Non-alcoholic fatty liver disease increases the risk of biochemical recurrence in high-grade metastatic prostate cancer patients

Author(s):  
Jie Cui ◽  
Wei zhang ◽  
Zhenlong Wang ◽  
Yanxiang Chang ◽  
Hongyi Zhang

Abstract Background Non-alcoholic fatty liver disease (NAFLD) has been reported to be helpful to identify high-risk individuals of developing prostate cancer. In the retrospective cohort study, our aim is to investigate the relationship between NAFLD and biochemical recurrence in metastatic prostate cancer patients. Methods We retrospectively investigated 602 patients with metastatic prostate cancer receiving androgen deprivation therapy. Liver fat was estimated with liver-to-spleen ratio by CT scans. The relationship between NAFLD and biochemical recurrence was investigated with Cox models. The model for biochemical recurrence was adjusted for multiple variables. Results NAFLD was significantly associated with biochemical recurrence in patients with Gleason score ≥ 4 + 3 when adjusting for each of body mass index (hazards ratio [HR] = 1.38; 95% confidence interval [CI] = 1.08–1.77; p = 0.01), visceral adipose tissue (HR = 1.36; 95% CI = 1.07–1.74; p = 0.01), hypertension (HR = 1.41; 95% CI = 1.10–1.80; p = 0.01) and diabetes mellitus (HR = 1.42; 95% CI = 1.11–1.82; p = 0.01), using age and prostate-specific antigen level as potential confounder. The 2-year biochemical recurrence rate in Gleason score ≥ 4 + 3 patients with and without NAFLD was 84.0% (100/119) and 72.2% (130/180), respectively (p = 0.018). The median biochemical recurrence free survival of Gleason score ≥ 4 + 3 patients with and without NAFLD were 17 and 21 months, respectively (p = 0.005). Conclusions NAFLD is an independent risk factor for biochemical recurrence in patients with high-grade metastatic prostate cancer. If validated in prospective studies, future research should test whether treatment of NAFLD can lead to better prognosis.

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Benedetta M. Motta ◽  
Christoph Grander ◽  
Martin Gögele ◽  
Luisa Foco ◽  
Vladimir Vukovic ◽  
...  

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is characterized by triglyceride accumulation in the hepatocytes in the absence of alcohol overconsumption, commonly associated with insulin resistance and obesity. Both NAFLD and type 2 diabetes (T2D) are characterized by an altered microbiota composition, however the role of the microbiota in NAFLD and T2D is not well understood. To assess the relationship between alteration in the microbiota and NAFLD while dissecting the role of T2D, we established a nested study on T2D and non-T2D individuals within the Cooperative Health Research In South Tyrol (CHRIS) study, called the CHRIS-NAFLD study. Here, we present the study protocol along with baseline and follow-up characteristics of study participants. Methods Among the first 4979 CHRIS study participants, 227 individuals with T2D were identified and recalled, along with 227 age- and sex-matched non-T2D individuals. Participants underwent ultrasound and transient elastography examination to evaluate the presence of hepatic steatosis and liver stiffness. Additionally, sampling of saliva and faeces, biochemical measurements and clinical interviews were carried out. Results We recruited 173 T2D and 183 non-T2D participants (78% overall response rate). Hepatic steatosis was more common in T2D (63.7%) than non-T2D (36.3%) participants. T2D participants also had higher levels of liver stiffness (median 4.8 kPa, interquartile range (IQR) 3.7, 5.9) than non-T2D participants (median 3.9 kPa, IQR 3.3, 5.1). The non-invasive scoring systems like the NAFLD fibrosis score (NFS) suggests an increased liver fibrosis in T2D (mean − 0.55, standard deviation, SD, 1.30) than non-T2D participants (mean − 1.30, SD, 1.17). Discussion Given the comprehensive biochemical and clinical characterization of study participants, once the bioinformatics classification of the microbiota will be completed, the CHRIS-NAFLD study will become a useful resource to further our understanding of the relationship between microbiota, T2D and NAFLD.


BMJ Open ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. e039804
Author(s):  
Chen Huanan ◽  
Li Sangsang ◽  
Adwoa Nyantakyiwaa Amoah ◽  
Bo Yacong ◽  
Chen Xuejiao ◽  
...  

ObjectiveNon-alcoholic fatty liver disease (NAFLD) is one of the major causes of liver-related diseases but relationship between triglyceride glucose (TyG) and NAFLD in the elderly is not reported yet. In this study, we investigated the role of TyG index for predicting the incidence of NAFLD in the elderly.Design and settingThis is a prospective cohort study in Henan, China, from 2011 to 2018.Participants and methodsIn total, 46 693 elderly who participated in a routine physical examination programme from 2011 to 2018 were included in this study. TyG index was calculated as ln (fasting triglyceride (mg/dL)×fasting plasma glucose (mg/dL)/2), while NAFLD was defined as hepatic steatosis after excluding other causes based on the results of abdominal ultrasonography; Cox regression model was performed to explore the relationship between TyG index and NAFLD. Also, mediation effect was used to analyse the role of the TyG index in WHtR (waist-to-height ratio) and NAFLD.ResultsDuring the 149 041 person-years follow-up, a total of 5660 NAFLD events occurred (3.80/100 person-years). After adjusting for potential confounding factors, quartiles 4 of TyG index significantly increased the incidence of NAFLD compared with quartile 1, the HRs and 95% CI were 1.314 (1.234 to 1.457). In addition, TyG index played a partial mediating role in the relationship between WHtR and NAFLD and indirect effect was 1.009 (1.006 to 1.011).ConclusionHigher TyG index was associated with higher risk of NAFLD in the aged, and therefore, TyG index may be a novel predictor for incidence of NAFLD. Further, regular examination and evaluation of the TyG index might be useful for controlling the occurrence of NAFLD.


Diabetologia ◽  
2019 ◽  
Vol 63 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Martijn C. G. J. Brouwers ◽  
Nynke Simons ◽  
Coen D. A. Stehouwer ◽  
Aaron Isaacs

Abstract Non-alcoholic fatty liver disease (NAFLD) is highly prevalent among individuals with type 2 diabetes. Although epidemiological studies have shown that NAFLD is associated with cardiovascular disease (CVD), it remains unknown whether NAFLD is an active contributor or an innocent bystander. Plasma lipids, low-grade inflammation, impaired fibrinolysis and hepatokines are potential mediators of the relationship between NAFLD and CVD. The Mendelian randomisation approach can help to make causal inferences. Studies that used common variants in PNPLA3, TM6SF2 and GCKR as instruments to investigate the relationship between NAFLD and coronary artery disease (CAD) have reported contrasting results. Variants in PNPLA3 and TM6SF2 were found to protect against CAD, whereas variants in GCKR were positively associated with CAD. Since all three genes have been associated with non-alcoholic steatohepatitis, the second stage of NAFLD, the question of whether low-grade inflammation is an important mediator of the relationship between NAFLD and CAD arises. In contrast, the differential effects of these genes on plasma lipids (i.e. lipid-lowering for PNPLA3 and TM6SF2, and lipid-raising for GCKR) strongly suggest that plasma lipids account for their differential effects on CAD risk. This concept has recently been confirmed in an extended set of 12 NAFLD susceptibility genes. From these studies it appears that plasma lipids are an important mediator between NAFLD and CVD risk. These findings have important clinical implications, particularly for the design of anti-NAFLD drugs that also affect lipid metabolism.


2014 ◽  
Vol 8 (4) ◽  
pp. e356-e363 ◽  
Author(s):  
Mehmet Boyraz ◽  
Nihal Hatipoğlu ◽  
Erkan Sarı ◽  
Arzu Akçay ◽  
Necati Taşkın ◽  
...  

2021 ◽  
Vol 74 (4) ◽  
pp. 1007-1010
Author(s):  
Tetyana V. Koval ◽  
Ivan V. Chopey ◽  
Mykhaylo M. Hechko ◽  
Artur V. Kurakh

The aim: To analyze the relationship between non-alcoholic fatty liver disease and changes in the gut microbiota. Materials and methods: The publications of domestic and foreign editions in the databases of the United European Gastroenterology (UEG) Journal, PubMed, MEDLINE, Web of Science were processed and analyzed. Conclusions: In recent years, non-alcoholic fatty liver disease was placed among the important diseases in gastroenterology. During this time, more and more data appear on the link between changes in the human intestinal microbiome and the development of metabolic diseases, including NAFLD. Contemporary research has indeed found evidence of such a relationship. Thus, some strains of microorganisms have been identified in more detail, which directly or indirectly affect the development or course of the above-mentioned disease. For a better understanding of the strategies for the treatment of pathologies, it is necessary to delve into the study of etiological factors, therefore, NAFLC cannot be considered a pathology that has been sufficiently studied. Indeed, recent data indicate that the development and severity of the course of the disease are not always associated with the physiological processes already known to us.


Author(s):  
Xiongfeng Pan ◽  
Atipatsa C. Kaminga ◽  
Jihua Chen ◽  
Miyang Luo ◽  
Jiayou Luo

The magnitude of the effect of fetuin-A and fetuin-B on non-alcoholic fatty liver disease (NAFLD) remains undefined. Therefore, the aim of this study was to synthesize previous findings to obtain a reliable estimation of this relationship. This study was registered in PROSPERO with the number CRD42019126314. Studies published not later than March 2019, examining the relationship between fetuin-A, fetuin-B, and NAFLD, were identified by a systematic search in the electronic databases of the Web of Science, PubMed, Embase, and Cochrane Library. Pooled estimates of standardized mean difference (SMD), calculated using the random-effects model in a meta-analysis, were applied to estimate the strength of the association between fetuin-A, fetuin-B, and NAFLD. Thirty publications were identified and analyzed based on specified inclusion criteria. Collectively, they consisted of 3800 NAFLD participants and 3614 controls. Compared with the controls, significant higher values of the fetuin-A (SMD = 0.83, 95% CI: 0.59 to 1.07, Z = 6.82, p < 0.001) and fetuin-B (SMD = 0.18, 95% CI: 0.02 to 0.33, Z = 2.27, p = 0.023) were observed in NAFLD patients. Meanwhile, in the subgroup analysis, the effect value of fetuin-A in the NASH group was significantly higher than that in the NAFL group (p = 0.036). The findings of this study suggest that elevated fetuin-A and fetuin-B may independently indicate the occurrence of NAFLD. Nevertheless, further research is needed to confirm these results.


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