Page 50 - GALENIKA MEDICAL JOURNAL

kod MuSK MG je bio odličan. Pozitivan odgovor je zabeležen tek u razvoju i koja još uvek nema širu primenu u kliničkoj
kod 72–89% pacijenata 48, 52, 53 . praksi, ali je sigurno da smo na prekretnici, pa će ubrzo le-
čenje SAMG biti mnogo efikasnije i sa manje neželjenih efe-
Pored navedenih, danas postoje i drugi, brojni tzv. „novi kata .
48
lekovi“ sličnih mehanizama delovanja čija se efikasnost i be-
zbednost tek ispituju. Uopšteno, to je terapija koja je danas

Abstract

Acquired autoimmune myasthenia gravis (MG) is a prototype of autoimmune disease in which autoantibodies directed
against various antigens of the neuromuscular junction, leading to impaired neuromuscular transmission with clinical
presentation of fluctuating weakness and excessive fatigue of transverse striated skeletal muscles. In 85% of patients
with MG there are antibodies to the nicotine acetylcholine receptor of the postsynaptic muscle membrane (nAChR), in
5-8% of patients there are antibodies to muscle-specific tyrosine kinase (MuSK), in 1-2% of antibodies to low-density
lipoprotein receptor-related protein 4 (LRP4), while in the remaining 10% none of the mentioned autoantibodies can
be detected, and these patients are classified in the group of so-called “seronegative” MG. It is well known that this
antigenic specificity affects both the clinical presentation and the therapeutic response, course and prognosis of the
disease, which is why the early serological confirmation of the diagnosis is important. In this way, determining the exact
profile of autoantibodies can provide a significantly more efficient, personalized therapeutic approach for each patient,
and thus improve the prognosis and quality of life of these patients. In general, when a patient is diagnosed with MG,
the goal is to alleviate the symptoms of the disease as soon as possible, as well as to induce remission or minimal
manifestations of the disease in the following period. MG therapy can be roughly divided into symptomatic therapy,
which includes drugs that alleviate the symptoms of weakness and fatigue, causal therapy, which immunomodulates
the pathogenetic process that affects the course of MG and temporary therapeutic procedures to achieve rapid
improvement in patients to avoid or treatment of the most severe clinical manifestations, the so-called “crisis” of
MG. Symptomatic MG therapy involves the use of acetylcholinesterase inhibitors, represented by pyridostigmine
bromide. It works by relieving the symptoms of MG in a short period of time, 4-8 hours. Causal therapy acts on the
pathogenetic process on the basis of MG and it includes corticosteroids as first-line drugs and immunosuppressive
drugs: azathioprine, cyclosporine A, mycophenolate mofetil, etc, while temporary therapeutic procedures include
therapeutic plasma changes and intravenous immunoglobulins. All the above mentioned MG therapies are is effective
in most patients with this disease, but it should be emphasized that, on the one hand, to achieve its full effect usually
takes several months, and on the other hand, that such prolonged therapy is often followed by the occurrence of various
side effects that require its reduction or complete cessation. With advances in immunology, molecular biology, and rapid
drug development, new agents are being developed today that have much more selective immune targets, save the rest
of the immune system, have lower toxicity, and a much faster onset of action MG. Some of these drugs are already being
used successfully today, but we can freely say that the door to highly selective immunotherapy in MG has just been
opened and that this is certainly the therapy of the future.

Keywords: Myasthenia gravis, therapy, anticholinesterase therapy, Cyclosporine A, corticosteroids, azathioprine

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50 DOI: 10.5937/Galmed2202044L