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Background and Objectives: Chronic spontaneous urticaria (CSU) is a distressing skin condition, which manifests as red, swollen, itchy, and sometimes painful hives or wheals appearing on skin. Recently, CSU has been associated with bradykinin release, which was previously discovered to be the main trigger of hereditary angioedema attacks. To study the role of bradykinin receptors 1 (BR1) and 2 (BR2) in the etiopathogenesis of CSU. Materials and Methods: A total of 60 individuals, 30 patients with CSU and 30 healthy subjects, were recruited to the study. CSU was diagnosed in accordance with the standardized protocol of dermatological assessment of skin symptoms. The level of bradykinin receptors was determined in populations of CD3+, CD4+, and CD8+ lymphocytes as well as in CD14++CD16−, CD14++CD16+ and CD14+CD16+ monocytes. In addition, urticaria activity score summed over 7 days (UAS-7) was assessed and correlated with BR1 and BR2 expression. Results: A statistically significant higher concentration of BR1 expression in lymphocytes was found in patients with CSU, compared to the control group (p &lt, 0.001). Moreover, a statistically significant positive correlation was observed between UAS-7 and BR1/BR2 expression in CD14++CD16− cells (p = 0.03, R = 0.4). Conclusions: Bradykinin receptors are elevated in selected populations of lymphocytes in symptomatic CSU patients compared to healthy controls, indicating their role in the etiopathogenesis of the disease.

Introduction Bacillary angiomatosis (BA) is a rare, opportunistic infectious disease caused by the aerobic Gram-negative bacilli Bartonella henselae or Bartonella quintana. The main reservoir for those microbes are cats. The disease mostly affects immunocompromised patients with human immunodeficiency virus infection, after organ transplantation, undergoing corticosteroid and methotrexate therapy or with oncological history. Case report We represent the case of a 65-year-old man who reported to the Department of Dermatology with a high fever and numerous nodular skin lesions on the 5th month of kidney transplantation. At that time, his immunosuppressive therapy consisted of tacrolimus 6 mg/day, mycophenolate mofetil 2 g/day, and prednisone 5 mg/day. Laboratory tests revealed an increased leukocyte count and elevated values of acute-phase proteins, but blood cultures were negative. Skin biopsy was performed and BA was diagnosed. The patient was given oral doxycycline 100 mg twice a day. During antibiotic therapy, his body temperature normalized and skin lesions began to resolve. The patient continued the above treatment for the next 3 months with good tolerance, and no relapse occurred in 1 year. Conclusion BA should be listed among possible opportunistic infections in organ transplant recipients.

Atopic dermatitis (AD) and chronic spontaneous urticaria (CSU) are common chronic and recurrent dermatoses. The role of vitamin D in the immunological processes, including the development of inflammation, has been the subject of numerous studies. The feasible measurement of vitamin D serum concentration and possibly supplementation necessitates the assessment of its impact on the clinical severity of mentioned diseases.The aim of the study was to determine the relationship between blood serum vitamin D concentration and the severity of clinical symptoms in the group of adults suffering from AD or CSU.The study was conducted in 2018 on groups of patients suffering from AD or CSU. Serum vitamin D concentration was determined by electrochemiluminescence assay. Student's t-test was adopted to compare vitamin D levels between groups. Spearman's rank correlation coefficient was used to assess the correlation between vitamin D concentration and the severity of AD (according to the SCORAD scale) and CSU (according to the UAS 7 scale).There was not found any statistically significant relationship between the severity of skin lesions scores in the course of AD and CSU and serum vitamin D concentration.

Introduction: Psoriasis is a chronic inflammatory skin disease with immunologic etiology. Aim: To investigate the levels of the proinflammatory cytokines tumor necrosis factor \alpha ($TNF-\alpha$), interleukin 23 (IL-23) and IL-17 in patients with psoriasis and psoriatic arthritis with concomitant metabolic syndrome. Material and methods: This study included 60 patients with severe psoriasis. Results: In patients with arterial hypertension concomitant with psoriasis, no statistically significant differences in cytokine levels were observed. On the other hand, in the group of patients diagnosed with diabetes, an increased level of IL-17 was observed. In patients with lipid disorders, the results were similar to the results of patients with diabetes. Conclusions: It is very important to study immunologic mechanisms responsible for the presence and severity of psoriasis, in order to personalize the therapy in the future and optimize the effect of action on the basic disease and on concomitant disorders.

Introduction: The incidence of metabolic syndrome is estimated at 15-24% in the general population and at 30-50% in patients with psoriasis. A probable cause of the described correlation is a constant release in chronic dermatosis of proinflammatory cytokines and their influence on individual systems and organs. Aim: Assessment of the concentration of the proinflammatory cytokines (IL-12, IL-23, IL-17 and $TNF-\alpha$) in blood serum and their correlation with the intensity of skin lesions, the presence of psoriatic arthritis and the risk of development of obesity and metabolic syndrome. Material and methods: The concentrations of subunit p70 IL-12, IL-17 and IL-23, and $TNF-\alpha$ in subjects with psoriasis and metabolic syndrome were determined. Results: The level of the studied cytokines, IL-17, IL-23 and $TNF-\alpha$ was higher in patients diagnosed with psoriasis. Higher levels of IL-17, IL-23 and $TNF-\alpha$ were observed in patients with metabolic syndrome accompanying psoriasis. A higher level of IL-17 and IL-23 was found in sera of patients with psoriatic arthritis in comparison to normal psoriasis. Conclusions: In the study, a higher level of IL-17 and IL-23 was also shown in patients with psoriatic arthritis in comparison to patients with normal psoriasis. The effectiveness of anti-IL12/23 drugs in psoriatic arthritis is a confirmation of the obtained results of the studies. Additionally, the increased level of IL-17, both in patients with metabolic syndrome and with psoriasis, could indirectly indicate an increased cardiovascular risk in patients with affected joints in comparison to psoriasis affecting only the skin.

Introduction Hereditary angioedema (HAE) is a rare autosomal dominant disease caused by genetic dysfunction of C1 inhibitor (C1-INH) due to mutations in the SERPING1 gene. The disorder is mediated mainly by bradykinin. The clinical course of the disease is varied and not related to genetic changes. Objectives We aimed to evaluate redox homeostasis of peripheral blood mononuclear cells (PBMCs) in patients with HAE due to C1-INH deficiency (C1 INH HAE) by measuring the levels of reactive oxygen species (ROS) of PBMCs as well as plasma advanced glycation end products (AGEs) and advanced oxidation protein products (AOPPs). We also aimed to assess the effect of bradykinin on ROS levels. Patients and methods We enrolled 30 adults with C1-INH-HAE and 15 healthy individuals. The levels of ROS were measured by flow cytometry, while the plasma levels of AGEs and AOPPs were determined spectrophotometrically by enzyme‑ linked immunosorbent assays. Results Basal and hydrogen peroxide (H2O2)-induced ROS levels were higher in patients with HAE when compared with controls (P = 0.002 and P = 0.001, respectively), indicating abnormalities in redox homeostasis. Plasma AOPP and AGE levels were similar in both groups. Bradykinin reduced basal and H2O2-induced ROS generation in PBMCs only in patients with HAE (P = 0.03). Conclusions The higher basal and H2O2-induced ROS levels in patients with C1 INH HAE indicate redox imbalance. However, by reducing basal and H2O2-induced ROS levels, bradykinin shows antioxidant action in this disorder.

Introduction Chronic urticaria is a complex disease process in which chronic spontaneous urticaria (CSU) and chronic inducible urticaria are distinguished. Its etiopathogenesis still remains unknown. Some recent studies indicated a significant participation of vitamin D in the etiopathogenesis of urticaria. In 40-50% of patients with CSU on the basis of the positive result of the autologous serum skin test (ASST), autoimmunological background of the disease is diagnosed. Moreover, numerous test results confirm involvement of the coagulation system/fibrinolysis and non-infectious inflammatory factors in the pathophysiology of CSU. Aim To determine whether some factors may play a role in pathogenesis and contribute to the severity of chronic spontaneous urticaria. Material and methods One hundred and forty-two patients with diagnosed CSU were enrolled in the study. The activity of urticaria was assessed using the UAS-7 (Urticaria Activity Score). The study participants were divided into 4 groups depending on the UAS-7. ASST was performed and blood was collected to determine the biomarkers (CRP, vitamin D, D-dimers, fibrinogen, MPV, PLT). Results Statistical analysis was performed using Statistica 13. A statistically significant difference between groups with various activity of urticaria in D-dimer concentration average values (p < 0.05) was observed. Moreover, a statistically significant negative correlation between activity of urticaria and vitamin D concentration (p < 0.001) was noted. Conclusions Our results might support the possible involvement of both coagulation and fibrinolysis pathway and vitamin D in the urticaria pathomechanism. Further prospective studies in larger populations conducted at multiple centres are required to expand further our findings.

Allergy to house dust mite (HDM) such as Dermatophagoides pteronyssinus, nickel and infection by Staphylococcus aureus are frequent in atopic dermatitis. Understanding molecular mechanisms responsible for pathological reactivity of immune cells on these substances may enable to individualize and consequently improve treatment of atopic patients. Furthermore, better understanding of nickel action can also prevent from postoperative complications in patients sensitive to nickel with atopic dermatitis.

Introduction The tumor necrosis factor (TNF-α) was initially described as lymphotoxin or cachectin. The discovery of therapies blocking the action of TNF-α, in 1988, started a new era in the therapy. One of often reported adverse effects related to the use of TNF-α antagonists is induction of the formation of autologous antibodies and antibodies neutralizing anti-TNF drugs. The development of anti-TNF-induced lupus or classical drug-induced lupus is more rarely reported.

Introduction Protein contact dermatitis (PCD) is an IgE-dependent allergic reaction which, despite enormous progress in knowledge, remains a 'non-diagnosed' nosologic unit in contemporary medicine. Skin lesion, with a chronic and recurring course, are analogous with the clinical picture in allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD); skin patch tests, however, are usually negative. This makes the diagnostics difficult, prevents a correct diagnosis and treatment based on the avoidance of allergen. Case description A 48-year-old woman presented with erythemato-squamous skin lesions, accompanied by a strong itching, occurring on hands for about 6 months. The patient attributed the occurrence of skin lesions to household chores, above all - cooking and contact with food. The contact allergy was not confirmed. Positive results of the prick-by-prick test were observed for potato. Based on the above results, contact eczema induced by potato protein was diagnosed. Allergen elimination and use of emolients were prescribed. A complete remission of skin lesions was obtained. Discussion PCD is rarely diagnosed, which is why there is no substantial epidemiologic data. It is estimated that about 50% of cases are related to atopy. This occurs more often in patients with a damaged dermal-epidermal barrier. Most often, the same products eaten by subjects do not produce any effects. A correct assessment of the substance provoking the occurrence of skin lesions is very important, as most often the products concerned are those commonly used in the household. A detailed PCD diagnostics is very important for obtaining the optimal treatment results.

The term “microbiome” defines the collective genome of all commensal, symbiotic, and pathogenic microbes living in the human body. The composition of microbiota in the gut and skin is influenced by many factors such as the stage of life, nutrition, lifestyle, and gender. In the past few years, several scientific papers have demonstrated an implication of microbiota in many immune-mediated diseases, for example, diabetes, ulcerative colitis, and multiple sclerosis. The alterations in the proportion of gut microbiota have emerged as potential immunomodulators with the capacity to induce physiologic as well as pathologic immune responses against the human body, causing inflammation and destruction of tissues or organs. The microbiota influences the differentiation of adaptive immune cells not only in the gut but also in the skin. Alopecia areata (AA) is a dermatologic disorder which causes hair loss in most cases resistant to treatment. There are some clinical and experimental evidences indicating that AA is the demonstration of autoimmune attack against hair follicles. The factors that may implicate such an autoimmunity in AA still remain unknown. Despite more and more evidences demonstrate that human microbiome plays a key role in human health and diseases, to the best of our knowledge, no study has been conducted to analyze an implication of microbiome in the pathogenesis of AA. Undoubtedly, there is a need to performing a study which might explain the involvement of gut and skin microbiota in the unclear pathogenesis of AA and lead to alternative treatment options for numerous patients suffering from current treatment limitations.

In the course of radiation therapy different types of adverse reactions of the skin are observed in approximately 95% of patients. Among the various complications encountered after radiotherapy, radiation recall dermatitis (RRD) deserves special attention. Radiation dermatitis is a form of delayed hypersensitivity of irradiated skin, and the direct trigger factors are medicines – most chemotherapeutics. The reaction is an inflammatory dermatosis. It is limited to previously irradiated skin and appears a number of months after radiotherapy. The aetiology of RRD is still unclear. Its clinical presentation may vary from mild erythema to necrosis and ulceration. The article presents the case of a 50-year-old patient, who after radiotherapy for breast cancer, during the hormonal therapy (tamoxifen), developed RRD type skin reactions after skin application of Amol. The article presents a detailed differential diagnosis of skin changes of RRD type, and discusses the principles of treatment and prevention.

Introduction Palisaded neutrophilic and granulomatous dermatitis (PNGD) are terms which include such diseases as rheumatoid nodules, Churg-Strauss granuloma, and interstitial granulomatous dermatitis with arthritis. This heterogeneous group was first described in 1965. It is associated with immunological diseases. There are reported cases of coexistence with systemic lupus erythematosus, rheumatoid arthritis, Wegener's granuloma, inflammatory bowel disease, generalized vascular inflammation, and lymphoproliferative disorders. The etiology of the disease is unknown. It is probable that the deposition of immune complexes in blood vessels leads to cutaneus leukocytoclastic vasculitis, degeneration of collagen fibres and palisaded granulomatous inflammation. Ultimately, this leads to fibrosis of the skin. Objective The aim of the study is to present a patient with skin lesions and histopathological features of palisaded neutrophilic and granulomatous dermatitis during the course of infection Borrelia burgdorferi. Several cases of this disease have been reported worldwide (30 entries in the PubMed database). To-date, there have been no reports of PNGD in Polish literature. Materials and method The patient, aged 72, was admitted to hospital because of erythematous, indurated lesion of the skin on the side surface of the left thigh. Diagnosis of PNGD was made on the basis of typical histopathologic features due to clinical symptoms. Conclusions Clinical diagnosis of PNGD is difficult, and is based mainly on the histopathological picture. Systemic therapy is incorporated mainly due to the systemic disease. The patient requires further observation in the direction of associated systemic disorders.

Irritant contact dermatitis (ICD) is a common skin condition and a risk factor for allergic contact dermatitis. The prevalence of this disease in the general population varies between 1.7% and 6.3% and is increasing. The role of the patch test in detection of contact sensitivity is of prime importance. Patch tests should be used to identify topical agents that may be responsible for exacerbation or aggravation of eczema, especially in patients who do not improve despite adequate treatment. A 53-year-old woman suffering from recurrent, long-lasting dispersed eczematous skin lesions, mainly on her face and hands, was admitted to the Allergy Unit of the Dermatology Department of Jagiellonian University Medical College in Krakow for treatment, extended diagnostics and finding the reason for her illness. She was generally in a good physical condition and not taking any drugs. Skin symptoms were accompanied by an intensive itch and unrelated to work. After the discontinuation of treatment and after 2 months of full remission of skin lesions, patch tests were performed, using European standard (Chemotechnique Diagnostics) series. A positive, erythemato-papular reaction to both colophony and parabens, corresponding to “++”, was observed after 48 h. After 96 h, a strong intensification of the reaction was found only in the test site for colophony. Additionally, the reaction was accompanied by a local oedema with blisters and estimated as “+++”. In the test site for parabens, the 48-hour reaction was maintained (Figure 1). Figure 1 Positive results of the patch test Between the first and second test readings, eczematous lesions with faint borders, growing gradually but quickly, appeared on the face and hands of the patient (Figure 2). Figure 2 Erythemato-papular-oedematous rash localized on face On the basis of the symptoms of acute allergic contact dermatitis, the flare-up phenomenon was suspected. Systemic and topical corticosteroids were prescribed. The initial dose of steroids (prednisone) was 30 mg a day. After 24 h, in view of a clear, sustained improvement of the local state, the dose of prednisone was gradually reduced and finally the drug was stopped after 10 days. The appearance of multifocal eczematous lesions during the testing was considered a hardly predictable complication in the course of a standard diagnostic procedure. The flare-up dermatitis was first time described in 1981, in a patient with nickel contact eczema [1]. In the daily practice, patch tests remain a basic diagnostic procedure for distinguishing allergic contact dermatitis from irritant contact dermatitis. Their sensitivity and specificity reaches 70% [2]. Although the safety of patch tests is proven, we have to remember the risk of complications in some cases [1–3]. In the patient, we confirmed an allergic contact dermatitis for colophony and parabens, triggering the flare-up reactions of distant dermatitis. The flare-up reactions consist of the reactivation of a previous dermatitis following the patch testing [4]. It has been frequently described as related to nickel and also in patients with multiple contact allergies – differently from our patient [1, 5]. The pathogenesis of the flare-up phenomenon during the patch testing is not completely understood. Probably it is a result of a reactivation of specific memory T cells that remained in the previous area of contact [1, 6]. On the basis of the clinical picture, history and the results of patch testing, the colophony was suspected to be the main reason for the flare-up reaction, because of the strong reaction to it in the patch testing and because of its cross-reactivity with many environmental substances in our daily life. A contact allergy to cosmetics used by our patient was suspected, as the colophony may provoke cross-reactions with many substances often present in cosmetics, like the Balsam of Peru, resins or dihydroabietyl alcohol [7, 8]. The presented case reminds us that side effects may appear during patch testing, even though this method is considered to be very safe [1]. Therefore, it is necessary to perform these tests in medical centres with well-trained personnel, with the patient supervision available during the whole testing time.

It is very difficult to differentiate Melkersson-Rosenthal syndrom and macrochelitis granulomatosa. Two neurologists: Ernt Melkersson and Curt Rosenthal in 1928 and 1931 described classical symptoms of this syndrom: recurring facial paralysis, swelling of the face and lips and the development of folds and furrows in the tongue. In 1945 Miescher described a few cases of primary interstitial inflammation of the lips and gave them the name macrochelitis granulomatosa. Some patients had paralysis of the facial nerve, others folds of the tongue. In the present study the etiopatho-genesis, diagnostic and therapeutic problems are presented.

The study is aimed to determine the importance of type I and type IV allergy in eczema caused by allergy to nickel. The study was performed at 55 patients (42 women, 13 men, aged 16-58 yrs) suffering from hand dermatitis (19 cases), disseminated eczema (22 cases) and atopic dermatitis (14 cases) with positive skin patch test to 2.5% nickel sulphate. In each patients history of illness was analyzed, total serum IgE level (tIgE) was estimated and specific IgE (sIgE) for nickel and also absolute blood eosinophils and basophils counts were estimated for the evaluation of the atopy features. In each patient patch skin test with different nickel sulphate dilutions were performed as well as skin prick tests with different dilutions of nickel sulphate. The following oral provocation tests were carried out with the nickel sulphate in doses 0.56 mg, 1.12 mg, 2.24 mg, 5.6 mg and 11.2 mg. The test was stopped at the dose provoking the symptoms of illness. Positive family history, the increased tIgE serum level as well as absolute counts of eosinophils and basophils were present in some patients with atopic and contact dermatitis and they were not useful in differential diagnosis of this forms of skin allergy. Skin patch test with different concentrations of nickel sulphate was helpful to establish the degree of contact sensitivity in all patients. The oral provocation test with different dose of nickel sulphate also provoked symptoms in some patients in each observed groups, but the reaction to the lowest dose was observed only in patients with atopic dermatitis. Specific IgE to nickel as well as skin prick testing also with different dilutions of nickel sulphate are not useful in the diagnosis of nickel allergy. In the all examined patients they were negative. It seems that both types of allergy (type I and IV) may take part in the patho-mechanism of atopic and contact skin allergy with alternate prevalence of one of its depending on patient condition.

Prevalence of allergic diseases has been increasing over recent decades, especially in developed countries. The aim of this study was to assess prevalence of bronchial asthma and allergic rhinitis in children of Krakow at school age, depending on home and school environment conditions. The study was carried out in two stages: questionnaire based on ISAAC questionnaire and skin prick tests in children with symptoms suggesting allergic disease were performed. Altogether 532 children from 4 primary schools (2 in central and 2 in peripheral parts of the city) were included. Symptoms suggestive of allergic disease were reported by 304 children (57.1%), including asthma in 145 (27.2%) and allergic rhinitis in 288 children (54.1%). Asthma and allergic rhinitis was previously diagnosed in 19 (4%) and 138 (26%) children respectively. In younger age groups more children reported symptoms suggestive of asthma. Pupils from schools in the center of Krakow exposed to high level of traffic significantly more frequently reported asthma and had diagnosed allergic rhinitis. Increased prevalence of allergic rhinitis symptoms was observed in children exposed to passive smoking. Skin prick tests were positive only in 29.7% of children qualified for them. The results of the study suggest that in pupils with allergic rhinitis in whom skin prick tests are weakly positive for inhaled allergens, environmental factors may play an important role in the development of clinical symptoms.

C1 inhibitor deficiency can be hereditary (Type I and II) or acquired (Type I and II). Clinically it is manifested by recurrent attacks of angioedema which may involve skin, airways and digestive tract. The acquired form of C1 inhibitor deficiency is associated with lymphoproliferative or connective tissue disorders as well as with autoimmunization. Clinical symptoms are similar in all forms of C1 inhibitor deficiencies and they are connected with low serum level of C4 as well as with decreased activity of C1 inhibitor. In acquired angioedema additionally they are also decreased C1 and C1q and in type II C3 serum concentration is diminished. The drugs of choice are anabolics (danazol, stanazolol). Antifibrinolitic drugs are also used, especially in acquired forms of C1 inhibitor deficiency. The infusion of C1 inhibitor concentrate is used in acute emergency treatment.

The aim of the study was estimation of the IgE value, circulating immunocomplexes and the activity of complement system in allergic contact as well as atopic dermatitis in patients with skin nickel hypersensitivity. The study was done in 30 patients in the age range of 18-53 yrs suffering from allergic contact dermatitis (15 patients) and atopic dermatitis (15 patients) with positive skin patch test to nickel. The concentration of total IgE as well as specific IgE to mites, Phleum, Betula, Artemisia and the concentration of circulating complexes in the serum of patients were estimated. The activity of C1inh and CH50 was estimated in plasma of the patients. The results of the study indicated an increase of concentration of circulating immuno-complexes in 80% of the patients of both groups, an increase of total IgE in 50% of patients with atopic dermatitis and in 25% of the patients with contact dermatitis. There were no changes in the activity of C1inh and the value of CH50 in both groups of patients.