The Oxidative Stress in Knee Osteoarthritis Patients. An Attempt of Evaluation of Possible Compensatory Effects Occurring in the Disease Development.

Background and Objective: Osteoarthritis (OA) is a disorder of the musculoskeletal system resulting in worsening of life condition. The research revealed the involvement of oxidative stress into both OA pathogenesis and the effects of therapeutic agents applied in OA cases. The activities of the most important antioxidant enzymes, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and total antioxidant status (TAS), in blood of the knee OA patients were studied, with the aim of clarifying which enzymatic antioxidants are involved into osteoarthritis (OA)-related oxidative stress and whether any compensatory effects occur. The results were additionally analyzed with regard to gender. Methods: Whole blood SOD (U/mL), plasma GPx (U/L) and CAT (U/mL) activities as well as plasma TAS (mmol/L)) in knee OA patients were investigated. Sixty-seven patients (49 females and 18 males) with primary knee OA were enrolled. The control comprised 21 subjects (10 females and 11 males) free of osteoarthritis or inflammation. Results: TAS was decreased in OA subjects (4.39 0.53 vs. 4.70 0.60), with this effect being more significant in OA females (4.31 0.51 vs. 5.02 0.54). GPx was depressed in all OA patients (518 176 vs. 675 149). In both genders, GPx was decreased, significantly in males (482 185 vs. 715 105). SOD was decreased in all OA patients (109 32 vs. 127 42). CAT showed no difference in all OA subjects vs. control, while in OA females it was depleted (20.2 (11.6-31.6) vs. 38.5 (27.9-46.6)) and in OA men it increased (26.9 (23.3-46.5) vs. 14.0 (7.0-18.6)). Conclusions: The obtained results suggest that in men some compensatory mechanisms towards OA-related oxidative stress occurred. Based on the obtained data, the introduction of antioxidant supplements into OA therapy could be suggested with further research concerning the choice of agents.

The Influence of Manganese and Glutamine Intake on Antioxidants and Neurotransmitter Amino Acids Levels in Rats' Brain.

Depending on the concentration, Mn can exert protective or toxic effect. Potential mechanism for manganese neurotoxicity is manganese-induced oxidative stress. Glutamine supplementation could reduce manganese-induced neurotoxicity and is able to influence the neurotransmission processes. The aim of this study was to investigate whether the long term administration of manganese (alone or in combination with glutamine) in dose and time dependent manner could affect the selected parameters of oxidative-antioxidative status (superoxide dismutase and glutathione peroxidase activities, concentrations of vitamin C and malonic dialdehyde) and concentrations of excitatory (Asp, Glu) and inhibitory amino acids (GABA, Gly) in the brain of rats. The experiments were carried out on 2-months-old albino male rats randomly divided into 6 group: Mn300 and Mn500-received solution of MnCl2 to drink (dose 300 and 500 mg/L, respectively), Gln group-solution of glutamine (4 g/L), Mn300-Gln and Mn500-Gln groups-solution of Mn at 300 and 500 mg/L and Gln at 4 g/L dose. The control group (C) received deionized water. Half of the animals were euthanized after three and the other half-after 6 weeks of experiment. The exposure of rats to Mn in drinking water contributes to diminishing of the antioxidant enzymes activity and the increase in level of lipid peroxidation. Glutamine in the diet admittedly increases SOD and GPx activity, but it is unable to restore the intracellular redox balance. The most significant differences in the examined amino acids levels in comparison to both control and Gln group were observed in the group of rats receiving Mn at 500 mg/L dose alone or with Gln. It seems that Gln is amino acid which could improve antioxidant status and affect the concentrations of the neurotransmitters.

The influence of lithium and/or selenium on plasma amino acids profile in rats.

INTRODUCTION: Selenium belongs to essential microelements and is used in agriculture. Lithium is used in medicine and the possibility of its exposure by environmental pollution has been reported. Both elements have been found to be connected with amino acids metabolism. OBJECTIVE: The aim of the study was to compare the effect of lithium and selenium on plasma amino acids in rats, and to evaluate the influence of selenium in organisms exposed to lithium. MATERIAL AND METHODS: The effect of selenium (0.5 mg/kg b.w., orally as Na2SeO3) and/or lithium (2.7 mg/kg b.w., orally as Li2CO3) given for 6 weeks on the plasma profile of selected amino acids in rats was studied. The concentrations of amino acids were determined using ion exchange chromatography with the aid of an amino acids analyzer AAA400. RESULTS: A significant effect of lithium on plasma amino acids profile was found in rats, much greater than for selenium. Selenium treatment slightly increased Tau, Phe, Tyr, Ala, Trp, Ser and Gln, while Lys and Orn were enhanced in a significant way. In contrast, Li-treatment caused a well-marked increase in Phe, Orn, Ala, His, Trp, Asp and Gln, whereas all the others were only slightly increased. Co-treatment resulted in a significant increase in Orn and Trp, a slight enhancement of Phe, Lys and His, while the rest remained unchanged. CONCLUSIONS: A significant effect of lithium alone on plasma amino acids profile in animals was demonstrated, with a much less influence of selenium alone. Co-treatment generally resulted in a slight or no effect. The slight selenium influence seems important regarding its agricultural application and the growing interest in its supplementation. Results concerning lithium could contribute to the research regarding the mechanism of Li action.

Role of matrix metalloproteinases and their tissue inhibitors in the pathological mechanisms underlying maxillofacial cystic lesions.

Cystic lesions are considered to be one of the most common pathologies of the maxillofacial region, and matrix metalloproteinases (MMPs) may represent potential etiological factors. The aim of the present study was to elucidate the role of MMP-2 and MMP-9, and their endogenous tissue inhibitors, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2, respectively, in the pathogenesis of maxillofacial cystic lesions. A total of 25 patients diagnosed with radicular cysts (RCs; n=20), dentigerous cysts (n=3) and retention cysts (RtCs; n=7) were enrolled in the present study. Gelatin zymography was performed to assess the gelatinolytic activity of MMP-2 and MMP-9, and commercial ELISA kits were used to determine TIMP-1 and TIMP-2 concentrations. Gelatin zymography revealed the presence of both MMP-2 and MMP-9 in all types of samples analyzed. An increase in MMP-9 activity, TIMP-1 concentration and MMP-9/TIMP-1 ratio was observed in the fluid obtained from RCs compared with that obtained from RtCs. In conclusion, MMP-9 may be involved in the pathogenesis of RCs, whereas the activity of MMP-2 in the wall of RtCs was low, and this gelatinase did not appear to significantly affect the development of this type of lesion.

Leukocyte cell-derived chemotaxin-2 and fibroblast growth factor 21 in alcohol-induced liver cirrhosis.

BACKGROUND: The importance of early diagnosis of alcoholic liver disease underscores the need to seek better and especially non-invasive diagnostic procedures. Leukocyte cell-derived chemotaxin-2 (LECT2) has been widely studied to determine its usefulness in monitoring the course of non-alcoholic fatty liver disease but not for alcoholic liver cirrhosis (ALC). AIM: To determine the concentration of LECT2 in the blood serum of patients in relation to progressive stages of ALC, its relation to fibroblast growth factor 1 (FGF-1) and FGF-21, and to examine the possible wider use of LECT2 in diagnosing ALC. METHODS: A retrospective case-control study was conducted with 69 ALC cases and 17 controls with no ALC. Subjects were recruited from the region of Lublin (eastern Poland). Liver cirrhosis was diagnosed based on clinical features, history of heavy alcohol consumption, laboratory tests, and abdominal ultrasonography. The degree of ALC was evaluated according to Pugh-Child criteria (the Pugh-Child score). Blood was drawn and, after centrifugation, serum was collected for analysis. LECT2, FGF-1, and FGF-21 were determined using enzyme-linked immunosorbent assay kits. RESULTS: The LECT2 Levels in the control group were 18.99 ± 5.36 ng/mL. In the study groups, they declined with the progression of cirrhosis to 11.06 ± 6.47 ng/mL in one group and to 8.06 ± 5.74 ng/mL in the other (P < 0.0001). Multiple comparison tests confirmed the statistically significant differences in LECT2 Levels between the control group and both test groups (P = 0.006 and P < 0.0001). FGF-21 Levels were 44.27 ± 64.19 pg/mL in the first test group, 45.4 ± 51.69 pg/mL in the second (P = 0.008), and 13.52 ± 7.51 pg/mL in the control group. The difference between the control group and the second test group was statistically significant (P = 0.007). CONCLUSION: We suggest that LECT2 may be a non-invasive diagnostic factor for alcohol-induced liver cirrhosis. The usefulness of LECT2 for non-invasive monitoring of alcohol-induced liver cirrhosis was indirectly confirmed by the multiple regression model developed on the basis of our statistical analysis.

Oxidative stress-induced growth inhibitor 1 in alcohol-induced liver cirrhosis.

INTRODUCTION AND OBJECTIVE: Human oxidative stress-induced growth inhibitor 1 (OSGIN1) is a protein identified in 2001 which belongs to the OKL38 protein family. The aim of the study was to investigate the levels of this protein depending on the severity of alcohol-induced liver cirrhosis. MATERIAL AND METHODS: The study group consisted of 60 patients: 30 patients with cirrhosis in the P-Ch A and B stage and 30 in the P-Ch C stage. The control group consisted of 18 healthy individuals without liver diseases, who did not abuse alcohol. Oxidative stress induced growth inhibitor 1 (OSGIN1), fibroblast growth factor 1 (FGF1) and fibroblast growth factor 21 (FGF21) were determined in blood serum using enzyme-linked immunosorbent assay (ELISA) kits. All absorbance readings were conducted using an Epoch Microplate Spectrophotometer (BioTek Instrumentals, Inc., Winooski, VT, USA). OSGIN1, FGF1 and FGF21 concentrations were determined using Sandwich enzyme immunoassay kits (by Cloud Clone Corp., Katy, TX, USA). Statistica 13.3 (TIBCO Software, Inc.) was used for data analysis. RESULTS: The concentration of OSGIN1 was 0.028 ± 0.017 in the control group which increased with the advancement of liver cirrhosis (stage of Pugh-Child): 0.075 ± 0.098 in the P-Ch A + B group and 0.121 ± 0.134 in the P-Ch C stage. Multiple comparison tests confirmed statistically significant differences in OSGIN1 concentration between the control group and P-Ch C (p <0.02). Significant correlations were noted between OSGIN1 and FGF1 (r = 0.39; p = 0.004) and between OSGIN1 and FGF21 (r = 0.53; p <0.0001). CONCLUSIONS: The study revealed that the level of OSGIN1 increased significantly in the P-Ch C stage of liver cirrhosis. It is possible that OSGIN1 may be used for the non-invasive diagnosis of ALD, but its possible diagnostic value is still very uncertain.

Decreased nitric oxide serum level after pituitary adenoma resection.

BACKGROUND: Nitric oxide (NO) is synthesized by the conversion of Arginine (Arg) into the NO and Citrulline (Cit). Although the NO is involved into the pathogenesis of several physiological and pathological processes, the role of NO in pituitary adenomas (PA) progression is not determined. Our purpose was to evaluate the relationship between NO and PA as well as the effect of tumor resection on NO metabolites level in serum. METHODS: The study group consisted of 21 patients with PA, 18 patients with macroadenomas and 3 with microadenomas. Venous blood samples were collected at two time-points; 1) before the surgery and 2) 3-5 days after PA resection. Arg and Cit levels were determined by the automated ion-exchange chromatography with usage of Amino Acids Analyser (AAA 400). Commercially available kit for the evaluation of nitrate/nitrite serum levels was applied for indirect assessment of serum NO level. RESULTS: Significant decrease in NO concentration after the surgery was observed in comparison with the time-point 1. Arg level did not significantly change during the study period. Cit level was ranged below the detection limit of applied method. CONCLUSIONS: The decrease of NO level after the pituitary adenoma resection indicates the relationship between NO synthesis and PA occurrence.

Analysis of novel serum markers of fibrosis and angiogenesis in patients with alcoholic liver cirrhosis.

INTRODUCTION: Alcohol consumption causes acute and chronic liver injury. The clinical forms of alcohol liver disease (ALD) include steatosis, hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) associated with liver cirrhosis. OBJECTIVE: The aim of the study was to determine the levels of novel markers of fibrogenesis and angiogenesis in patients with alcoholic liver cirrhosis. Serum levels of angiopoietin-like peptide 4 (ANGPTL-4), asialoglycoprotein receptor 1 (ASGP-R1), and S100 calcium-binding protein A8 (S100A8) were assessed. Levels of hyaluronic acid (Hyal) and collagen IV (Coll IV) werealso determined at various stages of alcoholic liver cirrhosis. MATERIAL AND METHODS: The study group consisted of 72 patients with alcoholic liver cirrhosis, while the control group included 22 healthy subjects without a history of alcohol abuse. The degree of liver cirrhosis was evaluated according to the Pugh-Child criteria (Pugh-Child score). Based on thse scores, patients were assigned to one of three groups: Pugh-Child (P-Ch) A - 21 with stage A, P-Ch B - 23 with stage B and P-Ch C - 28 with stage C liver cirrhosis. Serum levels of markers were determined using ELISA. RESULTS: The study findings demonstrated higher levels of ANGPTL-4, ASGP-R1, S100A, hyaluronic acid and serum collagen IV in the group of patients with alcoholic liver cirrhosis, compared to the control group. Furthermore, their levels increased with the progression of alcoholic liver cirrhosis. CONCLUSIONS: The biomarkers analysed in the study may be useful for diagnosis and prognosis in patients with alcoholic liver cirrhosis.

PDGF-BB homodimer serum level - a good indicator of the severity of alcoholic liver cirrhosis.

INTRODUCTION: Liver cirrhosis is a chronic disease in which progressive fibrosis is noted. This process leads to changed architectonics of the liver parenchyma and the appearance of regenerative nodules, all of which are caused by pathological activation of the hepatic stellate cells. This process is enhanced on a molecular level by many cytokines, with platelet-derived growth factors (PDGFs) playing the key role. OBJECTIVE: The aim of the study was to assess serum concentrations of PDGFs active biodymers (PDGF-AA, PDGF-BB and PDGF-AB) in patients with alcoholic liver cirrhosis, and to correlate them with the stage of disease. MATERIAL AND METHODS: 64 patients with alcoholic cirrhosis and a control group of 16 healthy individuals were analysed. Liver cirrhosis was determined based on clinical image, history of the patients' alcohol consumption, laboratory findings and abdominal ultrasonography. The serum PDGF-AA, PDGF-BB and PDGF-AB concentrations were determined using ELISA kits. RESULTS: Serum concentration of PDGF-AA and PDGF-BB homodimers increases in patients with alcoholic liver cirrhosis (p=0.034 and p<0.0001, respectively), unlike the serum concentration of PDGF-AB heterodimer (p>0.05). When the stage of the disease increases, the concentrations of PDGF-AA and PGFD-BB in blood also oncrease. Furthermore, the serum level of both PDGF-AA and PDGF-BB correlates significantly with the severity of alcoholic liver cirrhosis (measured by Pugh-Child's scale), the correlation being stronger in the case of PDGF-BB levels than PDGF-AA (R=0.28; p=0.027 and R=0.26; p=0.038, respectively). CONCLUSIONS: The plasma levels of PDGF-AA and -BB may be indicators of alcohol-induced liver fibrosis process, and might be considered as future possible treatment targets, with PDGF-BB levels being an even better indicator than PDGF-AA levels.

Correlations among plasma silicon, magnesium and calcium in patients with knee osteoarthritis - analysis in consideration of gender.

INTRODUCTION AND OBJECTIVE: Osteoarthrits (OA) is a complex, chronic disorder of cartilage and bone, related to homeostasis of bioelements. The current study aimed at evaluation of correlations between plasma silicon, magnesium and ionized calcium in OA patients in consideration to gender. MATERIAL AND METHODS: The study comprised 59 patients aged 69.5±9.0 years (18 males aged 66.8±9.2; 41 females aged 70.7±8.8), admitted to the Trauma and Orthopaedic Ward of the Independent Public Health Care Centre in Leczna, Poland, due to OA and qualified to surgery. Control group consisted of 19 subjects without OA (54.5±8.6 years; 10 males aged 41.3±9.3; 9 females aged 69.1±14.9). Plasma concentrations of silicon and magnesium (spectrophotometric methods) and ionized calcium (potentiometric method) were determined. RESULTS: Silicon in OA patients was significantly increased vs. control. In OA males and OA females, silicon was enhanced vs. the respective controls, but it was statistically significant only in males. Magnesium in OA patients was not significantly different from control group. In females, a significant decrease vs. the respective control was observed. No significant differences were observed in the case of ionized calcium. Positive correlations between silicon and magnesium in healthy control, both in the whole group and in male and female subgroups, were noted, while no such effect was observed in OA subjects. CONCLUSIONS: The results might suggest some connection between higher OA incidence in women and the depleted magnesium in the organism. Silicon increase in OA patients, especially in men, may indicate its intense metabolism during the articular inflammatory process, likely dependent on sex hormones. It remains open whether the plasma Si increase is the effect or cause of OA.

Factors influencing serum chemerin and kallistatin concentrations in patients with alcohol-induced liver cirrhosis.

INTRODUCTION: In Poland, an increasing number of patients are hospitalized due to liver diseases. One of the common liver diseases is cirrhosis, which can be caused by alcohol, viral hepatitis, autoimmune processes and metabolic diseases. MATERIAL AND METHODS: The study included 99 patients with alcoholic cirrhosis from the Lublin region of Eastern Poland. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The concentrations of serum kallistatin and chemerin were determined using ELISA kits. OBJECTIVE: The aim of the study is to evaluate serum levels of kallistatin and chemerin in patients with different stages of alcoholic liver cirrhosis. RESULTS: The highest chemerin level was found in the control group - 182.6±80.4 ng/ml. In other stages of liver cirrhosis, the following levels were observed: 175.7±62.7 ng/ml in Child-Pugh stage A (Ch-P A), 150.2±59.7 ng/ml in Ch-P B and 110.3±73.6 ng/ml in Ch-P C. Significant differences in chemerin levels between controls and Ch-P C patients (p=0.01), as well as between the Ch-P A patients and Ch-P C patients (p=0.02), were demonstrated. The highest kallistatin level was demonstrated in the control group - 8.2±3.5 µg/ml. In other stages of liver cirrhosis, the following concentrations were found: 7.2±27 µg/ml in Ch-P A, 4.4±2.2 µg/ml in Ch-P B and 3.5±1.9 µg/ml in Ch-P C. Statistically significant differences were observed between controls and Ch-P B patients (p<0.001), controls and Ch-P C patients (p<0.001), Ch-P A and Ch-P B patients (p=0.01), as well as Ch-P A and Ch-P C patients (<0.001). CONCLUSIONS: The levels of chemerin and kallistatin decrease with progression of liver damage during alcoholic liver cirrhosis. The impairment of its synthetic function leads to reductions in levels of the adipokines studied.

Antioxidant Potential of Propolis, Bee Pollen, and Royal Jelly: Possible Medical Application.

Honeybees products comprise of numerous substances, including propolis, bee pollen, and royal jelly, which have long been known for their medicinal and health-promoting properties. Their wide biological effects have been known and used since antiquity. Bee products are considered to be a potential source of natural antioxidants such as flavonoids, phenolic acids, or terpenoids. Nowadays, the still growing concern in natural substances capable of counteracting the effects of oxidative stress underlying the pathogenesis of numerous diseases, such as neurodegenerative disorders, cancer, diabetes, and atherosclerosis, as well as negative effects of different harmful factors and drugs, is being observed. Having regarded the importance of acquiring drugs from natural sources, this review is aimed at updating the current state of knowledge of antioxidant capacity of selected bee products, namely, propolis, bee pollen, and royal jelly, and of their potential antioxidant-related therapeutic applications. Moreover, the particular attention has been attributed to the understanding of the mechanisms underlying antioxidant properties of bee products. The influence of bee species, plant origin, geographic location, and seasonality as well as type of extraction solutions on the composition of bee products extracts were also discussed.

Afamin and adropin in patients with alcohol-induced liver cirrhosis.

The aim of the study was to determine serum concentrations of afamin and adropin in patients with alcoholic liver cirrhosis and to define their correlation with the stage of disease. The study included 99 patients with alcoholic cirrhosis from the region of Lublin, (Eastern Poland). Liver cirrhosis was diagnosed based on clinical features, history of heavy alcohol consumption, laboratory tests and abdominal ultrasonography. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The serum afamin and adropin concentrations were determined using ELISA kits. The concentration of afamin was found to be significantly lower in patients with compensated alcoholic liver cirrhosis, i.e. P-Ch B (85.1±40.6 µg/ml) and P-Ch C (56.4±32.3 µg/ml) individuals, compared to the control group (135.9±43.6 µg/ml); p-value was <0.01 and <0.001, respectively. As far as adropin is concerned, a reverse relationship was demonstrated: the highest concentration was found in patients with P-Ch C (11.7±5.7 ng/ml) cirrhosis. Furthermore, the above concentration was significantly higher compared to patients with P-Ch A cirrhosis (7.2±2.8 ng/ml; p<0.05) and controls (7.5±2.6 ng/ml; p<0.05). The concentration of afamin decreases with the severity of alcoholic liver cirrhosis, which most likely results from impaired hepatic synthesis. Otherwise, the higher the stage of disease according to the Child-Pugh score, the higher the concentration of adropin.

Does Vitamin C Influence Neurodegenerative Diseases and Psychiatric Disorders?

Vitamin C (Vit C) is considered to be a vital antioxidant molecule in the brain. Intracellular Vit C helps maintain integrity and function of several processes in the central nervous system (CNS), including neuronal maturation and differentiation, myelin formation, synthesis of catecholamine, modulation of neurotransmission and antioxidant protection. The importance of Vit C for CNS function has been proven by the fact that targeted deletion of the sodium-vitamin C co-transporter in mice results in widespread cerebral hemorrhage and death on post-natal day one. Since neurological diseases are characterized by increased free radical generation and the highest concentrations of Vit C in the body are found in the brain and neuroendocrine tissues, it is suggested that Vit C may change the course of neurological diseases and display potential therapeutic roles. The aim of this review is to update the current state of knowledge of the role of vitamin C on neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis and amyotrophic sclerosis, as well as psychiatric disorders including depression, anxiety and schizophrenia. The particular attention is attributed to understanding of the mechanisms underlying possible therapeutic properties of ascorbic acid in the presented disorders.

Relationships between serum selenium and zinc concentrations versus profibrotic and proangiogenic cytokines (FGF-19 and endoglin) in patients with alcoholic liver cirrhosis.

INTRODUCTION AND OBJECTIVE: Liver cirrhosis is a disease involving the liver parenchyma, which is characterised by fibrosis and impaired architectonics of the parenchyma with regenerative nodules. The aim of the study was to determine the relationship between stage of alcoholic liver cirrhosis, concentrations of selenium, zinc and profibrotic and proangiogenic cytokines (FGF-19, ENG). MATERIAL AND METHODS: The study included 99 patients with alcoholic cirrhosis and 20 healthy subjects. Ion chromatography with UV/VIS detection was used for determination of zinc ions in the previously mineralized serum samples. The measurements of selenium were performed with the ContrAA700 high-resolution continuum source graphite tube atomic absorption spectrometer. ELISA was used to determine concentration of FGF-19 and ENG in serum samples. RESULTS: Concentrations of zinc and selenium were significantly decreased in cirrhotic patients (p<0.001 for both). The highest concentration of FGF-19 was found in Child-Pugh stage C liver cirrhosis patients (806.9±650.3 pg/ml), and was significantly higher than observed in controls (p=0.005) and stage A patients (compensated cirrhosis) (p=0.02). The highest concentration of ENG was demonstrated in the control group (3.24±148 ng/ml) while the lowest in patients with decompensated cirrhosis (7.32±5.39 ng/ml and 7.92±4.18 ng/ml for stage B and C; p=0.03 and p=0.02, respectively). The use of the multiple-variable model demonstrated that the independent factors affecting the concentration of ENG were the concentration of bilirubin (p=0.02), INR (p=0.01) and duration of alcohol abuse (p=0.02). The independent determinants of FGF-19 concentrations were found to be the stage (severity) of liver cirrhosis (p=0.04) and INR (p=0.03). CONCLUSIONS: Concentrations of zinc and selenium in serum of patients with alcoholic liver cirrhosis are not independently related to concentrations of FGF-19 and ENG.

Association between Serum Selenium Concentrations and Levels of Proinflammatory and Profibrotic Cytokines-Interleukin-6 and Growth Differentiation Factor-15, in Patients with Alcoholic Liver Cirrhosis.

According to some authors, serum selenium levels are strongly associated with the severity of liver diseases, including liver cirrhosis. The aim of this study was to determine the relationship between the concentration of selenium and pro-inflammatory and profibrotic cytokines-interleukin-6 (IL-6) and growth differentiation factor 15 (GDF-15) in patients with alcoholic liver cirrhosis. The parameters studied were determined in the serum of 99 patients with alcoholic liver cirrhosis divided based on the severity of disease according to the Child-Turcotte-Pugh criteria. In patients with liver cirrhosis, the serum selenium concentration was statistically lower, whereas serum IL-6 and GDF-15 concentrations were higher than those in the control group. Moreover, the concentration of selenium negatively correlated with the levels of GDF-15 and IL-6. The above results may indicate a role of selenium deficiency in the pathogenesis and progression of alcoholic liver disease.