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    • Different from our study results

    2019-04-15

    Different from our study results, a Korean study that enrolled 3827 patients showed that PC and MS were associated in women only. The possible explanations for this discrepancy were different population composition and a larger sample size compared with our current study. Also, our study showed that the association between PC and MS was less significant for participants above 60 years of age, especially in men. Older patients of each ethnicity consistently have lower PC than young adults, and the phenomenon may be explained by a survival advantage to having lower PC or diminished hematopoietic stem-cell reserve. Accordingly, the linkage between PC and MS in elderly patients might be weakened, but the curiously needs to be further elucidated. The role of PC in patients with fatty liver is intriguing. Obesity is characterized by chronic inflammation and associated with an increased risk of fatty liver, and insulin resistance is a universal finding in the disease. Meanwhile, PC is independently associated with insulin resistance, and the decrease in PC observed in obesity patients after bariatric surgery may reflect decreased hepatic inflammation. In contrast, a linear decrease of PC with increasing histological severity of hepatic fibrosis in fatty liver is noticed, especially in conditions of nonalcoholic steatohepatitis. PC is included in several noninvasive scores, which reveal a negative correlation with fibrotic levels in patients with fatty liver diseases. While MS is related to PC and fatty liver, the relationship between PC among patients with MS with or without fatty liver was not clarified. Based on this study, we found that PC was positively related with MS after adjustment for BMI, age, and gender. After dividing patients by the status of fatty liver, PC was still correlated with MS (Table 3). Our study demonstrated a J curve phenomenon between PC and MS, which is consistent with the concept that extreme values of PC are related to cardiovascular diseases. However, the phenomenon did not apply to the relationship between PC and fatty liver. The exact mechanism is not fully elucidated. However, previous studies showed that the grade of steatosis might reduce with the progression of hepatic fibrosis and reduced PC in patients with fatty liver disease. It may explain the lower PC being paired with increased fibrosis and reduced steatosis. The strengths of this study were the large sample size and detailed biochemical data, which provide robust evidence to elucidate the correlation between PC and MS. However, several limitations need to be addressed. First, our study population had a high socioeconomic status, and could afford the expense of a physical check-up in a medical center. Whether the results of this study could represent the general population in Taiwan requires further studies to be validated. Second, alcohol consumption was not recorded and assessed. However, the prevalence of alcoholism was reported to be 1.5% in Taiwanese communities; therefore, it might have little influence on the result. Third, PC can be influenced by other factors, including infection, medication, and hematological diseases. Given that the patients received physical check-ups in the hospital, the incidence of acute infection should be minimal. The incidence of drug-induced thrombocytopenia was also low, at about one or two cases per 100,000 per year. Primary hematological diseases account for <5% of patients with elevated PC. These factors might have had only a little impact on the current study. Fourth, whether patients had diabetes mellitus, hypertension, or dyslipidemia was unknown and whether they took medication to control these diseases was not documented, either. Fifth, the gold standard for the diagnosis of fatty liver is liver biopsy. However, the invasiveness of that procedure means that it is not feasible for the general population. The lack of biopsy results also prevented us from further analyzing the influence of fibrosis severity. In the present study, the diagnosis of fatty liver was made by ultrasonography and defined by at least two of three abnormal findings: diffusely increased echogenic liver greater than kidney or spleen, vascular blurring, and deep attenuation of ultrasound signal with a sensitivity of 89% and specificity of 93%.