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Rationale. Psoriasis is a prevalent chronic inflammatory disease with worldwide distribution affecting approximately 2% of the Caucasian population. There have been many population- and family-based studies that agree on the strong genetic component of this disease. Several studies have investigated the relationship between cytokine gene polymorphisms, psoriasis, and the occurrence of comorbidities but their data are conflicting. Objective. This study examines cytokine gene single-nucleotide polymorphisms (SNPs) in the context of psoriasis and metabolic syndrome, with a focus on the occurrence of comorbidities in psoriasis patients. The working hypothesis is that particular SNPs may predispose to an accelerated disease course and more comorbidities in psoriasis patients. Methods. This cross-sectional study was carried out in 2016 in the Dermatology Department of "Elias" University Emergency Hospital, Bucharest and included 82 psoriasis patients. Several clinical and laboratory parameters were recorded, and the presence of metabolic syndrome (MetS) was noted. Using real-time PCR, we tested for the following SNPs: rs361525, rs1800629, rs1800896, rs610604, rs17782313. Results. Disease severity was not significantly influenced by any of the five studied SNPs. Gene polymorphism of rs17782313 was found to influence the occurrence of psoriatic arthritis. In these patients, rs610604 and rs17782313 polymorphisms were associated with the presence of diabetes mellitus. Furthermore, rs17782313 influenced the presence of obesity, heterozygotes being more at risk. Our data suggested that MetS occurred independently of the five studied SNPs. Discussion. The influence of certain cytokine gene polymorphisms on multiple organ systems is justification enough for further analysis of the genetic and molecular mechanisms of metabolic syndrome development in psoriasis patients. [ABSTRACT FROM AUTHOR]

Background: Psoriasis vulgaris is a chronic inflammatory hyper-proliferative disease of the skin, scalp, nails, and joints. It has been hypothesized that prolactin (PRL) may modulate the skin immune system and be involved in the pathogenesis of psoriasis. Psoriasis exerts significant, negative impact on patients' quality of life. Relatively high rates of depression are reported in patients with psoriasis. Objectives: The aim of this work was to study the possible role of PRL in the pathogenesis of psoriasis and its correlation with the disease activity, clinically, molecular and emotional status of patients. Subjects and methods: A total of 41 samples were analyzed - 21 new patients with psoriasis vulgaris before treatment and 20 after therapy - were included in this study. In all patients, we determined skin disease activity according to the PASI index, the psychological impact measured with HAMA and HAMD scales and the quality of their life measured by DLQI. The concentration of prolactin in the serum was measured by enzyme-linked immunosorbent assay (ELISA), and the concentration of soluble receptor of IL-2 was measured with automated immune chemiluminescent system - IMMULITE procedure. Results: The PRL and sIL2R serum levels were significantly decreased after three months of therapy, at least 50% with a p value <0.00001. Clinical, hormonal, molecular correlations between before and after therapy were measured with a statistically significant result. Correlations between HAMA-PRL and DLQI-PRL before therapy were not statistically significant, only the relationship between HAMD and PRL was demonstrated. After treatment, we obtained a significant clinical, psychological and paraclinical (especially serum levels of prolactin and sIL2R) decreased and relevant response on all the patients treated and analyzed. Conclusion: Prolactin seems to have a role in the pathogenesis of psoriasis and may represent a cause and/or a consequence of psoriasis pathology. The most likely scenario is that PRL enhances interferon-induced chemokine production in keratinocytes, thereby facilitating cutaneous T-cell infiltration. This raises the intriguing light that PRL may offer a novel future therapeutic target in psoriasis and other skin diseases that worsen in response to psychological distress. [ABSTRACT FROM AUTHOR]

Introduction: The polypeptide hormone prolactin (PRL) represents the pituitary modulator of lactation and reproduction. Currently, we discuss the wide range of PRL actions "beyond the mammary horizon". Multiple studies had showed the role of PRL as a cytokine, with comparable structural motifs, similar receptor structures and signal transduction pathways. Almost two decades ago it was first hypothesized that PRL acts as a neuroendocrine modulator of both skin epithelial growth and the skin immune system. Moreover, it was described the PRL circuit between the skin and the central nervous system. Psoriasis vulgaris, an immunologically mediated skin disease, is a common disorder, having as main pathogenetic mechanisms the chronic inflammation and keratinocytes hyperproliferation. Psoriasis vulgaris is not a life threatening disease, but affects seriously the quality of life; there is still no causative treatment. Methods: After we describe the essentials of general PRL biology, the almost ubiquitous distribution of its receptors and the vast list of extrapituitary PRL-expressing tissues, our aim is to summarize clinical observations that provide insights into how PRL may impact on the psoriatic skin and define research for better characterize the complex role of PRL in human skin biology and pathology. Results: Focusing on psoriasis, as a stress-related disease, we then discuss the possible role of PRL/ PRLR in its pathology and may identify one potential biological marker and therapeutic targets for the management of this autoimmune skin disorder. Conclusion: This theory/concept can now be integrated into current views on the multilevel neuroendocrine-immune communication along the brain-skin axis in health and disease. Due to the pathogenic complexity, there is no curative treatment for psoriasis and pharmacological modulation of PRL may represent a future target to restrict the lesions in psoriatic patients. [ABSTRACT FROM AUTHOR]