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SOME PARAMETERS CELLS IMMUNITY AT THE PATIENTS VIRUS HEPATITIS WITH PARENTERAL MECHANISM OF INFECTION Nagoev B.S., Ivanova M.R.
Technique of research.
Results of research.
Table 1 Change of quantity of common number lymphocytes (CD3) at the patients virus hepatitis (%)
Table 2 Change of quantity Т-helpers (CD4) at the patients virus hepatitis (%)
Table 3 Change of quantity Т-supressors (CD8) at the patients virus hepatitis (%)
Table 4 Parameters of braking of migration leukocytes at the patients virus hepatitis (%)
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SOME PARAMETERS CELLS IMMUNITY AT THE PATIENTS VIRUS HEPATITIS WITH PARENTERAL MECHANISM OF INFECTION

Nagoev B.S., Ivanova M.R.

The Kabardino-Balkarian state university, Nalchik (Russia)



Virus hepatitis with parenteral mechanism of transfer of the activator are by one of major tasks of domestic public health services. The sharp growth registered disease by these infections in Russia [3, 4, 5] testifies to it. Hepatitis B and C on breadth of distribution, level disease, the weights of current and frequency of development of the chronic forms borrow one of conducting places in an infectious pathology of the man [2,6]. After was established, that a virus hepatitis B does not cause direct cytolysis hepatocytes, the research immune reactions of organism has got the large meaning for specification pathogenic mechanisms virus hepatitis В. Large attention is given to study secondary immunedeficiency in Т-cells depending part of immunity. Mechanisms of formation Т-cells immunedeficiency at virus hepatitis B and C remain not much study in this connection the task was put to determine immune specifity of current sharp virus hepatitis B, C and mixt-hepatitis B + C.

Technique of research. Under supervision there were 120 patients in the age of from 16 till 68 years, including virus hepatitis B (HBV) -48 men, virus hepatitis C (HCV) -45 and virus гепатитом B + С-27 of the patients. The diagnosis was confirmed clinical and epidemiological data, laboratory results and serological diagnostics. In the patients virus hepatitis B in blood found out HBsAg, anti-coreAg IgM, HBeAg, anti-HBeAg, DNA-HBV; at the patients virus hepatitis C defined in whey of blood anti-HCV Ig M, absence NS4, RNA-HCV; at the patients mixt-hepatitis B + C clinical and epidemiological data for the sharp process was diagnosed, and in whey of blood defined markers of both groups. As healthy 30 donors of republican station of transfusion of blood were surveyed. All hepatitis patients were surveyed in the period of heat of disease, at height of clinical displays, with expressed intoxication and icterus, in the period of recession icterus and before an extract of the patients from hospital. The parameters subpopulation of structure immune cells of peripheric blood, such as total number Т-lymphocytes (CD3), relative contents Т-helper (CD4), Т-supressor (CD8) were certain by a method monoclonic of antibodies with use the test - system “vector – best” (Russia). The given method was carried out according to the descriptions submitted in a management "Immune methods " (1987) [7] and instructions of the manufacturers of antibodies. Reaction of braking of migration leukocytes with use in quality mitogen konkanavalin-A (kon-A) spent on a method Braude N.I., Goldman I.L. (1967) [1].

Results of research. In the period heat of disease all patients had authentic decrease of total Т-lymphocytes (tab. 1). Before an extract of the patients from hospital, in the period early recovery there is an increase of total CD3-lymphocytes, however reaching level healthy only at the patients virus hepatitis В. Authentic distinctions in quantity common Т-lymphocytes, depending on etiology hepatitis was not received.
Table 1
Change of quantity of common number lymphocytes (CD3) at the patients virus hepatitis (%)
Group surveyed
Period
n
Xm
P
P1
Healthy
30
471,5
The patients HBV
I
48
381,3
0,001
III
45
431,5
0,05
The patients HCV
I
45
371,8
0,001
0,05
III
42
392,1
0,05
0,05
The patients
I
27
391,7
0,001
0,05
HBV+HCV
III
25
430,8
0,05
0,05

The note: here and in tab. 2-5. I- the period of heat of disease; II- of recession icterus; III-early recovery. Р- reliability of distinction in relation to a level healthy; Р1- reliability of distinction in relation to meanings at the patients sharp virus hepatitis В.

At research of quantity CD4-lymphocytes the same tendency- authentic decrease of their quantity at all patients virus hepatitis in the period of heat of disease (tab. 2) was defined. In the period early recovery, before an extract of the patients from hospital there was an increase of relative quantity Т-helpers, which did not reach a level of the donors in one surveyed group. Besides it is necessary to note, that at the patients virus hepatitis C and mixt-hepatitis b + C were defined is authentic lower meanings of quantity Т-helpers in the researched periods, than at the patients sharp virus hepatitis В.
Table 2
Change of quantity Т-helpers (CD4) at the patients virus hepatitis (%)
Group surveyed
Period
n
Xm
P
P1
Healthy
30
361,1
The patients HBV
I
48
281,1
0,001
III
45
300,5
0,01
The patients HCV
I
45
240,9
0,001
0,01
III
42
232,0
0,001
0,001
The patients
I
27
221,6
0,001
0,001
HBV+HCV
III
25
251,6
0,01
0,01


Different of change were ascertained at definition of relative quantity CD8-lymphocytes (tab. 3). In all surveyed groups during heat of disease there was an authentic increase of quantity Т-supressors. In the period early recovery the tendency to decrease of quantity CD8-lymphocytes is marked which reached a level of control group at the patients sharp virus hepatitis B and C whereas, at the patients mixt-hepatitis these parameters differed from a level healthy. The highest parameters Т-supressors in the researched periods were observed also at the patients mixt-hepatitis B + С.
Table 3
Change of quantity Т-supressors (CD8) at the patients virus hepatitis (%)
Group surveyed
Period
n
Xm
P
P1
Healthy
30
110,1
The patients HBV
I
48
180,9
0,001
III
45
141,2
0,05
The patients HCV
I
45
190,9
0,001
0,01
III
42
131,7
0,05
0,001
The patients
I
27
221,3
0,001
0,001
HBV+HCV
III
25
191,7
0,05
0,01


The definition of quantity Т-lymphocytes and their subpopulations does not give representation about their functional condition. Reaction of braking of migration leukocytes with use mitogen kon-A therefore was spent which concerns to the factors oppressing migration leukocytes. The following data were received. In the period of heat of disease, at height icterus and intoxication the authentic decrease of percent of migration leukocytes in all surveyed groups (tab. 4) is observed.
Table 4
Parameters of braking of migration leukocytes at the patients virus hepatitis (%)
Group surveyed
Period
n
Xm
P
P1
Здоровые
30
791,2
The patients HBV
I
48
371,3
0,001
II
45
451,2
0,001
III
41
611,1
0,001
The patients HCV
I
45
300,9
0,001
0,001
II
45
391,1
0,001
0,001
III
42
501,1
0,001
0,001
The patients
I
27
301,0
0,001
0,001
HBV+HCV
II
27
381,1
0,001
0,001
III
25
450,7
0,001
0,001


In the period of recession icterus, parallel to improvement of general state of health of the patients and reduction icterus there is a gradual increase of this parameter. Before an extract of the patients from hospital this tendency is kept. However, the parameters of percent of migration do not come in norm in one surveyed group. Authentically lower meanings of percent of migration leukocytes where defined at the patients sharp virus hepatitis C and mixt-hepatitis B + C (tab. 4).

Thus, available secondary immunedeficiency in Т-cells dependent a part of immunity at the patients virus hepatitis B, C, B+C tries to be compensated by amplification of functional activity lymphocytes. Greatest expressive of these tendencies is observed at the patients sharp virus hepatitis C and mixt-hepatitis B + С. It, apparently, is connected to more expressed virus loading and effect immune "away", which is described at a virus hepatitis C, that results to hyperreactivity lymphocytes, inclusion autoimmune of mechanisms and promote to chronic of process.

LITERATURE

  1. Braude N.I., Goldman I.L. // News AS USSR.-1967. - № 6.-P.851-860.
  2. Kogevnicova G.M., Juscuk N.D. // J. "The Treating doctor" .-1998. - № 4.-P.22-25.
  3. Michailov M.I., Popov O.V. // Clinical laboratory diagnoctic.-1997. - № 7.-P.9-11.
  4. Nagoev B.S., Gabrilovich M.I.,Sigageva L.F. et all // Epidemiology and infectious desease.-2000. - № 1.-P.28-30.
  5. Oniscenco G.G., Favorov M.O., Lvov D.K. // J. microbiol., epidemiol. and immunobiol..-1992. - № 11.-P.22-24.
  6. Sorinson S.N. Virus hepatitis.-SPb.: Teza, 1997.-325 p.
  7. Frimmel G. Immune methods.-Moscow: medicine, 1987.-472p.