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Comparative Analysis of the Informative Value of Radioimmunoassay and Laser Correlation Spectroscopy in Myasthenia Gravis

DOI: 10.1155/2014/718393

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Abstract:

The objective of this study was to compare informative value of traditional approach (anti-AChR antibody radioimmunoassay) and evaluation of metabolic shifts by laser correlation spectroscopy in myasthenia gravis. The method based on changes in spectral characteristics of laser radiation caused by scattering in a disperse system yields a histogram reflecting particle contribution into light scatter as a function of particle radius in nanometers. The spectrum of anti-AChR-positive serum is characterized by appreciably increased contribution of particles with a radius 4.6–6.2?nm. Binding of serum components with solubilized AChR confirms that this peak is determined by elevated concentration of antibodies to this receptor. The search for the relationship between the disease severity and the distribution pattern of subfraction serum components revealed three informative zones: 6–15, 27–67, and 127–223?nm. In patients without disturbances of vital functions, the contribution of the first zone particles into light scatter increases and that of the third zone particles decreases. Considerable differences attaining the level of statistical significance in zones 4–6 and 20?nm were revealed in the spectra of serum from patients with myasthenia gravis of the same severity with and without thymoma. This opens prospects for dynamic monitoring of the efficiency of therapy. 1. Introduction According to current concept of myasthenia gravis (MG) pathogenesis, autoimmune aggression towards certain molecular structures of the skeletal muscle and neuromuscular junction is the leading pathophysiological factor responsible for the development of clinical manifestations of this disease [1–3]. Numerous studies have demonstrated that postsynaptic nicotinic acetylcholine receptors (AChR) are more often attacked in MG: 80–85% myasthenia patients have elevated concentrations of antibodies to these receptors [4]. Pathophysiological role of antibodies to AChR has been confirmed in animal experiments reproducing the development of myasthenic process after immunization with AChR preparations or injection of the serum from myasthenic patients [5, 6]. Antibody-mediated autoimmune processes impair neuromuscular transmission due to loss of functionally active AChR, which impairs acetylcholine binding to the receptor and reduces the probability of the transmitter-receptor interaction. Moreover, antibody fixation to the postsynaptic membrane leads to destruction of junction folds and structural modification of the synapse. Hence, not only the density of AChR decreases, but also the

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