Preoperative Neutrophil-to-Lymphocyte Ratio as an Independent Predictor of 1-Year Graft Loss and Mortality After Orthotopic Liver Transplantation.

INTRODUCTION: Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are low-cost and readily available inflammation markers. Previously, we revealed that the high preoperative neutrophil level is a recipient-related risk factor for the primary liver graft dysfunction (PGD), associated with a higher risk of early retransplantation or death. Here we aimed to evaluate the prognostic significance of preoperative neutrophil level, as well as the NLR and PLR in predicting a 1-year outcome of the orthotopic liver transplantation (OLTx). MATERIALS AND METHODS: One hundred and thirty-four patients who underwent the OLTx between 2012 and 2017 were enrolled. Analysis included, inter alia, etiology of liver failure and preoperative blood morphology. In the statistical analysis, the logistic regression model and receiver operator characteristic analysis were applied. RESULTS: In 1-year follow-up, 11% of patients died and 5% were retransplanted. Acute liver failure (ALF; odds ratio [OR] = 8.62, P = .007), autoimmune hepatitis (AIH; R = 5.25, P = .006), neutrophil level (OR = 1.23, P = .0003), MELD (OR = 1.05, P = .038), and the NLR (OR = 1.16, P = .001) were significant predictors of these detrimental outcomes. The multivariate analysis revealed etiology (AIH, P < .001 or ALF, P = .006) and NLR (P = .008) as the only independent predictors of 1-year graft loss or patient's death. Receiver operator characteristic analysis pointed at the NLR above 5.48 as their highly sensitive and specific risk factor. The PLR was not a prognostic biomarker. CONCLUSION: Achieved results call for further studies on the influence of the preoperative balance between systemic inflammation and immunity, expressed with the NLR on the long-term liver graft function.

Circulating apelin level in relation to nutritional status in polycystic ovary syndrome and its association with metabolic and hormonal disturbances.

OBJECTIVE: The aim of the study was to analyse relationships between plasma apelin-36 and apelin-12 levels, nutritional status, insulin resistance and hormonal disturbances, as well as plasma adiponectin, leptin and resistin concentrations in PCOS women. STUDY DESIGN PATIENTS AND MEASUREMENTS: A cross-sectional study involving 87 PCOS (48 obese) and 67 non-PCOS women (36 obese). Anthropometric parameters and body composition were determined. Serum glucose, androgens, FSH, LH, SHBG, insulin, apelin-36, apelin-12, adiponectin, leptin and resistin were measured in the fasting state. RESULTS: Plasma apelin-36 and apelin-12 levels were significantly higher in normal weight women than in the obese women with PCOS (3·1 ± 2·2 vs 1·2 ± 0·7 µg/l, P < 0·001; 2·9 ± 2·4 vs 0·5 ± 0·7 µg/l; P < 0·001 respectively). Both plasma apelin-36 and -12 levels correlated positively with adiponectin levels, and inversely with leptin or resistin levels. There was a negative correlation between plasma apelin-36, apelin-12 and serum LH levels. In addition, an inverse correlation between apelin-12 level and LH to FSH ratio was found. In multiple regression analysis 9% of LH variability was explained by apelin-12 levels (ß = -0·14; P < 0·001). CONCLUSIONS: Nutritional status seems to have different effects on apelin release, particularly, its active isoform, in women with PCOS compared with women without PCOS. This may be partially caused by changes in leptin and resistin secretion and may enhance pituitary-ovarian axis disturbances. The association between both isoforms of apelin and insulin resistance seems to be bidirectional.

Circulating visfatin level and visfatin/insulin ratio in obese women with metabolic syndrome.

INTRODUCTION: Visfatin is an adipokine secreted by visceral adipose tissue with insulin-mimetic properties. Higher circulating visfatin levels were reported in type 2 diabetes. The aim of this study was to analyse circulating visfatin and insulin levels and the visfatin/insulin ratio in obese women with and without metabolic syndrome (MetS). MATERIAL AND METHODS: The study involved 92 obese women. Subjects were diagnosed with MetS according to IDF 2005 criteria. The MetS group consisted of 71 subjects (age: 52.8 ±9.4 years, body mass index [BMI]: 39.1 ±5.6 kg/m(2), waist circumference: 109.6 ±11.4 cm and fat mass: 52.0 ±12.8 kg) while the non-MetS group consisted of 21 subjects (age: 51.7 ±9.5 years, BMI: 36.3 ±5.2 kg/m(2), waist circumference: 104.7 ±11.0 cm and fat mass: 45.2 ±10.7 kg). In addition to anthropometric measurements and assessment of serum glucose and lipids, plasma concentrations of visfatin were estimated by enzyme-linked immunosorbent assay (ELISA) and of insulin by radioimmunoassay (RIA). Homeostatic model assessment insulin resistance (HOMA-IR) and visfatin/insulin ratio were calculated. RESULTS: In the MetS group significantly higher (p < 0.01) plasma concentrations of insulin and HOMA-IR values but similar visfatin levels were observed than in the non-MetS group. As a consequence of the significantly higher plasma insulin concentration the visfatin/insulin ratio was significantly lower in the MetS group (p < 0.05). The visfatin/insulin ratio correlated inversely with anthropometric parameters such as body mass, BMI, body fat and waist circumference (r = -0.41, p = 0.0003; r = -0.42, p = 0.0002; r = -0.29, p = 0.01; r = -0.23, p = 0.04, respectively). CONCLUSIONS: We conclude that the visfatin/insulin ratio declining with increasing visceral obesity may predispose to the development of insulin resistance.

Plasma visfatin and tumor necrosis factor-alpha (TNF-α) levels in metabolic syndrome.

BACKGROUND: Experimental studies have shown that tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) downregulate visfatin gene expression in adipocytes. On the other hand, the induction of cytokine production by visfatin in leucocytes and monocytes has also been described. AIM: To assess the possible interrelation between plasma concentrations of visfatin and TNF-α and TNF soluble receptor in obese women fulfilling, or not, the criteria of metabolic syndrome (MS). METHODS: Ninety two obese women were included in the study. Metabolic syndrome, based on IDF criteria (2005) was diagnosed in 71 subjects (mean age 53 ± 9 years; body mass index 39.1 ± 5.6 kg/m(2), waist circumference 109.6 ± 11.4 cm). The remaining 21 formed the non-MS subgroup (mean age 52 ± 9 years, body mass index 36.3 ± 5.2 kg/m(2), waist circumference 104.7 ± 11.0 cm). Fourteen healthy normal weight women served as controls. In all subjects, body composition was assessed by the bioimpedance method. RESULTS: In the MS subgroup, but not in the non-MS subgroup, visfatin levels were significantly higher than in controls. We did not observe any significant difference in plasma concentrations of visfatin, TNF-α or sTNFRs between the MS subgroup and the non-MS subgroup. Only in the MS subgroup and in the combined analysis of all study subgroups did plasma visfatin concentrations correlate significantly with TNF-α levels (R = 0.31, p = 0.01, R = 0.21, p = 0.03; respectively). Additionally, in the MS subgroup there was a positive correlation between visfatin levels and insulin resistance (R = 0.53, p = 0.01). CONCLUSIONS: Our findings suggest that visfatin in metabolic syndrome should be regarded as a proinflammatory factor indirectly favouring the development of insulin resistance.

[A little-known new components of the appetite control]. / Malo znane nowe ogniwa regulacji poboru pokarmu.

Appetite control is a complex process regulated by both neurotransmitters, such as: appetite- increasing neuropeptide Y (NPY), Agouti related peptide (AgRP), orexins A and B, as well as appetite-suppressing propiomelanocortin (POMC) and a peptide (CART) which transcription is regulated by cocaine and amphetamine. In addition, other factors are involved such as hormones of the alimentary tract (appetite-stimulating ghrelin and appetite-decreasing cholecystokinin, peptide YY, glucagon like peptide-1, oxyntomodulin, pancreatic peptide, enterostatin and amylin). In this process participates also leptin, an appetite-suppressing hormone produced by adipocytes. The authors focus on other, little-known neurotransmitters involved in the control of appetite: RFamide Peptide (QRFP43) and VGF-Derived Peptide, TLQP-21, as well as xenin, another hunger-decreasing hormone of the alimentary tract.