Letter to the Editor An absence of atherosclerosis progression in a type 2 diabetic patient with multiple atherosclerotic risk factors, complicated with liver cirrhosis Hidetaka Hamasaki a , Hidekatsu Yanai a,b, ⁎ a Department of Internal Medicine, National Center for Global Health and Medicine Kohnodai Hospital, Chiba, Japan b Clinical Research Center, National Center for Global Health and Medicine Kohnodai Hospital, Chiba, Japan article info Article history: Received 13 November 2013 Accepted 28 December 2013 Available online 10 January 2014 Keywords: Atherosclerosis Liver cirrhosis Platelet activation Type 2 diabetes To the Editor: Non-alcoholic fatty liver disease, which is a common comorbidity of type 2 diabetes, is recognized as one of the important risk factors for atherosclerosis and cardiovascular diseases (CVDs) [1]. However, patients with other chronic liver diseases have been reported to show a low prevalence of CVD and coronary atherosclerosis [2]. The underly- ing mechanisms for a low prevalence of atherosclerotic diseases in chronic liver diseases remain obscure. We have certified that we comply with the Principles of Ethical Publishing in the International Journal of Cardiology. A 50-year-old woman diagnosed as having type 2 diabetes and liver cirrhosis was admitted to our hospital for the evaluation of diabetic complications. She developed type 2 diabetes four years ago when she was admitted to our hospital for treatment for abdominal ascites due to alcoholic cirrhosis. She has been repeatedly hospitalized for treatment for diabe- tes since then. She has been treated with insulin therapy three years ago, and the total daily dose of insulin has been increasing gradually. On the admission, her height was 154.7 cm and weight 73.6 kg (body mass index was 30.7 kg/m 2 ). Her systolic and diastolic blood pressures were 107 and 67 mm Hg, respectively. The computed to- mography of abdominal fat demonstrated her visceral fat area was 234.2 cm 2 , suggesting the existence of severe visceral obesity (Fig. 1). She has smoked 40 tobaccos a day since she was ten years old. Her serum level of high-density lipoprotein cholesterol was significantly de- creased to 29 mg/dL (normal range: 40–85 mg/dL) and triglyceride was elevated to 157 mg/dL (normal range: 30–149 mg/dL). Her plasma glu- cose and HbA1c levels were significantly elevated to 481 mg/dL (normal range: 80–112 mg/dL) and 9.0% (normal range: 4.8–6.2%), respectively. In spite of a great amount of daily insulin use (total daily insulin dose, 190 units), her urinary C-peptide level was relatively high (157 μg/day, normal range: 29.2–167 μg/day), suggesting the existence of severe in- sulin resistance. She had multiple severe risk factors for atherosclerosis such as smoking, severe visceral obesity, severe insulin resistance, poor blood glucose control and dyslipidemia [3]. However, the brachial- ankle pulse wave velocity was 1198 cm/s (right) and 1177 cm/s (left), and augmentation index was 51%, denying the existence of evident atherosclerosis and/or arteriosclerosis. Stenosis and plaques were not detected in bilateral carotid arteries, and the intima-media thick- ness (IMT) of the carotid artery was 0.66 mm (right) and 0.68 mm (left) (Fig. 2), supporting the absence of atherosclerosis progression. She had severe thrombocytopenia due to liver cirrhosis and her platelet count significantly decreased to 3.5 × 10 4 /μL (normal range: 15.0–35.0 × 10 4 /μL). An increase in systemic platelet activation has been reported to be associated with atherosclerotic diseases by inducing inflammation and atherogenesis [4]. Platelet activation induces the formation of arachidonic acid which promotes vasocon- striction and platelet aggregation [5], contributing to atherosclerosis progression. Her serum arachidonic acid (86.4 μg/mL, normal range: 135.7–335.3 μg/mL) was significantly low. Serum platelet-derived growth factor (971 pg/mL, normal range: 942–7366 pg/mL) which leads to atherosclerosis progression was relatively low [6], possibly due to the small number of platelets. In conclusion, we experienced a type 2 diabetic patient with multiple atherosclerotic risk factors who showed an absence of athero- sclerosis progression, possibly due to severe thrombocytopenia by liver cirrhosis. Our observation indicates a significance of platelet activation for atherosclerosis progression. References [1] Brea A, Puzo J. Non-alcoholic fatty liver disease and cardiovascular risk. Int J Cardiol 2013;167:1109–17. [2] Otsubo R, Higuchi Mde L, Gutierrez PS, et al. Influence of chronic liver disease on coronary atherosclerosis vulnerability features. Int J Cardiol 2006;109:387–91. International Journal of Cardiology 172 (2014) e253–e254 ⁎ Corresponding author at: Department of Internal Medicine and Clinical Research Center, National Center for Global Health and Medicine Kohnodai Hospital, 1-7-1 Kohnodai, Chiba 272-8516, Japan. Tel.: +81 47 372 3501; fax: +81 47 372 1858. E-mail address: dyanai@hospk.ncgm.go.jp (H. Yanai). 0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.265 Contents lists available at ScienceDirect International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard