CNS diseases compared with those without (120.8 (13.1) pg/ml) and HIV negative control patients (133.1(14.8) pg/ml). Serum samples from patients with untreated HIV associated encephalopathy (HIVE, n = 3) contained the highest VEGF levels (583.9 (71.5) pg/ml). In two patients VEGF serum levels were reduced during antiretroviral therapy. However, regardless of effective viral suppression, patients with HIVE still had higher levels compared with HIV infected patients without HIVE. A relevant increase of serum VEGF was not observed in patients without HIVE though high HI viral load. We conclude that HIVE is associated with increased serum VEGF levels. Further studies are warranted to elucidate the role of VEGF in HIVE.
- CSF, cerebrospinal fluid
- HIVE, HIV associated encephalopathy
- VEGF, vascular endothelial growth factor
Footnotes
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This work was supported by a grant from the Ludwig Maximilians-University, Munich, to B Sporer (Förderprogramm für Forschung und Lehre).
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This study was in part presented at the conjoint meeting of the 4th International Symposium on NeuroVirology and the 10th Conference on Neuroscience on HIV Infection, June 2002, Düsseldorf, Germany.
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Competing interests: none declared







