[The effect of cladribine treatment on beta-2 microglobin in the cerebrospinal fluid and serum of patients with multiple sclerosis].

Multiple sclerosis (MS) is the most frequent demyelinating disease of the central nervous system (CNS). Lymphocytes seem to play a crucial role in the pathogenesis of the disorder. They are rich in, among others, beta-2Microglobulin (beta 2M)--a low molecular weight protein located extracellularly and associated with class 1 antigens of the major histocompatibility complex. beta-2M is considered as a marker for disease activity in immune disorders. Its precise role in pathology remains still unknown, but there is evidence that it may be involved in lymphocyte activation. Cladribine (2-chloro-2-deoxyadenosine, 2-CDA) is a potent lymphocytotoxic agent under investigation in the treatment in MS patients, earlier used in hairy-cell-leukemia therapy. Previous studies in MS populations showed beta 2-microglobulin to be moderately increased. Suspecting that beta 2M levels might indicate inflammatory events in CNS we determined CSF-beta 2M and serum beta 2M concentration in patients with relapsing-remitting MS (n = 15) before and after cladribine treatment as well as in a control group diagnosed as tension type headache (n = 10). There was a significant decrease in the CSF and sera beta 2M level in MS patients after cladribine treatment, associated with a slight but significant clinical improvement measured by Kurtzke's Expanded Disability Status Scale. We conclude that beta 2M is a sensitive marker of the CDA influence on the immune system in MS patients; however, increase in CSF and sera beta 2M is not specific as there was no statistically significant difference between MS and control patients.