Metabolic profile of liver transplant recipient with respect to the development of NAFLD – results of a pilot study
Irena Hejlová1, Monika Dezortová2, Petr Šedivý2, Miloslav Drobný2, Milan Hájek2, Monika Cahová3, Helena Daňková3, Eva Sticová4, Věra Lánská5, Pavel Trunečka6
1 Klinika hepatogastroenterologie, Transplantcentrum, IKEM, Praha
2 Pracoviště radiodiagnostiky a intervenční radiologie, Komplement, IKEM, Praha
3 Centrum experimentální medicíny, IKEM, Praha
4 Pracoviště klinické a experimentální patologie, Transplantcentrum, IKEM, Praha
5 Lékařská statistika, IKEM, Praha
6 Transplantcentrum, IKEM, Praha
Aims: Non-alcoholic fatty liver disease (NAFLD) of liver grafts occurs in 31–56% of liver transplant recipients, and its prevalence increases with time after transplantation. The aim of this prospective study was to analyze metabolic profile of liver transplant recipients with respect to development of NAFLD. Methods: The pilot part of the prospective study included 31 patients at 1–16 years after liver transplantation who underwent a protocol liver biopsy. We performed laboratory investigations of glucose and lipid metabolism, and determined liver fat content and subcutaneous and visceral fat volume by 1H MR spectroscopy and imaging. We determined the maximal mitochondrial capacity in musculus gastrocnemius by dynamic 31P MR spectroscopy. Results: In the liver biopsies, we found steatosis grade 2–3 in 12 (38.7%) patients, steatosis grade 1 in 13 (41.9%) patients, and no steatosis in six (19.4%) patients. With increasing steatosis grade, a positive correlation was found between BMI (p = 0.002), waist circumference (p = 0.004), subcutaneous fat volume (p = 0.023), visceral fat volume (p = 0.034), occurrence of metabolic syndrome (p = 0.006), fasting glucose (p = 0.043), glycated haemoglobin (p = 0.048) and C-peptide (p = 0.026). The proportion of smokers was lower in patients with steatosis than in those without steatosis (p = 0.001). Increases in the HOMA index (p = 0.10) and decreases in the QUICKI index (p = 0.10) did not reach statistical significance. With increasing steatosis grade, we found a trend towards a decrease in maximal mitochondrial capacity of skeletal muscles measured by 31P MR spectroscopy, but the differences were not statistically significant (p = 0.23). Histological grade of steatosis correlated well with steatosis grade measured by 1H MR spectroscopy (p = 0.0002). Conclusions: In this pilot study, we identified significant clinical, laboratory and MR parameters that could contribute to predicting NAFLD in liver transplant recipients.
KeywordsNAFLD, inzulinová rezistence, magnetic resonance, metabolic syndrome, mitochondrial capacity
To read this article in full, please register for free on this website.
Benefits for subscribers
Benefits for logged users
1. Bedogni G, Miglioli L, Masutti F et al. Prevalence of and risk factors for nonalcoholic fatty liver disease: the Dionysos nutrition and liver study. Hepatology 2005; 42 (1): 44–52.
2. Browning JD, Szczepaniak LS, Dobbins R et al. Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity. Hepatology 2004; 40 (6): 1387–1395.
3. Adams LA, Lymp JF, St Sauver J et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005; 129 (1): 113–121.
4. Söderberg C, Stål P, Askling J et al. Decreased survival of subjects with elevated liver function tests during a 28-year follow-up. Hepatology 2010; 51 (2): 595–602. doi: 10.1002/hep.23314.
5. Anstee QM, Seth D, Day CP. Genetic factors that affect risk of alcoholic and nonalcoholic fatty liver disease. Gastroenterology 2016; 150 (8): 1728–1744. doi: 10.1053/j.gastro.2016.01.037.
6. Hejlova I, Honsova E, Sticova E et al. Prevalence and risk factors of steatosis after liver transplantation and patient outcomes. Liver Transpl 2016; 22 (5): 644–655. doi: 10.1002/lt.24393.
7. Wallace TM, Matthews DR. The assessment of insulin resistance in man. Diabet Med 2002; 19 (7): 527–534.
8. Muniyappa R, Lee S, Chen H et al. Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am J Physiol Endocrinol Metab 2008; 294 (1): E15–E26.
9. Petersen KF, Dufour S, Befroy D et al. Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med 2004; 350 (7): 664–671.
10. Scheuermann-Freestone M, Madsen PL, Manners D et al. Abnormal cardiac and skeletal muscle energy metabolism in patients with type 2 diabetes. Circulation 2003; 107 (24): 3040–3046.
11. Šedivý P, Kipfelsberger MC, Dezortová M et al. Dynamic 31P MR spectroscopy of plantar flexion: influence of ergometer design, magnetic field strength (3 and 7 T), and RF-coil design. Med Phys 2015; 42 (4): 1678–1689. doi: 10.1118/1.4914448.
12. Thomsen C, Becker U, Winkler K et al. Quantification of liver fat using magnetic resonance spectroscopy. Magn Reson Imaging 1994; 12 (3): 487–495.
13. Hájek M, Dezortová M, Wagnerová D et al. MR spectroscopy as a tool for in vivo determination of steatosis in liver transplant recipients. MAGMA 2011; 24 (5): 297–304. doi: 10.1007/s10334-011-0264-9.
14. Kleiner DE, Brunt EM, Van Natta M et al. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology 2005; 41 (6): 1313–1321.
15. Zhang J, Zhao Y, Xu C et al. Association between serum free fatty acid levels and nonalcoholic fatty liver disease: a cross-sectional study. Sci Rep 2014; 4: 5832. doi: 10.1038/srep05832.
16. Larter CZ, Yeh MM, Haigh WG et al. Hepatic free fatty acids accumulate in experimental steatohepatitis: Role of adaptive pathways. J Hepatol 2008; 48 (4): 638–647. doi: 10.1016/j.jhep.2007.12.011.
17. Sorice GP, Muscogiuri G, Mezza T et al. Metabolic syndrome in transplant patients: an academic or a health burden? Transplant Proc 2011; 43 (1): 313–317. doi: 10.1016/j.transproceed.2010.09.099.