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Obstructive sleep apnea syndrome (OSAS) is a common but underdiagnosed condition with significant health and economic implications for society. Inflammatory mediators are proposed to be associated with the presence and severity of OSAS and contribute to morbidity and mortality. This paper details a prospective non-randomized case control study of a cohort of subjects, who underwent surgical treatment of OSAS and were enrolled to assess the sleep parameters and blood levels of selected inflammatory markers at pre-operative and post-operative time points, also comparing them to the levels in a control group. A total of 25 study subjects and 18 control subjects were enrolled. Median values and interquartile range (IQR) of the apnea-hypopnea index (AHI) in the study group pre-operatively and post-operatively were 34 (18.5-45.5) and 13.3 (7.5-27.3), while in the control group 1.4 (1.0-2.1) per hour. The mean (IQR) hs-CRP levels (mg/L) were 1.782 (0.941-5.594) and 1.980 (0.990-5.445) in the study group, pre-operatively and post-operatively, respectively, while 0.891 (0.767-1.436) in the control group. The mean (IQR) TNF-α levels (pg/mL) were 7.999 (6.137-9.216) and 6.614 (5.534-7.460) pre-and post-operatively, respectively, and were 6.000 (5.026-6.823) in the control group. Results demonstrated that both inflammatory markers, hs-CRP and TNF-α, are higher in subjects with OSAS compared to the controls, and their levels decrease, but are still higher than the controls, after successful surgical treatment. Further analysis including the body mass index and age demonstrated that these changes were significant for TNF-α, but not hs-CRP.

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INTRODUCTION: The incidence of hepatitis E virus (HEV) infections in Poland is largely unknown. This study aimed to describe seroprevalence of markers of HEV infection among patients with immunodeficiency of diverse etiology and patients with advanced chronic liver diseases. MATERIAL AND METHODS: Four hundred fifty patients were enrolled; among them, 180 persons were solid organ transplant recipients, 90 patients were HIV-infected and 180 persons had confirmed liver cirrhosis of different etiology. Serum anti-HEV-IgG, IgM antibodies and HEV-antigen were detected by ELISA (Wantai, China). RESULTS: In the group of transplant recipients, serum anti-HEV-IgG antibodies were detected in 40.6%, IgM in 1.1% and HEV-Ag in 2.8% of subjects. In the HIV-infected population 37.7% had anti-HEV-IgG, 1.1% had anti-HEV-IgM and none had HEV-Ag. Among patients with advanced chronic liver diseases the highest prevalence of anti-HEV-IgG was recorded in alcohol-related liver cirrhosis (52.1%) (p = 0.049). In the population of all liver cirrhotics anti-HEV-IgG seroprevalence was 48.3%, anti-HEV-IgM seroprevalence was 5.0% and HEV-Ag seroprevalence was 1.7%. Older age and male gender were significant risk factors associated with increased anti-HEV-IgG prevalence, p = 0.0004 and p = 0.02, respectively. CONCLUSIONS: In this large cohort a high seroprevalence of anti-HEV-IgG was detected in comparison to other European countries, with the highest rates in patients with alcoholic liver disease and in transplant recipients.

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INTRODUCTION: Minimal hepatic encephalopathy (MHE) is a common complication of liver cirrhosis not only leading to a decrease in the quality of life, but also predicting development of overt encephalopathy. The diagnosis of MHE usually relies on a combination of neuropsychological tests, while robust serum biomarkers are lacking. We aimed to assess serum concentrations of brain-derived neurotrophic factor (BDNF) in MHE patients. MATERIAL AND METHODS: Serum BDNF was assessed in 78 patients with liver cirrhosis (53 male, median age 55 years) and 40 healthy individuals. 43 subjects underwent extensive evaluation for MHE by psychometric hepatic encephalopathy score (PHES) and inhibitory control test (ICT) or critical flicker frequency (CFF). RESULTS: Serum BDNF was twofold lower in liver cirrhosis compared to healthy subjects [13.6 (7.8-22.6) vs. 33.0 (24.1-40.7) ng/ml, p < 0.001] and its decrease reflected a degree of liver insufficiency assessed by model for end-stage liver disease (MELD). BDNF showed a negative correlation with bilirubin (R = -0.35, p = 0.005) and international normalized ratio (INR) (R = -0.37, p = 0.003), and positive with platelets (PLT) (R = 0.36, p = 0.004), while no associations with age, sex, body mass index (BMI), waist-hip ratio (WHR), creatinine and ammonia were noted. Importantly, subjects with a diagnosis of MHE by at least two modalities showed the lowest levels of BDNF [10.9 (2.5-14.4) vs. 19.9 (9.3-29.4) ng/ml, p < 0.01]. Patients with self-reported sleep disturbances had significantly lower serum BDNF [13.0 (2.5-23.4) vs. 20.0 (8.4-31.3) ng/ml, p = 0.04]. CONCLUSIONS: The lowest serum BDNF concentration was noted in patients with MHE and sleep disturbances, which suggests a role in pathophysiology of hepatic encephalopathy but also as a potential biomarker.

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INTRODUCTION: Due to the lack of highly specific and sensitive methods for diagnosing ovarian cancer at advanced stages (according to the International Federation of Gynecology and Obstetrics (FIGO) classification stage III-IV), new noninvasive biomarkers are urgently needed. This study aims to investigate how the levels of plasma bioactive sphingolipids (ceramides, sphingosine-1-phosphate, sphingosine and sphinganine) are altered in serum, erythrocytes and platelets of patients with advanced serous ovarian cancer. MATERIAL AND METHODS: A total of 135 patients with advanced serous ovarian cancer and 159 women with normal ovarian morphology were enrolled. Plasma levels of sphingosine, sphingosine-1-phosphate, sphinganine, ceramide C14:0-Cer, C16:0-Cer, C18:1-Cer, C18:0-Cer, C20:0-Cer, C22:0-Cer, C24:1-Cer and C24:0-Cer were assessed by LC/MS/MS. RESULTS: Plasma concentrations of C16-Cer, C18:1-Cer and C18-Cer were significantly higher in the advanced ovarian cancer group than in the control group (1.5-fold, p = 0.021; 1.8-fold, p = 0.036 and 1.5-fold, p = 0.031, respectively). Plasma concentration of C18:1-Cer was significantly higher in erythrocytes of women with advanced serous cancer compared to the control group (p = 0.027). Plasma C16-Cer and C18:1-Cer levels and erythrocyte C18:1-Cer levels were able to distinguish patients with moderate/severe serous ovarian cancer from patients with mild ovarian cancer (AUC: 0.86, 0.898, 0.795, respectively). Plasma concentrations of C16, C18.1 and C18 significantly correlated with FIGO staging (p = 0.001, p = 0.024 and p = 0.005), and grading (p = 0.021, p = 0.021 and p = 0.033). CONCLUSIONS: Plasma concentrations of C16, C18.1 and C18 correlated with the progression of ovarian cancer (FIGO staging and grading). Plasma levels of C16-Cer and C18:1-Cer and erythrocyte C18:1-Cer levels could be used to distinguish patients with advanced serous ovarian cancer.

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Background: Minimal hepatic encephalopathy (MHE) refers to a number of neuropsychiatric and neurophysiological disorders in patients with cirrhosis who do not show abnormalities on physical examination or in clinical tests. The aim of this study was to determine the prevalence, risk factors, and predictive value of minimal hepatic encephalopathy and the usefulness of the inhibitory control test (ICT) in the diagnosis. Methods: Seventy patients (mean age 53 years, range 24-77) with liver cirrhosis were enrolled in the study. MHE was diagnosed based on PHES (psychometric hepatic encephalopathy score) and ICT. PHES and ICT were validated in a group of 56 control subjects. Results: Minimal hepatic encephalopathy was diagnosed using PHES in 21 patients (30%). ICT diagnosed MHE in 30 patients (42%), and the test had a sensitivity of 65% and a specificity of 57% compared to PHES. The ICT score (lures/target accuracy rate) correlated with the age of subjects (R = 0.35, p = 0.002) and only slightly with education (education in years R = -0.22, p = 0.06). MHE diagnosed with PHES or ICT was associated with a significantly higher model of end-stage liver disease (MELD) score in the follow-up. MHE diagnosed with ICT was correlated with a significantly higher incidence of symptoms of decompensated cirrhosis (p = 0.02) in the follow-up. Conclusions: ICT had moderate sensitivity and specificity in diagnosing MHE compared to PHES. Importantly, MHE detected with PHES or ICT was associated with poorer survival and a more severe progression of the disease.

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Objective: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a well- known risk factor of atherosclerotic vascular diseases which are common comorbidities in psoriasis. The aim of this study was to evaluate serum Lp-PLA2 level in psoriatic patients and elucidate possible associations with disease activity, metabolic or inflammatory parameters and systemic treatment.Methods: We enrolled 33 patients with active plaque-type psoriasis and 11 healthy controls. Blood samples were collected before and after 3 months of systemic treatment with acitretin or methotrexate. Serum Lp-PLA2 level were evaluated by enzyme-linked immunosorbent assay.Results: Serum Lp-PLA2 level in patients with psoriasis did not statistically differ comparing to the control group (p = .2). However, in patients with severe psoriasis Lp-PLA2 was significantly higher than in the controls before and after treatment (p = .03, p = .01, respectively). The lipase did not correlate with BMI (p = .22); however, a statistical significance was noted between psoriatics with obesity compared to the controls (p = .03). No significant effect of systemic treatment combined (p = .5) nor separately with acitretin (p = .5) or methotrexate (p = .1) on the Lp-PLA2 level was found, despite clinical improvement.Conclusion: Lp-PLA2 assay might be helpful in assessment of the risk of cardiometabolic comorbidities development especially in patients with severe psoriasis and obesity.

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Despite high biocompatibility of titanium and its alloys, this metal causes various side effects in the human body. It is believed that titanium biomaterials may induce an innate/adaptive immune response. However, still little is known about changes caused by titanium mandible implants, particularly with regard to bone healing. The latest studies showed disturbances in the antioxidant barrier, increased oxidative/nitrosative stress, as well as mitochondrial abnormalities in the periosteum covering titanium mandible fixations; nevertheless, the impact of titanium implants on free radical production, inflammation, and mandible apoptosis are still unknown. Because severe inflammation and apoptosis are among the main factors responsible for disturbances in osteointegration as well as implant rejection, this study is the first to evaluate pro-oxidant enzymes, cytokines as well as pro- and anti-apoptotic proteins in the periosteum of patients with a broken jaw, treated with titanium miniplates and miniscrews. The study group consisted of 29 patients with double-sided fracture of the mandible body requiring surgical treatment. We found significantly higher activity of NADPH oxidase and xanthine oxidase as well as enhanced rate of free radical production in the periosteum of patients in the study group compared to the control group. The markers of inflammation [interleukin 1 (IL-1), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), transforming growth factor ß (TGF-ß) and ß-glucuronidase (GLU)] as well as apoptosis [Bax, Bax/Bcl-2 ratio, caspase-3 (CAS-3) and nitric oxide (NO)] were significantly elevated in periosteum covering titanium fixations compared to the control group. In the study group, we also demonstrated an increased content of titanium on the periosteum surface, which positively correlated with CAS-3 activity. The study led us to the conclusion that titanium mandible implants increase the production of pro-inflammatory cytokines, and enhance free radical generation in the periosteum covering titanium miniplates and miniscrews. Additionally, exposure to Ti6Al4V titanium alloy induces apoptosis in the mandible periosteum. However, no clinical signs of the said phenomena have been observed.

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Psoriasis is a systemic disease associated with metabolic syndrome and cardiometabolic diseases. Adipocyte fatty acid-binding protein (A-FABP, FABP4) is a relevant mediator of lipid metabolism and several comorbidities development. Aim of the study was to explore the possible role of FABP4 in psoriasis and assess its relationship with disease activity, inflammation or metabolic disturbances, and impact of systemic treatment. Fasting blood samples were obtained from 33 patients with active plaque-type psoriasis before and after 12 weeks of therapy and from 11 healthy volunteers. Serum FABP4 concentrations were analyzed by the enzyme-linked immunosorbent assay (ELISA) and statistically analyzed for their correlations with clinical outcomes and the treatment introduced. Serum FABP4 levels were significantly increased in psoriatics compared to controls (p = 0.03). No relationship between the protein and psoriasis severity expressed through psoriasis area and severity index (PASI) was noted (p = 0.57). FABP4 did not correlate with CRP (p = 0.41), lipid profile, and body mass index (BMI) nor the glucose level or liver enzyme activity. FABP4 significantly correlated with morphotic blood elements. After total therapy, FABP4 did not statistically change (p = 0.07), but significantly decreased after administering acitretin (p = 0.03). FABP4 is a potential marker of psoriasis and clinical outcome after therapy with acitretin. Adipocyte-type FABP may be related to hematological disorders or obesity-mediated comorbidities in psoriasis.

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Still little is known about the redox abnormalities in patients with non-alcoholic fatty liver disease (NAFLD). The purpose of the study was to find the relationship between enzymatic and non-enzymatic antioxidants, redox homeostasis and oxidative damage in 67-patients with NAFLD. The study population was divided into patients with non-alcoholic fatty liver (early NAFLD, n = 29) and patients with non-alcoholic steatohepatitis (advanced NAFLD, n = 38). Redox biomarkers: enzymatic antioxidants (Cu - Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR)); non-enzymatic antioxidants and redox status (reduced glutathione (GSH), total antioxidant capacity (TAC)); and oxidative damage products (total oxidant status (TOS), advanced glycation end products (AGE), malondialdehyde (MDA), and DNA/RNA oxidative damage) were determined in the serum/plasma samples. The activity of SOD, GPx, GR and levels of GSH, TOS, AGE, MDA, and DNA/RNA oxidative damage were significantly elevated in early NAFLD and advanced NAFLD group compared to controls (p < .001). There was a positive correlation between AGE, TAC and ALT activity (R = 0.34, p = .04; R = 0.36, p = .03, respectively) in advanced NAFLD group. Interestingly, ROC analysis for AGE showed good discriminatory ratio for patients with minimal steatosis (BARD score 0-1) vs. moderate steatosis (BARD score 2-4), AUC = 0.76. Plasma AGE can be a potential non-invasive biomarker differentiating NAFLD patients.

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Cancer develops as a result of the loss of self-control mechanisms by a cell; it gains the ability to induce angiogenesis, becomes immortal and resistant to cell death, stops responding to growth suppressor signals, and becomes capable of invasion and metastasis. Sphingolipids-a family of membrane lipids-are known to play important roles in the regulation of cell proliferation, the response to chemotherapeutic agents, and/or prevention of cancer. Despite the underlying functions of sphingolipids in cancer biology, their metabolism in different malignant tumors is poorly investigated. Some studies showed marked differences in ceramide content between the tumor and the respective healthy tissue. Interestingly, the level of this sphingolipid could be either low or elevated, suggesting that the alterations in ceramide metabolism in cancer tissue may depend on the biology of the tumor. These processes are indeed related to the type of cancer, its stage, and histology status. In this paper we present the unique roles of bioactive sphingolipid derivative in selected gynecologic malignant and nonmalignant lesions.

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Fatty acid-binding proteins play an inconclusive role in lipid metabolism and cardiometabolic diseases (CMDs) which are closely related with psoriasis. Aim of the study was to investigate the diagnostic value of serum liver fatty acid-binding protein (FABP1) level and associations with disease severity, inflammation or metabolic parameters and influence of systemic treatment in psoriatic patients. The study included thirty-three patients with active plaque-type psoriasis and eleven healthy volunteers. Blood samples were obtained before and after 12 weeks of therapy with methotrexate and acitretin. Serum FABP1 concentrations were analyzed by the enzyme-linked immunosorbent assay. Statistical analysis was performed for correlation of FABP1 with anthropometric, metabolic or inflammatory indices and treatment used. Serum liver-type FABP levels were significantly increased in psoriatic patients compared to the controls (p < 0.001). No statistical correlations between FABP1 and PASI (p = 0.25) was noted, however patients with severe psoriasis had the highest level of FABP1. No significance with metabolic parameters was obtained, beside a positive significant relation with BMI after therapy (p = 0.03). Liver-type FABP significantly correlated with CRP (p = 0.01) and morphotic blood elements. Systemic treatment combined resulted in significant decrease of FABP1 (p = 0.04), regardless of the drug: p = 0.1 in acitretin group, p = 0.3 in methotrexate group. Liver-type FABP might be a novel marker of psoriasis and predictor of clinical response to systemic therapy. FABP1 could be involved in CMDs risk assessment and perhaps link psoriasis with hematological disorders.

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AIM OF THE STUDY: Recent reports provide evidence for the immunomodulatory properties of vitamin D. Decreased vitamin D levels may contribute to the progression of liver disease in hepatitis B virus (HBV) infection. This study aims to assess serum 25(OH)D in patients with chronic HBeAg-negative HBV (CHB) infection at different phases of disease. MATERIAL AND METHODS: Fifty-eighty patients with CHB, 10 with a history of HBsAg/anti-HBs seroconversion, were enrolled. The control group consisted of 9 healthy volunteers. Serum 25(OH)D concentration was assessed by ELISA. RESULTS: Serum 25(OH)D concentration was significantly lower in the CHB group in comparison to the HC group. It did not differ across the consecutive phases of the HBeAg-negative HBV infection. Negative correlations between serum 25(OH)D and alanine aminotransferase (ALT) as well as frequency of peripheral blood monocytes were observed. Serum 25(OH)D in samples collected in winter was significantly lower in comparison to the pool of samples collected in the summer. Serum 25(OH)D concentration was not associated with the phases of HBV-infection, HBV viral load, APRI or liver histology. CONCLUSIONS: Serum 25(OH)D is significantly decreased in HBV infection irrespectively of the phase of the infection and negatively correlates with serum ALT level, which may reflect the deterioration of liver function. Based on our results, we can conclude that the role of vitamin D in the immune control of HBV infection is probably irrelevant.

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INTRODUCTION: The changes of enzyme activity in the hepatocytes in the course of different liver diseases are reflected by increase of the corresponding enzyme activity in the plasma. For example, the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) correlate with the severity of the condition during cirrhosis. In this study we measured the activity of ADH isoenzymes and ALDH in the sera of patients with hepatitis C. MATERIAL AND METHODS: Serum samples were taken from 60 patients suffering from viral hepatitis C and from 66 control subjects. Total ADH activity and class III and IV isoenzymes were measured by the photometric method and ALDH activity, ADH I and II by the fluorometric method. RESULTS: The ADH activity was significantly higher in patients with hepatitis C than in healthy (p < 0.001). The total activity of ADH was 1284 mU/l in patients, and 745 mU/l (controls). The activity of isoenzymes classes ADH I and ADH II in the hepatitis C group increased respectively 55% (4.24 vs. 1.88 mU/l; p < 0.001) and 47% (26.63 vs. 14.11 mU/l; p < 0.001) in the comparison to the control. There was significant increase in the activity of ADH I isoenzyme (4.96 vs. 3.81 mU/l; p < 0.001) and ADH total (1833 vs. 1105 mU/l; p < 0.001) in patients with high viral load in comparison to patients with low viral load. CONCLUSIONS: The activity of class I and II ADH isoenzymes in the sera of patients with hepatitis C is increased, and it seems to be caused by the release of these isoenzymes from damaged liver cells.

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OBJECTIVE: YKL-40 is an inflammatory glycoprotein associated with atherosclerosis, cardiovascular disease, diabetes or metabolic syndrome which are common comorbidities in psoriasis. The aim of the study was to assess serum YKL-40 level in psoriasis and elucidate possible associations with disease activity, inflammatory or metabolic parameters and treatment. METHODS: A total of 37 individuals with active plaque-type psoriasis and 15 healthy controls were enrolled. Blood samples were collected before and after 2 weeks of therapy. Serum YKL-40 concentrations were evaluated by enzyme-linked immunosorbent assay (ELISA). The results were correlated with Psoriasis Area and Severity Index (PASI), body mass index (BMI), inflammatory and biochemical markers, lipid profile and topical therapy. RESULTS: Median YKL-40 serum levels were significantly increased in psoriatic patients in comparison to the controls (p < .0001). No significant correlations between investigated protein and metabolic parameters as BMI (p = .19), glucose (p = .32) nor lipids levels were found. Significant positive relation with CRP (p = .003) or alanine aminotransferase (p = .04) and no correlation with PASI (p = .2) were noted. Serum YKL-40 level remained unchanged (p = .5) after topical treatment, despite clinical improvement. CONCLUSIONS: YKL-40 might be a biomarker of psoriasis and inflammation in psoriatic patients, but not a reliable indicator of metabolic conditions, severity of psoriasis nor efficacy of the treatment.

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INTRODUCTION: N-terminal propeptide of procollagen type III (PIIINP) is generated during the synthesis of type III collagen. PIIINP can be measured in the serum as an indicator of liver fibrosis and cirrhosis. AIM: To evaluate the effect of liver diseases of different aetiologies and clinical severity of liver cirrhosis on the serum level of PIIINP. MATERIAL AND METHODS: Patients with alcoholic cirrhosis (AC) - 63 subjects, non-alcoholic cirrhosis (NAC) - 31 and toxic hepatitis (HT) - 33 were studied. Cirrhotic patients were classified according to the Child-Pugh scale. The samples were analysed using the ELISA method. RESULTS: The level of PIIINP was significantly higher in patients with alcoholic cirrhosis, non-alcoholic cirrhosis, and toxic hepatitis in comparison to the control group. There were no significant differences in the serum PIIINP levels between liver diseases and according to the severity of liver cirrhosis. PIIINP has the highest diagnostic power for the diagnosis of toxic hepatitis. The highest sensitivity was reached in alcoholic cirrhosis, but other diagnostic values (specificity, positive predictive value (PPV), negative predictive value (NPV), diagnostic accuracy (ACC)) in alcoholic cirrhosis were lower than that in toxic hepatitis. In the diagnosis of non-alcoholic cirrhosis PIIINP has low sensitivity, specificity, PPV, NPV, and ACC. CONCLUSIONS: The serum PIIINP shows the alterations in liver diseases in comparison to healthy controls, but not between diseases. Taking the above into account we can suggest that PIIINP may be a useful test for the detection of liver diseases.

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Non-alcoholic fatty liver disease (NAFLD) is a chronic progressive liver disease, coupled with metabolic syndrome, which may progress to non-alcoholic steatohepatitis (NASH). Diabetes, obesity, hypertension, hypercholesterolemia, and hypertriglyceridemia are considered to be the most common causes leading to the incidence of NAFLD. It is assumed that the accumulation of lipid deposits in hepatocytes leads to production of proinflammatory cytokines that triggers the development of liver inflammation. Regulatory T cells (Tregs) play a critical role in regulating inflammatory processes in NASH, while T helper type 17 (Th17) might functionally oppose Treg-mediated responses. In addition, important mediators of hepatic steatosis are fatty hormones known as adipokines. We aimed to describe the significance and interaction between Treg and Th17-related cytokines as well as adipokines in pathogenesis and its potential use as biomarkers of NAFLD, especially with respect to progression to NASH.

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BACKGROUND AND AIMS: Recent reports suggest an involvement of Th17 responses in inflammatory and autoimmune reactions in alcoholic liver disease (ALD). Our study aimed to assess serum levels of Th17-interleukins in ALD with regard to the frequency of liver-specific autoantibodies and degree of liver damage. METHODS: Ninety-five patients with ALD were enrolled. Serum concentrations of IL-17F, IL-17A, IL-22 were assessed by ELISA. The presence of autoantibodies AMA-M2, SLA/LP, LKM-1, LC1, anti-F-actin, anti-desmin and anti-myosin in serum was assessed by immunoblotting, ANA antibodies were detected by ELISA. The results were analysed with regard to the degree of hepatic damage. RESULTS: Serum IL-17F was significantly elevated in ALD patients compared to controls (p=0.03). There was a correlation between serum IL-17F and degree of liver failure evaluated by the MELD score (rs=0.23, p=0.03). Serum IL-22 also correlated with MELD score (rs=0.32, p=0.007) and CTP score (rs=0.28, p=0.02). Anti-F-actin antibodies were present in 19% and ANA-antibodies in 11% of the patients in the study group, and in no subjects in the control group. The prevalence of anti-F-actin autoantibodies was higher in subjects with more advanced liver diseases but also independently associated with IL-17A in the regression analysis. Furthermore, serum IL-22 in anti-F-actin(+)-patients was significantly higher compared to anti-F-actin(-)-patients (p=0.03). CONCLUSIONS: Elevation of serum IL-17A, IL-17F, IL-22 correlated with the progression of liver damage and also with presence of F-actin in ALD. Alcoholic liver disease may trigger autoimmunity and formation of autoantibodies, especially anti-F-actin, with possible engagement of Th17-related cytokines in this process.

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Chronic hepatitis B has highly a dynamic course with significant fluctuations of HBV-DNA and ALT impeding assessment of disease activity. New biomarkers of inflammatory versus noninflammatory stages of HBV infection are urgently needed. Cytokeratin 18 epitope M30 (M30 CK-18) is a sensitive marker of cell death. We aimed to investigate an association between serum M30 CK-18 and histological activity and phase of HBV infection. 150 Caucasian patients with HBV-infection were included in the study. Serum M30 CK-18 levels reflected phase of disease, being significantly higher in both HBeAg(+) and HBeAg(-) hepatitis B in comparison to HBsAg(+) carrier groups. The highest serum M30 CK-18 levels were observed in subjects with the most advanced stages of HBV. Moreover, its serum concentrations correlated with both inflammatory activity and fibrosis advancement (ANOVA P < 0.001). Importantly, serum M30 CK-18 levels were able to discriminate patients with mild versus moderate-advanced fibrosis (AUC: 0.86) and mild versus active liver inflammation (AUC: 0.79). M30 CK-18 serum concentration has good sensitivity and specificity in discriminating mild versus moderate/severe fibrosis and inflammation even in patients with normal ALT activity. This study suggests M30 CK-18 as a potential noninvasive marker of disease activity and also a marker of phase of persistent HBV infection.

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PURPOSE: The role of lipids in carcinogenesis through induction of abnormal cell lines in the human body is currently undisputable. Based on the literature, bioactive sphingolipids play an essential role in the development and progression of cancer and are involved in the metastatic process. The aim of this study was to determine the concentration of selected sphingolipids in patients with advanced ovarian cancer (AOC, FIGO III/IV, high grade ovarian cancer). METHODS: Seventy-four patients with ovarian cancer were enrolled. Plasma concentrations of C16-Cer, C18:1-Cer and C18-Cer were assessed by LC/MS/MS. The content of tissue sphingolipids was measured using a UHPLC/MS/MS. RESULTS: Plasma concentration of 3 ceramides: C16-Cer, C18:1-Cer and C18-Cer was significantly elevated in women with advanced ovarian cancer compared to control group (P=0.031; 0.022; 0.020; respectively). There were increases in concentration of 5 ceramides: C16-Cer, C18:1-Cer, C18-Cer, C24:1-Cer, C24-Cer (P=0.025; 0.049; 0.032; 0.005; 0.013, respectively) and S1P (P=0.004) in ovarian tissue of women with advanced ovarian cancer compared to healthy individuals. Importantly, significantly higher risk of ovarian cancer when the plasma concentration of C16-Cer>311.88ng/100µl (AUC: 0.76, P=0.0261); C18:1-Cer>4.75ng/100µl (AUC: 0.77, P=0.0160) and C18-Cer>100.76ng/100µl (AUC:0.77, P=0.0136) was noticed. CONCLUSIONS: Bioactive sphingolipids play an essential role in the development and progression of cancer and they also take part in the process of metastasizing. This study suggests that some sphingolipids can be used as potential biomarkers of advanced ovarian cancer and that they can play an important role in the pathogenesis of this disease.

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