Peculiarities of biochemical blood parameters and cytokine profile in patients with non-alcoholic fatty liver disease depending on the form of hypothyroidism

Main Article Content

V.P. Prysyazhnyuk
O.I. Voloshyn
N.V. Pashkovska


Background. The purpose of the study was to investigate the biochemical blood peculiarities and cytokine profile in non-alcoholic fatty liver disease (NAFLD) patients depending on the form of hypothyroidism. Material and methods. The study involved 188 NAFLD patients (average age 53.60 ± 12.34 years). Among the examined individuals 44 of them had diagnosed hypothyroidism in addition to NAFLD (20 patients had subclinical form and 24 patients had manifest hypothyroidism). A comparison group consisted of 144 NAFLD patients with thyroid normal functional activity. The control group consisted of 45 healthy individuals represented by their age and gender similar to the patients of the studied groups. Biochemical blood parameters, tumor necrosis factor α, interleukin-10, leptin, adiponectin blood levels were investigated in the observed patients and healthy individuals. Results. Total lactate dehydrogenase blood activity in NAFLD patients with subclinical and manifest hypothyroidism was found to be 13.5 % increased compared to the NAFLD patients with normal functional activity of the thyroid gland (p = 0.02 and p = 0.01, respectively). Higher alkaline phosphatase blood activity by 12.0 % (p = 0.03) was recorded in NAFLD and manifest hypothyroidism patients as compared to the patients with intact thyroid gland. Leptin blood concentration in NAFLD patients with subclinical as well as manifest hypothyroidism was 35.7 % and 72.1 % increased compared to NAFLD patients with normal thyroid functional activity (p = 0.04 and p = 0.009, respectively). Adiponectin blood level in NAFLD patients with manifest hypothyroidism was 2.1 lower (p = 0.004) in comparison with NAFLD patients with thyroid normal functional activity and 50.0 % lower (p = 0.009) as compared to the NAFLD patients with subclinical hypothyroidism. NAFLD and manifest hypothyroidism patients showed greater vertical size of the liver measured by midclavicular line on average by 9.1 mm (p = 0.004) as compared to NAFLD patients with unchanged thyroid gland functional activity and by 8.6 mm (p = 0.04) in comparison with the NAFLD patients with subclinical hypothyroidism. Conclusions. There were found higher total lactate dehydrogenase acti­vity and leptin blood level in NAFLD patients with subclinical and manifest hypothyroidism and higher alkaline phosphatase activity and lower adiponectin blood level in NAFLD patients with manifested hypothyroidism as compared
to NAFLD patients with normal functional activity of the thyroid gland. A significant increase in liver vertical size measured by midclavicular line was observed in NAFLD patients with manifest hypothyroidism as compared to the patients with normal thyroid function or subclinical hypothyroidism.

Article Details

How to Cite
Prysyazhnyuk, V., O. Voloshyn, and N. Pashkovska. “Peculiarities of Biochemical Blood Parameters and Cytokine Profile in Patients With Non-Alcoholic Fatty Liver Disease Depending on the Form of Hypothyroidism”. INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), vol. 13, no. 3, June 2017, pp. 115-20, doi:10.22141/2224-0721.13.3.2017.104106.
Clinical Thyroidology


Nakaz MOZ Ukraїni vіd 06.11.2014 № 826 ‘Pro zatverdzhennja ta vprovadzhennja mediko-tehnologіchnih dokumentіv zі standartizacії medichnoї dopomogi pri hronіchnih neіnfekcіjnih gepatitah’ [Order of Health Ministry of Ukraine N 826 dated 06.11.2014 ‘About a statement and introduction of medical and technological documents from standardization of medicare at chronic uninfectious hepatitis’]. Kyiv, 2014. (In Ukrainian).

Pankiv VI, Yuzvenko T.Y. Intercommunication of subclinical thyroid disfunction and metabolic syndrome. Clinical Endocrinology and Endocrine Surgery. 2015;3:54-9. (In Ukrainian).

Bellentani S, Scaglioni F, Marino M, Bedogni G. Epidemiology of non-alcoholic fatty liver disease. Dig Dis. 2010;28(1):155-61. doi: 10.1159/000282080.

Chou WY, Cheng YS, Ho CL, et al. Human spot 14 protein interacts physically and functionally with the thyroid receptor. Biochem Biophys Res Commun. 2007;357(1):133-8. doi: 10.1016/j.bbrc.2007.03.103.

EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388-1402. doi: 10.1016/j.jhep.2015.11.004.

Flores-Morales A, Gullberg H, Fernandez L, et al. Patterns of liver gene expression governed by TRbeta. Mol Endocrinol. 2002;16:1257-68. doi: 10.1210/mend.16.6.0846.

Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American association of clinical endocrinologists and the American thyroid association. Endocr Pract. 2012;18(6):988-1028. doi: 10.4158/EP12280.GL.

Grasselli E, Voci A, Demori I. et al. 3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver. Journal of Endocrinology. 2012;2:149-158. doi: 10.1530/JOE-11-0288.

Huang Y-Y, Gusdon AM, Qu S. Cross-talk between the thyroid and liver: A new target for nonalcoholic fatty liver disease treatment. World J Gastroenterol. 2013;19(45):8238-46. doi: 10.3748%2Fwjg.v19.i45.8238.

Ittermann T, Haring R, Wallaschofski H, et al. Inverse association between serum free thyroxine levels and hepatic steatosis: results from the Study of Health in Pomerania. Thyroid. 2012;22(6):568-74. doi: 10.1089%2Fthy.2011.0279.

Laukkarinen J, Sand J, Aittomäki S, et al. Mechanism of the prorelaxing effect of thyroxin on the sphincter of Oddi. Scand J Gastroenterol. 2002;37(6):667-73. PMID: 12126244.

Li G, Hu H, Shi W, et al. Elevated hematocrit in nonalcoholic fatty liver disease: a potential cause for the increased risk of cardiovascular disease? Clinical Hemorheology and Microcirculation. 2012;51(1):59-68. doi: 10.3233/CH-2011-1509.

Liedtke C, Trautwein C. The role of TNF and Fas dependent signaling in animal models of inflammatory liver injury and liver cancer. European Journal of Cell Biology. 2012;91(6-7):582-9. doi: 10.1016/j.ejcb.2011.10.001.

Mauss S, Berg T, Rockstroh J, et al. Hepatology. A clinical textbook. 7th edition. Hamburg; 2016. 710 p.

Pearce SH, Brabant G, Duntas LH, et al. 2013 ETA Guideline: management of subclinical hypothyroidism. Eur Thyroid J. 2013;2(4):215-28. doi: 10.1159/000356507.

Pergialiotis V, Konstantopoulos P, Prodromidou A, et al. Management of endocrine disease: The impact of subclinical hypothyroidism on anthropometric characteristics, lipid, glucose and hormonal profile of PCOS patients: a systematic review and meta-analysis. Eur J Endocrinol. 2017;176(3):159-66. doi: 10.1530/eje-16-0611.

Perra A, Simbula G, Simbula M, et al.Thyroid hormone (T3) and TRbeta agonist GC-1 inhibit/reverse nonalcoholic fatty liver in rats. FASEB J. 2008;22(8):2981-9. doi: 10.1096/fj.08-108464.

Perumpail RB, Liu A, Wong RJ, et al. Pathogenesis of hepatocarcinogenesis in non-cirrhotic nonalcoholic fatty liver disease: Potential mechanistic pathways. World Journal of Hepatology. 2015;7(22):2384-8. doi: 10.4254%2Fwjh.v7.i22.2384.

Thakran S, Sharma P, Attia RR, et al. Role of sirtuin 1 in the regulation of hepatic gene expression by thyroid hormone. J Biol Chem. 2013;288(2):807-18. doi: 10.1074/jbc.M112.437970.

Younossi ZM, Jarrar M, Nugent C, et al. A novel diagnostic biomarker panel for obesity-related nonalcoholic steatohepatitis (NASH). Obesity Surgery. 2008;18(11):1430-7. doi: 10.1007/s11695-008-9506-y.

Most read articles by the same author(s)

1 2 3 4 > >>