Éntravenous immunoglobulin in the treatment of multiple sclerosis
Éntravenous immunoglobulin in the treatment of multiple sclerosis
Éntravenous immunoglobulin in the treatment of Multiple Sclerosis
D.KountourisCenter of Neurological Diagnosis, Athens, Greece.
Archieves of Hellenic Medicine 1995;12(4):264. Multiple scierosis (MS) is a central nervous system (CNS) demyelinating disease in the pathogenesis of which autïimmune ìechallisms are implicated. The existing evidence of its immune-mediated etiology hás led to theralpeutic attempts to modify, generally and/or selectively, the immune system of these patients. Antiviral, anti-inflammatory, immunosuppresant, and immunomodulatory therapies have been considered, involving glucocorticoids, immunosuppresant drugs (e g azathioprine), physicalagents (e.g. irradiation), plasmapheresis and, most recently, interferon-beta.Despite the fact that the mechanism of immunomodulation induced by high-dose intravenous immunoglobulin (IVIG) has not been completely understood as yet, the beneficial effect that exerts in the clinical course of various autoimmune disorders justified its use in the treatmelnt of MS. Several open trials have been conducted till now with encouraging results.7-6 Patients with reldpsing-remitting, progressive, and/or steroid dependent MS have been included in these studies. Generally, IVIGwasadministered either in monthly doses of 500mg – 2 g/kg of body weight or in daily (loses of 400 mg/kg for 5consecutive days followed by the same bimonthly booster dose. Reduction in the rate and severity of acute exacerbations, improvement of the neurological disability and decrease of the Kurtzke Expanded Disability Status Scale was observed in the majority of MS patients after the treatment with IVIG compared to the controls. No significant short or long-term adverse effects were reported. According lo the results of the above studies the treatment with IVIG is expected to be more successful in the following subsets of the disease:
a. Young patients in remission b. relapsing optic neuritis
Stable steroid-unresponsive optic neuritis
Chronic progressive MS
e. Mild cases with participation of other systems. Significant experimental work has also been done in an attempt to clarify the code of action of IVIG, in MS. Achiron et al,’ using the rat model of experimental autoimmune encephalomyelitis (EAE), observed that IVIG supressed active EAE in relation to disease severity and duration, despite the presence of T-cell reactivity to specific antigens, while the treatment had no effect on passive EAE induced by adoptive transfer of myelin basic protein specific CD4+ T-cells. On the other hand, van Engelen et al 7 examined the possibility of polyclonal immunoglobulin to enhance the potential of myelin repair occuring in the evolution of the inflammatory-demyelinating lesion, using the Theiler’s virus model of CNS demyelination. They observed promotion of remyelination after passive transfer of CNS-specific antiserum and transfer of CNS-specific purified immunoglobulin. Mouse polyclonal immunoglobulin from normal non-syngeneic mice, comparable with the human immunoglobulin preparation, was also found to promote CNS remyelination in the Theiler’s virus model of MS. From the clinical point of view, Tensen et al 8 detected decreased numbers of B, T, and natural killer Iymphocytes in six MS patients after the treatment with IVIG. The Iymphocyte numbers reached their minimum values one week after the treatment but an immunosuppressive effect continued to be present alter 5 weeks. The above mentioned promising findings of both the clinical and the experimental studies as well as the apparent clinical safety of IVIG indicate that this is the time for randomised, double-blind, placebo-controlled clinical trials, with Iarge number of patients followed for long periods, to be conducted in order to determine the exact role of IVIG in the treatment of MS.9 Such a trial, including 76 patients, is already under progress by Noseworthy e t al 10
D. KountourisREFERENCES 1. YAN J, RlCHERT JR, SIRDOVSKY MD. High-dose immunoglobulin for multiple sclerosis. Lancet 1990, 336:692
2. ACHIRON A,PRAS E, GILAD R, ZIV I, MANDEL M, GORDON CR ET AL. OpencontroLled therapeutic trial of intravenous immunoglobulin in relapsing-remitting multiple sclerosis. Arch Neurol 1992,49:1233-1236 3. COOK SD,.TROIANO R, ROHOWSKY-KOCHAN C,JOTKOWITZ A,BIELORY L, MEHTA PD ET AL. Intravenous gamma globulin in progressive MS ACtd Neurol Scand 1992, 86:’171-1754. CROSS AH,TROTTER JL,HART WMJR.Caveat regarding immuno-globulin therapy in multiple sclerosis. Ann Neuro/ 1993, .3.3:600-601
5. UCCELLI A, CAPELLO E, FENOGLIO D, INCAGLIAIO M, VALBONESI M, MANCARDI GL. Intravenous immunoglobulin, plasmalym-phocytalpheresis and aIzathioprine in chronic progressive mult iple sclerosis Itali J Neurol Sci 1994, 15 :51 -53 6.ACHIRON A,GILAD R, MARGALIT R, GABBAY U,SAROVA-PINHAS I, COHEN IR ET AL. Intravenous gammaglobulin treatment in multiple sclerosis and experimental autoimmune encephalomyelitis: delineation of usage and mode of action. J Neurol Neurosurg Psychiatry 1994, 57(Suppl):57-61 7. VAN ENGELEN BG,MILLER DJ,PAVELKO KD,HOMMES OR,RODRIGUEZ M. Promotion of remyelination by polyclonal immuno-globulin in their’s virus-induced demyelination and in multiple sclerosis. J Neurol Neurosurg Psychiatry 1994, 57(5uppl):65 – 688. TENSEN RB, HAY KA, ABERG JA. Immunoglobulin G immunosup-pre ssion of multiple sderosis. Suppression of all three major Iymr)hocyte subsets. Arch Neurol 1993, 50:417-4209. SORENSEN PS. Treatment ol multiple sderosis with IVIg: potential effects s and methodology of clinical trials. J Neurol Neurosurg Psychiatry 1994, 57(Suppl):62-6410. NOSEWORTHY JH, O`BRIEN PC,VAN ENGELEN BG,RODRIGUEZ M.. Intravenous immunoglobulin therapy in mulliple sclerosis: progress from remyelitnation in Theiler`s virus model to a randomised, double-blind, placebo-controlled clinical trial. J Neurol Neurosurg Psychiatry 1994, 57(suppl)1):11-14
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