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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., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Aim: The aim of the study was to assess of sTNFαR1 concentration in the serum of patients with localized scleroderma (in comparison with a control group)., Material and Methods: This was a prospective study. The patients with localized scleroderma were divided into two groups: 21 persons treated with PUVA therapy and 20 persons treated with procaine penicillin. In the case of the patients treated with intramuscularly administered procaine penicillin (dose: 2,400,000 IU/day), achievement of a total dose of at least 30 million IU/day was considered as the end of the therapy. In the group of patients treated with photochemotherapy, the single initial dose during a PUVA session was 0.5 J/cm 2 and it was increased by 0.5 J/cm 2 every other day to reach the maximum value of 10 J/cm 2 , depending on the clinical condition. The study involved three sessions a week., Results: sTNFαR1 concentration in the serum of patients with localized scleroderma was significantly higher in comparison with the control group and correlated with the skin damage index. The difference in the determined particle level was higher in the group of patients undergoing photochemotherapy (median: 106.25 ng/ml) than in the group taking penicillin (median: 81.50 ng/ml). Patients treated with PUVA sessions demonstrated a greater decrease in sTNFαR1 concentration and an improvement of the clinical condition after therapy completion., Conclusions: The obtained results suggest a potential role of sTNFαR1 in the pathogenesis of localized scleroderma., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2020 Termedia Sp. z o. o.)

Introduction: Chronic spontaneous urticaria constitutes an interdisciplinary problem and its pathogenesis is still a subject of debate. Overweight and hyperlipidemia are supposed to be related to chronic spontaneous urticaria. Fatty tissue can be the source of adipokines., Aim of the Study: To assess the potential role of adiponectin in chronic spontaneous urticaria pathogenesis., Material and Methods: The study included 52 chronic spontaneous urticaria patients and 43 healthy controls. The patients were divided into two subgroups: patients with wheals only, and patients with urticaria and an accompanying angioedema. The adiponectin concentration was measured in all studied subjects., Results: No statistically significant difference in adiponectin level was determined between the studied groups and subgroups., Conclusions: We are among the first to present the results of study to determine a possible role of adipokines in chronic spontaneous urticaria pathogenesis. We did not observe any difference in adiponectin level. In our opinion, it is necessary to conduct further analyses in this field., Competing Interests: The authors declare no conflict of interest., (Copyright © 2020 Termedia.)

Psoriasis is a chronic, recurrent, inflammatory, and proliferative skin disease. Its etiology has not yet been fully assessed, but undoubtedly it is a multifaceted disease. The key role in its pathomechanism is played by genetic, immunologic, and environmental factors and stress. If traditional methods of psoriasis treatment (phototherapy, methotrexate, retinoids, cyclosporine A) fail, we reach for the following biopharmaceuticals - infliximab, etanercept, adalimumab, or ustekinumab. However, genetic engineering progress discovers new possibilities - the pending clinical trials involve IL-17, IL-23 antagonists, PDE4 and -3 and -1. Psoriasis etiopathogenesis mainly involves the IL-17A, IL-17F, and IL-17A/F subtypes, which affect the keratinocytes. The biological therapy molecularly oriented with the antagonists of interleukin 17 is based mainly on the influence onto the cytokine in the manner that prevents it from binding with the receptor. Three biopharmaceuticals are currently under third phase studies: two fully humanized antibodies neutralizing IL-17 - ixekizumab and secukinumab, and one human monoclonal antibody, brodalumab. The below work will be devoted to the analysis of possible undesirable symptoms, which were observed during the studies. We will try to review the latest literature concerning the most important clinical trials conducted in many centers., (© 2019 The International Society of Dermatology.)

The rapid progress of genetic engineering furthermore opens up new prospects in the therapy of this difficult-to-treat disease. IL-23 inhibitors, phosphodiesterase 4 (PDE4) inhibitors, and Janus kinase (JAK) inhibitors are currently encouraging further research. Two drugs which are IL-23 inhibitors are now in phase III of clinical trials. The aim of the action of both drugs is selective IL-23 inhibition by targeting the p19 subunit. Guselkumab is a fully human monoclonal antibody. Tildrakizumab is a humanized monoclonal antibody, which also belongs to IgG class and is targeted to subunit p19 of interleukin 23 (IL-23). Phosphodiesterase inhibitors exert an anti-inflammatory action and their most common group is the PDE4 family. PDE4 inhibits cAMP, which reduces the inflammatory response of the pathway of Th helper lymphocytes, Th17, and type 1 interferon which modulates the production of anti-inflammatory cytokines such as IL-10 interleukins. The Janus kinase (JAK) signaling pathway plays an important role in the immunopathogenesis of psoriasis. Tofacitinib suppresses the expression of IL-23, IL-17A, IL-17F, and IL-22 receptors during the stimulation of lymphocytes. Ruxolitinib is a selective inhibitor of JAK1 and JAK2 kinases and the JAK-STAT signaling pathway. This article is a review of the aforementioned drugs as described in the latest available literature., (© 2017 Wiley Periodicals, Inc.)

Treatment during pregnancy is problematic. The Food and Drug Administration established drug categories to help in the treatment process. First-generation antihistamines are considered safe but they have sedative properties. Second-generation antihistamines cause less adverse reactions but besides cetirizine and loratadine they belong to category C. All retinoids should be avoided during pregnancy due to the risk of fetal malformations. Antimalarial drugs should be considered based on the clinical data. Sulfones can be considered as safe for use during pregnancy only with proper monitoring. Prednisone is administered in pregnancy. Other glucocorticosteroids have a different safety profile. Cyclosporine A treatment should be reserved as rescue therapy in severe stages of the disease. Treatment during pregnancy should be precise when it comes to pregnant woman and safe for the fetus.

Psoriasis is a chronic immunological skin disease and patients with this disorder typically experience a significant decrease in their quality of life. The disease is traditionally managed with topical and systemic agents (retinoids, ciclosporin A, methotrexate), but these treatment options are often long-term and their effects can be inconsistent and not ideal. The use of biological drugs in dermatological treatment is relatively new and began in the early 2000s. It should be noted that, in most countries, in order for biological treatment to be administered, specific criteria must be met. The current treatment options for psoriasis and psoriatic arthritis include tumour necrosis factor alpha (TNF-α) blockers, interleukin (IL)-12 and IL-23 inhibitors, T cell inhibitors and B cell inhibitors. These classes of biological drugs are characterised by protein structure as well as high molecular weight and their effectiveness is evaluated based on the Psoriasis Area and Severity Index (PASI), Body Surface Area (BSA) and the Dermatology Life Quality Index (DLQI). TNF-α antagonists are one such class of biological drugs which includes infliximad, etanercept and adalimumab. Infliximab is a chimeric protein that is administered via intravenous infusions as a monotherapy in psoriasis vulgaris. Etanercept is indicated for use in both psoriasis vulgaris and psoriatic arthritis and it is the only drug that can be used as a treatment for children under the age of 8 with psoriasis. The drug is administered subcutaneously. Finally, adalimumab is a fully human monoclonal antibody that neutralises both free and membrane-bound TNF-α and is used in the treatment of psoriasis vulgaris and psoriatic arthritis. This article reviews the latest research in the use of TNF-α for the treatment of moderate to severe psoriasis and psoriatic arthritis. The results of research in this field are promising and confirm the effectiveness and safety of biological drugs as dermatological treatments for psoriasis. In particular, adalimumab, etanercept and infliximab are promising therapeutic options for patients with moderate to severe psoriasis and psoriatic arthritis who are unresponsive to conventional treatment strategies and they can significantly improve the quality of lives in patients with this disease., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)

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 (β = -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., (© 2012 John Wiley & Sons Ltd.)

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.

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.

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.