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28IMMUNOLOGICAL FEATURE OF THE BODY IN CHILDREN WITH DIFFUSED APPENDICULAR
PERITONITIS
1 "2 "l Abduvoyitov B.B. , Djalolov D.A. , Ishankulov R.T. ,
Khasanov A.B.4
1Abduvoyitov Bobur Bahodirovich - Medical School Student; Djalolov Davlatshokh Abduvokhidovich - Medical School
Student;
Ishankulov Rauf Tokhirovich - Medical School Student; 4Khasanov Aziz Batirovich - Medical School Student, DEPARTMENT OF PEDIATRIC SURGERY, SAMARKAND STATE MEDICAL INSTITUTE, SAMARKAND, REPUBLIC OF UZBEKISTAN
Abstract: an objective assessment of the intensity of inflammation, as well as the interaction of various parts of the immune system reflects the level of serum cytokines. Cytokines are a group of polypeptide mediators involved in the formation and regulation of protective reactions of the body during the introduction of pathogens and violation of the integrity of tissues. The study of the content ofpro-inflammatory cytokines IL-1fi and TNF-a in the serum of peripheral blood in sick children with diffused appendicular peritonitis (DAP) showed that in sick children with DAP, it increases dramatically. Keywords: diffused appendicular peritonitis, cytokines, phagocytosis, immunity.
Introduction. Common appendicular peritonitis is a frequent and most severe complication of acute appendicitis in childhood, occurring in 8-10% of all cases of the disease, and in children of the first 3 years of life is 4-5 times more often than at older age [4, 6, 9, 15]. In recent years, it has been possible to reduce mortality among patients hospitalized in the initial phases of the disease, but with neglected forms, mortality remains very high [1, 4, 10, 18].
This is due to the late diagnosis of acute appendicitis due to the abrasion of the clinical picture, the predominance of general symptoms over the local, inadequate experience of polyclinic
physicians, the broad prescription of antibiotics that mask appendicitis, but not prevent the progression of the inflammatory process in the abdominal cavity [2, 3, 5, 8, 17].
Despite a large program of basic experimental and clinical research on peritonitis, the mortality rate for this disease remains quite high, reaching up to 20% in children [4, 7, 11]. Most studies deal with the various aspects of complex pathophysiological changes observed in peritonitis, and the correction of these disorders [5, 12, 16].
The pathogenesis of diffuse peritonitis is a complex chain of functional and morphological changes in a number of systems and organs [13, 21]. Anatomical and physiological features of the children's body affect the course of appendicular peritonitis [14, 19, 22]. The smaller the child, the faster the purulent process spreads to all parts of the peritoneum [11, 20]. This is facilitated by the low plastic properties of the peritoneum, the hypoplasia of the greater omentum. Intoxication and metabolic disorders are growing faster, many of the body's reactions from defensive to pathological.
Regardless of the prevalence of peritonitis, the level of IL-1P increases by about 2.5 times, at the same time, the concentration of TNF-a increases by more than 3.6 times, which indicates a significant tension of the body's defenses aimed at separating the inflammatory process (table 1). Normally, the secretion of cytokines is negligible and is intended to ensure the interaction between the cells producing them, while it dramatically increases with inflammation.
Table 1. The concentration of serum cytokines in sick children
with RAP
Indicator Control group, n=15 Diffuse peritonitis, n=30 Spilled peritonitis, n=30 General group, PAn, n=60
IL-1ß pkg / ml 18,7±0,7 46,2±0,95* 45,8±1,1* 45,9±1,0*
TNF-a, pkg / ml 9,4±0,3 34,1±0,64* 35,1±0,8* 34,7±0,7*
Note: * differences regarding control group data, P<0,001.
Activation of cytokine producing cells occurs under the influence of endotoxins, microorganisms, hypoxia. The immune system ceases to control the secretion of cytokines and other inflammatory mediators. This leads to the fact that instead of restricting the inflammatory process and protecting the body, proinflammatory cytokines begin to have a destructive effect on tissue not only in the focus of infection, but also in other organs, which under certain conditions can lead to multiple organ failure, sepsis and septic shock.
The diffused purulent appendicular peritonitis is inevitably accompanied by a massive influx of microbial antigens and bacterial toxins into the biological environment of the child's body, simultaneously from three main sources: 1) purulent-destructive source of the abdominal cavity; 2) peritoneal exudate; 3) from the intestinal lumen against the background of its paresis. Infectious, resorption, retention and metabolic endotoxemia is the main cause of involvement in the pathological process of various immunoresistance mechanisms with the inclusion of neuroimmunohumoral factors, mechanisms of natural immunoresistance, early induced (non-specific) immune response and late adaptive immune response.
A significant decrease in the total number of lymphocytes was revealed, moreover due to the T-cell component. It is known that the decrease in T-cell immunity predisposes to the generalization of purulent-inflammatory processes and their unfavorable course.
T-lymphocytes play a major role in immune responses, because directly involved in the presentation of antigens. In DAP in children, we found noticeable changes in the content of both the common pool and T-lymphocyte subpopulations in the blood. In particular, in children with DAP, there was a significant decrease in the total number of lymphocytes by reducing the absolute number of T-lymphocytes by 2.4 times, mostly T-helper cells (CD4) - by 2.9 times compared with the control (Table 2).
The study of the content of immunoregulatory subpopulations of T-lymphocytes and their ratio (CD4 / CD8) in children with DAP revealed a significant decrease in both T-helper cells (CD4) and T-suppressors (CD8) - 1.9 times, and these changes were not only quantitative, but also qualitative: the percentage of CD4 decreased 2.1 times, and CD8 - 1.3 times relative to control indicators. Changes in regulatory subpopulations of T-lymphocytes are reflected in a decrease in the IRI to 1.28 in children with DAP. As it is known, the deficiency of the T-lymphocyte helper function leads to the body's resistance to antigenic stimulation, which contributes to the progression of the purulent-infectious process in the abdominal cavity and its generalization.
Table 2. Indicators of cellular and humoral immunity in children
with DAP
Control group, n=40 Children
Indicator with DAP, n=306
Common x109/l 2,951±0,18 1,910±0,29*
lymphocytes % 35,4±0,2 23,9±1,1*
CD3 x109/l 1,940±0,041 0,822±0,013*
Cr- lymphocytes) % 65,8±2,4 43,1±0,7*
CD4 x109/l 1,250±0,040 0,425±0,017*
(T- helpers) % 42,4±1,5 20,3±0,68*
CD8 x109/l 0,685±0,025 0,353±0,014*
(T- suppressors) % 8,18±0,37 6,42±0,35*
IRI 1,95±0,11 1,28±0,03*
CD16+ x109/l 0,237±0,015 0,358±0,011*
(natural killers) % 8,0±0,3 12,1±0,4*
phagocytic activity of neutrophils (FAN) 58,3±1,27 44,0±1,4*
spontaneous, %
CD19 x109/l 0,59±0,02 0,58±0,03
(B- lymphocytes) % 12,30±0,27 11,50±0,87
IgA, g/l 1,18±0,04 1,12±0,03
IgM, g/l 1,01±0,03 1,18±0,06*
IgG, g/l 9,0±0,1 8,5±0,3
CIRCULATING IMMUNE 64,2±0,8 114,5±1,1*
COMPLEX (CIC), UE.
Note: * - significantly compared with the control group, P <0,05.
In children with DAP, there is a significant increase in the number of natural killer (CD16 +) - 1.5 times compared with the control group. Multidirectional changes in T-cell immunity: the decrease in regulatory subsets of CD4 and CD8 against the background of an increase in CD16 is apparently due to the rapid response to antigenic stimulation of the body without increasing
119
cell proliferation and differentiation, and the fact that primary contact with the activation of natural killers is achieved through group interaction cells, not individual molecules.
The content of total B-lymphocytes in children with DAP did not significantly change relative to the control, although the level of IgM was significantly increased, which reflects the response to an acute microbial-inflammatory process in the abdominal cavity. The level of the circulating immune complex (CIC) in children with DAP was increased 1.7 times relative to the control. The accumulation of circulating immune complexes in the blood of children with RAP can contribute to their deposition in the endothelium and the basal membrane of blood vessels with subsequent activation of complement and lysosomal enzymes in various tissues, which causes the systemic inflammatory process.
Investigation of the phagocytic activity of neutrophils (FAN) in children with DAP found it significant decrease (1.33 times), indicating incomplete phagocytosis. It is possible that the presentation of the antigen and its binding to macrophages in the lymphoid organs of the abdominal cavity with DAP is ineffective; and soluble and primarily phagocytosed particles of microbial antigens become unacceptable for presentation to immunocompetent cells, since the process of phagocytosis in the DAP is inhibited. It is assumed that the mechanism of phagocytosis disorders is that a number of gram-negative bacteria using cell wall components (hyaluronic acid, etc.) block the process of phagosome fusion with lysosomes during phagocytosis, which leads to incomplete degradation of the antigen and incomplete phagocytosis; In addition, the excessive flow of microbial antigens into the biological environment of the macroorganism leads to an excessive release of 3,5,-cAMP, which, in turn, can inhibit the reaction of phagocytosis.
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