CC BY
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К^Ш /ребёнка
КёУчна пед1атр1я / Clinical Pediatrics
UDK 616.36-002.08+616-053.2+611.366 DOI: 10.22141/2224-0551.8.76.2016.90818
S.O. BABII, N.Yu. ZAVGORODNYA, I.S. KONENKO
SI «Institute of Gastroenterology of the National Academy of Medicine Sciences of Ukraine», Dnipro, Ukraine
MORPHOFUNCTIONAL CHANGES OF GALLBLADDER AND BIOCHEMICAL PARAMETERS OF LIPID METABOLISM IN CHILDREN WITH LIVER STEATOSIS
Abstract. Background. The aim of study was to investigate peculiarities of structural and functional disorders of gallbladder in children with non-alcoholic fatty liver disease. Materials and methods. The study was conducted in 51 children aged 10—17 years. Patients were divided into four groups: the 1st group consisted of 11 children with biliary normokinesia without steatosis; the 2nd group — 20 children with biliary hypokinesia without steatosis; 3rd group — 11 children with biliary normokinesia and steatosis, and the 4th group — 9 children with biliary hypokinesia and steatosis. Anthropometric parameters were measured: height, weight, abdominal circumference, body mass index. Functional state of gallbladder was investigated with the help of ultrasound. Such biochemical parameters, as total cholesterol, triacylglycerols, levels of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and very-low-density lipoprotein cholesterol were defined, atherogenic index was calculated according to Friedewaldformula. Results. Present study shows overweight (in 15 % of patients), obesity (in 85 % of patients), increase in the gallbladder volume by 30—50 % (p < 0.05), in the density of gallbladder wall by 12—16 % (p < 0.05) and its echogenicity by 24% (p < 0.05) in children with steatosis versus group without steato-sis and gallbladder normokinesia. Positive correlation between wall thickness and steatosis has been established. Thus, weight increase may potentially play a role in lipid disorders and biliary dysfunction. The 70 % of children with obesity had pathological changes of lipid levels, such as 74% — increased blood atherogenicity. Conclusions. Physicians must necessarily correct afunctional state of gallbladder during the treatment of obesity in children and adolescents. Only comprehensive approach to the treatment allows prevention of non-alcoholic fatty liver disease and its complications.
Keyworlds: biliary dysfunction; steatosis; obesity; dyslipidemia
Introduction
Since 1980, number ofpatients with obesity increased twice. In 2014 more than 41 million of children older than 5 years had overweight. Physicians set obesity apart as a systemic disease which is based on lipid and carbohydrate metabolism disorders [1]. In blood of patients with overweight level of free fatty acids is increased. It leads to fat accumulation in internal organs and visceral obesity. Therefore, overweight is a main etiological factor in the pathogenesis of metabolic disorders, such as nonalcoholic fatty liver disease (NAFLD) and functional gallbladder disorders (FGD) [2—4]. In Calasani's study (2012) among adult patients with NAFLD 90% had in-
creased body mass index (BMI) and visceral obesity, in 69 % of cases diabetes mellitus type 2 was diagnosed, in 50 % of cases — high level triacyl glycerides (TG) and low level of high density lipoprotein (HDL) in blood serum were found [5]. Such changes are common for pediatric patients. Clinical investigation showed NAFLD in one third of children with obesity, which was often accompanied by dyslipidemia, intolerance to carbohydrates and insulin resistance [6]. Etiology, development and diagnosis of steatosis in children are specific. The youngest age of steatosis diagnosis is 2 years [7]. Ecological and genetic factors play important role in NAFLD development [5].
© «Child's Health», 2016 © «Здоров'я дитини», 2016
© Publisher Zaslavsky O.Yu., 2016 © Видавець Заславський О.Ю., 2016
For correspondence: Svitlana Babii, State Institution «Institute of Gastroenterology of the National Academy of Medicine Sciences of Ukraine», Slobozhanskii Avenue, 96, Dnipro, 49074, Ukraine; e-mail: babiy.sveta@gmail.com
Для кореспонденци: Бабм Свгтлана Олександр1вна, ДУ «1нститут гастроентерологи НАМН УкраТни», пр. Слобожанський, 96, м. Днтро, 49074, Укра'ша; e-mail: babiy.sveta@gmail.com
KëiHNHa neAiaTpifl / Clinical Pediatrics
Our previous investigations demonstrated that more than 50 % of children with NAFLD had FGD [8]. The previous studies showed positive correlation between total obesity, fatty liver and fatty gallbladder in adults. Under these conditions the functional state of liver and gallbladder is low. The existing literature data describe a direct link between the overall adult obesity, fatty liver and fatty gallbladder, thus decreasing their functional ability. Unfortunately to date there is no detailed analysis of the relationship of these abnormalities in pediatric patients.
Aim of study — to investigate peculiarities of structural and functional disorders of gallbladder among children with non-alcoholic fatty liver disease.
Materials and methods
Study was conducted in children and adolescents searching for medical help with gastro-intestinal tract disorders in SD «Institute of Gastroenterology of the National Academy of Medicine Sciences of Ukraine». All patients had given their agreement to participation in the study.
The study was conducted in 51 children aged 10—17 years. Patients were divided into four groups: the 1st group consisted of 11 children with biliary normokinesia without steatosis; the 2nd group — 20 children with biliary hypokinesia without steatosis; 3rd group — 11 children with biliary normokinesia and steatosis, and the 4th group — 9 children with biliary hypokinesia and steatosis.
Anthropometric parameters were measured: height, weight, waist circumference, body mass index:
BMI = [body mass, kg]/[height, m]2 [9].
Thickness of gallbladder wall and its volume were measured in all patients with ultrasound (SH-2000
Honda Electronics) in real time scale, on an empty stomach. Analysis of changes in abdominal organs included size measurement, profile, acoustic structure and echogenicity by generally accepted methods [10].
We had studied gallbladder function with ultrasound on the background of choleretic breakfast. As choleretic breakfast we used more physiological routine food loading: 40 g of wheat bread, 20-25 g of butter, 150-200 ml black tea with 5 g of sugar [11].
Gallbladder volume was measured: with empty stomach and after breakfast (5, 10, 45 and 60th minutes).
Decreasing of gallbladder volume on 45th or 60th minutes after breakfast for 34-64 % was the evidence of gallbladder normokinesia, less than 33 % — hypokinesia [11].
Diagnosis of liver steatosis was realized by measurement of the controlled attenuation parameter (CAP) with FibroScan®502 Touch F60156 (Echosens, France). This parameter was correlated with the degree of fatty liver. Its level higher than 232 db/m2 confirmed that total amount of fatty hepatocytes was more than 10 %.
Such biochemical parameters as total cholesterol (CH), triacylglicerols (TG), phospholipids (PL), levels of high density lipoprotein-cholesterol (HDL), low density lipoprotein-cholesterol (LDL) and very low density lipo-protein-cholesterol (VLDL), atherogenic coefficient (AC) were analysed with Cormey test-kits (Poland) and biochemical analyzator Stat Fax 1904 Plus, Awareness Technology (USA) calculated according to Friedewald formula.
Data of NCEP (American National Cholesterol Education Program) and NHANES (The National Health and Nutrition Examination Survey, USA) were used as lipid metabolism reference criteria in children. The normal CH levels for 1-19-year-old children were 2,96-4,4 mmol/l, TG — 0,40-0,9 mmol/l, HDL — 0,99-1,59 mmol/l, LDL — 1,63-2,59 mmol/l and VLDL — 0,22-0,40 mmol/l.
Table 1. Anthropometric and sonographic parameters in children depending on functional state
of gallbladder and presence of steatosis
Parameters S(-) S(+)
Group 1st, normokinesia Group 2nd, hypokinesia Group 3rd, normokinesia Group 4th, hypokinesia
n = 11 n = 20 n = 11 n = 9
Age, years 9,80 ± 1,21 11,91 ± 0,69 12,33 ± 0,92 13,29 ± 1,08
Height, cm 145,50 ± 6,90 158,45 ± 2,43 165,42 ± 5,46* 161,14 ± 4,89
Weight, kg 44,55 ± 3,49 54,84 ± 1,93 83,17 ± 5,47* 75,03 ± 7,69*
Waist circumference, cm 65,83 ± 1,45 76,27 ± 8,34 99,17 ± 4,03* 85,86 ± 2,90*
Body mass index, kg/m2 21,30 ± 0,82 22,37 ± 0,68 30,43 ± 1,04** 27,43 ± 1,75*
Subcutaneous fat, mm 18,10 ± 0,11 26,11 ± 2,05 24,94 ± 2,61* 29,05 ± 2,15*
Epigastric fat, mm 6,50 ± 0,10 4,86 ± 0,28 8,20 ± 1,50* 7,02 ± 0,40
Intraperitoneal fat 1, mm 38,30 ± 2,13 29,22 ± 3,26 47,21 ± 4,41 48,60 ± 2,30*
Intraperitoneal fat II, mm 49,40 ± 2,40 40,89 ± 3,64 58,50 ± 4,37 61,15 ± 4,05*
Intraperitoneal fat III, mm 17,40 ± 0,38 18,06 ± 1,69 22,41 ± 2,48* 20,45 ± 5,15
Fatty index 0,35 ± 0,08 0,44 ± 0,11 0,41 ± 0,05 0,88 ± 0,16**
Notes: * — р < 0,05; ** — р < 0,01 — significance of differences between parameters in compare with group I.
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3AopoBbe peSeHKa, p-ISSN 2224-0551, e-ISSN 2307-1168
№ 8(76) • 2016
KAiHNHa neAiaTpin / Clinical Pediatrics
Data from all groups were compared using the Student unpaired t-test by SPSS 9.0 for Windows. Difference average values were considered as probable in p < 0,05 and p < 0,01 [13].
Results
Study showed no difference in patients age and height between groups (table 1), but body weight was significantly increased in groups 3rd and 4th on average 45 % in comparison with 1st group.
High body weight led to BMI increasing by 26 % in children with steatosis in comparison with children without steatosis. Abdominal type of obesity was presented in children with overweight. In 3rd group waist circumference increasing in 1,8 times was observed, subcutaneous fat increasing — by 59 % and intraperitoneal fat increasing — by 10—57 %. So, patients from groups 3rd and 4th were characterized by overweight (15 % of cases) and obesity (85 % of cases) (p < 0,05). In 1st and 2nd groups obesity was observed in 43 and 24 % respectively.
Increasing of gallbladder volume by 30—50 % (p < 0,05), density of gallbladder wall by 12-16 % (p < 0,05) and its echogenicity by 24 % (p < 0,05) in children with steatosis was observed in comparison with group without steatosis and normokinesia of gallbladder (table 2).
Positive correlation between wall thickness and steatosis has been established: r = 0,39 (t = 2,76; p = 0,03) and r = 0,35 (t = 2,4; p = 0,01). Thus, weight increase may potentially play a role in lipid disorders and biliary dysfunction. It was confirmed with 63 % of gallbladder hypokinesia in children with obesity [6].
Decreasing of gallbladder motility directly influenced on digestion and absorption of lipids in the intestine, such as total lipid metabolism in organism [2]. About 70 % of children with obesity had a pathological changes of lipid levels, such as 74 % — increasing of blood atherogenicity.
In our study hypercholesterinemia was observed in every group, its frequency was 50 % higher among patients with gallbladder hypokinesia: 60 % patients in 1st group and 29 % patients in 4th respectively (fig. 1).
Thus, hypertriacylglycerolemia prevalenced among patients with steatosis (fig. 2). It could be related to high triacylglycerides production in the liver as a main mechanism of steatosis development.
Analysis of the lipid fraction ratio in the blood serum depending on gallbladder functional state and liver steatosis in children showed changes in TG, PL, HDL, LDL, VLDL, CH/PL levels and AC. The mild atherogenic dyslipidemia was found in the 3rd group. There were increasing in 1,4 times TG level (p < 0,05), VLDL — in 1,5 times (p < 0,05) and increasing of CH/PL rate in 1,3 times (p < 0,05), in comparison with 1st group (table 3).
Dyslipidemia in patients from 4th group was combined with decreased PL level in blood serum in 1,5 times (p < 0,05), HDL — in 1,5 times (p < 0,05) and CH/PL ratio increasing in 3,6 times (p < 0,05) compared with
1st group.
Discussion
Low gallbladder motility with increased volume and wall thickness were found in children with steatosis. This disorder was accompanied by atherogenic changes in lipid fractions (high TG and VLDL levels). They were more severe in groups with steatosis. So, obesity and overweigh are underlying causes in NAFLD development, and FGD leads to the complication of disease. It also does not exclude the deterioration functional status of the gallbladder due to general obesity.
Our data demonstrated an increasing of gallbladder volume and wall thickness in children with steatosis. Significant increase of these parameters in III and IV groups in comparison with I group was showed. Also, motility of gallbladder in these groups was less than in children without steatosis.
Figure 1. Percent of patients with Figure 2. Percent of patients with
hypercholesterinemia in groups hypertriacylglycerolemia in groups
Table 2. Parameters of gallbladder structure in children depending on functional state of gallbladder
and presence of steatosis
Parameters S(-) S(+)
Group 1st, normokinesia Group 2nd, hypokinesia Group 3rd, normokinesia Group 4th, hypokinesia
n = 11 n = 20 n = 11 n = 9
Volume, cm3 16,64 ± 1,61 20,44 ± 2,14 21,77 ± 2,97* 24,80 ± 3,88*
Wall thickness, mm 1,89 ± 0,10 1,87 ± 0,16 2,15 ± 0,19* 2,24 ± 0,23*
Increased wall echogenicity, % 27 30 36 45*
Notes: * — р < 0,05.
Клшнна пед1атр1я / Clinical Pediatrics
Table 3. Parameters of lipid metabolism in children depending on functional state of gallbladder
and presence of steatosis
Parameters S(-) S(+)
Group 1st, normokinesia Group 2nd, hypokinesia Group 3rd, normokinesia Group 4th, hypokinesia
n = 11 n = 20 n = 11 n = 9
CH, mmol/l 4,28 ± 0,20 4,50 ± 0,30 3,99 ± 0,24 4,04 ± 0,24
TG, mmol/l 0,49 ± 0,11 0,70 ± 0,11* 0,72 ± 0,12* 0,93 ± 0,15*
PL, mmol/l 2,79 ± 0,20 2,41 ± 0,35 2,39 ± 0,26* 1,95 ± 0,46*
HDL, mmol/l 1,08 ± 0,09 0,97 ± 0,06 0,95 ± 0,08 0,74 ± 0,12**
LDL, mmol/l 3,02 ± 0,18 2,85 ± 0,19 2,71 ± 0,22 2,79 ± 0,23
VLDL, mmol/l 0,22 ± 0,48 0,32 ± 0,05* 0,33 ± 0,05** 0,43 ± 0,07*
CH/PL 1,65 ± 0,19 1,81 ± 0,22 2,04 ± 0,05* 5,98 ± 0,45**
AC 3,12 ± 0,30 3,70 ± 0,39* 3,54 ± 0,54* 4,25 ± 0,53**
Notes: * — р < 0,05; ** — р < 0,01 — significance of differences between parameters in compare with group I.
Correlation between NAFLD and FGD can be explained by lipotoxicity effect which leads to lipid accumulation outside of adipose tissue. Free fatty acids and cholesterol play the key role in this mechanism [14]. It is assumed, that cholesterol increase and relation of cholesterol to phospholipids is a cause of low gallbladder motility because of humoral response inhibition by neuronal transmitters such as acetylcholine, cho-lecystokinin and neuronal peptide Y [15—17]. It was evidenced in the experiments with animals. Blocking of intestinal absorption of cholesterol led to decrease of lipids level in gallbladder wall and improved gallbladder motility [18].
Other eventual mechanism of low gallbladder motility in NAFLD is an effect of hyperproduction of cyto-kines in adipocytes which leads to visceral organ inflammation.
Numerous studies showed the fact that adipocytes is capable to produce inflammatory molecules, including TNF-a, IL-6 and cause inflammation in other organs [19-21].
So, inflammation in patients with overweight and obesity cause weak function of gallbladder wall and decrease absorption and secretion ability [22, 23]. Our results proved this conception because patients with NAFLD in our research groups often had a high BMI and enlarged gallbladder volume.
Overweight is one of the causes of gallbladder hypokinesia. We suggest that two mechanisms may play role in development of gallbladder hypokinesia in steatosis. They are based on accumulation of fat in gallbladder wall and decreasing of humoral response to neurotransmitters action as a result of cholesterol/phospholipids relation disruption and inflammation. In our opinion, physicians must necessarily correct a functional state of gallbladder during treatment of obesity in children and adolescent. Only complex approach of treatment allows prevention of non-alcoholic fatty liver disease and its complications [24].
Conclusions
1. Overweight and abdominal type of obesity play key role in the development of fatty liver in children.
2. Decreased gallbladder contractility lead to dislipi-demia, such as hypercholesteremia development whereas steatosis is associated with hypertriacylglycerolemia.
3. Hepatic steatosis formation is associated with gallbladder volume elevation, gallbladder wall thickness and echogenicity increasing, gallbladder motility impairment probably due to fat accumulation and cholesterol/ phospholipids relation disruption.
4. We recommend an obligatory functional gallbladder state correction in children with fatty liver.
Conflict of interests. Authors declare the absence of conflict of interests.
Reference
1. Факторы риска развития стеатоза печени у детей / [М.Ю. Степанов, Н.Ю. Завгородняя, О.Ю. Лукьяненко та íh.]// Гастроэнтерология. — 2016. — № 2. — С. 5-9.
2. Auen D. Body mass index, abdominal fatness and the risk of gallbladder disease / D. Auen, T. Norat, L.J. Vatten // Europian Journal ofEpidemiology. — 20)15. — № 30. — С. 1009-1019.
3. Cholelithiasis and markers of nonalcoholic fatty liver disease in patients with metabolic risk factors/[T. Koller, J. Kollerova, T. Hla-vaty et al.]// Scandinavian Journal ofGastroenterology. — 2012. — № 47. — P. 197-203.
4. Tsai C.J. Steatocholecystitis and fatty gallbladder disease / C.J. Tsai // Digestive Diseases and Sciences. — 2009. — № 54. — P. 1857-1863.
5. The diagnosis and management of non-alcoholic fatty liver disease: practice Guideline by the American Association for the Study of Liver Diseases, American College ofGastroenterology, and the American Gastroenterological Association / [N. Chalasani, Z. Younossi, J.E. Lavine et al.]//Hepatology. — 2012. — № 55. — P. 2005-2023.
6. Завгородняя Н.Ю. Характеристика функционального состояния желчного пузыря и структурных изменений печени при неалкогольной жировой болезни печени у детей/Н.Ю. Завгородняя, О.Ю. Лукьяненко//Гастроэнтерология. — 2016. — № 2. — С. 81-94.
7. Prevalence of fatty liver in children and adolescence / [J.B. Schwimmer, R. Deustch, T. Kahen et al.] // Pediatric. — 2006. — № 118. — P. 1388-1393.
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KAiHiHHa пед1атр1я / Clinical Pediatrics
8. Бюхштт маркери порушень лШдного обмшу при cmeamo3i печшки у дтей / [Н.Ю. Завгородня, С. О. Бабш, 1.А. Клетна та iH.]// Здоровье ребенка. — 2015. — № 8. — С. 38-42.
9. Colak Y. Impaired Gallbladder Motility and Increased Gallbladder Wall Thickness in Patients with Nonalcoholic Fatty Liver Disease [Electronic resource] / Y. Colak, G. Bozbey, T. Erim, O.T. Caklili et.al. // Journal of Neurogastroenterology and Motility. — 2016. — Mode of access.: http://www.jnmjournal.org/journal/ view.html?uid=1094&vmd=Full&
10. Пальмера П.Е. Руководство по ультразвуковой диагностике / Под ред. П.Е.С. Пальмера. — Женева: Всемирная ОЗО, 2000. — 334 с.
11. Гончаренко Н.И. Моторно-эвакуаторная функция желчного пузыря у детей с хроническими гепатитами и портальной гипертензией / Н.И. Гончаренко // Перинатология и педиатрия. — 2011. — № 1. — С. 76-79.
12. Утфжований клтчний протокол медичног допомоги дг-тям i3 функцюнальними розладами жовчного мiхура та сфшк-тера Оддi: Наказ Мтстерства охорони здоров 'я Украгни № 59 вiд 29.01.2013р.
13. Петри А. Наглядная статистика в медицине/А. Петри, К. Сэбин. — Москва: ГЭОТАР-Мед, 2003. — 144 с.
14. Day С.Р. Steatohepatitis: a tale of two «hits»? / С.Р. Day, O.F. James //Gastroenterology. — 1998. — № 114. — P. 842-845.
15. Nonalcoholic Fatty gallbladder disease: the influence of diet in lean and obese mice/[M.I. Goldblatt, D.A. Swartz-Basile, H.H. Al-Azzawi et al.] // Journal of gastrointestinal surgery: official journal of the Society for Surgery of the Alimentary Tract. — 2006. — № 10. — P. 193-201.
16. Excess membrane cholesterol alters human gallbladder muscle contractility and membrane fluidity / Q. Chen, J. Amaral, P. Bian-cani, J. Behar // Gastroenterology. — 1999. — № 116. — P. 678-685.
17. Effect of ursodeoxycholic Acid alone and ursodeoxycholic Acid plus domperidone on radiolucent gallstones and gallbladder contractility in humans [Electronic resource] / [I. Tuncer, M. Harman, Y. Colak et al.]// Gastroenterology Research and Practice. — 2012. — Mode of access: https://www.hindawi.com/journals/grp/2012/159438/
18. Ezetimibe ameliorates cholecystosteatosis / [A. Mathur, J.J. Walker, H.H. Al-Azzawi et аI.]// Surgery. — 2007. — № 142. — P. 228-233.
19. Alexopoulos N. Visceral adipose tissue as a source of inflammation and promoter of atherosclerosis / N. Alexopoulos, D. Katritsis, P. Raggi//Atherosclerosis. — 2014. — № 233. — P. 104-112.
20. Jung U.J. Obesity and its metabolic complications: the role of adipokines and the relationship between obesity, inflammation, insulin resistance, dyslipidemia and nonalcoholic fatty liver disease / U.J. Jung, M.S. Choi // International Journal of Molecular Sciences. — 2014. — № 15. — С. 6184-6223.
21. Makki K. Adipose tissue in obesity-related inflammation and insulin resistance: cells, cytokines, and chemokines [Electronic resource] / K. Makki, P. Froguel, I. Wolowczuk // ISRN Inflammation. — 2013. — Mode of access: https://www.hindawi.com/journals/ isrn/2013/139239/
22. Resistin-like molecule alpha reduces gallbladder optimal tension / [H.H. Al-Azzawi, A. Mathur, D. Lu et al.] // Journal of gastrointestinal surgery: official journal of the Society for Surgery of the Alimentary Tract. — 2007. — № 11. — P. 95-100.
23. Human Adipocytes Induce Inflammation and Atrophy in Muscle Cells During Obesity /[V. Pellegrinelli, C. Rouault, S. Rodriguez-Cuenca et al.]// Diabetes. — 2015. — № 64. — P. 3121-3134.
24. Просоленко К.О. Сучаст тдходи должування неалкоголь-ног жировог хвороби печшки на фот метаболiчного синдрому / К.О. Просоленко//Лжи Украгни. — 2012. — № 3. — С. 30-34.
Received 29.11.2016 ■
Бабгй С.О., Завгородня Н.Ю., Коненко I.C.
ДУ «1нститут гастроентерологй НАМН Украгни», м. Днпро, Украгна
МОРФОФУНКЦЮНАЛЬЖ ЗМШИ ЖОВЧНОГО MiXyPA i BiOXiMiHHi ПАРАМЕТРИ AiniAHOrO ОБМШУ В ДЛЕЙ 3i СТЕАТОЗОМ ПЕЧШКИ
Резюме. Метою нашого дослщження було дослщити за-лежшсть м1ж функцюнальним станом i структурними змь нами жовчного м1хура, а також лшщним обмшом у дгтей 3i стеатозом печ1нки. MaTepiarn та методи. Пщ спостере-женням перебувала 51 дитина вжом вщ 10 до 17 ротв, яы за даними ультразвукового дослщження моторно-еваку-аторно! функци жовчного м1хура та транз1ентно1 еласто-графи печшки були розподшеш на 4 групи: I — 11 дгтей 1з нормоынез1ею жовчного м1хура без стеатозу печ1нки, що обрано як групу пор1вняння; II — 20 дней 1з гшоыне-з1ею жовчного м1хура без стеатозу печшки; III — 11 дней 1з нормокшез1ею жовчного м1хура i стеатозом печ1нки; IV — 9 дгтей 1з гшокшез1ею жовчного м1хура з1 стеатозом печшки. Оцшювали антропометричш дат: р1ст, вагу, окружшсть тали, 1ндекс маси тала. Функцюнальний стан жовчного м1хура i його характеристики визначали за до-помогою ультразвуково! д1агностики. Як дослщш маркери лшщного спектра сироватки кров1 використано вмют загального холестерину, триглщервддв, лшопротещв ви-соко! та низько! щшьноста, лшопротещв дуже низько!
щшьноста 1 розраховано коефщент атерогенноста. Результата. Установлено, що для пащентав з1 стеатозом печ1нки характерними були надм1рна вага (у 15 % пащентав), ожи-ршня (у 85 % хворих), збшьшення об'ему жовчного мгху-ра на 30—50 % (р < 0,05), щшьноста станок — на 12—16 % (р < 0,05) 1 ехогенноста станки — на 24 % (р < 0,05) пор1вня-но з групою без стеатозу 1 нормокгнез1ею жовчного м1хура. Виявлено позитивний зв'язок м1ж товщиною стшки та на-явнютю стеатозу. Отже, збшьшення ваги може бути одним 1з чиннишв розвитку розлад1в бшарно! системи та лшщного обмшу. Виявлено, що в 70 % д1тей з ожиршням на-явш патолопчш змши р1вня лшщв, у тому числ1 в 74 % — збшьшення атерогенних властивостей кров1 Висновки. Призначаючи л1кування при ожиршш в д1тей та пщлитав, слщ обов'язково здшснювати корекщю функцюнально-го стану жовчного м1хура. Тшьки комплексний пщхщ до лжування дасть змогу запоб1гти розвитку неалкогольно! жирово1 хвороби печшки.
Ключовi слова: бшарна дисфунк^; стеатоз печшки; ожиршня; дислiпiдемiя
Бабий С.А., Завгородняя Н.Ю., Коненко И.С.
ГУ «Институт гастроэнтерологии НАМН Украины», г. Днепр, Украина
МОРФОФУНКЦИОНААЬНЫЕ ИЗМЕНЕНИЯ ЖЕЛЧНОГО ПУЗЫРЯ И БИОХИМИЧЕСКИЕ ПАРАМЕТРЫ ЛИПИДНОГО ОБМЕНА У ДЕТЕЙ СО СТЕАТОЗОМ ПЕЧЕНИ
Резюме. Целью нашего исследования было изучить за- турными изменениями желчного пузыря, а также липид-висимость между функциональным состоянием и струк- ным обменом у детей со стеатозом печени. Материалы и
КлШчна пед1атр1я / С!1п1са! Pediаtrics
методы. Под наблюдением находился 51 пациент в возрасте от 10 до 17 лет, которые по данным ультразвукового обследования моторно-эвакуаторной функции желчного пузыря и транзиентной эластографии печени были разделены на 4 группы: I — 11 детей с нормокинезией желчного пузыря без стеатоза печени, которую выбрали в качестве группы контроля; II — 20 детей с гипокинезией желчного пузыря без стеатоза печени; III — 11 детей с нормокинезией желчного пузыря и стеатозом печени и IV — 9 детей с гипокинезией желчного пузыря со стеатозом печени. Оценивали антропометрические данные: рост, вес, окружность талии, индекс массы тела. Функциональное состояние желчного пузыря определяли с помощью ультразвуковой диагностики. В качестве исследуемых маркеров липидного спектра сыворотки крови использовали содержание общего холестерина, триглицеридов, липопротеидов высокой и низкой плотности, липопротеидов очень низкой плотности и рассчитывали коэффициент атерогенности. Результаты. Установлено, что для пациентов со стеатозом характерными
были лишний вес (у 15 % пациентов), ожирение (у 85 % пациентов), увеличение объема желчного пузыря на 30— 50 % (р < 0,05), плотности стенок — на 12-16 % (р < 0,05) и эхогенности стенки — на 24 % (р < 0,05) в сравнении с группой без стеатоза и с нормокинезией желчного пузыря. Выявлена положительная связь между толщиной стенки и наличием стеатоза. Таким образом, избыток веса может быть одним из факторов развития нарушений липидного обмена, а также билиарной дисфункции. Выявлено, что у 70 % детей с ожирением имеются в наличии патологические изменения уровня липидов, в том числе у 74 % детей — увеличение атерогенных свойств крови. Выводы. Назначая лечение при ожирении детей и подростков, следует обязательно осуществлять коррекцию функционального состояния желчного пузыря. Только комплексный подход к лечению даст возможность предотвратить развитие осложнений неалкогольной жировой болезни печени.
Ключевые слова: билиарная дисфункция; стеатоз печени; ожирение; дислипидемия
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Здоровье ребенка, р-^БЫ 2224-0551, е-^БЫ 2307-1168
№ 8(76) • 2016
