Treating patients with schizophrenia deficit with erythropoietin?
Article first published online: 21 JUN 2012
DOI: 10.1111/j.1440-1819.2012.02359.x
© 2012 The Authors. Psychiatry and Clinical Neurosciences © 2012 Japanese Society of Psychiatry and Neurology
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How to Cite
Fond, G., Macgregor, A., Attal, J., Larue, A., Brittner, M., Ducasse, D. and Capdevielle, D. (2012), Treating patients with schizophrenia deficit with erythropoietin?. Psychiatry and Clinical Neurosciences, 66: 375–382. doi: 10.1111/j.1440-1819.2012.02359.x
Publication History
- Issue published online: 26 JUL 2012
- Article first published online: 21 JUN 2012
- Received 16 February 2012; revised 25 April 2012; accepted 28 April 2012.
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Keywords:
- cognition;
- erythropoietin;
- neuroprotection;
- oxydative stress;
- schizophrenia
This systematic review summarizes and critically appraises the literature on the effect of erythropoietin (EPO) in schizophrenia patients and the pathophysiological mechanisms that may explain the potential of its use in this disease. EPO is mainly known for its regulatory activity in the synthesis of erythrocytes and is frequently used in treatment of chronic anemia. This cytokine, however, has many other properties, some of which may improve the symptoms of psychiatric illness. The review follows the preferred reporting items for systematic reviews and meta-analysis (PRISMA) statement guidelines. Three databases (Medline, Web of Science, and Cochrane) were searched combining the search terms ‘erythropoietin AND (psychotic disorders OR schizophrenia)’. Seventy-eight studies were included in qualitative synthesis, a meta-analytic approach being prohibited. The findings suggest that several EPO cerebral potential properties may be relevant for schizophrenia treatment, such as neurotransmission regulation, neuroprotection, modulation of inflammation, effects on blood–brain barrier permeability, effects on oxidative stress and neurogenesis. Several potentially detrimental side-effects of EPO therapy, such as increased risk of thrombosis, cancer, increased metabolic rate and mean arterial blood pressure leading to cerebral ischemia could severely limit or halt the use of EPO. Overall, because the available data are inconclusive, further efforts in this field are warranted.

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