Научная статья на тему 'PHYSIOLOGICAL INDICATORS IN CHILDREN WITH VARIOUS FORMS OF ENCEPHALOPATHY'

PHYSIOLOGICAL INDICATORS IN CHILDREN WITH VARIOUS FORMS OF ENCEPHALOPATHY Текст научной статьи по специальности «Клиническая медицина»

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Ключевые слова
OXIDATIVE STRESS / MITOCHONDRIAL DYSFUCTION / HEMATOLOGICAL AND BIOCHEMICAL INDICATORS OF BLOOD / NEURODEGENERATIVE DISORDERS

Аннотация научной статьи по клинической медицине, автор научной работы — Ussіpbek B.A., Paiziyeva T.R., Toibekov A.S., Orazbekova G.O., Murzakhmetova M.K.

Encephalopathy is a group of diseases whose main manifestation is gradual dystrophy of brain tissue. To treat the disease, it is important to eliminate the main factor that is gradually destroying the brain. These can be liver or kidney function failure, atherosclerosis, traumatic brain injury, diabetes mellitus and many other causes. This article therefore focuses on the assessment of physiological indicators in children with encephalopathy. The results of biochemical and hematological blood parameters, as well as changes in the respiratory and cardiovascular systems before and after rehabilitation are presented. The study of encephalopathy in children and adults caused by cardiovascular pathology, metabolic disorders and brain injury is a priority for modern paediatrics and neurology. The results of a study of biochemical and hematological indicators before and after rehabilitation showed a positive trend.

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Текст научной работы на тему «PHYSIOLOGICAL INDICATORS IN CHILDREN WITH VARIOUS FORMS OF ENCEPHALOPATHY»

Vestnik KazNMU №3-2020

UDK 574.577

Physiological indicators in children with various forms of encephalopathy

B.A. Ussipbek1, T.R. Paiziyeva1, A.S. Toibekov2, G.O. Orazbekova3, M.K. Murzakhmetova1

1Al-Farabi Kazakh National University, Almaty, Kazakhstan

2NJSC "S.D. Asfendiyarov Kazakh National Medical University", Almaty, Kazakhstan 3Clinic "Dostar Med", Almaty, Kazakhstan

Encephalopathy is a group of diseases whose main manifestation is gradual dystrophy of brain tissue. To treat the disease, it is important to eliminate the main factor that is gradually destroying the brain. These can be liver or kidney function failure, atherosclerosis, traumatic brain injury, diabetes mellitus and many other causes.

This article therefore focuses on the assessment of physiological indicators in children with encephalopathy. The results of biochemical and hematological blood parameters, as well as changes in the respiratory and cardiovascular systems before and after rehabilitation are presented. The study of encephalopathy in children and adults caused by cardiovascular pathology, metabolic disorders and brain injury is a priority for modern paediatrics and neurology.

The results of a study of biochemical and hematological indicators before and after rehabilitation showed a positive trend. Keywords: oxidative stress, mitochondrial dysfuction, hematological and biochemical indicators of blood, neurodegenerative disorders

Mitochondria contain numerous redox transporters and centres involved in redox reactions. Mitochondria are capable not only of restoring oxygen to water, but also of single-electron restoration of oxygen to the radical of superoxide anion, the precursor of other active oxygen forms. As a result of the imbalance between the production of active oxygen forms and the activity of antioxidant control systems, a state of intracellular oxidative stress occurs, which is accompanied by an increased rate of free radical formation, often resulting in cell death. Oxidative stress, which leads to oxidative damage and mitochondrial DNA dysfunction, appears to determine the severity of neurodegenerative disorders. One of the most common neurodegenerative disorders is encephalopathy, which is characterised by a decrease in nerve tissue volume and brain dysfunction [1, 2]. In this regard, it is of interest to study the biochemical and hematological indicators in children with encephalopathy and changes in the respiratory and cardiovascular systems before and after rehabilitation.

Oxidative stress is a failure of the body's antioxidant system, in which cells are exposed to excessive levels of reactive oxygen forms and other free radicals. This leads to selective death of specialised cells, reduced functionality of organs and tissues and determines the development of diseases of the cardiovascular, bone and nervous systems. The main cause of oxidative stress is mitochondrial dysfunction, which is induced by the imbalance between the production of active oxygen forms and their disposal by the antioxidant control system. On the other hand, mitochondria, as the central link in intracellular signal transmission, maintain the functional state and cellular composition of the body's tissues, organs and systems, controlling cell proliferation, differentiation and apoptosis [3]. At the same time, mitochondrial dysfunction and the accumulation of mitochondrial mutations in tissues have been found to contribute significantly to aging processes and to the pathogenesis of a number of diseases characterized by neurodegeneration [4]. Mutations lead to increased generation of free radicals, reduced ATP levels and energy deficiency in cells. Studies by a number of authors testify to mitochondrial dysfunction and ultrastructural and biochemical mitochondrial abnormalities in encephalopathy [5].

Encephalopathy is a general term used to refer to noninflammatory brain diseases. It is characterised by a decrease in nerve tissue volume and brain dysfunction. Encephalopathy of the brain can be congenital or acquired. Congenital encephalopathy is caused by genetic disorders or abnormal brain development during intrauterine development or brain damage during childbirth. Acquired encephalopathy is divided into several

species. Depending on the cause of the disease, the following types of acquired encephalopathy are distinguished:

- Post-traumatic encephalopathy develops due to brain injury. It is often detected in athletes. It happens that the signs of the disease appear long after head trauma.

- Toxic encephalopathy causes prolonged adverse effects on the brain of toxic substances such as alcohol, certain medicines, heavy metals and poisons.

- Discirculatory encephalopathy is caused by insufficient blood supply to the brain.

- Residual encephalopathy occurs due to the death of cells in the central nervous system.

- Liver and uremic encephalopathy is caused by severe liver and kidney diseases.

- Pancreatic encephalopathy occurs in pancreatic diseases.

- Hypoglycemic and hyperglycemic encephalopathy occurs in diabetes.

- Radiation encephalopathy results from radiation damage.

- Vascular encephalopathy occurs when the blood supply to the brain is chronically impaired. They develop due to atherosclerosis of brain vessels, hypertension, etc [6-9].

Encephalopathy is a group of diseases whose main manifestation is gradual dystrophy of brain tissue. To treat the disease, it is important to eliminate the main factor that is gradually destroying the brain. This can be liver or kidney function failure, atherosclerosis, traumatic brain injury, diabetes mellitus and many other causes [10,11].

The study of encephalopathy in children and adults due to cardiovascular pathology, metabolic disorders and brain injury is a priority for modern paediatrics and neurology. Vascular and post-traumatic encephalopathy in children and adults has been shown to have a tendency to decrease individual phospholipid fractions in the blood serum [12]. In metabolic encephalopathy in children and adults, an increase in phospholipid fractions -leucine, sphingomyelin and serum phosphatidylcerin - has been detected, indicating a delay in myelin decay in such patients. Elevated levels of total free amino acids were found, especially in metabolic encephalopathy in children and adults. Correlation between amino acid and phospholipid metabolic rates and their relation to the brain mediator system in various forms of encephalopathy in children and adults was revealed. The aim of our study is to study physiological and biochemical indicators in children with residual encephalopathy [13]. Materials and methods of research

The work was carried out at the Department of Biophysics and Biomedicine of the Faculty of Biology and Biotechnology of the

BecTHHK KasHMV №3-2020

Al-Farabi Kazakh National University and the Almaty Regional Children's Clinical Hospital.

The object of the study is children aged 2 and 8 years. Diagnosis was made only by qualified doctors, based on the results of clinical and diagnostic tests - collection of anamnesis of the patient, external examination, laboratory and instrumental diagnostics.

The blood chemistry of children was determined using Biochem SA, (HTI, USA). Hematological blood parameters were determined using the Abacus Junior Vet automatic hematology analyser manufactured by DIATRON (Austria).

Treatment carried out: LFK, massage, classes with a speech therapist, electrophoresis with magnesium sulphate, vitamins B6 and B12, diet, etc. The rehabilitation period was 10 days. The results obtained were statistically processed using the Microsoft Excell programme. The reliability of the differences was judged by the Student's t-criterion with the determination of the P-value level by tables. Differences at significance level P < 0.05 were considered reliable. The results and their discussion

Complaints on admission: irritability, emotional instability, stammering, headaches, sleep disturbance, fatigue, apathy, decreased mental ability, memory, concentration disorder. Past medical history: According to mothers (or fathers), children are sick from birth. Perinatal anamnesis is burdened. Children regularly receive outpatient and inpatient treatment. Children are hospitalised as planned through the portal. They were diagnosed with: residual encephalopathy, astheno-neurotic syndrome.

Table 1 - Average hematological index of blood in children with relapsing e

Past medical history: children from 1, 2, 3 pregnancies, various urgent spontaneous births. Rating on the Apgar scale: 7-9 points. Many of the maternity hospitals were discharged in satisfactory condition: they grew and developed according to their age. Immunoprophylaxis was carried out according to the calendar. Contact with infectious patients, viral hepatitis, tuberculosis and other diseases were denied.

Objective data: general average severity condition due to neurological symptoms. Well-being is not affected. Normostenic physique. Skin coverings of normal colour, clean. Lymph nodes are not enlarged. Vesicular breathing in the lungs, no wheezing. Heart tones are clear, rhythm is correct. Both groups have a soft stomach, painless on palpation. The liver and spleen on palpation are not painful, not enlarged. Stool and diuresis are normal. Neurological status: consciousness is clear, response to examination is adequate, attention is diffuse, there may be signs of delayed psycho-speech development. On the FMN side, with no features, muscle tone is reduced diffusely, CDS alive D=S. Coordination is not affected, slight changes are possible. Mild disturbance of fine motor skills of the hands. The study identified biochemical and hematological indicators of children's blood. Hematological and biochemical blood parameters were studied in children with normal and residual encephalopathy. Children who turned to the hospital received a 1-month rehabilitation.

Hematological indices of children aged two and eight are shown in Table 1.

before rehabilitation

Parameters Norm 1 group - Group II -

2 years 8 years

(n*=15) (n*=18)

Hemoglobin g/l 110-140 110,01±0,17 109,02±0,21

Erythrocytes, 1012 l 3,5-4,5 4,45x1012 n 4,82x1012 n

Hematocrit, % 37-44 26,03±0,05 25,5±0,08

Erythrocyte sedimentation rate, mm / h 4-12 10,04±0,04 5,01±0,07

Platelets, 109/n 160-390 203x109/n 307x109/n

Leukocytes, 109/n 5-12 6,44x109/n 9,5x109/n

Monocytes, % 2-10 8,6±0,1 7,4±0,08

Lymphocytes, % 26-60 32,8±0,14 37,01±0,38

*Note: n - number of children in the group.

Compared to the normal indicator, the average hemoglobin indicator for two-year-old children is 110.01 ±0.17 g/l, while for eight-year-old children it is 109.02±0.21 g/l. This indicates that hemoglobin levels in Group I and Group II children are normal, meaning that the respiratory and circulatory systems in children are sufficient. The number of erythrocytes in Group I is 4,45x1012 litres within the normal range, while in Group II it is 4,82x1012 litres slightly above the normal range. The hematocrit in Group I is 26.03±0.05%, in Group II it is 25.5±0.08% and in both groups a significant decrease from the norm can be observed. The rate of erythrocyte sedimentation in Group I was 10.04±0.04 mm/hour, while in Group II it was 5.01±0.07 mm/hour. The rate of erythrocyte sedimentation in children aged two and eight years differed twofold, although within the normal range.

Platelets in Group I 203x109/l, Group II 307x109/l, and leukocytes in Group I 6,44x109/l, Group II 9,5x109/l. Although the content of platelets and white blood cells in the second group is 1.5 times

higher, if we compare them with the norm, we can note that these figures are within the norm.

The table shows that the content of monocytes and lymphocytes in Groups I and II does not differ significantly and is within the normal range.

Table 2 shows the results of the blood chemistry of children with residual encephalopathy. Glucose content in Group I was 3.5±0.05 mol/l, in Group II - 4.8±0.05 mol/l, and urea in Group I - 4.06±0.03 mmol/l, in Group II - 6.2±0.03 mmol/l. It should be noted that glucose and urea indices in children aged eight are 1.5 times higher than in Group I, but when compared to the norm, these indices are within the norm.

According to data from two groups: Group I, 2 years old, and Group II, 8 years old. The total protein index in Group I was 67.3±0.04 g/l, while in Group II it was 65.6±0.05 g/l. From the table, the total protein indicators in the two groups studied are practically the same and are within normal limits.

Vestnik KazNMU №3-2020_

Table 2 - Indicators of biochemical parameters in children suffering from residual encephalopathy before rehabilitation

Parameters Norm 1 group - Group II -

2 years 8 years

(n*=15) (n*=18)

Total protein, g/l 62-82 67,3±0,04 65,6±0,05

Creatinine, Mmole/l 35-110 45,2±0,04 67,3±0,08

Glucose, moth/l 3,3-6,1 3,5±0,05 4,8±0,05

Urea, mmole/l 4,3-7,3 4,06±0,03 6,2±0,03

Cholesterol, mmole/l 3,7-6,5 4,1±0,03 3,8±0,04

*Note: n - number of children in the group

The results of the creatinine study revealed that the creatinine level in Group I was 45.2±0.04 mmol/l, while in Group II it was 67.3±0.08 mmol/l. It can be seen that creatinine content in the second group is 1.5 higher in children of eight years old than in children of the first group (within the norm). Table 2 shows that the cholesterol content of 4.1±0.03 mmol/l in Group I is higher than that of Group II - 3.8±0.04 mmol/l, indicators are also within the normal range.

Figure 1 shows the results of a study of aminotransferase in children aged 2 and 8 of patients with residual encephalopathy. The figure shows that in the first group the AST content is practically the same as the norm, while AST is 1.2 times higher than the norm. According to the data, AST in both groups is the same, i.e. 13±0.07 |_imol/l in Group I and 13±0.05 |_imol/l in Group II. While the AST content in Group I is 16±0.05 |_imol/l, and in Group II it is 29±0.07 |jmol/L Therefore, the AST index in Group II is 1.8 times higher than the index of this enzyme in Group I.

35 30 25 20 15 10 5 0

Norm

I group

II group

□ ALT

□ AST

Figure 1 - ALT and AST performance in normal and I and II groups Axis abbreviated: group names; ordinate abbreviated: amino transfer concentration in mmol/l.

The results of the study of total bilirubin in children aged 2 and 8 are shown in Figure 2.

14 12 10 8 6 4 2 0

Norm

b)

I group II group

3,5 3 2,5 2 1,5 1

0,5 0

Norm

I group II group

Figure 2 - Total bilirubin (a) and direct bilirubin (b) in normal I and II groups Axis: group names; ordinate: bilirubin concentration (a) and direct bilirubin concentration (b) in mmol/l.

a)

The levels of total bilirubin (a) and direct bilirubin (b) are within the normal range in both Group I and Group II. Accordingly, the normal amount of total bilirubin was 3.4-20.7 jimol/l, in Group I -

11±0.03 jimol/l, in Group II - 10±0.04 jimol/l. The content of direct bilirubin in Group I was 2.8±0.04 imol/l, and in Group II - 1.3±0.05 imol/l, which is also within the normal range of 0.83-3.4 imol/l.

_Вестник КазНМУ №3-2020

Table 3 shows the results of biochemical parameters in children parameters changed slightly after rehabilitation, but comparison

suffering from residual encephalopathy before and after of both groups before and after rehabilitation showed a positive

rehabilitation. The table shows that all studied biochemical trend in changes in all studied parameters.

Table 3 - Biochemical indicators in children with residual encephalopathy before and after rehabilitation

Parameters Before rehabilitation After rehabilitation

1 group - Group II - 1 group - Group II -

2 years 8 years 2 years 8 years

(n*=15) (n*=18) (n*=15) (n*=18)

Total protein, g/l 67,3±0,04 65,6±0,05 64,5±0,03 65,2±0,04

Glucose, moth/l 3,5±0,05 4,8±0,05 3,1 ±0,05 4,5±0,02

Urea, Mmole/l 4,06±0,03 6,2±0,03 4,05±0,03 6,01±0,03

Creatinine, Mmole/l 45,2±0,04 67,3±0,08 47,5±0,03 65,5±0,04

ALT, mE/l 13±0,07 13±0,05 12±0,05 11,5±0,03

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AST, mE/^ 16±0,05 29±0,07 14,5±0,05 27,5±0,04

Total bilirubin, 11±0,03 10±0,04 9,5±0,04 9,2±0,05

l_imol/l

Direct bilirubin, 2,8±0,04 1,3±0,05 2,7±0,03 1,1 ±0,05

micromol/l.

Cholesterol, mmole/l 4,1±0,03 3,8±0,04 3,9±0,02 3,7±0,03

*Note: n - number of children in the group.

The results of the study of biochemical indicators in children aged 2 and 8 years before and after rehabilitation showed an improvement compared to the results obtained before rehabilitation. As can be seen from the table, the total protein index in children 2 and 8 years old after rehabilitation decreased by 1.2 times, which is a positive trend. Compared to the normal indicator, glucose content in children in groups I and II after rehabilitation did not change significantly. Rehabilitation took place over a period of 10 days, at which time the children's temperature varied from 35.6 to 36.9C, i.e. it can be noted that before and after rehabilitation the temperature was within normal limits.

Figures 3 and 4 show the definition of respiratory rate (BR) and heart rate (HRC) in children. As can be seen from the figure, average respiratory rates were obtained for children before rehabilitation. Before rehabilitation, the breathing rate in Group I children was on average 22 per minute, which is slightly lower than normal. And after rehabilitation, the children's breathing rate is within normal limits. The pre-rehabilitation breathing rate for Group II children was 19 per minute; after rehabilitation, the average breathing rate was 22 times per minute, which is within the normal range when compared to the normal rate.

35 30 25 20 15 10 5 0

Hh

Г-Н

□ I group

□ Iigroup

Norm

Before rehabilitation After rehabilitation

Figure 3 - Breathing rate in children with residual encephalopathy, min Axis abbreviated: group names; Axis ordinate: respiration rate, min.

160 140 120 100 80 60 40 20 0

□ I group

□ Iigroup

Norm

Before rehabilitation After rehabilitation

Figure 4 - Heart rate rate in children with residual encephalopathy, s/min Axis abbreviated: group names; Axis ordinate: heart rate, s/min

According to the data, heart rate in Group I children showed moderate heart rate only after rehabilitation. And before rehabilitation, the rates were above the normal limit. All heart rate results obtained in Group II before and after rehabilitation did not exceed the normal heart rate (Figure 4).

Discharge status: The overall discharge status of the children was satisfactory. The treatment was well received. Psycho-emotional background has improved. Mood has improved. Sleep and appetite are not impaired. Neurological status: consciousness is clear. They react calmly to the examination. Meningial signs negative. Tonus and muscle strength sufficient. Gait is normal. Rehabilitation took place within 10 days. In children aged 2 and 8 suffering from encephalopathy under the influence of neurodegenerative disorders, hematological and biochemical blood indicators before and after rehabilitation showed a positive trend.

The results of respiratory rate and heart rate in children of I and II groups after rehabilitation are within the normal range. Body temperature in children during rehabilitation remained normal. Possible progressive course and clinical polymorphism of residual organic encephalopathy in children require individual approach. With a large volume of affected cells, refusal of treatment or inability to completely eliminate the damaging factor on neurons, the consequences cannot be avoided. As a result, timely and comprehensive diagnostics, taking into account clinical and laboratory indicators, is a key factor in the effectiveness of rehabilitation in children.

In conclusion, diseases associated with mitochondrial dysfunction can present multiple symptoms, even when the same mutation is detected. The importance of timely diagnosis of mitochondrial diseases, finding clinical and paraclinical criteria for these diseases in the preliminary stage, dogenetic, is necessary to select adequate metabolic therapy and prevent worsening of the condition or disability of patients with these rare diseases.

REFERENCES

1 Allen C.L., Bayraktutan U. Oxidative stress and its role in the pathogenesis of ischaemic stroke // Int. J. Stroke Off. J. Int. Stroke Soc. - 2009. - № 4. - P.461-470.

2 Ikonomidou C., Kaindl A.M. Neuronal death and oxidative stress in the developing brain // Antioxid. Redox Signal. - 2011. - № 14.- P. 1535 - 1550.

3 Doyle K.P., Simon R.P., Stenzel-Poore M.P. Mechanisms of ischemic brain damage // Neuropharmacology. - 2008. - № 55. - P. 310-318.

4 Solovieva E.Y., Chipova D.T. From the conception of "oxidizing stress" to the conception of "cell signaling modulation" // Zh. Nevrol. Psikhiatr. Im. S.S. - 2015. - № 115. - P. 105-111.

5 Hole P.S., Darley R.L., Tonks A. Do reactive oxygen species play a role in myeloid leukemias? // Blood. - 2011. - № 117. -P. 5816-5826.

6 Ferri C.P., Prince M., Brayne C., Brodaty H., Fratiglioni L., Ganguli M et al Global prevalence of dementia: a Delphi consensus study // Lancet (London, England). - 2005. - № 366(9503). - P. 2112-2117.

7 Liu Y., Li W., Hu L., Liu Y., Li B., Sun C., Zhang C., Zou L. Downregulation of nitric oxide by electroacupuncture against hypoxicischemic brain damage in rats via nuclear factor KB/neuronal nitric oxide synthase // Mol. Med. Rep. - 2015. -№11. - P. 837-842.

8 Yu L., Yi J., Ye G., Zheng Y., Song Z., Yang Y., Song Y., Wang Z., Bao Q. Effects of curcumin on levels of nitric oxide synthase and AQP-4 in a rat model of hypoxia-ischemic brain damage // Brain Res. - 2012. - № 1475. - P. 88-95.

9 Kuzmanic S. R., Primorac D., Resic B., Pavlov V., Capkun V., Punda H., Lozic B., Zemunik T. Association of NOS3 gene variants and clinical contributors of hypoxic-ischemic encephalopathy // Braz. J. Med. Biol. Res. Rev. Bras. Pesqui. Med. E Biol. Soc. Bras. Biofisica. - 2014. - № 47.- P. 869-875.

10 Drobyshevsky A., Yu L., Yang Y., Khalid S., Luo K., Jiang R., Ji H., Derrick M., Kay L., Silverman R.B., et al. Antenatal insults modify newborn olfactory function by nitric oxide produced from neuronal nitric oxide synthase // Exp. Neurol. - 2012. -№237. - P. 427-434.

11 Robertson N.J., Faulkner S., Fleiss B., Bainbridge A., Andorka C., Price D., Powell E., Lecky-Thompson L., Thei L., Chandrasekaran M. et al. Melatonin augments hypothermic neuroprotection in a perinatal asphyxia model // Brain J. Neurol. - 2013. - №136. - P.90-105.

12 Hattori F., Oikawa S. Peroxiredoxins in the central nervous system // Subcell Biochem.-2007.-№ 44. - P. 357-374.

13 Jalland C. M., Scheffler K., Benestad S. L., Moldal T., Ersdal C., Gunnes G., Suganthan R., Bjoras M., Tranulis M. A., Neil3 induced neurogenesis protects against prion disease during the clinical phase // Sci Rep. - 2016.-№ 6.-P. 37844.

Вестник КазНМУ №3-2020

Б.А. Ycin6eK1, Т.Р. Пайзиева1, А.С. Тойбеков2, Г.О. Оразбекова3, М.К. Мурзахметова1 'Казахский национальный университет имени аль-Фараби, Алматы, Казахстан 2 НАО «Казахский национальный медицинский университет» им. С.Д. Асфендиярова, Алматы, Казахстан

3Клиника «Достар Мед», Алматы, Казахстан

ФИЗИОЛОГИЧЕСКИЕ ПОКАЗАТЕЛИ У ДЕТЕЙ С РАЗЛИЧНЫМИ ФОРМАМИ ЭНЦЕФАЛОПАТИИ

Резюме: Энцефалопатия представляет собой группу заболеваний, основным проявлением которых является постепенная дистрофия мозговой ткани. Для лечения болезни важно устранить основной фактор, который постепенно разрушает мозг. Это может быть недостаточность функции печени или почек, атеросклероз, перенесенные черепно-мозговые травмы, сахарный диабет и множество других причин.

В связи с этим, данная статья посвящена вопросу оценки физиологических показателей у детей больных энцефалопатией. Представлены результаты биохимических и гематологических показателей крови, а также изменения

дыхательной и сердечно-сосудистой систем до реабилитации и после реабилитации.

Изучение энцефалопатии у детей и взрослых, обусловленных сердечно-сосудистой патологией, нарушением обмена веществ и черепно-мозговой травмой, является приоритетной задачей современной педиатрии и неврологии.

Результаты исследования биохимических и гематологических показателей до и после реабилитации показали положительную тендецию.

Ключевые слова: окислительный стресс, митохондриальная дисфукция, гематологические и биохимические показатели крови, нейродегенеративные нарушения.

Б.А. Yciпбек1, Т.Р. Пайзиева1, А.С. Тойбеков2, Г.О. Оразбекова3, М.К. Мурзахметова1 'эл-Фараби атындат Казак ¥лттык университетi, Алматы, Казакстан 2 С.Д. Асфендияров атындаFы Казак ¥лттык Медицина Университетi, Алматы, Казакстан 3«Достар Мед» клиникасы, Алматы, Казакстан

БАЛАЛАРДАРЫ ЭНЦЕФАЛОПАТИЯНЫН, eРТYРЛI ТYРЛЕРIНIH, ФИЗИОЛОГИЯЛЫК К0РСЕТК1ШТЕР!

Тушн: Энцефалопатия - непзп керЫа ми улпасынын бiртiндеп бузылуынан пайда болатын аурулар тобы Ауруды емдеу ушлн миды бiртiндеп бузатын непзп факторды жою манызды болып табылады. Бул бауыр немесе буйрек жеткшказдН атеросклероз, ми жарак,аты, к,ант диабет жэне баск,а да кептеген cебептерiнен болуы мумюн. ОcыFан байланысты, бул макала энцефалопатиямен ауыратын балалардаFы физиологиялык керcеткiштердi баFалауFа арналFан. Каннын биохимиялык, жэне гематологиялык, керcеткiштерi, сондай-ак, тыныс алу жэне журек-тамыр жYЙелерiнiн езгеруiн реабилитацияFа дешн жэне реабилитациядан кейiнгi нэтижелерi уcынылFан. Балалар мен ереcектердегi жYрек-к,ан тамырлары патологиясынан, метаболизмнiн бузылуынан жэне ми

жарак,атынан туындаFан энцефалопатияны зерттеу к^рп педиатрия мен неврологияныц басым баFыты болып табылады.

РеабилитацияFа дейiнгi жэне кешнп канныц биохимиялык жэне гематологиялык керсетюштерд^ зерттеу нэтижелерi оц нэтиже керсетл.

Изучение энцефалопатии у детей и взрослых, обусловленных сердечно-сосудистой патологией, нарушением обмена веществ и черепно-мозговой травмой, является приоритетной задачей современной педиатрии и неврологии.

ТYЙiндi сездер: тоть^у стреа, митохондрия дисфукциясы, канныц гематологиялык жэне биохимиялык керсетюштер^ нейродегенеративтi бузылыстар

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