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Lupus
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Autonomic nerve dysfunction in systemic lupus erythematosus: evidence for a mild involvement

L. Altomonte

Divisione di Reumatologia, Istituto di Medicina Intema e Geriatria, Università Cattolica S. Cuore, Roma, Italia

L. Mirone

Divisione di Reumatologia, Istituto di Medicina Intema e Geriatria, Università Cattolica S. Cuore, Roma, Italia

A. Zoli

Divisione di Reumatologia, Istituto di Medicina Intema e Geriatria, Università Cattolica S. Cuore, Roma, Italia

M. Magaro

Divisione di Reumatologia, Istituto di Medicina Intema e Geriatria, Università Cattolica S. Cuore, Roma, Italia

Neurologic manifestations are known to occur in patients with systemic lupus erythematosus (SLE) and significantly affect the clinical course of the disease. Nevertheless, the prevalence, pattern and severity of autonomic impairment in such patients have yet to be defined.

In the present study a series of 38 female SLE patients was assessed for the presence of autonomic dysfunction. Five noninvasive standardized cardiovascular reflex tests were used. The grading system proposed by Ewing and Clarke was applied to classifying autonomic impairment according to severity. Seventeen out of 38 patients, that is 44.7%, had evidence of autonomic impairment. Most of the patients had a mild degree of dysfunction. No correlation was found for the duration of the disease while an apparent lack of the commonly described chronological sequence of autonomic involvement was observed.

We suggest that in SLE patients the prevalence of autonomic impairment, when investigated, does not significantly differ from that of other SLE-associated neurological events. The contribution of a direct immunological damage to components of neural pathways in the pathogenesis of the autonomic involvement can be postulated. Clinical consequences of autonomic impairment in patients with systemic lupus erythematosus need to be elucidated.

Key Words: autonomic neuropathy • systemic lupus erythematosus

Lupus, Vol. 6, No. 5, 441-444 (1997)
DOI: 10.1177/096120339700600505


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This article has been cited by other articles:


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