• Features of a functional state of the liver in children with Crohn’s disease
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Features of a functional state of the liver in children with Crohn’s disease

SOVREMENNAYA PEDIATRIYA.2016.6(78):103-106; doi 10.15574/SP.2016.78.103 

Features of a functional state of the liver in children with  Crohn's disease


Berezenko V. S., Tkalik E. N., Dyba M. B., Mostovenko R. V.

SI «Institute of Pedietrics, Obstetrics and Gynecology of NAMS of Ukraine», Kyiv, Ukraine

National children's specialized hospital «OKHMATDYT», Kyiv, Ukraine


Objective: Investigation of the functional state of the liver in the children with Crohn's disease activity and taking into account the length of bowel disease.


Patients and methods. The study has involved 45 children with Crohn's disease in an age of 3 to 18 years old. Clinical study was conducted under the order of 
Ministry of Health of Ukraine (No.59 from 29.01.2013). We examined the degree of the alanine aminotransferase (ALT), the aspartate aminotransferase, (AST), the g'glutamyl transpeptidase (GGT), the alkaline phosphatase (ALP), the direct bilirubin, the crude protein, the proteynohramma, for the study of liver parenchyma used ultrasound.


Results. It was found that an increase in transaminases more than one episode had 42.2% of children with CD. Violation of the functional state of the liver in children with CD is describe by predominantly cytolytic syndrome — a severe form of the disease increased ALT>40 IU/l were observed in 50% (n=6), and at moderate form — in 9% (n=3) children (χ2=9,2; p=0.008); increase in AST>40 IU/l more likely to have children with a severe form of the disease — 58,3% (n=7) than with moderate 12,2% (n=4) (χ2=10,18; p=0.001). Cytolytic option biochemical changes significantly more likely to have children with a severe form of the disease than the disease of moderate severity, — 8 (80%) and 3 (33,3%) (χ2=8,03; p=0.008), respectively.


Conclusions. Violation of the functional state of the liver mainly in the form of a periodic hypertransaminasemia occurred in 42.2% of children with CD. The children with CD have version prevails cytolytic violation functional state of the liver, the frequency is higher in children with a severe form of CD (р<0,05).


Key words: children, Crohn's disease, liver functional status, activity, duration of illness.


REFERENCES

1. Berezenko VS. 2010. K voprosu ob osobennostyah techeniya, diagnostyky i lecheniya bolezny Krona u detey. Sovremennaya pediatriya. 5(33): 167—175.

2. Mazankova LN, Halif IL, Vodylova OV. 2008. Bolezh’ Krona u detey. Monographiya: 96.

3. Mendes FD, Levy C, Enders FB et al. 2007. Abnormal hepatic biochemistries in patients with inflammatory bowel disease. Am J Gastroenterol. 102: 344—50. https://doi.org/10.1111/j.1572-0241.2006.00947.x; PMid:17100965

4. Zhengtao Liu, Shuping Que, Jing Xu et al. 2014. Alanine Aminotransferase — Old Biomarker and New Concept. A Review Int J Med Sci. 11(9): 925—935. https://doi.org/10.7150/ijms.8951; PMid:25013373 PMCid:PMC4081315

5. Thia KT, Loftus EV, Sandborn WJ et al. 2008. An update on the epidemiology of inflammatory bowel disease in Asia. Am J Gastroenterol. 103: 3167—3182. https://doi.org/10.1111/j.1572-0241.2008.02158.x; PMid:19086963

6. Bargiggia S, Maconi G, Elli MJ. 2003.Sonographic prevalence of liver steatosis and biliary tract stones in patients with inflammatory bowel disease: study of 511 subjects at a single center. Clin Gastroenterol. 36: 417—20. https://doi.org/10.1097/00004836-200305000-00012

7. Kim HY, Kim CW, Lee CD et al. 2014. Can «healthy» normal alanine aminotransferase levels identify the metabolically obese phenotype? Findings from the Korea national health and nutrition examination survey 2008—2010. Dig Dis Sci. 59(6): 1330—7. https://doi.org/10.1007/s10620-013-2995-0; PMid:24705695

8. McGowan CE, Jones P, Long MD et al. 2012. Changing shape ofdisease: nonalcoholic fatty liverdisease in Crohn's disease — A caseseries and review of the literature. Inflamm Bowel Dis. 18: 49—54. https://doi.org/10.1002/ibd.21669; PMid:21351214 PMCid:PMC3137748

9. Clinical guideline Hepatitis B (chronic): full guideline DRAFT (January 2013) National Institute for Health and Clinical Excellence.

10. Thin LW, Lawrance IC, Spilsbury K et al. 2014. Detection of liver injury in IBD using transient elastography. J Crohns Colitis. 8: 671—677. https://doi.org/10.1016/j.crohns.2013.12.006; PMid:24529605

11. Barbero-Villares A, Mendoza Jimenez-Ridruejo J, Taxonera C et al. 2012. Evaluation of liver fibrosis by transient elastography (Fibroscan®) in patients with inflammatory bowel disease treated with methotrexate: a multicentric trial. Scand J Gastroenterol. 47: 575—579. https://doi.org/10.3109/00365521.2011.647412; PMid:22229701

12. Vavricka SR, Schoepfer A, Scharl M et al. 1996. Extraintestinal Manifestations of Inflammatory Bowel Disease. Clinical patterns of familial inflammatory bowel disease. Gut. 38: 738—741. https://doi.org/10.1136/gut.38.5.738

13. Parente F, Pastore L, Bargiggia S et al. 2007. Incidence and risk factors for gallstones in patients with inflammatory bowel disease: a large case-control study. Hepatology. 45: 1267—74. https://doi.org/10.1002/hep.21537; PMid:17464998

14. Khan N, Abbas AM, Whang N et al. 2012. Incidence of liver toxicity in inflammatory bowel disease patients treated with methotrexate: a metaanalysis of clinical trials. Inflamm Bowel Dis. 18: 359—67. https://doi.org/10.1002/ibd.21820; PMid:21751301

15. Pusateri AJ, Kim SC, Jennifer L et al. 2015. Incidence, Pattern, and Etiology of Elevated Liver Enzymes in Pediatric Inflammatory Bowel Disease. JPGN. 60(5): 592—597. https://doi.org/10.1097/mpg.0000000000000672

16. Goyal A, Hyams JS, Trudy Lerer et al. 2014. Liver Enzyme Elevations Within 3 Months of Diagnosisof Inflammatory Bowel Disease and Likelihood of Liver Disease. JPGN. 59(3): 321-323.

17. Cappello M, Randazzo C, Bravati I et al. 2014. Liver Function Test Abnormalities in Patients with Inflammatory Bowel Diseases: A Hospital-based Survey. Clinical Medicine Insights: Gastroenterology. 7: 25—31. PMid:24966712 PMCid:PMC4069044

18. Loftus EV. 2004. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastoenterology. 126; 6: 1504—1517. https://doi.org/10.1053/j.gastro.2004.01.063

19. Maloy K ,. Powrie F. 2011. Intestinal homeostasis and its breakdown in inflammatory bowel disease. Nature. 474: 298—306. https://doi.org/10.1038/nature10208; PMid:21677746

20. Saich R, Roger C. 2008. Primary sclerosing cholangitis, autoimmune hepatitis and overlap syndromes in inflammatory bowel disease. World J Gastroenterol. 21; 14(3): 331—337.

21. Saich R, Chapman R. 2008. Primary sclerosing cholangitis, autoimmune hepatitis and overlap syndromes in inflammatory bowel disease. World J Gastroenterol. 14: 331—337. https://doi.org/10.3748/wjg.14.331; PMid:18200656 PMCid:PMC2679122

22. Candelli M, Nista EC, Pignataro G et al. 2003. Steatohepatitis during methylprednisolone therapy for ulcerative colitis exacerbation. J Intern Med. 253: 391—2. https://doi.org/10.1046/j.1365-2796.2003.01108.x; PMid:12603510

23. Gizard E, Ford AC, Bronowicki JP et al. 2014. Systematic review: the epidemiology of the hepatobiliary manifestations in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 40: 3—15. https://doi.org/10.1111/apt.12794; PMid:24815622

24. Bernstein CN, Blanchard JF, Rawsthorne P et al. 2001. The prevalence of extraintestinal diseases ininflammatory bowel disease: apopulation-based study. Am J Gastroenterol. 96: 1116-22. https://doi.org/10.1111/j.1572-0241.2001.03756.x; PMid:11316157

25. Venkatesh PGK, Navaneethan U, Shen B. 2011. Hepatobiliary disorders and complications of inflammatory bowel disease. Journal of Digestive Diseases. 12: 245—56. https://doi.org/10.1111/j.1751-2980.2011.00511.x; PMid:21791019

26. Yarur AJ, Czul F, Levy C. 2014. Hepatobiliary manifestations of inflammatory bowel disease. Inflamm Bowel Dis. 20: 1655—1667. https://doi.org/10.1097/MIB.0000000000000065; PMid:24874461