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Gaybiyev Akmal,
assistant professor, of Department of Neurology and Neurosurgery
Samarkand State Medical Institute Djurabekova Aziza, professor, Samarkand State Medical Institute, Head of Department of Neurology and Neurosurger
Utaganova Guljahon, assistant professor of Department of Neurology and Neurosurgery Samarkand State Medical Institute Igamova Saodat, assistant professor of Department of Neurology and Neurosurgery Samarkand State Medical Institute E-mail: [email protected]
MODERN METHODS OF DIAGNOSTICS OF POLYNEUROPATHY
Abstract: This article describes the methods of diagnosis for polyneuropathy of small fibers, sensitive disorders and disorders of the autonomic nervous system prevail. In the study, 35 children with an increased incidence of anti-ganglioside antibodies GM1 IgM, GD1b IgG and HLA IgG in children with polyneuropathy were examined. The results of the study showed that this method of investigation is a differential diagnosis.
Keywords: polyneuropathy of small fibers, dysesthesia, anti-ganglioside antibodies, hyperalgesia.
Relevance. In most cases, with polyneuropathies (PNP), decreases during the course of the disease [4]. Antibodies
nerve fibers of all sizes are involved in the pathological process, but in some cases the lesion is limited primarily to either large or small fibers. With PNP, mainly small nerve fibers are affected, which is manifested by such symptoms as decreased sensitivity to needle pricks, temperature sensitivity in the presence of dysesthesia in the form of painful burning, a disorder of the autonomic nervous system.
The motor strength, balance and tendon reflexes are relatively well preserved. The main indications for the detection of anti-ganglioside antibodies are Guillain-Barre syndrome, including Miller-Fisher syndrome, multifocal motor neuropathy, sensory neuropathy. According to the literature, antibodies to monosialoganglioside GM1 IgM are associated with multifocal motor neuropathy with a frequency of occurrence of 40-70% [1; 2; 3]. In addition, an elevated antibody titer to monosialoganglioside GM1 is found in patients with Ginein-Barre syndrome in 22-30% of cases.
The titre correlates with the activity of the disease. In the acute phase, the titer increases to maximum values and
to dsialoganglioside GD1b IgG are described in rare cases in patients with sensory neuropathy [5]. However, this process is not fully understood.
The purpose of the study was to study the diagnostic criteria of polyneuropathy.
Materials and methods. Two groups of patients were examined. The first group consisted of 20 patients with acute diseases of the peripheral nervous system. 15 patients were allocated to the control group. The kit contains strips used for blotting, which are covered with parallel strips of highly purified antigens. In the first stage of the reaction, the strips are incubated with a sample of the diluted serum or plasma of the patient. In case the sample is positive, specific antibodies of classes IgM and IgG will bind to the corresponding antigenic bands. To detect bound antibodies, a second incubation is carried out using an enzyme conjugate (antibodies to human IgG, labeled with alkaline phosphatase), which is capable of causing the development of a color reaction.
Table 1.- The frequency of detection of antineuronal anti-ganglioside antibodies in the examined patients in two groups
Groups examined GM1 GD1b HLA
Patients with acute PNS diseases (I group, n = 20) 18 16 14
Control group (group II, n = 15) 1 0 0
Medical science
The results of the study showed that in the group of patients with acute peripheral nervous system (PNS) diseases we detected a higher incidence of antineuronal anti-ganglio-side antibodies GM1 IgM, GD1b IgG and HLA IgG - 85.7%, 84.3% and 68.3% respectively Table 1, 2). It was also found that at least one type of antibody is present in 94.3% of patients in Group I (Table 2).
The rates of detection of antineuronal anti-ganglioside antibodies GM1 IgM, GD1b IgG, HLA IgG or at least one type of antibodies in the first group significantly differed both from the parameters of the second group (Table 3).
The increased detection rate of antineuronal anti-ganglioside antibodies GM1 IgM, GD1b IgG, HLA IgG, or
at least one type of antibody in the group of patients with acute peripheral nervous system diseases proves the high diagnostic significance of qualitative determination of the invitro antibodies IgM and IgG classes to seven ganglio-sides: GM1, GD1b, HLA in the serum and plasma of patients with acute diseases of the peripheral nervous system. According to the literature [6; 7; 8] antibodies to monosia-loganglioside GM1 IgM are associated with multifocal motor neuropathy with a frequency of occurrence of 40-70%. In addition, elevated titers of antibodies to monosialogan-glioside GM1 IgM are found in patients with Ginein-Barre syndrome in 22-30% of cases.
Table 2.- Frequency of detection (in%) of the most common antineuronal anti-ganglioside antibodies in the examined patients
Groups examined GM1 IgM GD1b IgG HLA At least 1 type of antybodies
I group (n=20) 85.7 84.3 68.3 94.3
II group (n=15) 5.0 7.0 5.5 6.0
Table 3.
Type of antybodies I group (n =20) II group (n = 15)
GM1 IgM I group P = 0.048 P = 0.09
II group P = 0.48
GD1b IgG I group P = 0.036 P = 0.004
II group P = 0.35
At least 1 type of antybodies I group P = 0.088 P = 0.01
II group P = 0.18
As can be seen from (Table 3), according to our data, the frequency of occurrence of the same antibody in patients with acute diseases of the peripheral nervous system is 25.7%. Antibodies to disi-angloglioside GD1b IgG are described in patients with sensory neuropathy. In the group of patients with acute diseases of the peripheral nervous system, the frequency of occurrence of this antibody 34.3% has significant differences with the incidence of antibodies to dysialoglanglioside
GD1b IgG 10.0% in group II (P = 0.036). antibodies with Guillain-Barre syndrome.
Conclusions. Thus, we detected an increased occurrence of antibodies GM1 IgM, GD1b IgG and HLA IgG in patients with polyneuropathy, which can serve as a new diagnostic criterion for this autoimmune disease, which proves its genetic predisposition.
References:
1. Cross A. H., Golumbek P. T. Neurologic manifestations of celiac disease: proven, or just a gut feeling? Neurology. 2013.-No. 27.- P. 1566-1568.
2. Kopishinskaya S. V., Gustov A. V. Neuromuscular disorders in celiac disease patients. European Journal of Neurology. 2010. Sep. P. 37-38.
3. Goddard C. J. R., Gillett H. R. Complications of celiac disease: are all pensions at risk? Postgrad. Med. J. 2016.- No. 82.-P. 705-712.
4. Koning F. The molecular basis of celiac disease. J. Mol. Recognit. 2003.- No 16.- P. 333-336.
5. Lepers S., Couignoux S., Colombel J. F., Dubucquoi S. Celiac disease in adults: new aspects. Rev. Med. Interne. 2004.-No. 25.- P. 22-34.
6. Pengiran Tengah D. S., Wills A. J., Holmes G. K. Neurological complications of coeliac disease. Postgrad. Med. J. 2002.-No. 78.- P. 393-398.
7. Vaknin-Dembinsky A., Eliakim R., Steiner I. Neurological deficits in patients with celiac disease. Arch. Neurol. 2002.-No. 59.- P. 647-648.
8. Zelnik N., Pacht A., Obeid R., Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2014.-No. 6.- P. 1672-1676.
9. Briani C., Zara G., Toffanin E., Ruggero S. Neurological complications of celiac disease and autoimmune mechanisms: preliminary data of a prospective study in adult patients. Ann. N. Y. Acad. Sci. 2015.- No. 1051.- P. 148-155.
