Introduction

Patients with non-alcoholic fatty liver disease (NAFLD) are at a higher risk of developing cardiovascular disease (CVD).

Aims & Methods

This study aimed to determine if there is an association between increased steatosis and fibrosis with a higher risk of CVD in patients with diabetes mellitus (DM). This study enrolled 288 patients with DM who were over 40 years of age, between January and August 2023, after excluding viral hepatitis, cirrhosis, and cancers. Patients provided written informed consent and underwent clinical measurements and answered questions about their past medical history. The following measurements and data were taken: body weight (BW), body mass index (BMI), waist circumference (WC), laboratory data, presence of hypertension, dyslipidemia, alcohol consumption, and smoking. The degree of steatosis was estimated using the fatty liver index {FLI, (e^{(0.953×ln(triglyceride, TG)+0.139×BMI+0.718×ln(gamma-glutamyltrasnsferase, GGT)+0.053×WC-15.745)})/(1+ e^{(0.953×ln(TG)+0.139×BMI+0.718×ln(GGT)+0.053×WC-15.745)})×100}, hepatic steatosis index {HSI, 8x(alanine aminotransferase (ALT)/aspartate aminotransferase (AST) ratio+BMI (+2, if female; +2, if diabetes mellitus)}, and controlled attenuation parameter (CAP by FibroScan^®). The degree of fibrosis was estimated using the fibrosis-4 (FIB-4) index, NAFLD fibrosis score (NFS), and liver stiffness (LS by FibroScan^®). CVD was defined as ischemic heart disease or hemorrhagic or ischemic stroke. The past history of CVD was asked and reported by trained nurses and chart review.

Results

The mean age was 60±9 years old, and the proportion of males was 54.9% (n=158). The mean CAP and LS values were 273±48 dB/m and 6.8±3.5 kPa, respectively. The CAP values were correlated with BW (r=0.473, p<0.001), BMI (r=0.618, p<0.001), WC (r=0.565, p<0.001), FLI (r=0.603, p<0.001), and HSI (r=0.622, p<0.001). The LS values were correlated with BW (r=0.230, p<0.001), BMI (r=0.446, p<0.001), WC (r=0.371, p<001), and FIB-4 (r=0.419, p<0.001). The LS values were not correlated with NFS. Ninety three (32.3%) patients had CVD and 57 patients were male. The mean age (62±9 vs. 58±9 years, p=0.001), BW (73.2±13.2 vs. 69.1±12.9 kg, p=0.013), BMI (27±4.1 vs. 25.6±3.7 kg/m², p=0.004), and WC (91.5±10 vs. 87.7±9.6 cm, p=0.002) were higher in patients with CVD than in those without CVD. The prevalence of HTN (81.7% vs. 41.5%, p<0.001) and dyslipidemia (75.3% vs. 61.5%, p=0.021) were also higher in patients with CVD. However, the prevalence of alcohol consumption (18.3% vs. 26.7%) and smoking (48.4% vs. 47.7%) were not different between the two groups. The CAP value (275±48 vs. 271±49 dB/m), FLI (51±29 vs. 43±27), and HSI (39±6 vs. 38±6) were not different between the two groups. The LS value (7.4±3.8 vs. 6.5±3.3 kPa, p=0.049) and FIB-4 (1.5±0.9 vs. 1.2±0.7, p=0.006) were higher in patients with CVD than those without CVD. However, NFS (-0.8±1.2 vs. -1.1±3.1, p=0.335) was not different between the two groups. Multivariate logistic regression analysis revealed that age [odds ratio (OR): 1.059, 95% confidence interval (CI): 1.023-1.095, p=0.001], hypertension (OR: 4.843, 95% CI: 2.611-8.985, p<0.001), and BW (OR: 1.032, 95% CI: 1.008-1.056, p=0.008) were significant risk factors for CVD. However, the LS and FIB-4 were not risk factors for CVD.

Conclusion

In contrast to the steatosis, the fibrosis estimated by LS and FIB-4 were associated with the risk of CVD in patients with DM. However, multivariate analysis did not show the LS and FIB-4 as risk factors for CVD.

Introduction

Patients with diabetes mellitus (DM) are at increased risk of developing cardiovascular disease (CVD). Hepatic fibrosis is common among patients with DM and is associated with liver-related events. However, its impact on CVD risk remains unclear.

Aims & Methods

This study aimed to prospectively assess the association between hepatic fibrosis and CVD risk in patients with DM.
A total of 323 patients with DM were prospectively enrolled from January 2022, excluding those with viral hepatitis, overt cirrhosis, or cancer. Clinical measurements and CVD history were recorded. The following parameters were assessed: body weight (BW), body mass index (BMI), waist circumference (WC), laboratory data [aspartate aminotransferase, alanine aminotransferase (ALT), gamma-glutamyl transferase, platelet count, hemoglobin A1C, cholesterol, and triglycerides], presence of hypertension (HTN), dyslipidemia, alcohol consumption, smoking status, liver steatosis measured by the controlled attenuation parameter (CAP) using FibroScan®, and current anti-DM medications. Hepatic fibrosis was quantified by liver stiffness measurement (LSM) using FibroScan®, assessed at baseline and after two years. CVD was defined as ischemic heart disease or ischemic/hemorrhagic stroke.

Results

A total of 277 patients completed the two-year follow-up and underwent repeat LSM. The mean age was 57±12 years, and 56.3% were male. The baseline mean LSM was 6.9±3.7 kPa. A history of CVD was present in 86 (31%) patients, while 6 (3.2%) developed new CVD events during follow-up. Among the new CVD cases, 3 were cardiac events, and 3 were neurovascular events. LSM decreased in 157 patients (d-LSM group) and increased in 120 patients (i-LSM group). The mean LSM change was -1.7±2 kPa in the d-LSM group and +1.5±1.3 kPa in the i-LSM group. The d-LSM group had significantly higher baseline ALT (39±30 vs. 32±21 IU/L, p=0.018), CAP (281±51 vs. 264±49 dB/m, p=0.005), and LSM (7.9±4.2 vs. 5.7±2.3 kPa, p<0.001) than the i-LSM group. Alcohol consumption was more prevalent in the i-LSM group (30.8% vs. 17.8%., p=0.011). There were no significant differences between the two groups in mean age (57±13 vs. 57±10 years, p=0.738), male proportion (51.6% vs. 62.5%, p=0.07), BW (72±16 vs. 72±14 kg, p=0.93), BMI (26.7±4.7 vs. 26.1±4.1 kg/m², p=0.233), WC (90±12 vs. 89±10 cm, p=0.816), HTN (58% vs. 48.3%, p=0.111), dyslipidemia (68.2% vs. 62.5%, p=0.326), laboratory results excluding ALT, or smoking status (45.2% vs. 49.2%, p=0.515). The use of metformin (91.1% vs. 95.8%, p=0.121), pioglitazone (1.9% vs. 2.5%, p=1.0), and insulin (7% vs. 9.2%, p=0.51) did not differ significantly between the two groups. When stratified by LSM change, the incidence of new CVD was 2% (1/49) in patients with a decrease LSM of ≤-2 kPa, 2% (4/198) in those with changes between -2 and +2 kPa, and 3.3% (1/30) in those with an increase of ≥+2 kPa (p=0.897).

Conclusion

Hepatic fibrosis, as measured by LSM, can change dynamically in patients with DM. Although this was an observational study, a decrease in LSM was not associated with a reduced risk of CVD. Therefore, LSM monitoring may have limited value in assessing CVD risk in this population.

Introduction

Patients with diabetes mellitus (DM) are at an increased risk of developing cardiovascular disease (CVD). Hepatic steatosis is common among patients with DM, but its impact on CVD risk remains unclear.

Aims & Methods

This study aimed to prospectively assess the association between a reduction in hepatic steatosis and a lower risk of CVD in patients with DM.
A total of 323 patients with DM were prospectively enrolled from January 2022, after excluding those with viral hepatitis, overt cirrhosis, and cancer. Clinical measurements and CVD history were recorded. The following parameters were assessed: body weight (BW), body mass index (BMI), waist circumference (WC), laboratory data (aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, platelet count, hemoglobin A1C, cholesterol, and triglycerides), presence of hypertension (HTN), dyslipidemia, alcohol consumption, smoking status, liver stiffness measurement (LSM by FibroScan®), and current anti-DM medications. Hepatic steatosis was quantified using the controlled attenuation parameter (CAP) measured by FibroScan® at baseline and after two years. CVD was defined as ischemic heart disease or ischemic/hemorrhagic stroke.

Results

A total of 277 patients completed the two-year follow-up and underwent repeat CAP assessment. The mean age was 57±12 years, and 56.3% were male. The baseline mean CAP was 274±18 dB/m. A history of CVD was present in 86 (31%) patients, while 6 (3.2%) developed new CVD events during follow-up. Among the new CVD cases, 3 were cardiac events, and 3 were neurovascular events. CAP scores decreased in 176 patients (d-CAP group) and increased in 101 patients (i-CAP group). The mean CAP change was -33±29 dB/m in the d-CAP group and +24±18 dB/m in the i-CAP group. The mean age was higher in the d-CAP group than in the i-CAP group (58±12 vs. 55±12 years, p=0.012). The baseline mean CAP was higher in the d-CAP group than in the i-CAP group (284±50 vs. 255±47 dB/m, p<0.001). There were no significant differences in male proportion (58% vs. 53.5%, p=0.468), BW (71±14 vs. 73±17 kg, p=0.258), BMI (26.1±4.2 vs. 27±4.9 kg/m², p=0.14), WC (89±10 vs. 90±12 cm, p=0.397), laboratory data, HTN (56.8% vs. 48.5%, p=0.182), dyslipidemia (66.5% vs. 64.4%, p=0.72), alcohol consumption (24.4% vs. 21.8%, p=0.616), smoking status (48.9% vs. 43.6%, p=0.395), or baseline LSM (6.9±3.8 vs. 6.9±3.5 kPa, p=0.988) between the two groups. The use of metformin (93.2% vs. 93.1%, p=0.972) and pioglitazone (2.3% vs. 2%, p=1.0) did not differ significantly, but insulin use was lower in the d-CAP group than in the i-CAP group (5.1% vs. 12.9%, p=0.022). When stratified by CAP change, the incidence of new CVD was 0% (0/55) in patients with CAP reduction of ≤-40 dB/m, 2% (4/201) in those with changes between -40 and +40 dB/m, and 9.5% (2/21) in those with CAP increases of ≥+40 dB/m (p=0.037).

Conclusion

Hepatic steatosis, as measured by CAP, can change dynamically in patients with DM. Although this was an observational study, a marked decrease in CAP score was associated with a lower risk of CVD in patients with DM. Therefore, CAP monitoring may be a valuable tool for assessing CVD risk. Efforts to reduce hepatic steatosis, as reflected by CAP reduction, may contribute to CVD prevention in this population.

Introduction

Patients with nonalcoholic fatty liver disease (NAFLD) have a higher risk of chronic kidney disease (CKD).

Aims & Methods

This study aimed to investigate whether the degree of steatosis and fibrosis is associated with an increased risk of CKD in patients with diabetes mellitus (DM). Between January and August 2023, 324 patients with DM were enrolled in the study, after excluding those with viral hepatitis, cirrhosis, and any cancers. Patients provided written informed consent, underwent several clinical measurements, and provided past medical histories. Body weight (BW), body mass index (BMI), waist circumference (WC), laboratory variables including serum creatinine and estimated glomerular filtration rate {eGFR, 175 × Serum Cr^-1.154× age^-0.203 × 1.212 (if patient is black) × 0.742 (if female)}, presence of hypertension, and dyslipidemia were investigated. The degree of steatosis was estimated using the fatty liver index {FLI, (e^{(0.953×ln(triglyceride, TG)+0.139×BMI+0.718×ln(gamma-glutamyltrasnsferase, GGT)+0.053×WC-15.745)})/(1+ e^{(0.953×ln(TG)+0.139×BMI+0.718×ln(GGT)+0.053×WC-15.745)})×100}, hepatic steatosis index {HSI, 8x(alanine aminotransferase (ALT)/aspartate aminotransferase (AST) ratio+BMI (+2, if female; +2, if diabetes mellitus)}, and controlled attenuation parameter (CAP by FibroScan^®). The degree of fibrosis was estimated using fibrosis-4 (FIB-4) index, NAFLD fibrosis score (NFS), and liver stiffness (LS by FibroScan^®). CKD was defined as eGFR less than 60 mL/min/1.73m².

Results

The mean age of the patients was 57±12 years, and 54.9% (n=178) were male. The mean CAP and LS values were 276±50 dB/m and 7.0±3.7 kPa, respectively. CAP values were correlated with BW (r=0.524, p<0.001), BMI (r=0.625, p<0.001), WC (r=0.592, p<0.001), FLI (r=0.637, p<0.001), and HSI (r=0.653, p<0.001). LS values were correlated with BW (r=0.364, p<0.001), BMI (r=0.531, p<0.001), WC (r=0.46, p<001), and FIB-4 (r=0.3, p<0.001), but not correlated with NFS. Twenty-nine (8.9%) patients had CKD, of whom 14 were male. Patients with CKD were older (mean age: 63±11 vs. 56±12 years, p=0.005) and had a higher prevalence of hypertension (79.3% vs. 49.8%, p=0.002) compared to those without CKD. AST (29±22 vs. 30±20 IU/L), ALT (36±39 vs. 37±27 IU/L), GGT (40±30 vs. 44±73 IU/L), and HbA₁C (7.3±1.3 vs. 7.3±1.4%) were not different between the two groups. The prevalence of dyslipidemia (75.9% vs. 63.4%), BW (73±15 vs. 72±15 kg), BMI (28±4 vs. 27±5 kg/m²), and WC (92±11 vs. 90±11 cm) were also not different between the two groups. CAP value (273±55 vs. 276±50 dB/m), FLI (49±29 vs. 48±29), and HSI (40±7 vs. 39±7) were not different between the two groups. LS value (7.0±2.2 vs. 7.0±3.8 kPa), NFS (-1.0±1.3 vs. -1.2±2.6), and FIB-4 (1.3±0.6 vs. 1.2±0.8) were also not different between the two groups. Multivariate logistic analysis revealed that age [odds ratio (OR): 1.047, 95% confidence interval (CI): 1.008-1.088, p=0.019] and hypertension (OR: 3.260, 95% CI: 1.274-8.339, p<0.014) were the independent risk factors for CKD.

Conclusion

The steatosis estimated by CAP and the fibrosis estimated by LS were not associated with the risk of CKD in patients with DM.

Introduction

As the most common form of chronic liver disease, the increasing prevalence of non-alcoholic fatty liver disease (NAFLD) is a global concern. NAFLD and obesity are independently related to an increased risk for atherosclerotic cardiovascular disease (ASCVD), the primary cause of mortality in NAFLD patients. Even though many subjects with NAFLD are normal weight, it still remains uncertain whether their ASCVD risk is of major importance.

Aims & Methods

The aim of this study is to assess and compare the ASCVD risk between lean and obese patients with NAFLD. Normal weight and obese patients were evaluated between January 2020 and February 2023 and their data was analyzed. NAFLD was diagnosed by vibration-controlled transient elastography (VCTE) with controlled attenuation parameter (CAP) and the American College of Cardiology/American Heart Association guidelines was used to evaluate the ASCVD risk. Moreover, medical history and biochemical data were collected.

Results

In total, 221 patients were included in the final analysis. In the obese group, 164 (63.8%) patients were diagnosed with NAFLD, compared to 57 (12.3%) in the lean population. In comparison to those with obese NAFLD, subjects with lean NAFLD had significantly higher ASCVD scores (mean 15.3% vs 22.7%, p<0.001). Moreover, subjects with lean NAFLD and significant liver fibrosis had a higher risk of ASCVD events, compared to their obese counterparts (OR, 2.51 vs 1.95, p=0.034). On the other hand, in terms of liver stiffness measurements, the prevalence of at least significant liver fibrosis was substantially higher in the obese group. Regarding the presence of the components of the metabolic syndrome, the prevalence of type 2 diabetes mellitus was higher the obese group, while changes in the lipid profile and higher systolic blood pressure were more frequently found in lean subjects.

Conclusion

The ASCVD scores of subjects with lean NAFLD were significantly higher than those with obese NAFLD. The presence of significant liver fibrosis was a notable risk factor associated with an ASCVD event in both study groups, but the effects were more pronounced in individuals with a low body mass index.​

Introduction

Patients with type 2 diabetes (T2D) have a high prevalence of non-alcoholic fatty liver disease (NAFLD) (1). The most validated non-invasive method to assess liver steatosis and fibrosis is transient elastography (TE), whereas some new ultrasound-based technologies still lack substantial clinical evidence in this setting (2,3). In this line we aimed to evaluate performance of Shear Wave Measurement (SWM) and Attenuation (ATT) Measurement by Fujifilm to diagnose liver steatosis and fibrosis in the cohort of patients with T2DM, using TE as the reference.

Aims & Methods

Consecutive outpatients with T2D (N=147) were referred for controlled attenuation parameter (CAP) and liver stiffness measurements (LSM) to assess the presence of liver steatosis and fibrosis by using TE. The presence of any grade of liver steatosis was considered in patients with CAP≥297 dB/m, and advanced fibrosis in those with LSM≥10 kPa by TE, which served as the reference method (4,5). All consented patients also underwent SWM and ATT (by Fujifilm Arietta 65), as the investigated methods, and their results were compared to LSM and CAP as measured by TE. All measurements were performed in fasting patients, whereas patients with conditions that might have influenced the results of LSM (ALT>5xULN, congestive liver disease, biliary obstruction, infiltrative liver neoplasms) were excluded.

Results

Of 147 included patients with T2D, 76 (51.7%) were females, average age 66, median Body Mass Index 30.5 kg/m², 113 (76,9%) had arterial hypertension, 111 (75,5%) dyslipidemia, 27 (18.4%) were smokers, 26 (17.7%) reported risky alcohol consumption. As for TE, M probe was used in 104 (70.7%) patients, median LSM was 5.9 kPa, median CAP 290 dB/m. Any grade of steatosis (CAP≥297 dB/m) was detected in 62 (42,2%) patients, and advanced fibrosis (LSM≥10 kPa) in 17/145 (11.6%) patients by using TE. Median SWM was 5.5 kPa, and median ATT 0.62 dB/cm/MHz. We observed good correlation between LSM as measured by TE and SWM (Pearson's R=0.68, 95 CI: 0.58-0.76, p<0,001), whereas SWM produced lower (mean -0,7 unit, Bland-Altman) LSM values in comparison to TE. SWM had AUROC of 0.905 at the LSM cut-off ≥ 8.3 kPa (Youden) to diagnose advanced fibrosis (sen. 76.5%, specif. 93.8%). LSM by SWM optimized for ruling-in and ruling-out advanced fibrosis were respectively ≥10.1 kPa (specif. 97%) and <6.2 kPa (sens. 94.1%). Presence of advanced fibrosis would be missed in 23.5%, 41.2% and 5.8% patients by using reported LSM cut-offs (≥ 8.3, ≥10.1 and <6,2 kPa respectively). In multivariate analysis only platelet count (OR 0.979; CI 0.96-0.998, p=0.03) and LSM as measured by TE (OR 1.197; CI 1.031-1.391, p=0.02) were significantly associated with LSM measured by SWM. Correlation between ATT and CAP was poor (Pearson' R=0.31, 95 CI: 0.16-0.45, p<0.001), as was the overall diagnostic performance of ATT to diagnose any grade of liver steatosis (AUROC 0.673 at the cut-off ≥0.66 dB/cm/MHz (Youden); sens. 56.5%, specif. 75.3%). ATT cut-offs optimized for ruling-in and ruling-out any steatosis were ≥0.75 dB/cm/MHz (specif. 89.4%), and <0.50 dB/cm/MHz (sens. 88.7%) respectively. Presence of any steatosis would be missed in 43.5%, 62.9% and 11.2% by using reported ATT cut-offs (≥0.66, ≥0.75 and <0.50 dB/cm/MHz respectively).

Conclusion

SWM reliably recognizes presence of advanced liver fibrosis in patients with T2D. The diagnostic performance of ATT was suboptimal, and this should be further investigated by using more reliable reference methods, such as liver biopsy or magnetic resonance.

References

1. Leite NC, Villela-Nogueira CA, Pannain VLN et al. Histopathological stages of non-alcoholic fatty liver disease in type 2 diabetes: Prevalences and correlated factors. Liver Int. 2011 doi: 10.1111/j.1478-3231.2011.02482.x.
2. Tovo CV, Villela-Nogueira CA, Leite NC, Panke CL, Port GZ, Fernandes S, et al. Transient hepatic elastography has the best performance to evaluate liver fibrosis in non-alcoholic fatty liver disease (NAFLD). Annals of Hepatology [Internet]. 2019 May [cited 2019 Dec 6];18(3):445–9.
3. Dietrich C, Bamber J, Berzigotti A, Bota S, Cantisani V, Castera L, et al. EFSUMB Guidelines and Recommendations on the Clinical Use of Liver Ultrasound Elastography, Update 2017 (Long Version). Ultraschall in der Medizin - European Journal of Ultrasound. 2017 Apr 13;38(04):e16–47.
4. Petroff D, Blank V, Newsome PN, Shalimar, Voican CS, Thiele M, et al. Assessment of hepatic steatosis by controlled attenuation parameter using the M and XL probes: an individual patient data meta-analysis. The Lancet Gastroenterology & Hepatology. 2021 Mar;6(3):185–98.
5. Franchis R de, Bosch J, Garcia-Tsao G, Reiberger T, Ripoll C, Abraldes JG, et al. Baveno VII – Renewing consensus in portal hypertension. Journal of Hepatology [Internet]. 2021 Dec 29;0(0). Available from: https://www.journal-of-hepatology.eu/article/S0168-8278(21)02299-6/fulltext

Introduction

Fatty liver is sensitive to ischemia-reperfusion injury [1, 2]. At the microcirculatory level, the structural and functional properties of red blood cells (RBCs) play a key role, since the degree of hypoxia in liver tissue depends on their ability to deform, tendency to form aggregates, and hemolysis [3], which, in turn, is a factor in fibrogenesis [4].

Aims & Methods

Research objective is as follows: To study the associations of viscoelastic, electrical parameters of RBCs and levels of FAs of their membranes, serum in patients with fatty liver disease.
84 men (average age 48.4±13.9 years) with fatty liver disease (FLD) of various genesis (alcoholic, non-alcoholic, of mixed genesis: alcoholic+metabolic), various necroinflammatory activity with fibrosis F0-1 (FibroScan® 502 (Echosens, France) have been examined. The study of RBC electrical, viscoelastic parameters has been performed by dielectrophoresis. The content of FAs in RBC membranes and blood serum has been determined using gas chromatography-mass spectrometry (Agilent 7000B, USA).

Results

It has been found, that RBC indices reflecting their deformation ability (amplitude of deformation at 10⁶ Hz, degree of deformation at 0.5x10⁶ Hz), membrane state (capacitance), surface charge value (dipole moment, speed of cell movement to electrodes), RBC resistance (polarisability) were directly correlated with the levels of n-3 PUFAs in RBC membranes, blood serum, both their total content and concentrations of individual FAs (C20:5n-3, C22:5n-3, C22:6n-3), the level of monounsaturated oleic FAs, as well as two SFAs (C15:0, 17:0). On the contrary, the associations with the predominant part of SFAs, both individual (especially highly accurate: with C16:0, C18:0) and total content, MUSAs, USAs, including ratios of n-6/n-3 PUFAs, SFAs/UFAs, SFAs/PUFAs, were inverse (p=0,02-0,0000001).
The summarized rigidity was related with high strength of association and statistical significance to RBC content of C16:0 (r=0.674, p<0.000001), C18:0 (r=0.443, p<0.000006), C18:2n-6 (r=0.345, p=0.0006) FAs, total SFAs (r=0.640, p<0.000001), the ratios of n-6/n-3 PUFAs (r=0.605, p<0.000001), SFAs/PUFAs (r=0.428, p=0.000015).
Correlations with RBC levels of C16:0 (r=0.551, p<0.000001), C18:2n-6 (r=0.470, p=0.000042) were the closest for membrane conductivity levels, total SFAs (r=0.484, p<0.000001), USAs (r=0.468, p<0.000001), MUSAs (r=0.504, p<0.000001), n-6 PUFA (r=0.414, p=0.00003), as well as for ratio of n-6/n-3 PUFAs (r=0.568, p<0.000001).
Associations of high strength and statistical significance for RBC aggregation index have been found concerning RBC C16:0 (r=0.691, p<0.000001), C18:0 (r=0.486, p<0.000001), for the total UFAs' content (r=0.672, p<0.000001), the ratios n-6/n-3 PUFAs (r=0.611, p<0.000001), SFAs/UFAs (r=0.475, p<0.000001), SFAs/PUFAs (r=0.478, p<0.000001).
RBC destruction indices have been found to be directly related to the total UFAs' content in both RBC membranes and serum, RBC levels of C20:3n-6 (r=0.205, p=0.046), and inversely related to the content of C15:0 (r=-0.224, p=0.028), C17:0 (r=-0.151, p=0.039) and C18:1;c9 (r=-0.206, p=0.045).

Conclusion

The identified associations indicate a dependence of RBC parameters on the levels and ratios of FAs in their membranes, serum. Deterioration of blood rheological properties in patients with FLD is a factor associated with increasing hypoxia in liver tissue with potential for fibrogenesis and progression. The ability to modulate electrical, viscoelastic parameters of RBCs by exposure of FAs, including dietary FAs, defines new additional treatment targets for patients with FLD.

References

1. Farrell GC, Teoh NC, McCuskey RS. Hepatic microcirculation in fatty liver disease. Anat Rec (Hoboken). 2008 Jun;291(6):684-92. DOI: 10.1002/ar.20715
2. Patrono D, De Stefano N, Vissio E, et al. How to Preserve Steatotic Liver Grafts for Transplantation. J Clin Med. 2023 Jun 12;12(12):3982. DOI: 10.3390/jcm12123982
3. Brun JF, Varlet-Marie E, Myzia J, et al. Metabolic Influences Modulating Erythrocyte Deformability and Eryptosis. Metabolites. 2021 Dec 21;12(1):4. DOI: 10.3390/metabo12010004
4. Ramalho FS, Fernandez-Monteiro I, Rosello-Catafau J, Peralta C. Hepatic microcirculatory failure. Acta Cir Bras. 2006;21 Suppl 1:48-53. doi: 10.1590/s0102-86502006000700012