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Multiple Sclerosis, Vol. 13, No. 9, 1100-1106 (2007)
DOI: 10.1177/1352458507078684

Fulminant central nervous system demyelination associated with interferon-{alpha} therapy and hepatitis C virus infection

R. Höftberger

Institute of Neurology, Medical University of Vienna, Austria

F. Garzuly

Department of Pathology, Markusovszky Hospital, Szombathely, Hungary

H.P. Dienes

Department of Pathology, University of Köln, Germany

J. Grubits

Department of Neurology, Elisabeth Hospital, Sopron, Hungary

B. Rohonyi

Department of Pathology, Elisabeth Hospital, Sopron, Hungary

G. Fischer

Institute of blood group serology, Medical University of Vienna, Austria

Z. Hanzely

National Institute of Neurosurgery, Department of Neuropathology, Budapest, Hungary

H. Lassmann

Center for Brain Research, Division of Neuroimmunology, Vienna, Austria

H. Budka

Institute of Neurology, Medical University of Vienna, Austria, herbert.budka{at}meduniwien.ac.at

Hepatitis C virus (HCV) infection is common in the general population and may coincide with disease in the central and peripheral nervous system. Interferon-{alpha} (IFN-{alpha}) is used as treatment for HCV infection. The therapeutic benefit is assumed to result from activation of natural killer cells and CD8+ T cells. Despite its beneficial effects, it has been associated with a number of autoimmune disorders, such as chronic inflammatory demyelinating polyneuropathy and multiple sclerosis. Several clinical reports including magnetic resonance imaging exist, but neuropathological confirmation of MS associated with IFN-{alpha} therapy and HCV infection is lacking. We report a case of a female patient with chronic HCV infection who developed `acute MS'-like demyelinating disease after IFN-{alpha} administration, with extensive lesions throughout brain and thoracic spinal cord. The patient died after a disease duration of 6 months. Brain autopsy revealed Baló-like demyelinating plaques with positive HCV sequences within florid lesions. The development of fulminant demyelinating disease after administration of IFN-{alpha} suggests that autoimmune mechanisms such as T cell mediated tissue damage might be initiated or aggravated by IFN-{alpha} therapy. Additionally, the presence of HCV RNA within the demyelinated lesion indicates a possible role in triggering or propagating disease. Multiple Sclerosis 2007; 13: 1100—1106. http://msj.sagepub.com

Key Words: CD8+ T cells • concentric sclerosis (Baló) • hepatitis C virus • interferon-{alpha} • multiple sclerosis (MS)


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