Serum fetuin-A Levels Research Articles

Assessment of serum fetuin-A and its gene polymorphism as a marker of insulin resistance in polycystic ovary syndrome

Background/aim Polycystic ovary syndrome (PCOS) is a prevalent endocrine condition affecting 5–10% of reproductive-aged women, the cause of which is unknown. Chronic anovulation, polycystic ovaries, and hyperandrogenism are symptoms of PCOS. It is linked to hirsutism, obesity, and increased probability of cardiovascular disease, metabolic syndrome, and diabetes mellitus. A risk factor for cardiovascular disease is PCOS that is undiagnosed or untreated. Our aim in this study is to investigate serum fetuin-A level and its gene as potential biomarkers for screening of insulin resistance in PCOS. Patients and methods This study involved 100 female participants from outpatient clinic, Department of Obstetrics and Gynecology, Zagazig University Hospital, Egypt. They were split into two groups (each 50). The first group included healthy fertile women without symptoms of hyperandrogenemia as a control. The second group included women with PCOS. Fasting blood sugar levels, cholesterol, high-density lipoprotein cholesterol and triglycerides have been estimated by enzymatic colorimetric technique while low-density lipoprotein cholesterol was calculated. Enzyme-linked immunosorbent assays have been used to measure serum concentrations of luteinizing hormone, follicular-stimulating hormone, testosterone, and fetuin-A, while PCR has been used to extract DNA and genotype common functional polymorphisms in fetuin-A. Results The present results revealed a considerable rise in glucose, insulin, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), cholesterol, triglyceride, low-density lipoprotein cholesterol, luteinizing hormone, testosterone, and fetuin-A and significant decrease in follicular-stimulating hormone and high-density lipoprotein cholesterol in PCOS patients. Also, there was significant higher frequency of the fetuin-A gene variant rs1071592 AA genotype and A allele compared to controls. Conclusions Fetuin-A has a potential diagnostic value as a biomarker for insulin resistance in PCOS associated with metabolic syndrome. Additionally, ‘CG’ allele can be considered a risk factor for PCOS.

Humoral and cellular factors inhibit phosphate-induced vascular calcification during the growth period.

Hyperphosphatemia is an independent and non-classical risk factor of cardiovascular disease and mortality in patients with chronic kidney disease (CKD). Increased levels of extracellular inorganic phosphate (Pi) are known to directly induce vascular calcification, but the detailed underlying mechanism has not been clarified. Although serum Pi levels during the growth period are as high as those observed in hyperphosphatemia in adult CKD, vascular calcification does not usually occur during growth. Here, we have examined whether the defence system against Pi-induced vascular calcification can exist during the growth period using mice model. We found that calcification propensity of young serum (aged 3 weeks) was significantly lower than that of adult serum (10 months), possibly due to high fetuin-A levels. In addition, when the aorta was cultured in high Pi medium in vitro, obvious calcification was observed in the adult aorta but not in the young aorta. Furthermore, culture in high Pi medium increased the mRNA level of tissue-nonspecific alkaline phosphatase (TNAP), which degrades pyrophosphate, only in the adult aorta. Collectively, our findings indicate that the aorta in growing mouse may be resistant to Pi-induced vascular calcification via a mechanism in which high serum fetuin-A levels and suppressed TNAP expression.

Alpha 2-Heremans-Schmid glycoprotein gene polymorphism (rs4918) is associated with coronary artery calcification in incident peritoneal dialysis patients.

Coronary artery calcification (CAC) is a common and severe complication in peritoneal dialysis (PD) patients, and it progresses in a majority of patients. Fetuin-A, encoded by the alpha 2-Heremans-Schmid glycoprotein (AHSG) gene, is a serum calcification inhibitor. The study aimed to examine the role of AHSG gene polymorphism rs4918 in CAC and CAC progression of PD patients. Incident PD patients at Huashan Hospital Fudan University in China from August 2007 to July 2018 were recruited in this prospective study and followed up for 2 years. Patients underwent CAC measurements at recruitment and 2 years later. AHSG gene polymorphism rs4918 and serum fetuin-A were determined at baseline. The demographic characteristics, clinical data, and laboratory data were collected during the follow-up period. Binary logistic regression was performed to explore the association between rs4918 with CAC and CAC progression. A total of 202 PD patients (112 men, 55.4%) were recruited, with a mean age of 54 ± 16 years. The multivariate logistic regression identified genotype GG as an independent risk factor that correlates to CAC (odds ratio [OR]=2.153; 95% CI: 1.182-3.925; p=.012) and CAC progression (OR=2.482; 95% CI: 1.422-4.330; p=.001). The serum fetuin-A level was influenced by the rs4918 variants of AHSG, with a dose-dependent effect depending on the number of the G allele. AHSG gene polymorphism rs4918 affects serum fetuin-A levels and is significantly associated with both CAC and CAC progression in a cohort of patients receiving PD.

Serum fetuin-A and RANKL levels in patients with early stage breast cancer.

Breast cancer (BC) is the primary cause of mortality due to cancer in females around the world. Fetuin-A is known to increase metastases over signals and peroxisomes related with growing. Receptor activator of nuclear factor-kB ligand (RANKL) takes part in cell adhesion, and RANKL inhibition is used in the management of cancer. We aimed to examine the relationship between serum fetuin-A, RANKL levels, other laboratory parameters and clinical findings in women diagnosed with early stage BC, in our population. Women having early stage BC (n=117) met our study inclusion criteria as they had no any anti-cancer therapy before. Thirty-seven healthy women controls were also confirmed with breast examination and ultrasonography and/or mammography according to their ages. Serum samples were stored at -80°C and analysed via ELISA. Median age of the patients was 53 (range: 57-86) while it was 47 (range: 23-74) in the healthy group. Patients had lower high-density lipoprotein levels (p=0.002) and higher neutrophil counts (p=0.014). Fetuin-A and RANKL levels did not differ between the groups (p=0.116 and p=0.439, respectively) but RANKL leves were found to be lower in the favorable histological subtypes (p=0.04). In this study, we found no correlation between serum fetuin-A levels and clinical findings in patients diagnosed with early stage BC. However, RANKL levels are found to be lower in subgroups with favorable histopathologic subtypes such as tubular, papillary and mucinous BC and there was statistically significant difference.

Post-translational modifications glycosylation and phosphorylation of the major hepatic plasma protein fetuin-A are associated with CNS inflammation in children.

Fetuin-A is a liver derived plasma protein showing highest serum concentrations in utero, preterm infants, and neonates. Fetuin-A is also present in cerebrospinal fluid (CSF). The origin of CSF fetuin-A, blood-derived via the blood-CSF barrier or synthesized intrathecally, is presently unclear. Fetuin-A prevents ectopic calcification by stabilizing calcium and phosphate as colloidal calciprotein particles mediating their transport and clearance. Thus, fetuin-A plays a suppressive role in inflammation. Fetuin-A is a negative acute-phase protein under investigation as a biomarker for multiple sclerosis (MS). Here we studied the association of pediatric inflammatory CNS diseases with fetuin-A glycosylation and phosphorylation. Paired blood and CSF samples from 66 children were included in the study. Concentration measurements were performed using a commercial human fetuin-A/AHSG ELISA. Of 60 pairs, 23 pairs were analyzed by SDS-PAGE following glycosidase digestion with PNGase-F and Sialidase-AU. Phosphorylation was analyzed in 43 pairs by Phos-TagTM acrylamide electrophoresis following alkaline phosphatase digestion. Mean serum and CSF fetuin-A levels were 0.30 ± 0.06 mg/ml and 0.644 ± 0.55 μg/ml, respectively. This study showed that serum fetuin-A levels decreased in inflammation corroborating its role as a negative acute-phase protein. Blood-CSF barrier disruption was associated with elevated fetuin-A in CSF. A strong positive correlation was found between the CSF fetuin-A/serum fetuin-A quotient and the CSF albumin/serum albumin quotient, suggesting predominantly transport across the blood-CSF barrier rather than intrathecal fetuin-A synthesis. Sialidase digestion showed increased asialofetuin-A levels in serum and CSF samples from children with neuroinflammatory diseases. Desialylation enhanced hepatic fetuin-A clearance via the asialoglycoprotein receptor thus rapidly reducing serum levels during inflammation. Phosphorylation of fetuin-A was more abundant in serum samples than in CSF, suggesting that phosphorylation may regulate fetuin-A influx into the CNS. These results may help establish Fetuin-A as a potential biomarker for neuroinflammatory diseases.

The Correlation between Fetuin-A Levels And Nafld Fibrosis Score (NFS)

Abstract. Fetuin-A is a plasma glycoprotein expressed in the liver. Fatty liver accumulation because changing fetuin-A expression leads to nonalcoholic fatty liver disease (NAFLD). The benefits of serum fetuin-A as a predictor of fibrosis biomarkers in NAFLD patients remain unclear. Non-invasive scoring system predicting fibrosis among patients with NAFLD is the NAFLD fibrosis score (NFS). Objective. This study aims to find the correlation between circulating fetuin-A levels and NFS in NAFLD patients. Methods. Eighty subjects (male, 52; female, 26) followed this cross-sectional study. NAFLD is diagnosed with an abdominal ultrasound. The serum levels of fetuin-A measured by ELISA. NFS is used to identify the probability of fibrosis in subjects. The correlation between Fetuin-A levels and NFS was determined using Pearson correlation tests. A p-value < 0.05 was significant. Results. There was significant difference in fetuin-A levels (p < 0.001) between NAFLD degree I (421.71 pg/mL), NAFLD degree II (494.88 pg/mL), and NAFLD degree III (692 pg/mL). The NFS low probability score in 46 subjects and NFS indeterminate score in 34 subjects. Serum concentrations of fetuin-A correlate significantly with NFS (r = 0.478, p < 0.001). Conclusion. There is a positive correlation between serum levels of fetuin-A and NFS.

Evaluation of Fetuin-A level in diabetic retinopathy

BackgroundDiabetic retinopathy (DR) is a micro-vascular consequence of diabetes mellitus (DM) that manifests clinically as retinal ischemia, neovascularization, altered retinal permeability, and macular edema. In the adult population, DR is now considered a leading cause of blindness. Fetuin-A is a multifunctional glycoprotein that, because of its dual role in insulin resistance and angiogenesis, could be an early trigger of DR pathogenesis.ObjectiveThis study aimed to evaluate the level of Fetuin-A in diabetic patients with and without retinopathy and demonstrate if it could be used as an early indicator of DR.Patients and methodsA case–control study enrolled 45 participants selected from Al-Zahraa University Hospital, between March 2021 and October 2021, they were divided into three groups: Group 1: healthy control group (n=15); Group 2: type 2 diabetic patients without DR (n=15); and Group 3: type 2 diabetic patients with DR (n=15). All groups were age- and sex-matched and were investigated by enzyme-linked immunosorbent assay (ELISA) to evaluate serum level of Fetuin-A.ResultsThere was a highly significant difference of FBG, 2HPP, and HbA1c between the studied groups (p< 0.001), while there was no significant difference between the three studied groups regarding Fetuin-A. There were no significant correlation between Fetuin-A, glycemic parameters, and diabetic duration in Groups 2 and 3.ConclusionFetuin-A has no significant role in the pathogenesis of diabetic retinopathy.

Serum Calcification Propensity T50 Associates with Disease Severity in Patients with Pseudoxanthoma Elasticum.

Pseudoxanthoma elasticum (PXE) is a currently intractable genetic disorder characterized by progressive ectopic calcification in the skin, eyes and arteries. Therapeutic trials in PXE are severely hampered by the lack of reliable biomarkers. Serum calcification propensity T50 is a blood test measuring the functional anticalcifying buffer capacity of serum. Here, we evaluated T50 in PXE patients aiming to investigate its determinants and suitability as a potential biomarker for disease severity. Fifty-seven PXE patients were included in this cross-sectional study, and demographic, clinical, imaging and biochemical data were collected from medical health records. PXE severity was assessed using Phenodex scores. T50 was measured using a validated, nephelometry-based assay. Multivariate models were then created to investigate T50 determinants and associations with disease severity. In short, the mean age of patients was 45.2 years, 68.4% was female and mean serum T50 was 347 min. Multivariate regression analysis identified serum fetuin-A (p < 0.001), phosphorus (p = 0.007) and magnesium levels (p = 0.034) as significant determinants of T50, while no correlations were identified with serum calcium, eGFR, plasma PPi levels or the ABCC6 genotype. After correction for covariates, T50 was found to be an independent determinant of ocular (p = 0.013), vascular (p = 0.013) and overall disease severity (p = 0.016) in PXE. To conclude, shorter serum T50—indicative of a higher calcification propensity—was associated with a more severe phenotype in PXE patients. This study indicates, for the first time, that serum T50 might be a clinically relevant biomarker in PXE and may thus be of importance to future therapeutic trials.

High Fetuin-A Levels in Children with Celiac Disease

Fetuin-A is a multifunctional non-collagen protein that plays a role in bone mineralization. Celiac disease is a chronic inflammatory disorder of the small intestine due to exposure to gluten. In this research, it was aimed to investigate levels of Fetuin-A and its relationship with bone mineral density in children with celiac disease. The study was conducted on 59 children with celiac and 29 healthy children. The celiac disease group was composed of three groups, newly diagnosed, gluten-free diet compliant and, non- gluten- free diet compliant patients. Serum Fetuin-A concentrations were measured by an enzyme-linked immuno- sorbent assay kit. Measurement of bone mineral density was performed a dual-energy x-ray absorptiometry. Serum Fetuin-A levels were 136.85 ± 38.09 μg/L and 112.95 ± 44.39 μg/L in the celiac disease and healthy control groups, respectively. There was a statistically significant difference between groups in levels of serum Fetuin-A (P < .05). A significant positive correlation was observed between serum Fetuin-A and bone mineral density Z-score in the celiac patients. Increased Fetuin-A levels and positive correlation between Fetuin-A and bone mineral density in children with celiac disease suggest that Fetuin-A may be a biomarker for celiac disease.

Differential Diagnosis between Takotsubo Syndrome and Acute Coronary Syndrome-A Prospective Analysis of Novel Cardiovascular Biomarkers for a More Selective Triage.

Introduction: Takotsubo syndrome (TTS) is clinically indistinguishable from an ACS. Despite the implementation of clinical scoring systems and novel biomarkers, coronary angiography currently remains necessary for differential diagnosis. Methods: 93 patients with chest pain and the suspicion of TTS were enrolled in two study centers. Fetuin-A, IGFBP-2, Galectin-3, and TNF α were determined in serum samples, collected within 24 h after the onset of symptoms. Serum levels of biomarkers were analyzed for the differential diagnostic value between TTS and ACS. Results: Compared to TTS, patients with ACS had significantly lower serum levels of Fetuin-A and IGFBP-2. The cut-off value of Fetuin-A for the identification of TTS compared to ACS was 55.74 μg/mL (sensitivity: 100.0%, specificity: 82.6%, PPV: 63.2%, NPV: 100.0%). An optimal cut-off value for IGFBP-2 for the differential diagnosis between TTS and ACS was determined as 171.77 ng/mL (sensitivity: 76.0%, specificity: 82.6%, PPV: 76.4%, NPV 72.7%). Conclusion: Fetuin-A and IGFBP-2 might facilitate the triage between TTS and ACS and could be therefore of great benefit for the guidance of treatment.

Serum fetuin-A level is independent of Helicobacter pylori postinfection status in systemic lupus erythematosus.

Helicobacter pylori is a common pathogen causing gastric inflammation and malignancy. Fetuin-A is a multifunctional protein that is involved in the regulation of calcification, insulin resistance and inflammation. Reports on serum levels of fetuin-A in acute H. pylori infection are contradictory. We intended to see whether H. pylori post-infection status has a long-term effect on serum fetuin-A levels in a well-characterized series of systemic lupus erythematosus cases. In this cross-sectional study 117 patients with systemic lupus erythematosus were enrolled. Helicobacter infection status and serum fetuin-A concentration were determined by ELISA and radial immunodiffusion, respectively. H. pylori positive patients had higher serum fetuin-A concentration than negative ones: 517 (456-603) vs. 476 (408-544) mg L-1, median (25-75% percentiles), P = 0.020. No other parameters differed between these groups. During univariate regression analysis fetuin-A levels were associated with Erythrocyte sedimentation rate (ESR), White blood cell count (WBC), C-reactive protein (CRP), serum total protein, albumin, and the SLEDAI index at the time of diagnosis but only serum albumin remained a significant determinant in multivariate regression study.

IDF21-0491 The effects of HIIT and MICT on glycemic control and serum levels of fetuin-A in type 2 diabetic patients

Background: Regular physical activity is a key element in the management of type 2 diabetes. Cytokines play a central role in the therapeutic effects of exercise. Fetuin-A, as a hepatokine, with known effects on carbohydrate metabolism, is affected by exercise and possibly its intensity in healthy individuals and increased in plasma of patients with type 2 diabetes.

Evaluation of the serum visfatin eotaxin and fetuin-A levels of patients with type 2 diabetes mellitus

Objective: The aim of this study was to determine the serum visfatin, eotaxin and fetuin-A levels in patients with normal BMI and overweight type 2 diabetes mellitus (T2DM).&#x0D; Material and Method: This study perform in 30 T2DM patients and in 20 healthy subjects. Test subjects were divided into four groups as two diabetics and two controls. Diabetics with a body mass index (BMI) of 26.2-29.9 kg/m2 were included in the overweight diabetic group (OD), and those with a body mass index of 20.9-24.9 kg/m2 were included in the normal BMI diabetic group (ND). The volunteers in the control group were also divided into two groups as overweight (OC) and normal BMI (NC). Smoking and alcohol users were not included in the study. In addition, patients with significant diabetic complications such as retinopathy, hypertension, neuropathy, renal failure, and cardiovascular disease were excluded from the study. The serum visfatin eotaxin and fetuin-A levels were measured using the ELISA method. The Mann-Whitney U test was used to compare the data of the groups, while Spearman’s analysis was applied for the correlations.&#x0D; Results: The visfatin levels of the OD and ND were significantly higher compared to those of their control groups (p

Serum levels of fetuin-A as a novel biomarker for disease activity in patients with Takayasu arteritis and granulomatous polyangiitis.

The aim of the present study was to investigate serum fetuin-A (Fet-A) levels in patients with Takayasu arteritis (TA) and granulomatous polyangiitis (GPA) and to analyze the relationship between serum Fet-A levels and disease activity scores. Thirty-two TA and 28 GPA patients presented to the rheumatology clinic at Gazi University and met the criteria of American College of Rheumatology 1990 and 2012 International Chapell Hill meeting, respectively, and 20 healthy control subjects were included in the present study. We collected data on serum C-reactive protein (CRP), albumin, calcium, and phosphate levels as well as erythrocyte sedimentation rates. Calcification risk index (CRI) was calculated for each patient. The Birmingham Vasculitis Activity Score (BVAS) and Indian Takayasu Clinical Activity Score (ITAS), were used to assess disease activity in GPA and TA patients respectively. Serum Fet-A levels were significantly lower in the overall vasculitis group compared to control group (p = 0.015). In subgroup analysis, Fet-A levels were significantly lower in those with active disease, compared to control group (p = 0.001, for active TA (n = 18) and GPA (n = 17), respectively). However, there was no significant difference in serum Fet-A levels in inactive cases versus control subjects (p = 0.061, for inactive TA (n = 14) and GPA (n = 11), respectively). Serum Fet-A levels negatively correlated with BVAS (r = - 0.675) and ITAS scores (r = - 0.385), as well as with CRP and CRI. Our results suggest that serum Fet-A level could be a novel biomarker for assessment of activity status in patients with GPA or TA. Key Points • Serum Fetuin-A is negative acute phase protein and systemic calcification inhibitor synthesized in hepatocytes and secreted by various inflammation. • Serum Fetuin-A was negatively correlated with CRP, BVAS, and ITAS scores and significantly decreased in vasculitis patients with high disease activity. • Serum Fetuin-A could be a promising and useful biomarker for the assessment of disease activity for vasculitis, also that it might also be a predictor of long-term cardiovascular progression.

Impact of the fetuin gene polymorphisms in coronary artery calcification and mortality of patients with chronic kidney disease and renal transplant

Fetuin A is a major systemic inhibitor of vascular calcifications. The aim of this study was to examine association of single nucleotide polymorphisms (SNP) in the gene for fetuin-A with fetuin-A serum levels, coronary arteries calcification (CAC) and mortality in renal transplant (RT) and chronic kidney (CKD) patients. This study included 88 patients (42 stable RT patients at least 6 months after transplantation and 46 CKD patients, stage 2-5 not requiring dialysis) followed five years. Detection and analysis of fetuin A gene polymorphisms in positions C742T (Thr248Met; rs4917) and C766G (Thr256Ser; rs4918) were performed using PCR method. Respondents with allele 742T had at the same time 766G. Combined genotypes TT/GG had lower serum fetuin A levels than CT /CG and CC/CC. Predictors of CAC in univariate analysis were age (p=0,000), serum fetuin-A levels (p=0.011) and rs 4917 polymorphism (p=0.021) while multivariate determined age (p=0.001) and fetuin-A levels (p=0.031). Patients who were homozygous for variant 742T and 766G (combined genotype TT/GG) had lowest survival rate. Our results suggest that allele 742T and 766G in gene for fetuin-A were associated with lower serum fetuin-A levels, higher CAC occurrence and higher mortality rate in RT and CKD patients.

Fetuin-A to adiponectin ratio is an independent indicator of subclinical atherosclerosis in patients with newly diagnosed type 2 diabetes mellitus

AimsThe purpose of this research was to explore the associations of fetuin-A, adiponectin, and fetuin-A/adiponectin ratio (F/A ratio) with subclinical atherosclerosis as evaluated by carotid intima-media thickness (CIMT) in cases with newly diagnosed type 2 diabetes mellitus (T2DM). MethodsA total of 283 newly diagnosed T2DM patients were enrolled in this study. Serum fetuin-A and adiponectin levels were determined with an ELISA method. Other clinical and biochemical parameters were also collected. ResultsSignificant linear increases in waist-to-hip ratio (WHR), systolic blood pressure (SBP), diastolic blood pressure, homoeostasis model assessment of insulin resistance, C-reactive protein (CRP) and F/A ratio, and a significant linear decrease in adiponectin with increasing tertiles of CIMT were observed (P for trends <0.05). However, no significant correlation between fetuin-A and CIMT was detected (P > 0.05). In multivariate logistic regression models, WHR, SBP and F/A ratio were independently correlated with higher CIMT. Receiver operating characteristic curve analysis indicated that F/A ratio had a better predictive power for higher CIMT than adiponectin and fetuin-A, with an area under the curve of 0.802, 0.713 and 0.646, respectively. ConclusionF/A ratio is an independent indicator of subclinical atherosclerosis in patients with newly diagnosed T2DM.

Study of risk factors for the osteoporosis development in rheumatoid arthritis in real clinical practice

Introduction. Osteoporosis is a common complication of rheumatoid arthritis. Its development is associated with the mechanisms underlying in the progression of autoimmune inflammatory diseases and therapeutic approaches used for them. The study of risk factors for osteoporosis can contribute to the clarification of its pathogenesis components, as well as the development of new methods for prevention, diagnosis and treatment of this condition.Aim. To study the role of anamnestic, clinical and laboratory factors for secondary osteoporosis in women with rheumatoid arthritis.Materials and methods. 102 women with rheumatoid arthritis were enrolled in our study. Exclusion criterias were type 2 diabetes mellitus, hepatic cirrhosis, hepatocarcinoma and level of alanine aminotransferase ≥ than 3 upper limit ofnormal. The cumulative dose, duration and daily dose of glucocorticoids (GC) were determined by patient intake. All patients undergone standard clinical and immunological examination. Serum fetuin-A, 25-hydroxycalciferol, C-telopeptide of collagen I type, N-terminal propeptide of collagen I type levels were determined using ELISA. X-ray of afflicted joints and dual-energy x-ray absorptiometry were performed. Statistical analysis was performed using conventional methods. Forced data entry was used to perform multiple logistic regression. Hereinafter data is presented as odds ratio (OR) and 95% confirmation intervals (CI).Results. OR for osteoporosis were higher in women of age ≥ 58.5 years (OR 1,07 (1.02–1.12)), body mass index (BMI) ≤ 27 kg/m2 (OR 1.1 (1.01–1.2)), cumulative dose of GC ≥ 7.6 g (OR 1.09 (1.02–1.17), serum fetuin-A levels ≤ 660 μg/ml (OR 1,05 (1,01–1,09) and if the duration of GC intake is more than 3 months (hereinafter if dose of glucocorticoids is ≥ 5 mg for prednisolone daily) (OR 12.3 (4.12–36.5). Adjusted OR for osteoporosis were higher in women of age ≥ 58.5 years old (adjOR 1.08 (1.01–1.16), serum fetuin-A levels ≤ 660 μg/ml (adjOR 1.08 (1.01–1.15) andif the duration of GC intake is ≥ than 3 months (adjOR 12.1 (1.44–102.3).Conclusions. Women with RA of ≥ than 58.5 years old, duration of GCs intake more than 3 months and serum fetuin-A levels ≤ than 660 μg/ml had higher odds for osteoporosis.These are independent factors for osteoporosis in women with rheumatoid arthritis, whichshould be used in patient’s management.

Liver fibrosis indices are related to diabetic peripheral neuropathy in individuals with type 2 diabetes

The association between nonalcoholic fatty liver (NAFL) or liver fibrosis and diabetic peripheral neuropathy (DPN) has not been well studied. We aimed to investigate the association of NAFL or liver fibrosis indices and DPN in individuals with type 2 diabetes. In this observational study, we included 264 individuals with type 2 diabetes, and calculated non-alcoholic fatty liver disease (NAFLD) liver fat score, NAFLD fibrosis score, and Fibrosis-4 (FIB-4) index to evaluate the status of NAFLD or liver fibrosis. DPN was diagnosed when the Michigan Neuropathy Screening Instrument—Physical Examination score was ≥ 2.5. The NAFLD fibrosis score and FIB-4 index were significantly higher in individuals with DPN than in those without DPN. Logistic analyses showed that the NAFLD fibrosis score and FIB-4 index were associated with DPN after adjustment for covariates (adjusted odds ratio 1.474 and 1.961, respectively). In the subgroup analysis, this association was only significant in the group with a high NAFLD liver fat score (> − 0.640). Serum levels of fetuin-A, a hepatokine, were decreased in individuals with abnormal vibration perception or 10-g monofilament tests compared with their counterparts. The present study suggests that liver fibrosis might be associated with DPN in individuals with type 2 diabetes.

Fetuin-A in newly detected type 2 diabetes mellitus as a marker of non-alcoholic fatty liver disease.

Fetuin-A has been implicated in the causation of metabolic disorders such as obesity, diabetes, and hepatic steatosis. Numerous studies have shown the association between levels of fetuin-A in type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD). The levels of fetuin-A in newly detected type 2 diabetic (NDD)patients and its relationship with the presence of NAFLD have not been studied. To study the fetuin-A levels in patients with NDD and its relationship with NAFLD. A total of 60 NDD patientswere studied. The diagnosis of NAFLD was made on the basis of transient elastography. Serum fetuin-A and serum fasting insulin were measured along with other investigations. The percentage of patients with NAFLD in NDD was 53.33%. Fetuin-A levels were significantly higher in NDD with NAFLD compared to those without NAFLD. There was no association of fetuin-A with age, systolic and diastolic blood pressure, fasting blood sugar (FBS), hemoglobin (Hb)A1c, fasting insulin, homeostatic model assessment-insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and markers of advanced fibrosis. Fetuin-A levels beyond 1166.5 mcg/mL could predict the development of NAFLD with odds ratio (OR) of 4.33 (95%CI: 1.364-13.77), which remained significant after adjustment for various confounding factors. Fetuin-A is a reliable marker of NAFLD in NDD and is positively associated with insulin resistance (IR). The observation in this study suggests that high serum fetuin-A levels in patients with NAFLD do not merely reflect the effects of insulin resistance, but also a more extensive distortion of liver architecture.

Níveis mais Baixos de Fetuína-A Sérica estão Associados a um Maior Risco de Mortalidade em Dez Anos em Pacientes com Infarto do Miocárdio por Supradesnivelamento do Segmento ST

ResumoFundamento A fetuína-A é um fator anti-inflamatório e anticalcificação envolvido no curso da doença arterial coronariana (DAC). Em alinhamento com essas funções, investigou-se a fetuína-A como marcador de risco cardiovascular em vários estudos. Porém, a associação entre a fetuína-A e o prognóstico dos pacientes com DAC ainda é controversa.Objetivos O presente estudo foi conduzido para identificar a associação entre o nível de fetuína-A sérica e doença cardiovascular (DCV) de longo prazo e a mortalidade global por infarto do agudo do miocárdio por supradesnivelamento do segmento ST (STEMI).Métodos Foram cadastrados no estudo cento e oitenta pacientes consecutivos com STEMI. A população do estudo foi dividida em subgrupos (mais baixo, ≤288 µg/ml; e mais alto, >288 µg/ml) de acordo com a mediana do nível de fetuína-A. Dados de acompanhamento clínico foram obtidos por contato telefônico anual com pacientes ou familiares. As causas das mortes também foram confirmadas pelo banco de dados de saúde nacional. P-valores bilaterais <0,05 foram considerados estatisticamente significativos.Resultados Durante um acompanhamento médio de 10 anos, foram registradas 71 mortes, das quais 62 foram devidas a DCV. Identificou-se um índice de mortalidade global e por DCV significativamente mais alto no grupo com nível de fetuína-A mais baixo que no grupo com nível de fetuína-A mais alto (44% versus 24%, p= 0,005; 48% versus 31%, p= 0,022, respectivamente). Nas análises de risco proporcionais por regressão de Cox, detectou-se que a fetuína-A era um preditor independente de mortalidade global e por DCV.Conclusões A baixa concentração de fetuína-A está associada ao prognóstico de longo prazo ruim pós-STEMI, independentemente de fatores de risco cardiovascular tradicionais. Nossos achados fortaleceram estudos prévios demonstrando consistentemente o papel determinante dos mediadores anti-inflamatórios em síndromes coronárias agudas.