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for Myasthenia! MYASTHENIA GRAVIS
Neurochemical, neuroautonomic and neuropharmacological assessments carried out on all our myasthenia gravis (MG) patients showed that they presented a neural sympathetic deficit plus excessive adrenal-sympathetic activity. These abnormalities were registered during the basal (supine-resting) state, as well as after several stress tests (orthostasis, exercise, oral glucose and buspirone). In addition, MG patients showed increased levels of free-serotonin (f5HT) in the plasma, supposedly associated with the increased platelet aggregability which we found in all MG patients. As the above trio of neurochemical disorders (low noradrenergic-activity + high adrenergic-activity + increased f-5HT plasma levels) is known to favor Th-1 immunosuppression + Th-2 predominance, we outlined a neuropharmacological strategy for reverting the above neurochemical disorder. This treatment provoked sudden (acute), and late sustained improvements. Acute effects have been attributed to the increase of alpha-1 activity at the spinal motoneuron level. Late improvements always paralleled a significant normalization of immunological disorders.Complete normalization was registered only in non-thymectomized MG patients.
In a preliminary, report we published the successful therapeutic results obtained in eight myasthenia gravis (MG) patients receiving neuropharmacological treatment (Lechin, van der Dijs et al., 1997a). In the present study, we presented the results obtained in a series of 52 consecutive MG patients given the same therapy aimed at enhancing noradrenergic (NA) neural transmission.
The rationale of our neuropharmacological approach rests on two fundamental findings: first, all our MG patients showed a neurochemical deficiency of central and peripheral noradrenergic (NA) activity (Lechin, van der Dijs et al., 1985a, 1985b, 1990a, 1990b, 1995a, 1995b, 1996a, 1996b, 1996c, 1996e), and second, those MG patients who had not previously been submitted to surgical and/or chemical immunosuppression all showed an immunological Th-2 disorder, confirming data obtained by many other researchers (Barnard, Mahon et al., 1996; Faxvaag, Espevik et al., 1995; Romagnani, 1996). We decided, therefore, to attempt a two-pronged neuropharmacological therapy addressed to increasing NA neural, but not adrenal, sympathetic activity. This decision was adopted for the following reasons: it has been exhaustively demonstrated that NA neural activity stimulates the immune system, in particular macrophages and Th-1 cytokines, whereas adrenal glands sympathetic activity displays opposite effects and, in addition, is associated with excessive humoral immunity (Th-2 profile) and Th-2 cytokines (Kouassi, Li et al., 1990; Madden, Moynihan et al., 1994b; Spengler, Allen et al., 1990). Neuropharmacological manipulations were designed to stimulate the locus coeruleus (LC) NA neurons. Further-more, considering that all our MG patients showed high free serotonin in plasma rather than in platelets (raised f-5HT plasma levels), possibly associated with the increased platelet aggregability that all them presented, we assumed that eliminating the well-known Th-1 immunosuppressant effects of f-5HT would aid in reverting the autoimmune disorders underlying MG disease (Fuchs, Campbell et al., 1988; Jackson, Walker et al., 1998; Paegelow, Werner et al., 1985; Sternberg, Wedner et al., 1987; Walker and Codd, 1985; Warren, Kane et al., 1990) also included into the Th-2 autoimmune diseases (MokhtarianShirazianet al., 1993).
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