Serum fetuin-A Concentrations Research Articles

Effect of Fetuin-A and oxidative stress on the occurrence of unexplained infertility.

Unexplained infertility refers to a diagnosis in which all standard examinations are usually normal and is statistically seen in approximately 30-40% of infertile couples and endometriosis encountered in 25-50% of patients with unexplained infertility. Unexplained infertility is thought to be closely associated with endometriosis and serum and peritoneal fluid levels of Fetuin-A is increased in patients with endometriosis. Fetuin-A is proposed as a diagnostic marker for endometriosis and has anti-inflammatory effects on several diseases. Oxidative stress also is central to the etiopathogenesis of infertility in women. The aim of this study was to evaluate serum Fetuin-A and oxidative stress parameter concentrations impact on unexplained infertility. In the study, serum Fetuin-A, IL-1β, CA I, TAS, TOS levels, and PON and ARE enzyme activities were measured using the Enzyme-Linked ImmunoSorbent Assay in the sera of diagnosed unexplained infertility females (n=44) and controls (n=41). There was no statistically significant difference between unexplained infertile patients and control groups in terms of serum IL-1β, CA I, OSI, and PON levels (p>0.05). Serum Fetuin-A and ARE levels were significantly higher in unexplained infertility compared with the control, whereas serum TAS and TOS levels were lower (p<0.05, p<0.01, p<0.05, p<0.05, respectively). It is thought that increased Fetuin-A levels may be a response to the inflammatory process and increased ARE activity may be a sign of the impaired oxidant-antioxidant balance in unexplained infertility. This may contribute to the pathogenesis of infertility, and the data obtained will make a significant contribution to new works to be done in this sense.

Serum fetuin-A is decreased in cirrhotic patients with Wilson's disease.

Wilson's disease may lead to cirrhosis, but timely medical treatment could slow down its progression. Clinical markers helping early diagnosis are essential. Decreased fetuin-A concentration has been reported in cirrhosis of different etiologies. The aim of this study was to investigate whether decreased serum fetuin-A concentration could identify patients with Wilson's disease who developed cirrhosis. In this cross-sectional study we determined the serum fetuin-A concentration of 50 patients with Wilson's disease. We analyzed the data of patients with liver involvement, comparing cirrhotic and non-cirrhotic patients. Among patients with liver involvement those with cirrhosis had significantly lower fetuin-A and albumin level, white blood cell and platelet count. Fetuin-A negatively correlated with disease duration, bilirubin level, positively with total protein and albumin concentration, but not with copper and ceruloplasmin concentrations or markers of systemic inflammation. In multivariate analysis with fetuin-A and the Nazer score or its parameters only fetuin-A was a significant determinant of having cirrhosis. In receiver operator curve analysis among patients with liver involvement the fetuin-A level of 523 μg/ml was associated with cirrhosis with 82% sensitivity and 87% specificity. The presence of the H1069Q mutation was not associated with alteration in fetuin-A concentration. The serum concentration of fetuin-A is a sensitive marker of liver cirrhosis in Wilson's disease, independently of the H1069Q mutation, ceruloplasmin concentration or systemic inflammation.

Liver Fetuin-A at Initiation of Insulin Resistance

Hepatokines (liver secreted proteins with possible distant action) are emerging potential players in insulin resistance in type 2 diabetic patients. Here, we explored the effect of a high-fat diet on the expression of fetuin-A, one of those candidate liver proteins, and its relationship with liver macrophage activation. Mice were fed a normal diet or a high-fat diet for 3 days, known to initiate steatosis and liver insulin resistance. A preventive liver macrophage depletion was obtained by intravenous injection of clodronate-loaded liposomes. The mRNA and protein expression of fetuin-A was evaluated by qPCR, Western blot and immunofluorescence on different insulin-sensitive tissues (liver, adipose tissue, and muscle). Short-term high-fat diet-induced steatosis, liver macrophage activation, and hepatic insulin resistance together with a significantly increased expression of liver AHSG (α2-HS glycoprotein/fetuin-A) mRNA and serum fetuin-A concentration. On immunofluorescence, fetuin-A was mostly expressed in centrilobular hepatocytes. This increase in fetuin-A under high-fat diet was not evidenced in other peripheral insulin-sensitive tissues (skeletal muscle and adipose tissue). The mRNA expression of α2-HS glycoprotein was 800 times higher within the liver compared with the adipose tissue or the muscle. Liver macrophage depletion that significantly ameliorated insulin sensitivity was associated with a significant decrease in α2-HS glycoprotein mRNA expression. In conclusion, this study demonstrated liver fetuin-A overexpression at the initiation of high-fat diet feeding, concurrent with hepatic steatosis and insulin resistance. Targeting liver macrophages in this setting reduced liver α2-HS glycoprotein expression suggesting that fetuin-A acts as an hepatokine with proinsulin resistance effects.

Evaluation of Fetuin-A and Insulin Resistance among Iraqi Type 2 Diabetic Patients with and without Ischemic Heart Disease

Background: Diabetes mellitus (DM) is a metabolic disorder in which hyperglycemia is a characteristic feature due to impairment in insulin secretion, defective insulin action, or both reasons. One long-term complication is the ischemic heart disease (IHD) which is a major cause of morbidity and mortality. Insulin and fetuin-A are hormones that play a role in glucose metabolism regulation. Insulin is responsible for regulating glucose passage to the cells, while fetuin-A blocks insulin binding to its receptor, which is linked to insulin resistance in metabolic syndrome. Higher fetuin-A level patients have 4 times greater risk of developing IHD compared to patients with lower fetuin-A levels. Studies found that both hormones participate in the development of T2DM and IHD, beside their role in the pathophysiology of metabolic syndrome. Aim of the study: Evaluate serum fetuin-A concentrations in type2 diabetic (T2D) patients with and without IHD and compare them with healthy individuals. Assess serum glucose, insulin levels, and HOMA-IR in T2D patients and IHD and compare them with healthy individuals. Subjects and Methods: A case control study, that included 120 patients (60 have T2DM with IHD and 60 having T2DM without IHD age ranged from 30 to 70 years patient, who attended Al-Yarmouk Teaching Hospital and Iraqi Center for Myocardial Infarction, Medical City Hospital, Baghdad during the period from November 2020 until February 2021 and compare result with 60 healthy control which age ranged from 30 to 70 years. Female: male ratio is almost 1:1 in the three studied groups. The diagnosis of MI is based on medical reports, laboratory, and clinical tests for heart disease. Patients with neuropathy, retinopathy, thyroid dysfunction and liver diseases were excluded from the study. BMI, FBS, serum insulin, HOMA-IR, and fetuin-A were measured or calculated for each participant. Result: a statistical difference in BMI between participants is found; 46.70% of T2DM in the IHD group are obese. No significant association between disease duration and development of IHD is found. All the included markers showed statistical differences in mean ± SD between the diabetic and control group; fetuin-a mean ± SD level was 27.63 13.31, 12.39 ± 5.61 and 9.93 ± 5.1 in T2DM with IHD, T2DM without IHD and control group, respectively. There was no statistical association between the markers and fetuin-A except a moderate positive correlation with insulin. Conclusion: Fetuin-A can be used as a predictor of IHD development in diabetic patients.

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.

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.

A Study of Fetuin A in Fatty Liver (NAFLD) With and Without Chronic Kidney Disease

Abstract Background Obesity and insulin resistance are known risk factors for both chronic kidney disease (CKD) and nonalcoholic fatty liver disease (NAFLD). Further studies identify mechanisms common to both diseases linked through an inter-organ communication orchestrated by fetuin-A and adiponectin. Aim of the Work to determine the serum level of Fetuin A in cases of non- alcoholic fatty liver disease (NAFLD), as compared to normal controls. Also, as a main objective, is to determine the serum level of Fetuin A in cases of chronic kidney disease (CKD), as compared to normal controls, and try to correlate it to the severity of the disease. Patients and Methods This cross sectional cohort study was conducted on 80 persons divided into 4 groups: Group I: Includes 20 Healthy adult normal controls, Group II: Includes 20 adult patients with NAFLD, Group III: Includes 20 adult patients with CKD &amp; NAFLD and Group IV: Includes 20 adult patients with CKD. Results We detected that there is statistically significant difference between the four studied groups regarding Weight, Height &amp; BMI (P &amp;lt; 0.05). However there is a statistically insignificant difference between the four studied groups regarding Age &amp; Gender (P &amp;gt; 0.05). That there is statistically significant difference between the four studied groups regarding Serum Feutin-A (P &amp;lt; 0.05). There is statistically significant positive correlation between Serum Feutin-A &amp; (Weight, BMI, Systolic BP, Urea, Creatinine, Sodium, Calcium, Phosphorous, Cholesterol, Triglyceride, LDL, ALT, AST, FBS, 2hr PP &amp; RBS); In addition to that there is a statistically significant negative correlation between Serum Feutin-A &amp; (Height, HDL &amp; Albumin) (P &amp;lt; 0.05). There is statistically significant negative correlation between Serum Feutin-A &amp; (HDL) in Group I “Adult Normal Controls” (P &amp;lt; 0.05). The results revealed a statistically significant positive correlation between Serum FeutinA &amp; (FBS); In addition to that there is a statistically significant negative correlation between Serum Feutin-A &amp; (Diastolic BP) (P &amp;lt; 0.05). We detected that there is statistically significant positive correlation between Serum Feutin-A &amp; (FBS), (2 hr PP)(RBS), Serum urea &amp;Creatinine and potassium.; In addition to that there is a statistically significant negative correlation between Serum Feutin-A &amp; (Diastolic BP) and (Systolic BP) (P &amp;lt; 0.05). We detected that there is statistically significant positive correlation between Serum Feutin-A &amp; (LDL, Calcium, Triglyceride &amp; Creatinine); In addition to that there is a statistically significant negative correlation between Serum Feutin-A &amp; (HR) (P &amp;lt; 0.05). Conclusions Fetuin-A is a glycoprotein in the liver and a potent inhibitor of vascular calcification in the blood circulation in patients with chronic renal failure and end-stage kidney failure. It is also known as a vascular disease marker in patients with type 2 diabetes. It is increased during insulin resistance and non-alcoholic fatty liver, as well. Serum Fetuin-A concentrations are significantly reduced in patients with CKD. This decrease in Fetuin-levels is progressive, beginning from the early stages of CKD.

Fetuin-A Deficiency but Not Pentraxin 3, FGF-21, or Irisin, Predisposes to More Serious COVID-19 Course.

Analysis of liver biopsy specimens showed that SARS-CoV-2 might have led to liver damage. This study aimed to evaluate the role of selected hepatokines and myokines in the development and progression of COVID-19. Seventy patients with laboratory-confirmed COVID-19 and 20 healthy volunteers were enrolled in the study. Irisin, pentraxin 3, fetuin-A, and FGF-21 serum concentrations and biochemical parameters were assessed using an immunoenzymatic method with commercially available enzyme immunoassay (EIA) or enzyme-linked immunosorbent assay (ELISA) kits. Serum fetuin-A concentrations were significantly decreased in COVID-19 patients compared to healthy volunteers. The serum concentration of FGF-21 was significantly increased in obese COVID-19 patients compared to overweight ones. Moreover, the FGF-21 level was higher in COVID-19 patients diagnosed with metabolic syndrome than in patients without metabolic syndrome. PTX3 concentration was higher in COVID-19 patients with higher HOMA-IR values than those with lower HOMA-IR values. COVID-19 patients with HOMA-IR ≤ 3 and >3 had significantly lower fetuin-A levels than the control group. Irisin concentration was significantly decreased in the HOMA-IR ≤ 3 COVID-19 subgroup when comparing with the control group. Lower levels of fetuin-A observed in COVID-19 patients despite higher HOMA-IR, CRP, and ferritin levels, pneumonia, patients requiring ICU care suggests that fetuin-A deficiency predisposes to more severe COVID-19 course. Upregulated pentraxin 3 may be used as a potential predictor of COVID-19 severity.

Low Levels of Serum Fetuin-A and Retinol-Binding Protein 4 Correlate with Lipoprotein Subfractions in Morbid Obese and Lean Non-Diabetic Subjects.

Background: Fetuin-A and retinol-binding protein 4 (RBP4) are secreted as both hepatokine and adipokine. These are involved in insulin resistance, obesity-related dyslipidemia, and atherosclerosis. To date, correlations of circulating fetuin-A and RBP4 with lipoprotein subfractions as well as high-density lipoprotein (HDL)-linked proteins have not been entirely investigated in morbid obese and lean non-diabetic subjects. Methods: One-hundred obese non-diabetic patients (body mass index, BMI: 42.5 ± 8.1 kg/m2) along with 32 gender and age-matched normal weight controls (BMI: 24.5 ± 2.5 kg/m2) were enrolled in our study. Serum fetuin-A and RBP4 were measured by ELISA. Lipoprotein subfractions were distributed by Lipoprint gelelectrophoresis. Results: Serum fetuin-A and RBP4 were unexpectedly lower in obese patients (p < 0.01 and p < 0.01, respectively) compared to controls and correlated with each other (r = 0.37; p < 0.001). Fetuin-A had positive correlations with HDL-C (r = 0.22; p = 0.02), apolipoprotein AI (apoAI) (r = 0.33; p < 0.001), very-low density lipoprotein (VLDL) subfraction (r = 0.18; p = 0.05), and large HDL subfraction levels (r = 0.3; p = 0.001) but did not show correlation with carbohydrate parameters in all subjects. RBP4 correlated positively with HDL-C (r = 0.2; p = 0.025), apoAI (r = 0.23; p = 0.01), VLDL subfraction (r = 0.37; p < 0.001), intermediate HDL subfraction (r = 0.23; p = 0.01), and small HDL subfraction (r = 0.21; p = 0.02) concentrations, as well as C-peptide levels in overall participants. Backward stepwise multiple regression analysis showed that serum fetuin-A concentration is best predicted by RBP4 and large HDL subfraction. In model 2, VLDL subfraction was the independent predictor of serum RBP4 level. Conclusions: Our data may indicate a potential role of fetuin-A and RBP4 in impaired lipoprotein metabolism associated with obesity.

Independent Dose-Response Associations between Fetuin-A and Lean Nonalcoholic Fatty Liver Disease.

Patients with lean NAFLD make up an increasing subset of liver disease patients. The association between lean NAFLD and feutin-A, which serves as a hepatokine and adipokine, has never been examined. Our study aimed to explore the association of serum fetuin-A among lean and non-lean patients. The study comprised 606 adults from the community, stratified into lean or non-lean (BMI </≥ 24 kg/m2) and NAFLD or non-NAFLD (scoring of ultrasonographic fatty liver indicator, US-FLI ≥ 2/< 2). Multivariate logistic regression analyses were performed to estimate the odds ratio of having NAFLD among the tertiles of fetuin-A after adjustment. The least square means were computed by general linear models to estimate marginal means of the serum fetuin-A concentrations in relation to the NAFLD groups. The odds ratio (OR) of having NAFLD for the highest versus the lowest tertile of fetuin-A was 2.62 (95% CI: 1.72–3.98; p for trend < 0.001). Stratifying by BMI, the OR of having lean NAFLD for the highest versus the lowest tertile of fetuin-A was 2.09 (95% CI: 1.09–3.98; p for trend 0.026), while non-lean NAFLD had no significant association with the fetuin-A gradient after adjustments. Fetuin-A was positively associated with lean NAFLD after adjusting for central obesity and insulin resistance.

Do fetuin-A/apha2-Heremans Schmid-glycoprotein levels have an association with recurrent pregnancy loss?

Objective Fetuin-A is a hepatokine which is previously found related to fertility and pregnancy outcomes. We aimed to investigate if recurrent pregnancy loss (RPL) is associated with increased fetuin-A levels. Materials and methods Serum fetuin-A concentrations were measured and compared in 30 non-pregnant women with a history of unexplained recurrent miscarriage, 29 women who had a history of unexplained recurrent miscarriage and were admitted to our clinic due to miscarriage during the study period and 30 fertile women who have no history of miscarriage or any other pregnancy complications with at least two previous healthy children. Results The median serum fetuin-A levels of group I, II, and III were 59.45, 62.73, and 44.52, respectively (p=.065). Serum fetuin-A levels significantly increased in group II compared to group III (p=.011). No significant differences in the levels of fetuin-A of group I compared to either group II (p=.433) or group III (p=.268). Conclusions The etiology of RPL is still a subject that is not clarified. Fetuin-A levels may have a relationship with RPL.

Association of fetuin-A levels and left ventricular diastolic dysfunction in patients on haemodialysis.

To identify the relationship between serum fetuin-A levels and left ventricular diastolic dysfunction (LVDD) among maintenance haemodialysis patients. In a cross-sectional study, 75 dialysis patients with end-stage renal disease (ESRD) were recruited, and fetuin-A levels were detected using an enzyme-linked immunosorbent assay (ELISA). Echocardiography measurements were recorded according to the recommendations of the American Society of Echocardiography. The ratio of early diastolic transmitral inflow velocity (E) to early diastolic annular velocity (E') was measured using tissue Doppler imaging and E/E' > 15 was defined as diastolic dysfunction. The association of serum fetuin-A concentrations with echocardiographic parameters was analysed by calculating the bivariate linear correlation. A binary logistic regression analysis was conducted to determine the variables associated with LVDD. Compared to patients without diastolic dysfunction, patients with diastolic dysfunction were older, a higher percentage had a history of coronary artery disease, and presented with a high systolic pressure, high parathyroid hormone level, high N-terminal pro-brain natriuretic peptide (NT-proBNP) level, high LV mass index, high left atrium diameter, and low serum creatinine and fetuin-A levels. Serum fetuin-A levels showed a negative correlation with E/E' (r = -0.299, P = 0.009). Fetuin-A levels were considered an independent predictor of diastolic dysfunction. A decrease in the serum fetuin-A level is associated with an increased risk of LVDD in patients on haemodialysis.

Serum Calcification Propensity in Children on Chronic Hemodialysis

Serum Calcification Propensity in Children on Chronic Hemodialysis

Recurrent implantation failure is associated with increased levels of fetuin-A/alpha2-Heremans-Schmid-glycoprotein

ObjectiveRecurrent implantation failure is defined as the absence of implantation, after two or three consecutive cycles of in-vitro fertilization (IVF), intracytoplasmic sperm injection or frozen embryo replacement. Human fetuin-A/alpha2-Heremans-Schmid-glycoprotein is a plasma protein secreted by the liver that modulates insulin action in adipocytes. Increased fetuin-A promotes adipocyte dysfunction which results in decreased adiponectin and increased fatty acids and inflammatory cytokines. Fatty acids and inflammatory cytokines were previously reported in implantation failure. Also, fetuin-A inhibits receptor tyrosine kinase activity in trophoblast growth factors which decrease trophoblast viability and invasion. In this study, we aimed to find the association between fetuin-A and implantation failure. Study designA total of 78 women were included in this case-control study. Serum fetuin-A concentrations were measured in 42 women with recurrent IVF failure and 36 healthy women with regular cycles. ResultsThe mean serum fetuin-A levels of implantation failure and control women were 257.77 ± 32.18 and 219.59 ± 48.86 respectively with a p-value <0.001 (independent samples t-test). Our results showed a statistically significant difference between serum fetuin-A levels of implantation failure women and controls. ConclusionSo far reasons for implantation failure are only partially understood. The current study reveals the association between implantation failure and fetuin-A. Further studies with large population sizes are needed to investigate whether fetuin-A can be used as a marker before controlled ovarian stimulation began or regulation of fetuin-A levels with treatment or lifestyle interventions can improve implantation success.

Serum fetuin-A levels and association with hematological parameters in chronic kidney disease and hemodialysis patients

Abstract Aim The objective of the current study is to examine the association between serum fetuin-A concentrations and some other inflammation markers neutrophil to lymphocyte ratio (NLR), mean platelet volume (MPV) and C reactive protein (CRP) in patients with chronic kidney disease (CKD) and hemodialysis. Methods The study subjects are composed of healthy volunteers (n = 47) and two patient groups; CKD patients (n = 26) and hemodialysis patients (n = 33). We measured serum glucose, urea, creatinine, total protein, albumin, sodium, potassium, calcium, phosphorus, iron, alkaline phosphatase, parathyroid hormone, ferritin and CRP levels by auto-analyzer and fetuin-A levels by ELISA method. Also, complete blood count parameters were analyzed and NLR was calculated. Results There were significant differences in serum fetuin-A concentrations, NLR and MPV values among three groups (p &lt; 0.001, p &lt; 0.001, p &lt; 0.001). The correlation analyses revealed that fetuin-A negatively correlated with urea, creatinine, ferritin, and CRP concentrations (r: 0.349, 0.367, 0.399, 0.550, respectively, p &lt; 0.05). Conclusion Fetuin-A is lower in CKD and hemodialysis patients than the control group; supporting as a negative acute phase reactant. Determination of serum fetuin-A, NLR and MPV might be useful to assess inflammation in CKD and hemodialysis patients.

Serum fetuin-A, tumor necrosis factor alpha and C-reactive protein concentrations in patients with hereditary angioedema with C1-inhibitor deficiency

Background and aimsHereditary angioedema with C1-inhibitor deficiency (C1-INH-HAE) is characterized by localized, non-pitting, and transient swelling of submucosal or subcutaneous region. Human fetuin-A is a multifunctional glycoprotein that belongs to the proteinase inhibitor cystatin superfamily and has structural similarities to the high molecular weight kininogen. Fetuin-A is also known a negative acute phase reactant with anti-inflammatory characteristics. In this study we aimed to determine serum fetuin-A, C-reactive protein (CRP) and tumor necrosis factor alpha (TNFα) concentrations in patients with C1-INH-HAE during symptom-free period and during attacks and compare them to those of healthy controls. Further we analyzed possible relationship among these parameters as well as D-dimer levels which was known as marker of HAE attacks.Patients and methodsSerum samples of 25 C1-INH-HAE patients (8 men, 17 women, age: 33.1 ± 6.9 years, mean ± SD) were compared to 25 healthy controls (15 men, 10 women, age: 32.5 ± 7.8 years). Serum fetuin-A and TNFα concentrations were determined by ELISA, CRP and D-dimer by turbidimetry.ResultsCompared to healthy controls patients with C1-INH-HAE in the symptom-free period had significantly decreased serum fetuin-A 258 μg/ml (224–285) vs. 293 μg/ml (263–329), (median (25–75% percentiles, p = 0.035) and TNFα 2.53 ng/ml (1.70–2.83) vs. 3.47 ng/ml (2.92–4.18, p = 0.0008) concentrations. During HAE attacks fetuin-A levels increased from 258 (224–285) μg/ml to 287 (261–317) μg/ml (p = 0.021). TNFα and CRP levels did not change significantly. We found no significant correlation among fetuin-A CRP, TNFα and D-dimer levels in any of these three groups.ConclusionsPatients with C1-INH-HAE have decreased serum fetuin-A concentrations during the symptom-free period. Given the anti-inflammatory properties of fetuin-A, the increase of its levels may contribute to the counter-regulation of edema formation during C1-INH-HAE attacks.

There is No Association between Premature Ovarian Insufficiency and Levels of Fetuin-A/α2-Heremans-Schmid Glycoprotein.

Objective:Fetuin-A is a well-known negative acute-phase protein and has been used liberally to predict vascular disease. The aim of this study was to evaluate the association between serum human fetuin-A/alpha2-Heremans–Schmid glycoprotein levels and idiopathic premature ovarian insufficiency (POI).Methods:A total of 75 women were included in this case–control study between January 2013 and December 2013. Serum fetuin-A concentrations were measured in 36 women with idiopathic POI and 39 healthy women with regular cycles. Blood samples were drawn after a 12-h overnight fast and were kept at −80°C for subsequent assay. The serum levels of fetuin-A were assessed by commercial ELISA kits (BioVendor Laboratory Medicine Inc., Brno, Czech Republic) and serum concentration values were expressed as μg/ml.Results:The mean serum fetuin-A levels of idiopathic POI and control women were 229.02 ± 27.79 and 232.37 ± 65.56, respectively, with P = 0.771 (independent samples t-test). Our results showed no statistically significant difference between serum fetuin-A levels of idiopathic POI women and controls.Conclusion:The mean values of serum fetuin-A in idiopathic POI women were not significantly different from controls, which implies that there is no significant association between serum fetuin-A levels and idiopathic POI.

Serum levels of fetuin-A are negatively associated with log transformation levels of thyroid-stimulating hormone in patients with hyperthyroidism or euthyroidism: An observational study at a medical center in Taiwan.

Fetuin-A is a protein with various biological functions. It plays a role in insulin resistance and arterial calcium deposition. Thyroid dysfunction may affect energy expenditure, glucose metabolism, and the risk of cardiovascular diseases. In the present study, we compared the serum fetuin-A concentrations in hyperthyroid patients with those in euthyroid patients.We recruited 30 newly-diagnosed hyperthyroid patients (the HY group) and treated them with anti-thyroid regimens as clinically indicated. We recruited 30 euthyroid individuals (the EU group) as controls. We compared laboratory parameters at the baseline and at 6 months. We then determined the associations between the levels of fetuin-A and free thyroxine (fT4), thyroid-stimulating hormone (TSH), or log transformation of TSH (logTSH).At the baseline, the HY patients had significantly higher serum fetuin-A levels than the EU patients (median [Q1, Q3]: 735.4 [537.9, 843.4] ng/mL vs 561.1[449.2, 670.5] ng/mL, P = .010). At 6 months, the serum fetuin-A levels of the HY patients decreased but were still higher than those of the EU patients (698.4 [627.6, 924.3] ng/mL vs 616.5 [498.2, 727.7] ng/mL, P = .002). At baseline, the serum levels of fetuin-A were negatively associated with logTSH (β = –53.79, P = .010). At 6 months, the levels of fetuin-A were positively associated with fT4 (β = 86.91, P = .039), and negatively associated with logTSH (β = –104.28, P < .001). Changes to the levels of fetuin-A within 6 months were negatively associated with changes to logTSH (β = –57.80, P = .019). The negative associations between fetuin-A levels and logTSH at baseline and at 6 months, and the changes during the 6 months remained significant after adjustment for sex and age (β = –51.72, P = .016; β = –103.11, P < .001; and β = –59.36, P = .020, respectively).The patients with hyperthyroidism had higher serum fetuin-A levels than the patients with euthyroidism. In patients with hyperthyroidism, the serum fetuin-A concentrations decreased after the anti-thyroid treatment. In the present study, serum fetuin-A concentrations were negatively associated with logTSH.

The importance of fetuin-A in vascular calcification in children with chronic kidney disease.

The status of the cardiovascular (CV) system in children with chronic kidney disease (CKD) is significantly influenced by increasing stiffness of the arterial wall. This largely depends on the shortage of local and systemic inhibitors of soft tissue calcification. The aim of the study was to evaluate the role of fetuin-A in conjunction with other factors in the progressive hardening of the vascular wall in these children. We examined serum fetuin-A concentrations in relation to renal function, dialysis modality, and other clinical and biochemical markers promoting vascular calcification. Twenty children on peritoneal dialysis (PD), 20 on hemodialysis (HD), 36 treated conservatively, and 26 healthy subjects were enrolled into a cross-sectional study. In all children, fetuin-A and numerous clinical and biochemical parameters were measured. The fetuin-A concentration was significantly lower in children on hemodialysis (HD) vs children on peritoneal dialysis (PD), conservatively treated subjects, and the control group. In sick children, fetuinA concentration negatively correlated with dialysis vintage, PWV/ht, phosphate concentration, calcium phosphate product (CaxP), cumulative doses of calcium, and vitamin D3. In the whole study population, fetuin-A negatively correlated with blood pressure (BP), pulse wave velocity indexed to height (PWV/ht), intact parathyroid hormone (iPTH), high sensitivity C-reactive protein (hsCRP), and cholesterol concentrations. In children with CKD, the decreased concentration of fetuin-A is related to other vascular calcification risk factors. Serum fetuin-A concentration may play a role in the identification of vascular disease risk factors in this population.

Serum Fetuin-A levels in obese children with biopsy proven nonalcoholic fatty liver disease

Background and aimsFetuin-A has been proposed as a marker of liver damage in adults with obesity-related NAFLD. The aim of this study was to test serum fetuin-A concentrations in obese children with NAFLD diagnosed either by ultrasonography or by liver biopsy and to determine its applicability as predictive tool in pediatric NAFLD. Methods and resultsMetabolic parameters and fetuin-A levels were investigated in 81 obese children with NAFLD diagnosed by biopsy, 79 obese children with NAFLD defined by liver ultrasonography and 23 lean subjects.Serum fetuin-A correlated significantly with age, waist circumference, systolic blood pressure, fasting insulin and 2-h postload insulin during OGTT, HOMA-IR, ISI, CRP, and apo B levels. Obese children with NAFLD detected by ultrasonography had significantly higher fetuin-A levels compared to those with normal liver. In obese children who underwent liver biopsy, no significant differences were detected in fetuin-A levels between subject with nonalcoholic steatohepatitis and those with simple steatosis. Fetuin-A was not different between obese and lean children. ConclusionFetuin-A is not related with the degree of liver damage in obese children with NAFLD and its routine measurement as marker of liver disease severity is therefore not recommended.