De novo nealkoholová tuková choroba pečene po transplantácii pečene – diagnostikovaná pomocou magnetickej rezonancie

Download PDF English version

Authors: Skladaný Ľ. ¹; Adamcova-Selcanova S. ¹; Ciefova J. ¹; Bystrianska N. ¹; Skvarkova B. ¹; Bachova B. ¹; Koller T. ²
Authors‘ workplace: HEGITO – Hepatology, Gastroenterology and Liver Transplantation Division of the Department of Internal Medicine II, Faculty of Medicine, Slovak Medical University, F. D. Roosevelt Hospital, Banska Bystrica, Slovakia ¹; 5th Department of Internal Medicine, Comenius University Faculty of Medicine, University Hospital Bratislava Ruzinov, Bratislava, Slovakia ²
Published in: Gastroent Hepatol 2020; 74(2): 116-122
Category: Hepatology: original article
doi: https://doi.org/10.14735/amgh2020116

Overview

Východiská: Nealkoholová tuková choroba pečene (NAFLD) je jednou z najčastejších príčin chronického ochorenia pečene a zároveň indikácií transplantácie pečene (LTx). NAFLD, ktorá vznikne po LTx pre inú indikáciu sa nazýva de novo NAFLD.

Cieľ: Určiť výskyt de novo NAFLD za pomoci diagnostiky magnetickej rezonančnej (MR) spektroskopie (MRS).

Metódy: Prospektívna analýza údajov za sebou idúcich pacientov po LTx v intervale medzi januárom 2015 a decembrom 2019. Do štúdie boli zaradení pacienti transplantovaní pre cirhózu pečene na podklade inej etiológie ako NAFLD. Vylúčení boli pacienti po LTx pre NAFLD, so závažnými komplikáciami < 2 mesiace po LTx a tý, ktorí zomreli < 3 mesiace po LTx. Sledovali sme demografické a antropometrické charakteristiky, laboratórne parametre potrebné na výpočet indexu tuku v pečeni (FLI – fatty liver index) a MRS v mesiacoch 3, 6, 12, 24 po LTx. NAFLD bola diagnostikovaná pri FLI ≥ 60 a pri MRS obsah tuku v pečeni ≥ 5%

Výsledky: V sledovanom intervale bolo vykonaných 164 LTx u 153 pacientov, vylúčili sme 6 pacientov (4 %) po LTx pre NAFLD a 52 pacientov (34 %) podľa vopred stanovených kritérií. Do definitívnej analýzy sme zaradili 95 pacientov (62 %), s vekom 50,4 rokov (18–70), 38 % žien, s MELD (model for end stage liver disease) 15,7 bodov, s Child-Pugh skóre 8,9 bodov.

Etiológia: Alkoholová choroba pečene 44 pacientov ( 46 %), primárna sklerotizujúca cholangitída 16 (17 %), autoimunitné ochorenia 12 (13 %), rôzne 8 (9 %), hepatocelulárny karcinóm 7 (7 %), vírusové hepatitídy 3 (3 %), sekundárna biliárna cholangitída 3 (3 %), Wilsonova choroba 2 (2 %). Body mass index (BMI) kg/ m², v čase LTx, mesiace 3, 6, 12: 25,76; 24,6; 24,95; 26,5 (p < 0,01); FLI (mesiace 3, 6, 12, 24): 48,663 ± 5,878; 51,628 ± 6,166; 50,901 ± 7,075; 55,211 ± 13,832; MRS (> 5 % tuku, mesiace 6, 12, 24): 26,5; 32,1; 42,9 (p = 0,368); MRS (% tuku, medián, mesiace 6, 12, 24): 3,45; 4 (p = 0,045); 5 (p = 0,08). MR elastografia (≥ 2,88 kPa, mesiace 6, 12, 24): 26,8; 29,6 (p = 0,07); 46,2 (p = 0,1).

Záver: V sledovanej kohorte sme identifikovali so stúpajúcim trendom BMI zároveň vzostup obsahu Etiology po LTx. Šesť mesiacov po LTx sme pomocou MRS detegovali viac ako 5 % tuku v pečeni u 1/4 pacientov. V čase 6 a 12 mesiacov po LTx bola fibróza prítomná u 26 a 29 % pacientov. Klinický význam zatiaľ nepoznáme.

Klíčová slova:

transplantácia pečene – FLI – MR spektroskopia – MR elastografia – de novo NAFLD

Sources

1. Younossi ZM, Koenig AB, Abdelatif D et al. Global epidemiology of nonalcoholic fatty liver disease – meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology 2016; 64(1): 73–84. doi: 10.1002/ hep.28431.

2. Brunt EM, Wong VW, Nobili V et al. Nonalcoholic fatty liver disease. Nat Rev Dis Primers 2015; 17(1): 15080. doi: 10.1038/ nrdp.2015.80.

3. De Franchis R, Baveno VI Faculty. Expanding consensus in portal hypertension: report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension. J Hepatol 2015; 63(3): 743–752. doi: 10.1016/ j.jhep.2015.05.022.

4. EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO). J Hepatol 2016; 64(6): 1388–1402. doi: 10.1016/ j.jhep.2015.11.004.

5. Wong RJ, Aguilar M, Cheung R et al. Nonalcoholic steatohepatitis is the second leading etiology of liver disease among adults awaiting liver transplantation in the United States. Gastroenterology 2015; 148(3): 547–555. doi: 10.1053/ j.gastro.2014.11.039.

6. Davidson JA, Wilkinson A. International Expert Panel on New‐Onset Diabetes after Transplantation. New‐Onset Diabetes After Transplantation 2003 International Consensus Guidelines: an endocrinologist’s view. Diabetes Care 2004; 27(3): 805–812. doi: 10.2337/ diacare.27.3.805.

7. Pham PT, Pham PM, Pham SV et al. New onset diabetes after transplantation (NODAT): an overview. Diabetes Metab Syndr Obes 2011; 4: 175–186. doi: 10.2147/ DMSO.S19027.

8. Watt KD, Pedersen RA, Kremers WK et al. Evolution of causes and risk factors for mortality post‐liver transplant: results of the NIDDK long‐term follow‐up study. Am J Transplant 2010; 10(6): 1420–1427. doi: 10.1111/ j.1600-6143.2010.03126.x.

9. Bhagat V, Mindikoglu AL, Nudo CG et al. Outcomes of liver transplantation in patients with cirrhosis due to nonalcoholic steatohepatitis versus patients with cirrhosis due to alcoholic liver disease. Liver Transpl 2009; 15(12): 1814–1820. doi: 10.1002/ lt.21927.

10. Yalamanchili K, Saadeh S, Klintmalm GB et al. Nonalcoholic fatty liver disease after liver transplantation for cryptogenic cirrhosis or nonalcoholic fatty liver disease. Liver Transpl 2010; 16(4): 431–439. doi: 10.1002/ lt.22004.

11. Contos MJ, Cales W, Sterling RK et al. Development of nonalcoholic fatty liver disease after orthotopic liver transplantation for cryptogenic cirrhosis. Liver Transpl 2001; 7(4): 363–373. doi: 10.1053/ jlts.2001.23011.

12. Charlton M, Kasparova P, Weston S et al. Frequency of nonalcoholic steatohepatitis as a cause of advanced liver disease. Liver Transpl 2001; 7(7): 608–614. doi: 10.1053/ jlts.2001.25453.

13. Hejlova I, Honsova E, Sticova E et al. Prevalence and risk factors of steatosis after liver transplantation and patients outcomes. Liver Transpl 2016; 22(5): 644–655. doi: 10.1002/ lt.24393.

14. Dureja P, Mellinger J, Agni R et al. NAFLD recurrence in liver transplant recipients. Transplantation 2011; 91(6): 684–689. doi: 10.1097/ TP.0b013e31820b6b84.

15. Seo S, Maganti K, Khehra M et al. De novo nonalcoholic fatty liver disease after liver transplantation. Liver Transpl 2007; (13)6: 844–847. doi: 10.1002/ lt.20932.

16. Dumortier J, Giostra E, Belbouab S et al. Non-alcoholic fatty liver disease in liver transplant recipients: another story of „seed and soil”. Am J Gastroenterol 2010; 105(3): 613–620. doi: 10.1038/ ajg.2009.717.

17. Galvin Z, Rajakumar R, Chen E et al. Predictors of de novo nonalcoholic fatty liver disease after liver transplantation and associated fibrosis. Liver Transpl 2019; 25(1): 56–67. doi: 10.1002/ lt.25338.

18. Burke A, Lucey MR. Non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and orthotopic liver transplantation. Am J Transplant 2004; 4(5): 686–693. doi: 10.1111/ j.1600-6143.2004.0 0432.x.

19. Mikolasevic I, Orlic L, Hrstic I et al. Metabolic syndrome and non‐alcoholic fatty liver disease after liver or kidney transplantation. Hepatol Res 2016; 46(9): 841–852. doi: 10.1111/ hepr.12642.

20. Fatty Liver Index. [online]. Available from: https:/ / www.mdapp.co/ fatty-liver-index-fli-calculator-356/ .

21. Bedogni G, Bellentani S, Miglioli L et al. The fatty liver index: a simple and accurate predictor of hepatic steatosis in the general population. BMC Gastroenterol 2006; 6: 33. doi: 10.1186/ 1471-230X-6-33.

22. Machado MV, Cortez-Pinto H. Non-invasive diagnosis of non-alcoholic fatty liver disease. A critical appraisal. J Hepatol 2013; 58(5): 1007–1019. doi: 10.1016/ j.jhep.2012.11.021.

23. Idilman IS, Aniktar H, Idilman R et al. Hepatic steatosis: quantification by proton density fat fraction with MR imaging versus liver biopsy. Radiology 2013; 267(3): 767–775. doi: 10.1148/ radiol.13121360.

24. Gu J, Liu S, Du S et al. Diagnostic value of MRI-PDFF for hepatic steatosis in patients with non-alcoholic fatty liver disease: a meta-analysis. Eur Radiol 2019; 29(7): 3564–3573. doi: 10.1007/ s00330-019-06072-4.

25. Newsome PN, Sasso M, Deeks JJ et al. FibroScan-AST (FAST) score for the non-invasive identification of patients with non-alcoholic steatohepatitis with significant activity and fibrosis: a prospective derivation and global validation study. Lancet Gastroenterol Hepatol 2020; 5(4): 362–373. doi: 10.1016/ S2468-1253(19)30383-8.

26. Yin M, Talwalkar JA, Glaser KJ et al. Assessment of hepatic fibrosis with magnetic resonance elastography. Clin Gastroenterol Hepatol 2007; 5(10): 1207–1213. doi: 10.1016/ j.cgh.2007.06.012.

27. Loomba R, Wolfson T, Ang B et al. Magnetic resonance elastography predicts advanced fibrosis in patients with nonalcoholic fatty liver disease: a prospective study. Hepatology 2014; 60(6): 1920–1928. doi: 10.1002/ hep.27362.

28. Morisaka H, Motosugi U, Ichikawa S et al. Magnetic resonance elastography is as accurate as liver biopsy for liver fibrosis staging. J Magn Reson Imaging 2018; 47(5): 1268–1275. doi: 10.1002/ jmri.25868.

29. Kim H, Lee K, Lee KW et al. Histologicallyproven non-alcoholic fatty liver disease and clinically related factors in recipients after liver transplantation. Clin Transplant 2014; 28(5): 521–529. doi: 10.1111/ ctr.12343.

30. Vallin M, Guillaud O, Boillot O et al. Reccurent or de novo non-alcoholic fatty liver disease after liver transplantation: natural history based on liver biopsy analysis. Liver Transpl 2014; 20(9): 1064–1071. doi: 10.1002/ lt.23936.

31. Shaker M, Tabbaa A, Albedawi M et al. Liver transplantation for nonalcoholic fatty liver disease: new challenges and new opportunities. World J gastroenterol 2014; 20(18): 5320–5330. doi: 10.3748/ wjg.v20.i18.5320.

32. Skladany L’, Mesarosova Z, Bachova B et al. Alcohol-related liver disease as a new risk factor for post-transplant diabetes after liver transplantation. Transplant Proc 2019; 51(10): 3369–3374. doi: 10.1016/ j.transproceed.2019.07.021.