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  Vol. 57 No. 8, August 2000 TABLE OF CONTENTS
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{beta}-Endorphin Concentrations in Peripheral Blood Mononuclear Cells of Patients With Multiple Sclerosis

Effects of Treatment With Interferon Beta

Maira Gironi, MD; Vittorio Martinelli, MD; Elena Brambilla; Roberto Furlan, MD; Alberto E. Panerai, MD; Giancarlo Comi, MD; Paola Sacerdote, PhD

Arch Neurol. 2000;57:1178-1181.

Context  It has been reported that the opioid peptide {beta}-endorphin (BE) has immunosuppressive effects. Interferon beta (IFN-{beta}) is a well-established therapy for multiple sclerosis (MS), but immunological mechanisms underlying its beneficial effects in MS are partially undefined.

Objectives  To determine BE levels in peripheral blood mononuclear cells (PBMCs) of patients with relapsing-remitting MS during different phases of disease activity and the possible modulating effects of IFN-{beta} treatment on PBMC BE synthesis in patients with MS.

Design  We measured BE levels in blood samples collected from 6 patients with MS who had not experienced clinical changes during the previous 3 months (patients with stable MS) and from 7 patients with MS during a clinical relapse. We also surveyed BE levels in PBMC samples from 8 patients with MS before treatment and for 6 months after the beginning of IFN-{beta} administration. The control group was 13 healthy subjects.

Results  Low PBMC BE levels were detected in patients with stable MS and in those entering IFN-{beta} treatment compared with control subjects. Increased BE concentrations were observed in MS patients experiencing a clinical relapse compared with patients with stable MS. During IFN-{beta} treatment, the levels of BE in PBMC samples from patients with MS increased significantly (after 1 month, P = .02; after 3 months, P = .007; and after 6 months, P = .16).

Conclusions  A reduction of BE levels was present in patients with clinically inactive MS. Treatment with IFN-{beta} seems to induce an increase of this opioid in PBMCs of MS patients. The increase of BE concentration during a clinical relapse may represent a possible control mechanism aimed at counterbalancing the inflammatory phase of the disease.


From the Department of Neuroscience, San Raffaele Scientific Institute (Drs Gironi, Martinelli, Furlan, and Comi and Ms Brambilla), and Department of Pharmacology, University of Milan, (Drs Panerai and Sacerdote), Milan, Italy.


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