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DOI 10.1016/s1386-6532(01)00196-2

Медицинская библиотека · Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2001

Cerebrospinal fluid S-100beta and its relationship with AIDS dementia complex.

Pemberton L A, Brew B J

Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

BACKGROUND

The astrocyte is thought to be important in AIDS dementia complex (ADC) pathogenesis on the basis of ADC neuropathology and cell culture models putatively because HIV can infect astrocytes leading to a compromise of their physiological detoxifying and neuronal support functions. Confirmatory in vivo data are lacking. Currently, the only widely available marker of the astrocyte is the protein S-100beta.

OBJECTIVE

The aims of this study were to determine whether cerebrospinal fluid (CSF) levels of S-100beta correlate with the presence, severity and rapidity of ADC progression.

STUDY

DESIGN

Fourty nine CSF samples from HIV-1 seropositive individuals with either no ADC (ADC stage 0) or varying degrees of ADC (ADC stages 1-3) were analysed in this study. An immunoradiometric assay was used to quantify levels of S-100beta in the CSF. All individuals in this study were receiving antiretroviral therapy. In addition, individuals with ADC were grouped as either rapid ADC progressors or slow ADC progressors depending on the period of time from ADC diagnosis to death.

RESULTS

CSF S-100beta levels in individuals with either ADC stage 2 or 3 were significantly elevated compared to those with stage 0 or 1. Moreover, CSF S-100beta levels were significantly higher in individuals with rapid ADC progression compared with slow progressors.

CONCLUSIONS

This study shows that CSF S-100beta levels predict those patients in whom ADC will progress rapidly.

Для цитирования: Pemberton L A, Brew B J. Cerebrospinal fluid S-100beta and its relationship with AIDS dementia complex.. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology. 2001. DOI: 10.1016/s1386-6532(01)00196-2.

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