Abstract
Background: The levels and function of circulating progenitor cells (CPCs) may be affected by chronic metabolic diseases. Aim: To investigate the levels and functions of CPCs in patients with non-alcoholic fatty liver disease (NAFLD) and coronary artery disease (CAD). Methods: In this retrospective study, patients (n=82) undergoing elective coronary angiography for diagnosis of CAD were included. NAFLD was defined as presence of hepatic steatosis by ultrasound in the absence of other causes of liver disease and excessive alcohol use. After coronary angiography, patients were divided into NAFLD with CAD (n=24), NAFLD without CAD (n=13), only CAD (n=31) and Non-NAFLD and Non-CAD (n=14). CPCs were quantified by flow cytometry based on the expression of (CD34+, CD133+, CD34+CD133+) in presence or absence of the hematopoietic marker (CD45). We assessed serum levels of angiogenic growth factors (AGFs) (pg/ml) by Multiplex assay. Results: The levels of the CD45-CD34+ and CD45-CD133+ were higher in NAFLD patients with CAD (median, 15% and 2%, respectively) than NAFLD patients without CAD (median, 9% and 1%, respectively, all p ≤ 0.05). After age adjustment, only CD45-CD34+ circulating progenitor cells remain associated with increased risk of CAD in patients with NAFLD [OR: 8.71 (1.21-62.51)]. In contrast, the levels of the serum vascular endothelial growth factor-C (VEGF-C) was lower in NAFLD patients with CAD (median, 69 pg/ml) than NAFLD without CAD (median, 146 pg/ml) (p=0.01). Conclusions: Our results indicate that high levels of non-hematopoietic CPCs and low levels of AGFs may be associated with increased risk of CAD in NAFLD patients.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is regarded as the most common form of chronic liver disease in the United States and likely globally [1,2]
Clinical and laboratory data was collected for each patient, and subjects without NAFLD or coronary artery disease (CAD) were considered to be controls
BMI and Triglyceride levels were significantly higher in patients with NAFLD
Summary
Non-alcoholic fatty liver disease (NAFLD) is regarded as the most common form of chronic liver disease in the United States and likely globally [1,2]. NAFLD prevalence is estimated to be between 10 and 38% of the general population [3,4]. It is considered to be the hepatic manifestation of the metabolic syndrome [5,6]. The most common cause of morbidity and mortality among NAFLD patients is CVD, and this is generally mediated by early atherosclerosis. Previous studies have suggested that a common pathogenic mechanism exists between NAFLD and CVD [7,8,9]. The levels and function of circulating progenitor cells (CPCs) may be affected by chronic metabolic diseases
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