Zygmunt Adamski

New insights into the role of T cells in pathogenesis of psoriasis and psoriatic arthritis

Abstract Psoriasis is a chronic, relapsing, autoimmune disorder of the skin affecting 2–3% of general population. Approximately 30% of psoriasis patients are also affected with the psoriatic arthritis, a chronic inflammatory spondyloarthritis. The review aims to present the current knowledge on immunopathogenesis of both diseases to emphasize the involvement of various T helper cell subsets. An extensive literature search in electronic databases was performed on the topic of different Th cell subsets’ involvement in the pathogenesis of psoriasis and psoriatic arthritis. Studies were assessed and selected to present the recent progress in the area. Current data strongly suggest that both PsO and PsA are T cell-mediated diseases, with a key role of various proinflammatory cytokines in their development. The involvement of T cells is highlighted by the superior efficacy of biologic therapies targeting T cell-derived proinflammatory cytokines in both diseases. Initially, PsO and PsA were thought to be Th1-mediated diseases; however, in the last years, several studies have shown the important role of other T cell subsets, including Th17, Th22, Th9 and Treg cells, in the pathogenesis of both diseases, which has led to the development of new therapies.

The effects of the microbiota on the host immune system

Abstract The human gastrointestinal track harbors hundreds of species of commensal organisms, collectively known as microbiota. The composition of the intestinal microbiota is changeable by various factors, such as host genotype, diet, antibiotics, pathogen infections, among others. Changes in these factors can cause microbiome disruption known as dysbiosis, leading to the outgrowth of potential pathogenic bacteria or decrease in the number of beneficial bacteria. Dysbiosis has been implicated in numerous inflammatory and autoimmune diseases. This review is focused on host–microbiota interactions, specifically on influence of bacterial-derived signals on immune cell function and the mechanisms by which these signals modulate the development and progression of inflammatory and autoimmune diseases.

The effect of cigarette smoking on the clinical course of inflammatory bowel disease

Introduction Cigarette smoking is considered an important risk factor for developing Crohns disease (CD), contributing to a more severe course of the disease. Conversely, smoking is believed to have a beneficial effect on the course of ulcerative colitis (UC), a second major condition of inflammatory bowel disease (IBD). Aim To investigate the effect of tobacco use on the clinical course of IBD. Material and methods A group of 95 adults with IBD were enrolled to the study. Demographic and clinical data of patients as well as their smoking status were analysed based on their medical history. Values were considered significant when p ≤ 0.05. Results Current smokers constituted the majority of CD patients. They tended to develop a more severe course of the disease, compared to former smokers and non-smokers. Current smokers suffered a moderate-to-severe form of the disease and required immunosuppressive therapy more frequently. They were also hospitalised and underwent surgeries more frequently than patients from other investigated subgroups. The study failed, however, to fully confirm the beneficial effect of smoking on the clinical outcome of UC. The investigated non-smokers and former smokers suffered a more severe disease, but the analysis did not find any statistical differences in the frequencies of hospitalisations nor immunosuppressant usage among the investigated subgroups. Conclusions The study confirmed a detrimental effect of smoking on the outcome of CD, but failed to fully confirm its beneficial effect on UC.

Inhibitors of phosphodiesterase 4 (PDE 4): A new therapeutic option in the treatment of psoriasis vulgaris and psoriatic arthritis

Abstract Psoriasis vulgaris and psoriatic arthritis are inflammatory diseases in which inflammation and sustained inducing lesions result from immune disorders associated with overactivity of T cells that produce multiple proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α) and interleukin (IL): IL-2, IL-12, IL-17, IL-22 or IL-23. Modern treatment of these diseases is focused on reducing the inflammatory process responsible for the development of the disease. In recent years, the treatment of psoriasis is developing at a dynamic rate. Such therapeutic advances are contributed to the possibility of patient therapy through the use of some registered biologic agents, such as TNF-α inhibitors (infliximab, etanercept and adalimumab), and an inhibitor of the p40 subunit common to IL-12 and IL-23 (ustekinumab). In addition to the already registered medications for the indications mentioned above, there is a large group of preparations that are currently undergoing clinical trials in Europe, Canada and the United States, which provides hopes of therapy efficacy and safety.

Factors affecting response to biologic treatment in psoriasis

Psoriasis is a chronic, immune‐mediated inflammatory skin disease, affecting approximately 2–4% of the population in western countries. Patients with a more severe form of the disease are typically considered for systemic therapy, including biologics. In spite of the overall superiority of biologic agents, the treatment response may differ substantially among individual patients. As with other medical conditions, a range of factors contribute to response heterogeneity observed in psoriasis. Proper identification of these factors can significantly improve the therapeutic decisions. This review focuses on potential genetic and nongenetic factors that may affect the treatment response and outcomes in patients with psoriasis.

Basal cell carcinoma – diagnosis

Basal cell carcinoma is the most common skin cancer in the Caucasian population. The cancer arises in sun exposed areas of the skin. The incidence of morbidity is high and it is still growing. The metastatic rate is low, but the enlarging tumor may cause severe tissue disfigurement and a poor cosmetic outcome. The diagnosis is usually clinical but there are many subtypes of this carcinoma and correct diagnosis is the clue to appropriate treatment of the lesion. The main problem in basal cell carcinoma management is the high recurrence rate.

Selected biologic markers of inflammation and activity of Crohn’s disease

Abstract The study aimed to compare the accuracy of selected biologic markers in assessing the disease activity in patients with Crohn’s disease (CD). The analysis included serum IL-2, IL-6, IL-17, TNF-α, IFN-γ, hsCRP, peripheral CD4 + CD25 + FOXP3 + regulatory T cells, as well as fecal calprotectin and lactoferrin. A group of 55 adults with CD was enrolled to the study. Disease activity was assessed using Crohn’s Disease Endoscopic Index of Severity (CDEIS), which currently represents the gold standard for the evaluation of endoscopic activity. For clinical activity scoring, the Crohn’s Disease Activity Index (CDAI) was used. Concentrations of investigated markers were estimated by means of flow cytometry and enzyme-linked immunosorbent assays, and the results were correlated with both indices. The study demonstrated that both fecal markers, i.e. calprotectin (r = 0.827, p < 0.001) and lactoferrin (r = 0.704, p < 0.001), correlate closely with CDEIS score, and might be used to evaluate the severity of CD in clinical setting. The correlation of those markers with CDAI was also significant, with r = 0.742 for calprotectin (p < 0.001) and r = 0.675 for lactoferrin (p < 0.05). As for the other investigated markers, only hsCRP (r = 0.672, p < 0.001) and IL-17 (r = 0.296, p < 0.005) correlated closely with CDEIS. The correlation of the markers with CDAI was also significant, though weaker, with r = 0.518 for hsCRP (p < 0.001) and r = 0.296 for IL-17 (p < 0.05). The study showed that IL-17, despite its vague role in the pathogenesis of CD, might be a useful marker, comparable with hsCRP, in assessing the activity of the disease.

Itching sensation in psoriatic patients and its relation to body mass index and IL-17 and IL-31 concentrations

Introduction According to available data, pruritus is a common symptom of psoriasis, however its characteristics and pathogenesis are not clearly understood. Aim The main aim of this study was to assess itching sensation among patients suffering from psoriasis, including its incidence and severity. All factors triggering and worsening pruritic symptoms were also carefully analyzed. The authors assessed the relationship of itch with body mass index (BMI) and severity of disease. Moreover, serum levels of interleukin 17 (IL-17) and IL-31 were analyzed in relation to Psoriasis Activity and Severity Index, BMI and severity of pruritus. Material and methods The study group consisted of 60 patients with plaque-type psoriasis. Analysis of impact of pruritus on the quality of life and worsening factors was based on the questionnaire. The severity of pruritus was assessed with the use of two independent scales. Serum IL-17 and IL-31 levels were measured in 30 patients suffering from psoriasis and in 10 healthy controls using immunoassay tests. Results 88.3% of analyzed patients complained of itch and the most common factor which exacerbated pruritus was stress (39.6%). Pruritus in psoriasis was independent of gender, illness duration and extent of skin lesions. The average intensity of pruritus was assessed as moderate and did not correlate significantly with BMI level, IL-17 and IL-31. Conclusions Since the pathogenesis of pruritus in psoriasis is not fully understood, further investigation in this area needs to be conducted. Pruritus may be considered as a characteristic feature of psoriasis and, besides the skin lesions, should be a target in dermatological treatment to improve patients quality of life.

Long-term evaluation of ink clearance in tattoos with different color intensity using the 1064-nm Q-switched Nd:YAG laser

The aim of the study was to evaluate the efficacy of tattoo removal treatments using the 1064‐nm Q‐switched (QS) Nd:YAG laser.

Usefulness of selected laboratory markers in ulcerative colitis

IntroductionThis study aimed to compare the accuracy of selected laboratory markers in assessing disease activity in patients with ulcerative colitis (UC). The analysis included serum IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α, IFN-γ, hsCRP, peripheral regulatory T cells, as well as fecal calprotectin and lactoferrin.Patients and methodsA group of 45 adults with UC was enrolled in the study. Disease activity was assessed using the Mayo endoscopic index, while for clinical activity scoring, the Clinical Activity Index (CAI) was used. Concentrations of markers investigated were estimated by means of flow cytometry and enzyme-linked immunosorbent assays: the results were correlated with both indices.ResultsThe study demonstrated that both fecal markers, i.e. calprotectin (r = 0.880, P<0.001) and lactoferrin (r = 0.799, P<0.001) correlated closely with the Mayo endoscopic score, and might be used to evaluate the severity of UC in the clinical setting. The correlation of these markers with CAI was also significant, with r = 0.831 for calprotectin (P<0.001) and r = 0.672 for lactoferrin (P<0.05). As for the other markers investigated, only IL-6 (r = 0.598, P<0.001), IL-17A (r = 0.587, P<0.005), and TNF-α (r = 0.701, P<0.001) correlated closely with the Mayo endoscopic index. The correlation of the markers with CAI was also significant, though weaker, with r = 0.525 for IL-6 (P<0.001), r = 0.587 for IL-17A (P<0.05), and r = 0.624 for TNF-α (P<0.001).DiscussionDespite the fact, that UC is generally considered to be an IL-13-driven, Th2-like type of disease, markers of inflammation such as serum interleukin (IL)-6, IL-17, TNF-α, fecal calprotectin and lactoferrin might be useful in assessing disease activity.