4
sclerosis, we can use a lot of immunosuppressive and immunomodulatory agents -
corticosteroids, azathioprine, and methotrexate, total irradiation of lymphocytes. There
is known some effect of the oral administration of bovine myelin, resulting in reduction of
autoreactive T cells. Also used is intravenous administration of large doses of
immunoglobulin. However, character of changes in the immunological multiple sclerosis
status indicates immunodeficiency (decrease of T-lymphocytes and reduction ratio
CD4
+
/ CD8
+
, decrease of IgM), glucocorticoids may therefore contribute further
immunosuppression [Orlova Yu.Yu., 1999].
It is proved that injection of recombinant interferon
-1b promotes binding and
neutralizing antibodies in some patients with multiple sclerosis [Ric G.P.A. et al., 1999;
Plosker G.L., 2011]. However, anti-IFN-
β
molecules begin to form antibodies that
reduce the efficiency of the drug [Majorga C. et al., 1999; Sorensen P.S., 2008;
Applebee A., Panitch H., 2009; Zarkou S. et al., 2010]. In addition, there is a number of
detected and serious
side effects of such an interferon - the formation of subcutaneous
abscesses at the injection site, liver problems, flu-like reaction, weakness, stomatitis,
anorexia, decreased hemoglobin, neutrophils and platelets [Soria A. et al., 2007;
Nakamura Y., et al., 2008; Okushin H. et al., 2010; Sanford M. et al., 2011]. This often
forces to interrupt this treatment [Clerio M. et al., 2008]. It should be taken into account
relatively high cost of courses using interferon
-1b, reaching $400,000 [Bell C. et al.,
2007].
Considered to be promising as well are
selective inhibitors
of adhesion molecules
whose representative is a recombinant monoclonal antibody Natalizumab. Researchers
revealed, however, a downside to this treatment - the development of progressive
multifocal leukoencephalopathy [Clifford DB et al., 2010]. At the same time, using
plasmapheresis we had to remove the drug and to eliminate such complications [Khatri
BO et al., 2009; Tan. I.L. et al., 2011].
Along with this, the methods of efferent therapy are used, plasmapheresis, in
particular in combination with corticosteroids and cyclophosphamide [Khatri BO et al.,
1991; Weinshenker BG, 2000; Ohji S., Nomura K., 2008
; Schröder A.
et al., 2009;
Trebst C. et al., 2009; Hashimoto H., 2010]. Positive results were achieved by selective
Ig-apheresis with immunosorbents. I.M.Barbas and A.A.Skoromets (2003), the best
results are achieved with courses of hemocarboperfusion. V.I.Cherny et al. (2004) used
the software plasmapheresis - 2 sessions per week, and then at 1, 3, 6 months, a year.
Such tactics for 10 years, 7 patients allowed to achieve remission of multiple sclerosis.
We prefer the tactics of the initial course of 4-5 sessions of plasmapheresis,
followed by one session each month, which allows users to secure a positive result.
Success was achieved in the application of cascade plasmapheresis [Ramunni A. et al.,
2008].
Neuromyelitis optica, or
Devic’s disease
–
inflammatory disease characterized by
selective lesions of the optic nerve and spinal cord (extensive transverse myelitis with
5
paraplegia). Previously it was considered as severe variant of multiple sclerosis.
Usually, primary, visual disturbances occur with subsequent addition of the symptoms of
severe transverse myelitis - a couple and tetrapareses, disorders of pelvic organs
[Karim S., Majithia V., 2009]. Used for the treatment are steroids, immunoglobulins and
plasmapheresis to remove courses up to 2-3 liters of plasma per session [Watanabe S.
et al., 2007; Bonnan M. et al., 2009, 2012
; Magaña S.M.
et al., 2009; Trebst C. et al.,
2009; Ochi H., 2010; Wang K.C. et al., 2011; Pula JH, MacDonald CJ, 2012], followed
by a periodically repeated sessions of plasmapheresis (plasma exchange program or
intermittent plasmapheresis) [Miyamoto K., Kusunoki S., 2009]. This finds application
and cascade plasmapheresis [Yoshida H. et al., 2010].
Guillain-
Barré
syndrome. This is an acute severe disease of the central nervous
system, accompanied by progressive muscle weakness and paralysis, including
respiratory muscles, which often requires prolonged mechanical ventilation. In such
cases, when joining pneumonia, thrombocytopenia and bleeding, mortality can reach
12% [Netto AB et al., 2011]. At the heart of acute disseminated encephalomyelitis lie
demyelinating processes. Its connection with chronic demyelinating diseases still
debated, its pathogenesis is not clear, but the role of the immune system is undeniable.
Often, such a process is preceded by viral infections and vaccinations, sometimes an
infection caused by Campylobacter jejuni [Straub J. et al., 1997; Hao Q. et al., 1999;
Rogalewski A. et al., 2007]. At least 41% of patients identify this pathogen [Nachamkin
I. et al., 1999]. Some connections are found for acute disseminated encephalomyelitis
and previously suffered pneumonia caused by mycoplasma or bac. Legionella
[Hagiwara H., et al., 2009; de Lau LM et al., 2010].
Detection of antibodies indicates a possible molecular mimicry between epitopes of
the antigen of the infectious agent and the elements of the peripheral nerves, which
determines the pathogenesis of this syndrome. Among the patients with this disease
there is a large heterogeneity in the severity of neurological disorders of muscle
weakness, the degree of sensory disorders, demyelination and axonal degeneration.
Anti-GQ1b antibodies increases in severe ophthalmoplegia and Fisher syndrome, anti-
GM1 antibodies are more concerned with purely motor variant of the disease, anti -
GalNAcGD1a antibodies are detected more frequently in the gastro-intestinal infections
before clinical symptoms of Guillain-Barr
é
syndrome with the development of distal
paralysis [Hao Q. et al., 1999].
The widespread use of corticosteroids in the previous cases of treatment of Guillain-
Barr
é
syndrome has shown to be ineffective and was almost universally abandoned. In
current methods of choice are plasmapheresis and intravenous immunoglobulin, and
often a combination thereof. One group of researchers [Plasma Exchange /
Sandoglobulin Gullain-
Barré Syndrome Trial Group, 1997], considered it appropriate
immediately after plasmapheresis treatment with IVIG at a dose of 0.4 g / kg, which
should block the further development of antibodies. Total requires five sessions