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Rakhmanova Lola Karimovna, associate professor, of the Department of Childhood Illness No. 2 of the Tashkent Medical Academy Karimova Umida Nyrmatovna, asisstent, of the Department of Childhood Illness No. 2 of the Tashkent Medical Academy
PECULIARITIES OF IMMUNOPATHOLOGICAL SHIFTS WITH NEPHROTIC SYNDROME IN CHILDREN WITH ATOPIC DERMATITI
Abstract: Identified immune disorders in the initial period of nephrotic syndrome in CGN may indicate an imbalance in the mechanisms of controlling the inflammatory response, the lack of an adequate reaction of the antiinflammatory defense system of the body, therefore, is the pathogenetic basis of the formation of chronic glomerulonephritis, the progression of immunoinflammatory damage, including in the kidney tissue, and eventually leads to a worse prognosis of the disease.
Keywords: Atopic dermatitis, nephrotic syndrome, chronic glomerulonephritis.
The main manifestation of the nephrotic form of glomeru- same age. Clinical diagnosis was made based on anamnesis, lonephritis is nephrotic syndrome (NS), which is characterized by proteinuria (more than 2.5 g / day or 50 mg / kg body weight), oliguria, edema, hypoproteinemia, hypoalbuminemia, hyperlipidemia, hypercoagulability and develops as a major manifestation of acute glomerulonephritis and chronic [3].
Glomerulonephritis (GN) is a genetically determined immune-mediated inflammation with a predominant glomerular lesion and involvement in the pathological process of all renal structures, clinically manifested by renal and adrenal symptoms [9, 14]. In a series of parenchymal diseases of the kidneys, the GB occupies a dominant position, in which chronic glomerulonephritis (CGN) is more than 35% and is one of the most common causes of chronic renal failure (CRF) [10].
Atopic dermatitis (AD) is a chronically relapsing inflammatory skin disease caused mainly by IgE-mediated allergic reactions and genetically associated with atopy [3]. According to epidemiological studies, its prevalence reaches 20% in children of the first 2 years of life, varies from 5.5 to 30.8% in children 6-7 years and from 6.7 to 20.7% in children 13-14 years old. In children suffering from BP, involvement in the pathological process of virtually all organs and systems is noted. In this plan, serious attention is paid to blood pressure in children suffering from renal pathology [2, 3].
The aim of the study was to study immunopathological shifts in nephrotic syndrome in children with atopic dermatitis.
Materials and methods. Under our supervision were 40 children aged 7 to 11 years, suffering from a nephrotic form of CGN. Patients were divided into two groups: 1-group-CGN + AD (20 children); 2-group-CGN (20 children). The control group consisted of 25 practically healthy children of the
clinical and laboratory and functional research methods, immunological indicators, as well as blood pressure markers and the SCORAD index [2]. The state of cellular and humoral immunity, antigen-binding lymphocytes (ASL) of the kidneys was studied by the method of Garib F. Yu. and co-authors [7, 8]. Phagocytic activity of neutrophils (FAN) using a nitrous tetrazolium test using latex particles [5]. ELISA [6] studied immunoglobulin (Ig) E concentrations; circulating immune complexes (CEC) were determined by the precipitation method [4], interleukin-2 (IL-2) by Ortaldo J., et al. [10].
The material used for the study was venous blood taken in the morning on an empty stomach. The digital data was processed by the method of vibrational statistics with the calculation of the reliability of the numerical differences in the Student.
Results and its discussion. According to the results of the studies, it was found that 55.0% of the patients on the sex were CGD boys, 45% girls. At CGN + AD, 72.5% were boys, 27.5% were girls, who confirmed the literature that CGN and AD were 2 times more likely to be male. Duration of the disease - from the debut of GB at CGN-8 years, on average 4.1 ± 1.8 years; at CGN + AD-10 years, an average of 4.6 ± 2.0. According to mandatory diagnostic criteria, blood pressure was: hereditary predisposition to atopy - 88.0%, pathological course of pregnancy and childbirth in the mother - 76.0%, onset of the disease in early childhood - 71.1%, skin rashes on the flexor surfaces of the limbs - 64, 7%, the Denier-Morgan line-16.0%, the presence of concomitant diseases of the digestive system (gastroduode-nitis) - 54.0%, the nervous system (NDC) - 67.0%, which are consistent with literature data [12, 15]. Evaluation of the severity of BP in patients with SCORARAD index showed that in
PECULIARITIES OF IMMUNOPATHOLOGICAL SHIFTS WITH NEPHROTIC SYNDROME IN CHILDREN WITH ATOPIC DERMATITI
children with CGN + AD a large percentage were of moderate and severe form, in the complicated course of CGN in children, a large percentage was CGN + AD.
Clinical manifestations of HC with CGN and CGN + AD were characterized respectively: the onset of the disease is gradual (70.0%, 51.0%), "chalky" pallor (62.2%, 46.4%), lethargy (70.0%; 79.0%), a decrease in appetite (88.0%, 92.0%), edema (more common up to ascites) (65.9%, 76.9%), A / D increase (36.2%; 58.7%), hydrothorax (12.0%, 18.5%), tachycardia (79.3%, 89.5%), nausea (26.0%, 38.5%), hepatomegaly (14.5%%, 27.5%), positive symptoms of effleurage in the projection of the kidneys (58.0%, 76.5%), oliguria (100.0%, 100.0%), anuria (4.5%, 13.0%), headache (47.9%, 76.8%); proteinuria (100.0%, 100.0%), hypoproteinemia (88.9%, 95.0%), disproteinemia (86.4%, 94.5%), hypercoagulability (74.0%, 82.0%), and hypercholesterolemia (37.0%, 49.0%), which were more pronounced in children diagnosed with CGN + AD. The main disease in children with CGN and CGN + AD was accompanied by anemia (59.5%, 68.5%), chronic tonsillitis (67.5%, 83.0%), helminthiosis (30.0%, 48.0), gastroduodenitis (22.5%, 35.0%), bronchitis (10.0%, 15.0%), DZHVP (7.5%, 17.5%), GSH (17.5%, 22.5%).
According to the results of the study of partial renal functions in children of both groups, a statistically significant increase in daily proteinuria (more than 2.5-3.0 g / day), erythro-cyturia, leukocyturia, cylinduria (P < 0.001-0.01), (P < 0.001), hyperlipidemia (P < 0.001-0.01), increased fibrinolytic activity of the blood, hypercoagulability (P < 0.01), an increase in urea and creatinine in the blood serum (P< 0.001) hypoproteinemia, hypoalbuminemia and hypergammaglothulinemii (P < 0.01).
The results of immunological studies showed that, in comparison with the control group, a statistically significant decrease in the T-lymphocyte count (CD3) was observed in the children of HC with CGN (1-group) and CGN + AD (2-group) at the time of exacerbation (before treatment). T-suppressors (CD 8), T-helpers (CD4) and FAN (P <0.001-0.01), a significant increase in the number of B-lymphocytes (CD19) and ASL of the kidneys (P <0.001), an increase in serum IgE P < 0.001) as well as a significant increase in IL-2 production (P < 0.001) and CEC concentration (P < 0.001). Immunopathological shifts were more pronounced in children of the 2-group compared to group 1 (Table).
Immunopathological shifts of HC in CGN in children with BP are explained by the fact that the nature of GN is an immune-
mediated inflammation involving the activation of Thl or Th2 cells and the corresponding cytokines, including IL-2. IL-2 stimulates the synthesis of other cytokines (IL-4, IL-6, IFN-y) and autocrine-acting on Thl cells and paracrine to the Th2 cell subpopulation, affecting the Thl / Th2 balance. The cytokine imbalance between Th1 and Th2 determines the direction ofviola-tions of the immune response [1]. The ability of T-cell clones to maintain production by plasma IgE cells is directly proportional to IL-4 production, and the content of this cytokine in the blood in children with allergic diseases (n: AD) correlates with clinical manifestations, including the disease period, duration of the disease, IgE in the blood. The increased ability to produce IL-4 under the stimulation of IL-2 seems to be one of the defects that promote the prolongation and prolongation of IgE production in patients with atopic diseases. The starting role in the development of the immunopathological process in the NS probably belongs to the activation of the complement system, hyperproduction and the elimination of the CEC, which accumulate on the basal membrane of the glomerular vessels, cause the development of a local inflammatory reaction. Importantly, both the formation of local inflammation and immunopathological changes in the body as a whole play an important role in the activation of the humoral and cellular link of immunity with a disruption in the production of cytokines, including IL-2 [3].
After the traditional therapy in dynamics (after 6 months), the patients improved clinical and laboratory and immuno-logical parameters, which resulted in an increase in the relative content of CD3, CD4, CD8, FAS, IgA, (P < 0.001-0.01) kidney, IgM, IgE and the concentration of CIC in the blood (P < 0.01-0.01), as well as a decrease in IL-2 production (P < 0.05), compared with pre-treatment data.
In one year of follow-up, the children of group 1 (CGN+AD) had incomplete normalization of peripheral blood and urine parameters (hemoglobin, leukocytes, ESR, proteinuria, erythrocyturia, leukocyturia, diuresis and shortening of the period of clinical remission compared to children in group 2. During this period, 8 (40.0%) of 20 patients had an exacerbation of the disease in group 1 (CGN+AD), in children of the 2nd group (CGN), the exacerbation of the disease was in 5 (25.0%) of 20 patients The results suggest that HC in CGN in children with BP is more severe lo and difficult to conventional treatment and requires the inclusion of additional adequate therapy.
Table 1.- Dynamics of immunopathological shifts of HC in children with CGN with AD (M ± m)
Indicators Control group, n = 25 before treatment, n = 40 After treatment
1-group, CGH + AD, n=20 1-group, CGH n=20
1 2 3 4 5
CA3,% 56.21 ± 0.98 32.16 ± 1.21* 35.11 ± 1.12# 46.32 ± 0.36#
1 2 3 4 5
СД4% 34.50 ± 1.40 15.00 ± 1.41* 18.05 ± 1.44 25.13 ± 1.15#
СД8,% 18.64 ± 0.49 12.21 ± 0.85* 12.21 ± 1.08 14.22 ± 1.14#
СД19,% 11.16 ± 0.73 28.03 ± 0.46* 23.02 ± 0.64 18.07 ± 0.69#
АСЛ почек - 8.63 ± 0.36 5.25 ± 0.45* 2.17 ± 0.22#
IgE, МЕ/мл 109.67 ± 60.11 588.68 ± 85.37* 396.73 ± 62.44* 162.28 ± 55.18#
ЦИК, ед.опт.пл. 0.002 ± 0.004 0.01 ± 0.006* 0.084 ± 0.001 0.043 ± 0.006#
ФАН,% 50.50 ± 1.11 34.25 ± 1.45* 38.09 ± 0.34 46.42 ± 0.47#
ИЛ-2, (ИС) 2.8 ± 0.07 3.8 ± 0.05* 3.4 ± 0.04 2.9 ± 0.13#
Note: * - the reliability of the differences compared to a healthy group; # - the reliability of the differences between 1 and 2 group. ASL is compared with the difference before treatment (P < 0.001-0.01)
Conclusions. 1. Immunopathological shifts of HC in rameters ofASL of kidneys and IgE, the concentration of CIC
children with CGN and AD are characterized by a deficiency in the blood serum, hyperproduction of IL-2 may serve as a
of cellular and humoral immunity in the form of a decrease in criterion for early immunodiagnosis of HC in children with
CD3, CD4, CD8, FAN, an increase in the number of CD19, CGN with AD.
ASL of the kidneys, an increase in IgE serum, CEC concentra- 3. HC in children with CGN with AD is more severe and
tion and hyperproduction of IL-2, which persist even in the difficult to treat, which requires the inclusion of additional
period of remission. adequate therapies.
2. The preservation of immunopathological shifts in the period of remission of diseases, such as an increase in the pa-
References:
1. Automonova O. I. Cytokine-mediated mechanisms of the pathogenesis of clinical variants of glomerulonephritis: Diss... cand.med.nauk.- Cheboksary,- 2016.- 183 p.
2. Atopic dermatitis in children: diagnosis, treatment and prevention: The program of the Union of Pediatricians of Russia.-M.,- 2000.- 75 p.
3. Balabolkin II Modern aspects of pathogenesis and therapy of atopic dermatitis in children // Pediatrics.- Vol. 94.- No. 4.-P. 177-183.
4. Belokrinitsky D. B. Methods of clinical immunology. In: Laboratory methods of research in the clinic, Ed. Menshikov V V.M.: Medicine,- 1987.- P. 277-310.
5. Bumagina T. K. Determination of phagocytic activity of neutrophils with the help of latex // Immunology.- 1981.- No. 2. - P. 44-45.
6. Vlagov G. S. The method of enzyme immunoassay using a set of reagents produced by ZAO Vector-Best.- Novosibirsk,-1991.
7. Gharib F. Yu. The method of defining lymphocytes // Rasmi akhborotnoma.- 1995.- No. 1.- 90 p.
8. Gharib F. Yu. Clinical value of the determination of ASL in patients with typhoid and other diseases. Method. Rec.-Tashkent.- 1983.
9. Ignatova M. S. Diagnosis and treatment of nephropathy in children. Guide for physicians M. C. Ignatova. ON. Korovin 7 - M.,- 2007.- 332 p.
10. Ortaldo J. Effects of natural and recombinand Il-2 on regulation ofJEN production and Nk activity // J. Immunol.- 1984.-Vol. 133.- No. 2.- P. 779-784.
