#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Metabolic profile of liver transplant recipient with respect to the development of NAFLD – results of a pilot study


Authors: I. Hejlová 1;  M. Dezortová 2;  P. Šedivý 2;  M. Drobný 2;  M. Hájek 2;  M. Cahová 3;  H. Daňková 3;  E. Sticová 4;  V. Lánská 5;  P. Trunečka 6
Authors‘ workplace: Klinika hepatogastroenterologie, Transplantcentrum, IKEM, Praha 1;  Pracoviště radiodia­gnostiky a intervenční radiologie, Komplement, IKEM, Praha 2;  Centrum experimentální medicíny, IKEM, Praha 3;  Pracoviště klinické a transplantační patologie, Transplantcentrum, IKEM, Praha 4;  Lékařská statistika, IKEM, Praha 5;  Transplantcentrum, IKEM, Praha 6
Published in: Gastroent Hepatol 2016; 70(4): 325-330
Category: Hepatology: Original Article
doi: https://doi.org/10.14735/amgh2016325

Overview

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.

Key words:
insulin resistance – magnetic resonance – metabolic syndrome – mitochondrial capacity – NAFLD – liver transplantation

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE „uniform requirements“ for biomedical papers.

Submitted:
11. 7. 2016

Accepted:
1. 8. 2016


Sources

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 Det 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.

Labels
Paediatric gastroenterology Gastroenterology and hepatology Surgery

Article was published in

Gastroenterology and Hepatology

Issue 4

2016 Issue 4

Most read in this issue
Login
Forgotten password

Enter the email address that you registered with. We will send you instructions on how to set a new password.

Login

Don‘t have an account?  Create new account

#ADS_BOTTOM_SCRIPTS#