Vitiligo exacerbated after herpes zoster.

21:13 EST 18th December 2014 | BioPortfolio

Summary of "Vitiligo exacerbated after herpes zoster."

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Affiliation

Department of Dermatology, Osaka University Graduate School of Medicine, Osaka, Japan.

Journal Details

This article was published in the following journal.

Name: The Journal of dermatology
ISSN: 1346-8138
Pages:

Links

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Medical and Biotech [MESH] Definitions

Pain in nerves, frequently involving facial SKIN, resulting from the activation the latent varicella-zoster virus (HERPESVIRUS 3, HUMAN). The two forms of the condition preceding the pain are HERPES ZOSTER OTICUS; and HERPES ZOSTER OPHTHALMICUS. Following the healing of the rashes and blisters, the pain sometimes persists.

An attenuated vaccine used to prevent and/or treat HERPES ZOSTER, a disease caused by HUMAN HERPESVIRUS 3.

HERPES ZOSTER but without eruption of vesicles. Patients exhibit the characteristic pain minus the skin rash, sometimes making diagnosis difficult.

An acute infectious, usually self-limited, disease believed to represent activation of latent varicella-zoster virus (HERPESVIRUS 3, HUMAN) in those who have been rendered partially immune after a previous attack of CHICKENPOX. It involves the SENSORY GANGLIA and their areas of innervation and is characterized by severe neuralgic pain along the distribution of the affected nerve and crops of clustered vesicles over the area. (From Dorland, 27th ed)

Inflammation of brain tissue caused by infection with the varicella-zoster virus (HERPESVIRUS 3, HUMAN). This condition is associated with immunocompromised states, including the ACQUIRED IMMUNODEFICIENCY SYNDROME. Pathologically, the virus tends to induce a vasculopathy and infect oligodendrocytes and ependymal cells, leading to CEREBRAL INFARCTION, multifocal regions of demyelination, and periventricular necrosis. Manifestations of varicella encephalitis usually occur 5-7 days after onset of HERPES ZOSTER and include HEADACHE; VOMITING; lethargy; focal neurologic deficits; FEVER; and COMA. (From Joynt, Clinical Neurology, 1996, Ch 26, pp29-32; Hum Pathol 1996 Sep;27(9):927-38)

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