Ailevi hiperkolesterolemisi olan kişilerde non-alkolik yağlı karaciğer hastalığı

Yıl 2020, , 219 - 224, 01.06.2020

Aynur Arslan , Özgür Şimşek , Aykut Turhan , Ayşe Çarlıoğlu , Şenay Arıkan Durmaz , Mustafa Utlu , Emine Kartal

https://doi.org/10.21601/ortadogutipdergisi.722778

Öz

Amaç: Karaciğer, kolesterol sentezinde ve katabolizmasında çok önemli rol oynar. Non-alkolik yağlı karaciğer hastalığı (NAYKH), gelişmiş ülkelerde kronik karaciğer hastalığının en sık sebebidir ve sıklıkla diabetes mellitus, hipertansiyon, dislipidemi ve obezite gibi metabolik hastalıklarla komorbidite gösterir. Bu çalışmanın amacı Ailevi Hiperkolesterolemide (AH) NAYKH görülme sıklığını araştırmaktır.
Gereç ve Yöntemler: 2017-2018 yılları arasında Erzurum Bölge Eğitim ve Araştırma Hastanesi Endokrinoloji Polikliniğine başvurmuş olan AH’li kişiler tek merkezli bu vaka kontrol çalışmasına alındı. AH’li toplam 30 kişi (17 Kadın 13 erkek), 39 kişiden oluşan (30 kadın, 9 erkek) kontrol grubu ile karşılaştırıldı. İki grup sayı ve cinsiyet yönünden denkti. Aile öyküsü kaydedildi. Tanı kan tetkikleri ve karaciğer ultrasonografisi ile kondu.
Bulgular: İki grup arasında yaş ve cinsiyet açısından anlamlı fark görülmedi. NAYKH, kontrol grubundaki 39 kişiden 12’sinde saptanırken, AH grubunda 30 kişiden 16’sında görüldü (p = 0,058). AH ve kontrol gruplarının sırasıyla toplam kolesterol (333,27 ± 58,46) (219,23 ± 82,84) (mg / dl) (p = 0,000), LDL (249,93 ± 45,43) (127,11 ± 46,52) (mg / dl) (p = 0,000) ve CRP (3,37 ± 4,16) (1,43 ± 1,96) (mg / L) (p = 0,014) düzeyleri arasında anlamlı fark bulundu.
Sonuçlar: AH ve kontrol grupları arasında NAYKH açısından anlamlı bir fark yoktur. Ultrasonografide NAYKH saptanmaması, AH’ye yaklaşımdaki ciddiyeti azaltmamalıdır.

Anahtar Kelimeler

hiperkolesterolemi, non alkolik yağlı karaciğer hastalığı, ultrasonografi

Non-alcoholic fatty liver disease in patients with familial hypercholesterolemia

Öz

Aim: The liver plays a crucial role in the synthesis and catabolism of cholesterol. Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the developed world and commonly associated with metabolic comorbidities such as diabetes mellitus, hypertension, dyslipidemia, and obesity. The aim of this study was to investigate the frequency of NAFLD in Familial Hypercholesterolemia (FH).
Material and Method: Between 2017 and 2018, individuals with FH who had been referred to the Department of Endocrinology at Erzurum Regional Training and Research Hospital were admitted to this single center case-control study. Total 30 individuals (17 female and 13 male) who have FH were compared to a control group included 39 participants (30 female and 9 male). The two groups were thought to be well matched in terms of sample size and gender distribution. Family history was registered. Diagnosis is made by blood tests and ultrasound imaging of liver.
Results: The two groups showed no significant differences in terms of age and gender. NAFLD was seen at 12 of 39 individuals in the control group. It was seen at 16 of 30 persons in the FH group (p = 0.058). Total cholesterol (mg / dl) (333.27 ± 58.46) (219.23 ± 82.84) (p = 0.000), LDL (mg / dl) (249.93 ± 45.43) (127.11 ± 46.52) (p = 0.000) and CRP (mg / L) (3.37 ± 4.16) (1.43 ± 1.96) (p = 0.014) levels were significantly different between the FH and control groups respectively.
Conclusion: There isn’t a significant difference between control and FH groups in terms of NAFLD. The absence of NAFLD on ultrasonography, should not reduce the severity and importance of FH, and the treatments should be made to prevent complications such as atherosclerosis.

Anahtar Kelimeler

hypercholesterolemia, non-alcoholic fatty liver disease, ultrasonography

Kaynakça

• Defesche JC, Gidding SS, Harada-Shiba M, Hegele RA, Santos RD, Wierzbicki AS. Familial hypercholesterolaemia. Nat Rev Dis Prim 2017; 7: 17093. (doi: 10.1038/nrdp.2017.93).
• Benedict M, Zhang X. Non-alcoholic fatty liver disease: An expanded review. World J Hepatol 2017; 9: 715-32. (doi: 10.4254/wjh.v9.i16.715).
• Younossi ZM, Blissett D, Blissett R, Henry L, Stepanova M, Younossi Y, et al. The economic and clinical burden of nonalcoholic fatty liver disease in the United States and Europe. Hepatology 2016; 64: 1577-86. (doi: 10.1002/hep.28785).
• Parekh S, Anania FA. Abnormal Lipid and Glucose Metabolism in Obesity: Implications for Nonalcoholic Fatty Liver Disease. Gastroenterology 2007; 132: 2191-207. (doi: 10.1053/j.gastro.2007.03.055).
• Rader DJ, Hobbs HH. Disorders of Lipoprotein Metabolism. In: Harrison’s Principles of Internal Medicine, LongoDL. Harrison TR, et al (eds). 18th ed. New York, NY: McGraw-Hill Medical; 2012: Chapter 356.
• Abdelmalek MF, Diehl AM. Nonalcoholic Fatty Liver Diseases and Nonalcoholic Steatohepatitis. In: Harrison’s Principles of Internal Medicine, Longo DL. Harrison TR, et al (eds). 19th ed. New York, NY: McGraw-Hill Medical; 2019; Chapter 364.
• Theise ND. Liver and gallbladder. In: Robbins & Cotran Pathologic Basis of Disease, Kumar V, Abbas A, Aster J (eds). 9th ed. Philadelphia, PA: Elsevier Saunders; 2015; 845-6.
• McCullough AJ. The clinical features, diagnosis and natural history of nonalcoholic fatty liver disease. Clin Liver Dis 2004; 8: 521-33. (doi: 10.1016/j.cld.2004.04.004).
• Saadeh S, Younossi ZM, Remer EM, et al. The utility of radiological imaging in nonalcoholic fatty liver disease. Gastroenterology 2002; 123: 745-50. (doi: 10.1053/gast.2002.35354).
• Assy N, Kaita K, Mymin D, Levy C, Rosser B, Minuk G. Fatty infiltration of liver in hyperlipidemic patients. Dig Dis Sci 2000; 45: 1929-34. (doi: 10.1023/a:1005661516165).
• Gokalp D, Tuzcu A, Bahceci M, Arikan S, Pirinccioglu AG, Bahceci S. Levels of proinflammatory cytokines and hs-CRP in patients with homozygous familial hypercholesterolaemia. Acta Cardiol 2009; 64: 603-9. (doi: 10.2143/AC.64.5.2042689).
• Nambi V, Ballantyne CM. Utility of statin therapy using high-sensitivity C-reactive protein as an indicator of coronary heart disease risk. Curr Atheroscler Rep 2005; 7: 22-8. (doi: 10.1007/s11883-005-0071-8).
• Cheng HM, Ye ZX, Chiou KR, Lin SJ, Charng MJ. Vascular stiffness in familial hypercholesterolaemia is associated with C-reactive protein and cholesterol burden. Eur J Clin Invest 2007; 37: 197-206. (doi: 10.1111/j.1365-2362.2007.01772.x).
• Brouwers MCGJ, Bilderbeek-Beckers MAL, Georgieva AM, van der Kallen CJH, van Greevenbroek MMJ, de Bruin TWA. Fatty liver is an integral feature of familial combined hyperlipidaemia: relationship with fat distribution and plasma lipids. Clin Sci 2007; 112: 123-30. (doi: 10.1042/CS20070314).
• Choi SH, Ginsberg HN. Increased very low density lipoprotein (VLDL) secretion, hepatic steatosis, and insulin resistance. Trends Endocrinol Metab 2011; 22: 353-63. (doi: 10.1016/j.tem.2011.04.007).
• Kirvar A, Ayaz T, Durakoglugil T, Baydur Sahin S, Sahin OZ, Durakoglugil E. The Association Between Non-Alcoholic Fatty Liver Disease with Carotid Intima Media Thickness. The Journal of Kartal Training and Research Hospital 2015; 26: 13-8. (doi: 10.5505/jkartaltr.2015.13284).
• Sun D-Q, Liu W-Y, Wu S-J, et al. Increased levels of low-density lipoprotein cholesterol within the normal range as a risk factor for nonalcoholic fatty liver disease. Oncotarget 2016; 7: 5728-37. (doi: 10.18632/oncotarget.6799).
• Imamoglu M. Classification of Hepatosteatosis with Ultrasonography and Analysis of the Effect of Hepatosteatosis Degree. Medical Journal of Mugla Sitki Kocman University, 2015; 2: 23-8.
• DeFilippis AP, Blaha MJ, Martin SS, et al. Nonalcoholic fatty liver disease and serum lipoproteins: The Multi-Ethnic Study of Atherosclerosis. Atherosclerosis 2013; 227: 429-36. (doi: 10.1016/j.atherosclerosis.2013.01.022).
• Lee L, Alloosh M, Saxena R, et al. Nutritional model of steatohepatitis and metabolic syndrome in the Ossabaw miniature swine. Hepatology 2009; 50: 56-67. (doi: 10.1002/hep.22904).
• Wouters K, van Gorp PJ, Bieghs V et al. Dietary cholesterol, rather than liver steatosis, leads to hepatic inflammation in hyperlipidemic mouse models of nonalcoholic steatohepatitis. Hepatology 2008; 48: 474-86. (doi: 10.1002/hep.22363).