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To assess the real-world clinical treatment outcomes with brodalumab in patients with moderate-to-severe plaque psoriasis in Greece.This was a longitudinal, retrospective, real-world analysis of data from medical records of 106 patients with moderate-to-severe plaque psoriasis, treated with brodalumab for up to 24 months at four University Dermatology Centers in Greece. Efficacy assessments of psoriasis severity [Psoriasis Area and Severity Index (PASI) and Body Surface Area affected (BSA) scores] and its impact on patients' quality of life (QoL) [Dermatology Life Quality Index (DLQI) score] were evaluated at different timepoints up to 24 months.Treatment with brodalumab reduced both mean PASI (14.0-1.5,Brodalumab is effective long term, improving disease severity and health-related QoL in patients with moderate-to-severe plaque psoriasis in a real-world setting.

Nipple pain and discomfort during or after breastfeeding remains one of the most common reasons for premature cessation of lactation among the affected women. The belief that yeasts, and especially

Acremonium is a large fungal genus that is comprised of approximately 150 species, found ubiquitously in nature. Although the majority are recognized as being saprophytes in soil and pathogens of plants, several species are emerging as causative agents of a variety of human infections, including mycetomas. Herein, we present a young man that was referred to our department with a painful subungual mass that developed following traumatic inoculation of Acremonium spp. In recent years, the role of Acremonium spp. has been increasingly recognized in localized infections, such as mycetoma, in humans. Other locally invasive as well as disseminated infections are also described. Optimal treatment of Acremonium spp. mycetoma is not well defined owing to the rarity of cases, thus posing a therapeutic challenge.

Background Malacoplakia is a rare acquired, infection-related granulomatous disorder, that may affect many systems, but typically occurs in the urinary tract. Cutaneous involvement is less prevalent, and most commonly presents with a perianal or genital region localization. Cutaneous malacoplakia is believed to be caused by an acquired bactericidal defect of macrophages in the setting of chronic infections and immunocompromised states. A diagnosis of cutaneous malacoplakia should be considered when encountering non-specific granulomatous lesions that are refractory to treatment. Histologic findings are marked by the presence of foamy macrophages containing the pathognomonic Michaelis-Gutman bodies. Objectives The aim of this review is to discuss the current perspectives on the pathophysiology, clinical features, diagnosis, and treatment of this disease. We would also like to emphasize that the integration of clinical information, microscopic findings, and exclusion of other cutaneous granulomatous processes is necessary to accurately diagnose this exceedingly rare disease and provide opportunity for therapeutic intervention. Patients/methods Data for this work were collected from the published literature and textbooks. Results Combined surgical excision and protracted antibiotic courses appear to have the highest success rate. Antibiotics should be culture specific, but drugs that easily permeate the macrophages appear to be the best choice.

Background:The introduction of Immune Checkpoint Inhibitors in the recent years has resulted in high response rates and extended survival in patients with metastatic/advanced malignancies. Their mechanism of action is the indirect activation of cytotoxic T-cells through the blockade of inhibitory receptors of immunomodulatory pathways, such as cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4), programmed cell death protein-1 (PD-1) and its ligand (PD-L1). Despite their impressive therapeutic results, they can also induce immune-related toxicity, affecting various organs, including the skin.Objective:To provide an updated summarized overview of the most common immune-mediated cutaneous side effects and their management.Method:English articles derived from the databases PubMed and SCOPUS and published between 2009 and 2018, were analyzed for this narrative review.Results:The most common adverse cutaneous reactions include maculopapular rash, lichenoid reactions, vitiligo and pruritus, with severity Grade 1 or 2. Less frequent but eventually life-threatening skin side effects, including Stevens-Johnson syndrome, Drug Reaction with Eosinophilia and Systemic Symptoms and Toxic Epidermal necrolysis, have also been reported.Conclusion:Basic knowledge of the Immune-Checkpoint-Inhibitors-induced skin toxicity is necessary in order to recognize these treatment-related complications. The most frequent skin side effects, such as maculopapular rash, vitiligo and pruritus, tend to subside under symptomatic treatment so that permanent discontinuation of therapy is not commonly necessary. In the case of life-threatening side effects, apart from the necessary symptomatic treatment, the immunotherapy should be permanently stopped. Information concerning the management of ICIs-mediated skin toxicity can be obtained from the literature as well as from the Summary of Product Characteristics of each agent.

Ribonuclease P (RNase P) is ubiquitous and essential Mg(2+)-dependent endoribonuclease that catalyzes the 5'-maturation of transfer RNAs. RNase P and the ribosome are so far the only ribozymes known to be conserved in all kingdoms of life. Eukaryotic RNase P activity has been detected in nuclei, mitochondria and chloroplasts and demonstrates great variability in sequence and subunit composition. In the last few years we have developed methodologies and pursued projects addressing the occurrence, distribution and the potential physiological role of RNase P in human epidermal keratinocytes. In view of the vital importance of lymphocytes for an effective immune system and their successful application after transfection with RNase P-associated external guide sequences in gene therapy, we concerned ourselves with the isolation and characterization of RNase P of peripheral human lymphocytes. We developed a method described herein, that will enable the study of the possible involvement of this ribozyme in the pathogenetic mechanisms of diverse autoimmune, inflammatory and neoplastic cutaneous disorders and may facilitate the further development of RNase P-based technology for gene therapy of infectious and neoplastic dermatoses.

The aim of this study was to determine whether imiquimod, a Toll-like receptor-7/8 agonist, in addition to its well-known topical action on the cutaneous immune response, might also induce alterations in the peripheral blood lymphocytes. A 62.5 mg quantity of imiquimod (5% cream) was applied topically under occlusion once daily every second day for 3 weeks to the skin of 10 healthy volunteers, age range 30–57 years. Ten sex- and age-matched healthy controls applied corresponding quantities of the vehicle under occlusion. Before, and one and 3 weeks after the start of treatment, peripheral blood lymphocyte subpopulations were measured by flow cytometry. Statistically significant alterations in the percentage or absolute numbers of peripheral blood lymphocyte subpopulations were found in the imiquimod-treated group compared with the control group. These alterations indicate for the first time that topical application of imiquimod induces alterations in peripheral blood lympho cyte subsets in healthy individuals, which may be of importance in the immunotherapy of neoplastic and infectious disorders and should be taken into careful consideration in patients who are treated with imiquimod.

Sir, Stevens-Johnson syndrome (SJS) is a rare and severe mucocutaneous disorder, most frequently caused by systemic drugs, with an incidence of 1–6 cases per million person-years (1). It is characterized clinically by a maculopapular and bullous eruption with epidermal necrosis and detachment, mucosal ulcers and erosions and constitutional signs and symptoms. SJS and toxic epidermal necrolysis (TEN) are presently regarded as clinical forms of the same disorder that share common aetiopathogenetic factors but mainly differ in: (i) the extent of epidermal detachment (SJS 30%); (ii) the prognosis (SJS = good; TEN = poor); and (iii) the mortality rate (SJS < 5% vs. TEN = 30–40%) (2, 3). Although the exact pathogenetic mechanisms of SJS and TEN at the molecular and cellular level remain to be elucidated, there is evidence suggesting a cytotoxic cell immune response against keratinocytes that is induced by various drugs, mostly sulphonamides, allopurinol, phenytoine, phenobarbital, carbamazepine, lamotrigine, non-steroidal anti-inflammatory drugs and nevirapine (4). Since it is of essential importance to recognize and report drugs capable of inducing severe adverse reactions, we describe herein the first case of SJS occurring in a HIVnegative patient during oral fluconazole treatment. CASE REPORT A 50-year-old Caucasian woman was admitted to the Department of Dermatology at the University of Patras Medical Center with a 3-day history of skin and mucosal lesions accompanied by high fever and malaise. The cutaneous manifestations had developed one week after the onset of treatment of vaginal candidiasis with 200 mg/day oral fluconazole (Flucodrug caps; Med-One, Athens, Greece). Apart from fluconazole, the patient had received no other medication and had no history or evidence of infectious, autoimmune or neoplastic disorders. Physical examination of the patient on admission revealed a confluent erythematoviolaceous, maculopapular and focally bullous pruritic skin rash with large numbers of targeted lesions over her face, upper trunk and the extremities. In a small area on her back, epidermal detachment was clearly seen (Fig. 1A). There were superficial ulcers and erosions in the oral mucosae, erosions and crusts on her oedematous lips (Fig. 1B) and a severe conjunctivitis. Blisters and epidermal detachment affected about 9% of the patient’s body surface. Apart from a vaginal culture positive for Candida albicans, all haematological, biochemical, immunological and serological investigations (including tests for HSV, HIV 1 & 2, hepatitis A, B and C, Toxoplasma, Epstein Barr virus, Fluconazole-induced Stevens-Johnson Syndrome in a HIV-negative Patient