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  Vol. 145 No. 8, August 2009 TABLE OF CONTENTS
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Progressive Multifocal Leukoencephalopathy, Efalizumab, and Immunosuppression

A Cautionary Tale for Dermatologists

Benjamin D. Korman, MD; Kenneth L. Tyler, MD; Neil J. Korman, MD, PhD

Arch Dermatol. 2009;145(8):937-942.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Progressive multifocal leukoencephalopathy (PML) is a rare opportunistic infection of the central nervous system caused by the JC (John Cunningham) virus.1 This virus is common and is generally innocuous in an immunocompetent host. However, in individuals with innate, acquired, or iatrogenic immunodeficiency, the JC virus can become active and infect oligodendrocytes, leading to their lysis. Oligodendrocyte lysis leads to central nervous system demyelination, which may then result in focal neurologic deficits including hemiparesis, visual field deficits, and cognitive impairment. Progressive multifocal leukoencephalopathy is usually irreversible and fatal.

Progressive multifocal leukoencephalopathy was first identified in 1958 in patients with lymphoma,2 but it was not until 1971 that the viral origin of this disease was recognized.1 It remained a very rarely reported clinical entity until the 1980s and the AIDS pandemic. Indeed, deaths due to PML as a whole . . . [Full Text of this Article]

EPIDEMIOLOGY, PATHOGENESIS, AND CLINICAL MANIFESTATIONS


DIAGNOSIS AND TREATMENT

IMMUNOSUPPRESSIVE AGENT–RELATED PML

COMMENT

AUTHOR INFORMATION


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