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Mechanizmy patogenetyczne IgE-zależne i IgE-niezależne w nadwrażliwości pokarmowej u dzieci i młodzieży

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Kaczmarski M., Plewa K., Mikusek I.
Pediatria i Medycyna Rodzinna
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2010
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vol. 6
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issue 4
260-267
EN
According to the current terminology of the European Academy of Allergy and Clinical Immunology, incorrect, repeated reaction to ingested or eaten food that is well tolerated by healthy individuals is called the body’s sensitivity. We share it, because of the pathogenetic mechanisms, to immune or non-immune. The first group includes patients with food allergy, in which symptoms are the result of the participation of IgE antibodies. The group responded with an adverse food allergy affects about 8% of young children and most can be attributed to their body’s reaction to cow milk. The most important allergens responsible for the process of sensitization and/or development of food hypersensitivity are considered: cow milk, egg, fish, crustaceans, shellfish, nuts, soy, wheat. Immunological mechanisms responsible for most clinical manifestations of food hypersensitivity, correspond to the classification determined by the Gell and Coombs and are or may be: IgE-dependent, IgE-independent or mixed. Clinical signs of food allergy are very rich. The diagnosis of food hypersensitivity is a difficult and iterative process, because we do not have an easy, cheap, sensitive and specific test to facilitate this task. The diagnosis of allergy is to prove the causal dependencies between the consumption of harmful food, and the onset of symptoms. From immunological methods we have the ability to recognize food allergy IgE-dependent and determination of serum total IgE and allergen specific IgE. This pathogenetic mechanism is detected by performing skin tests such as “prick” with food or air allergens. With respect to clinical response induced by IgE-independent mechanisms, we have the possibility of making atopy patch tests with food allergens. In food hypersensitivity there is no single universal diagnostic test. To bring the proper diagnosis the most important is the oral provocation and elimination test. The basis for the treatment of this disease is elimination diet.
PL
Według aktualnie obowiązującej terminologii Europejskiej Akademii Alergologii i Immunologii Klinicznej nadwrażliwość organizmu to nieprawidłowa, opaczna i powtarzająca się reakcja na spożyty lub spożywany pokarm, który jest dobrze tolerowany przez osoby zdrowe. Ze względu na mechanizm patogenetyczny dzielimy ją na immunologiczną lub nieimmunologiczną. Do pierwszej grupy należą chorzy z alergią pokarmową, u których objawy chorobowe są wynikiem udziału przeciwciał IgE. Alergicznie na szkodliwy pokarm reaguje około 8% małych dzieci, w większości nadwrażliwość pokarmowa jest u nich wywołana reakcją organizmu na białka mleka krowiego. Za najważniejsze alergeny odpowiedzialne za proces uczulenia i/lub rozwoju nadwrażliwości pokarmowej uważane są: białka mleka krowiego, białka jaja, ryby, skorupiaki, mięczaki, orzechy, soja, pszenica. Klinika alergii pokarmowej jest bardzo bogata. Rozpoznanie nadwrażliwości pokarmowej to trudny i wieloetapowy proces, gdyż nie dysponujemy łatwym, tanim, czułym i swoistym testem ułatwiającym to zadanie. Podstawą rozpoznania alergii jest udowodnienie zależności przyczynowo-skutkowej między spożyciem szkodliwego pokarmu a wystąpieniem objawów. Z metod alergologiczno-immunologicznych dysponujemy możliwością rozpoznawania alergii pokarmowej IgE-zależnej i oznaczenia w surowicy IgE całkowitej oraz alergenowoswoistych IgE. Ten mechanizm patogenetyczny reakcji wykrywa się poprzez wykonanie testów skórnych typu prick z alergenami pokarmowymi i/lub powietrznopochodnymi. W odniesieniu do reakcji klinicznych wywołanych mechanizmami IgE-niezależnymi dysponujemy możliwością wykonania płatkowych testów skórnych z alergenami pokarmowymi. W nadwrażliwości pokarmowej nie ma jednego, uniwersalnego testu diagnostycznego. Dla postawienia właściwej diagnozy decydujące znaczenie ma doustna próba prowokacji i eliminacji. Podstawą w leczeniu przyczynowym tej patologii jest dieta eliminacyjna.
2
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Retinol binding protein-4 as a serum biomarker of intrahepatic lipid content in obese children - preliminary report

88%
Romanowska A., Lebensztejn D. M., Skiba E., Tarasów E., Kaczmarski M.
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2011
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vol. 58
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issue 1
35-38
EN
Objectives: Obesity, insulin resistance and dyslipidemia are the most significant risk factors of non-alcoholic fatty liver disease (NAFLD) but the role of adipokines in the pathogenesis of this disease is not clear. Assessment of retinol binding protein (RBP-4) seems to be promising because data from animal and human studies suggest its role in the patomechanism of insulin resistance. Therefore, the aim of the study was to evaluate the serum levels of RBP-4 in children with NAFLD. Methods: Fasting serum level of RBP-4 was determined in 42 obese children with suspected liver disease and 20 lean controls. The degree of liver steatosis was graded in ultrasound according to Saverymuttu. The intrahepatic lipid content was assessed noninvasively in a semiquantitative fashion using 1HMR spectroscopy (1.5-T scanner with PRESS sequence). Results: Fatty liver was confirmed in 30 children by ultrasonography (16 of them had also increased alanine transaminase (ALT) activity). Serum concentrations of RBP-4 were significantly higher in obese children with NAFLD compared to controls. Significant correlations were found between RBP-4 level and ultrasonographic grade of liver steatosis, intrahepatic lipid content (1HMRS) and triglycerides level, while the serum level of RBP-4 was not significantly higher in children with advanced liver steatosis (grade 2-3, n = 11) compared to patients with mild steatosis (grade 1, n = 19). The ability of RBP-4 to differentiate children with advanced liver steatosis from those with mild steatosis was not significant. Conclusion: RBP-4 can be considered as a convenient serum marker of intrahepatic lipid content in obese children.
3
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Cytokeratin-18 and hyaluronic acid levels predict liver fibrosis in children with non-alcoholic fatty liver disease

76%
Lebensztejn D. M., Wierzbicka A., Socha P., Pronicki M., Skiba E., Werpachowska I., Kaczmarski M.
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2011
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vol. 58
|
issue 4
563-566
EN
Objectives: There is a need to replace liver biopsy with non-invasive markers that predict the degree of liver fibrosis in fatty liver disease related to obesity. Therefore, we studied four potential serum markers of liver fibrosis and compared them with histopathological findings in liver biopsy in children with non-alcoholic fatty liver disease (NAFLD). Methods: We determined fasting serum level of hyaluronic acid (HA), laminin, YKL-40 and cytokeratin-18 M30 in 52 children (age range 4-19, mean 12 years, 80 % of them were overweight or obese) with biopsy-verified NAFLD. Viral hepatitis, autoimmune and metabolic liver diseases (Wilson's disease, alpha-1-antitrypsin deficiency, cystic fibrosis) were excluded. Fibrosis stage was assessed in a blinded fashion by one pathologist according to Kleiner. Receiver operating characteristics (ROC) analysis was used to calculate the power of the assays to detect liver fibrosis (AccuROC, Canada). Results: Liver fibrosis was diagnosed in 19 children (37 %). The levels of HA and CK18M30 were significantly higher in children with fibrosis compared to children without fibrosis (p=0.04 and 0.05 respectively). The ability of serum HA (cut-off 19.1 ng/ml, Se=84 %, Sp=55 %, PPV=52 %, NPV=86 %) and CK18M30 (cut-off 210 u/l, Se=79 %, Sp=60 %, PPV=56 %, NPV=82 %) to differentiate children with fibrosis from those without fibrosis was significant (AUC=0.672 and 0.666, respectively). The combination of both markers was superior (AUC=0.73, p=0.002). Laminin and YKL-40 levels did not allow a useful prediction. Conclusions: Cytokeratin-18 and hyaluronic acid are suitable serum markers predicting liver fibrosis in children with NAFLD. Studying these markers may identify patients at risk of disease progression.
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