Profil faktora rizika od oštećenja jetre kod hospitalizovanih kardioloških bolesnika

  • Jovan Jovanović Clinical Center “Kragujevac”, Clinic for Cardiology, Kragujevac, Serbia
  • Dragan R. Milovanović University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Predrag Sazdanović University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Maja Sazdanović University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Milan Radovanović University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Ljiljana Novković University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Vladimir Zdravković Clinical Center “Kragujevac”, Clinic for Cardiology, Kragujevac, Serbia
  • Nemanja Zdravković University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Ivan Simić Clinical Center “Kragujevac”, Clinic for Cardiology, Kragujevac, Serbia
  • Dejana Ružić Zečević University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
  • Slobodan M. Janković University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia
Ključne reči: alkohol, pijenje, amjodaron, kardiovaskularne bolesti, jetra, oštećenje, hemijsko i lekovima izazvano, lekovi, toksičnost, hospitalizacija, gojaznost, faktori rizika

Sažetak


Uvod/Cilj. Oštećenje jetre, sa potencijalno ozbiljnim posledicama, nije retka pojava kod hospitalizovanih kardioloških bolesnika. Cilj studije bio je ispitivanje profila faktora rizika od oštećenja jetre kod bolesnika hospitalizovanih zbog pogoršanja akutne ili hronične kardiološke bolesti. Metode. Studija je bila opservacionog dizajna, tipa slučaj-kontrola, uz retrospektivno prikupljanje podataka uvidom u istorije bolesti odraslih bolesnika lečenih u tercijarnoj zdravstvenoj ustanovi. Slučajevi (n = 140) su bili bolesnici sa novonastalim oštećenjem jetre (koja se razvila tokom hospitalizacije), a po tri kontrolna bolesnika (n = 420), komparabilna po godinama i datumu hospitalizacije, pridruženi su svakom slučaju. Primarni ishod je bila hepatotoksičnost (simptomatska ili asimptomatska), a nezavisne varijable su bile predložene kao faktori rizika. Statistička analiza je uključivala deskriptivne metode, ispitivanje hipoteze i univarijantnu i multivarijantnu binarnu logističku regresiju, sa p ≤ 0.05. Rezultati. Od ukupne studijske populacije, 432 (77,1%) osobe su bile ženskog pola, a srednja vrednost godina bolesnika iznosila je 64,1 godina [standardna devijacija (SD) = 10,7; opseg 24–85]. Najčešće bolesti su bile koronarna bolest (n = 385), hipertenzija (n = 334) i aritmija (n = 115). Srednja vrednost Charlson Comorbidity Index-a (CCI) bila je 3.8 (SD = 1,7; opseg 1–10), što je bilo u skladu sa procenjenim CCI 10-ogodišnjim preživljavanjem od 54,4% (SD = 33,5%). U grupi slučajeva, 114 (81.4%) bolesnika imalo je hepatocelularni tip, 9 (6,4%) holestatski tip, a 17 (12,2%) mešoviti tip oštećenja jetre. Nezavisni prediktori hepatotoksičnog događaja su bili: prethodna povremena konzumacija alkohola [odds ratio (OR) 96,47; 95% interval poverenja (IP) 28,95–321,43; p < 0,001], upotreba amiodarona (OR 3,70; 95% IP 1,82–7,53; < 0,001), enoksaparina (OR 3,29; 95% IP 1,79–6,05; < 0,001) i atorvastatina (OR 2,67; 95% IP 1,33–5,38; 0,006), gojaznost (OR 2,78; 95% IP 1,15–6,71; 0,023) i ukupni CCI skor (OR 1,89; 95% IP 1,53–2,34; < 0,001). Zaključak. Glavni faktori povezani sa akutnim oštećenjem jetre kod bolesnika hospitalizovanih na kardiološkom odeljenju u institucijama tercijarne zdravstvene nege su konstitucionalne karakteristike i navike bolesnika (povremeni unos alkohola, gojaznost, CCI skor) i lekovi za koje se zna da imaju hepatotoksični potencijal (amjodaron, enoksaparin, atorvastatin).

Reference

Hahn KJ, Morales SJ, Lewis JH. Enoxaparin-Induced Liver In-jury: Case Report and Review of the Literature and FDA Ad-verse Event Reporting System (FAERS). Drug Saf Case Rep 2015; 2(1): 17.

Møller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J 2013; 34(36): 2804‒11.

Yu YC, Mao YM, Chen CW, Chen JJ, Chen J, Cong WM, et al. CSH guidelines for the diagnosis and treatment of drug-induced liver injury. Hepatol Int 2017; 11(3): 221-41.

Kullak-Ublick GA, Andrade RJ, Merz M, End P, Benesic A, Gerbes AL, et al. Drug-induced liver injury: recent advances in diagnosis and risk assessment. Gut 2017; 66(6): 1154–64.

Björnsson ES. Hepatotoxicity by drugs: the most common im-plicated agents. Int J Mol Sci 2016; 17(2): 224.

Kim SH, Kim SH, Lee JH, Lee BH, Yoon HJ, Shin DH, et al. Superoxide dismutase gene (SOD1, SOD2, and SOD3) poly-morphisms and antituberculosis drug-induced hepatitis. Aller-gy Asthma Immunol Res 2015; 7(1): 88‒91.

Cataldi A, Gonella D, Robutti N, Siri M, Buonocore S, Odetti P. Hepatotoxicity after intravenous amiodarone. Aging Clin Exp Res 2008; 20(6): 593‒6.

Diab OA, Kamel J, Abd-Elhamid AA. Predictors of intravenous amiodarone induced liver injury. Egypt Heart J 2017; 69(1): 45‒54.

Haque T, Sasatomi E, Hayashi PH. Drug-induced liver injury: pattern recognition and future directions. Gut Liver 2016; 10(1): 27‒36.

Gluck N, Fried M, Porat R. Acute amiodarone liver toxicity likely due to ischemic hepatitis. Isr Med Assoc J 2011; 13(12): 748‒52.

Douros A, Bronder E, Andersohn F, Klimpel A, Thomae M, Sarga-nas G, et al. Drug-induced liver injury: results from the hospi-tal-based Berlin Case-Control Surveillance Study. Br J Clin Pharmacol 2014; 79(6): 988‒99.

Nyblom H, Berggren U, Balldin J, Olsson R. High AST/ALT ra-tio may indicate advanced alcoholic liver disease rather than heavy drinking. Alcohol Alcohol 2004, 39(4): 336‒9.

Teschke R, Wolff A, Frenzel C, Schwarzenboeck A, Schulze J, Eick-hoff A. Drug and herb induced liver injury: Council for Inter-national Organizations of Medical Sciences scale for causality assessment. World J Hepatol 2014; 6(1): 17‒32.

Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new meth-od of classifying prognostic comorbidity in longitudinal stud-ies: development and validation. J Chronic Dis 1987; 40(5): 373‒83.

de Abajo FJ1, Montero D, Madurga M, García Rodríguez LA. Acute and clinically relevant drug-induced liver injury: a population based case-control study. Br J Clin Pharmacol 2004; 58(1): 71‒80.

Pollak PT, Shafer SL. Use of population modeling to define ra-tional monitoring of amiodarone hepatic effects. Clin Phar-macol Ther 2004; 75(4): 342‒51.

Massey VL, Beier JI, Ritzenthaler JD, Roman J, Arteel GE. Po-tential Role of the Gut/Liver/Lung Axis in Alcohol-Induced Tissue Pathology. Biomolecules 2015; 5(4): 2477‒503.

European Association for the Study of Liver. EASL clinical practi-cal guidelines: management of alcoholic liver disease. J Hepa-tol. 2012; 57(2): 399‒420.

Bertholet N, Winter MR, Cheng DM, Samet JH, Saitz R. How accurate are blood (or breath) tests for identifying self-reported heavy drinking among people with alcohol depend-ence? Alcohol Alcohol 2014; 49(4): 423‒9.

Marchesini G, Moscatiello S, Di Domizio S, Forlani G. Obesity-associated liver disease. J Clin Endocrinol Metab 2008; 93(11 Suppl 1): S74‒80.

Massart J, Begriche K, Moreau C, Fromenty B. Role of nonalco-holic fatty liver disease as risk factor for drug-induced hepato-toxicity. J Clin Transl Res 2017; 3(Suppl 1): 212‒32.

Targher G, Bertolini L, Poli F, Rodella S, Scala L, Tessari R, Zenari L, Falezza G. Nonalcoholic fatty liver disease and risk of future cardiovascular events among type 2 diabetic pa-tients. Diabetes 2005; 54(12): 3541‒6.

Ioannou GN, Weiss NS, Boyko EJ, Mozaffarian D, Lee SP. Ele-vated serum alanine aminotransferase activity and calculated risk of coronary heart disease in the United States. Hepatology 2006; 43(5): 1145‒51.

Targher G, Arcaro G. Non-alcoholic fatty liver disease and in-creased risk of cardiovascular disease. Atherosclerosis 2007; 191(2): 235‒40.

Tapper EB, Sengupta N, Bonder A. The Incidence and Outcomes of Ischemic Hepatitis: A Systematic Review with Meta-analysis. Am J Med 2015; 128(12): 1314‒21.

Yurkovich M, Avina-Zubieta JA, Thomas J, Gorenchtein M, Lacaille D. A systematic review identifies valid comorbidity indices de-rived from administrative health data. J Clin Epidemiol 2015; 68(1): 3‒14.

Reuben A, Koch DG, Lee WM. Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. mul-ticenter, prospective study. Hepatology 2010; 52(6): 2065‒76.

Jaiswal P, Attar BM, Yap JE, Devani K, Jaiswal R, Wang Y, et al. Acute liver failure with amiodarone infusion: A case report and systematic review. J Clin Pharm Ther 2018; 43(1): 129‒33.

Lahbabi M, Aqodad N, Ibrahimi A, Lahlou M, Aqodad H. Acute hepatitis secondary to parenteral amiodarone does not pre-clude subsequent oral therapy. World J Hepatol 2012; 4(6): 196‒8.

Hahn KJ, Morales SJ, Lewis JH. Enoxaparin-Induced Liver In-jury: Case Report and Review of the Literature and FDA Ad-verse Event Reporting System (FAERS). Drug Saf Case Rep 2015; 2(1): 17.

Hui CK, Yuen MF, Ng IOL, Tsang KW, Fong GC, Lai CL. Low molecular weight heparin-induced liver toxicity. J Clin Phar-macol 2001; 41(6): 691-4.

Arora N, Goldhaber SZ. Anticoagulants and transaminase ele-vation. Circulation 2006; 113(15): e698‒e702.

Harrill AH, Roach J, Fier I, Eaddy JS, Kurtz CL, Antoine DJ, et al. The effects of heparins on the liver: application of mecha-nistic serum biomarkers in a randomized study in healthy vol-unteers. Clin Pharmacol Ther 2012; 92(2): 214‒20.

Wild SH, Byrne CD. ABC of obesity: risk factors for diabetes and coronary heart disease. BMJ 2006; 333(7576): 1009‒11.

Zheng J, Woo SL, Hu X, Botchlett R, Chen L, Huo Y, Wu C. Metformin and metabolic diseases: a focus on hepatic aspects. Front Med 2015; 9(2): 173‒86.

Firneisz G. Non-alcoholic fatty liver disease and type 2 diabe-tes mellitus: the liver disease of our age? World J Gastroenter-ol 2014; 20(27): 9072‒89.

Saeedi Saravi SS, Hasanvand A, Shahkarami K, Dehpour AR. The protective potential of metformin against acetaminophen-induced hepatotoxicity in BALB/C mice. Pharm Biol 2016; 54(12): 2830‒7.

Ling S, Shan Q, Liu P, Feng T, Zhang X, Xiang P, et al. Metfor-min ameliorates arsenic trioxide hepatotoxicity via inhibiting mitochondrial complex I. Cell Death Dis 2017; 8(11): e3159.

Tan S, Vollmar N, Benson S, Sowa JP, Bechmann LP, Gerken G, et al. Liver injury indicating fatty liver but not serologic NASH marker improves under metformin treatment in poly-cystic ovary syndrome. Int J Endocrinol 2015; 2015: 254169.

Crowley MJ, Diamantidis CJ, McDuffie JR, Cameron CB, Stanifer JW, Mock CK, et al. Clinical outcomes of metformin use in populations with chronic kidney disease, congestive heart fail-ure, or chronic liver disease: a systematic review. Ann Intern Med 2017; 166(3): 191‒200.

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2021/03/04
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