IMMUNOADSORPTION IN MYASTHENIA-GRAVIS - MECHANISMS OF ACTION, IMMUNOLOGICAL MARKERS AND CLINICAL COURSE

Immunoadsorption (IAD) is an effective therapeutic method in severe generalised myasthenia gravis. This treatment is characterised by a semiselective withdrawal of immunological acting proteins. In contrast to plasmapheresis, the patient's own plasma-proteins are preserved. Using tryptophan-containing adsorber columns IAD is a reliable and well tolerated therapy. For the majority of patients with myasthenia gravis this procedure results in continual benefit. Usually bulbar symptoms and respiratory insufficiency show improvement within hours after the first treatment, whereas it may take days to weeks for muscles of trunk and extremities to gain in strength. Hitherto it is unknown how clinical improvement is achieved via IAD. Among other mechanisms, IAD certainly reduces immunopathogenetic autoantibodies against acetylcholine receptors, but there is a considerable antibody rebound a few days after IAD, although clinical benefit is continuously sustained. Presumably additional changes in the immunological system are caused by IAD. Sequential measurements of immunological markers (CD4, CD8, CD25posCD4) under treatment with IAD indicate that the reduction of humoral immunoproteins modulates significantly cellular parts of the immunological system by means of a stimulating process. Assuming that the acetylcholine receptor antibodies shift between extra- and intravascular space, several effects caused by IAD are understandable, e. g. the continuous clinical improvement in spite of the newly increasing antibodies against acetylcholine receptors.