SUMMARY -When taking diff erent drugs, their possible side eff ects on the skin should be considered, including skin reactions connected to photosensitivity. Th is photosensitivity caused by drugs can appear as phototoxic reactions (which occur more often) or photoallergic reactions (which occur less often and include allergic mechanisms). Th e following drugs stand out as medications with a high photosensitivity potential: nonsteroidal anti-infl ammatory drugs (NSAIDs), cardiovascular drugs (such as amiodarone), phenothiazines (especially chlorpromazine), retinoids, antibiotics (sulfonamides, tetracyclines, especially demeclocycline and quinolones), etc. In recent years, photosensitive reactions to newer drugs have appeared, e.g., targeted anticancer therapies such as BRAF kinase inhibitors (vemurafenib, dabrafenib), EGFR inhibitors, VEGFR inhibitors, MEK inhibitors, Bcr-Abl tyrosine kinase inhibitors, etc. In patients taking drugs over a longer period of time (e.g., NSAIDs, cardiovascular drugs, etc.), a particular problem arises when an unrecognized drug-induced photosensitivity on the skin manifests in summer months. When taking patient histories, the physician/dermatovenereologist should bear in mind that any drug the patient is currently taking may be the cause of skin reactions. Th erefore, patients who use potentially photosensitive drugs and treatments on a long term basis should be warned of the possibility of these side eff ects on their skin and advised to avoid direct exposure to sunlight and to use adequate photoprotection. If patients carefully protect themselves from the sun, it is often not necessary to stop treatments that include photosensitive drugs. If such reactions appear, anti-infl ammatory and antiallergic therapies should be introduced.

Many relatively common chronic inflammatory skin diseases manifest on the face (seborrheic dermatitis, rosacea, acne, perioral/periorificial dermatitis, periocular dermatitis, etc.), thereby significantly impairing patient appearance and quality of life. Given the yet unexplained pathogenesis and numerous factors involved, these diseases often present therapeutic challenges. The term “microbiome” comprises the totality of microorganisms (microbiota), their genomes, and environmental factors in a particular environment. Changes in human skin microbiota composition and/or functionality are believed to trigger immune dysregulation, and consequently an inflammatory response, thereby playing a potentially significant role in the clinical manifestations and treatment of these diseases. Although cultivation methods have traditionally been used in studies of bacterial microbiome species, a large number of bacterial strains cannot be grown in the laboratory. Since standard culture-dependent methods detect fewer than 1% of all bacterial species, a metagenomic approach could be used to detect bacteria that cannot be cultivated. The skin microbiome exhibits spatial distribution associated with the microenvironment (sebaceous, moist, and dry areas). However, although disturbance of the skin microbiome can lead to a number of pathological conditions and diseases, it is still not clear whether skin diseases result from change in the microbiome or cause such a change. Thus far, the skin microbiome has been studied in atopic dermatitis, seborrheic dermatitis, psoriasis, acne, and rosacea. Studies on the possible association between changes in the microbiome and their association with skin diseases have improved the understanding of disease development, diagnostics, and therapeutics. The identification of the bacterial markers associated with particular inflammatory skin diseases would significantly accelerate the diagnostics and reduce treatment costs. Microbiota research and determination could facilitate the identification of potential causes of skin diseases that cannot be detected by simpler methods, thereby contributing to the design and development of more effective therapies.

Urticaria is one of the most common dermatologic allergic diseases, but also holds a significant psychosocial burden due to possible long duration, frequent relapses, unknown cause or trigger and resistance to applied therapy. Many patients associate the onset and worsening of the disease with stressful experiences indicating it can be a psychosomatic disease within the psychoneuroimmunological approach. Apart from that, urticaria greatly affects the quality of life (QoL) of patients, disrupts their daily lives in all aspects, and is a dermatological disease with one of the highest prevalence of psychiatric comorbidities. Therefore, in this review article we discuss why a multidisciplinary approach, which includes both biological, psychological and social aspects of the disease, must be acknowledged for effective treatment. Finally, we provide suggestions for clinical management of patients suffering from urticaria.

Background: Because of the important role in regulating the immune system, increasing evidence suggests a possible implication of gut microbiota in Chronic spontaneous urticaria (CSU). Although the oral cavity is the first site of contact between microbiota and the immune system, the association between salivary microbiota and CSU has not yet been reported. Objective: This case-control study aimed to compare differences in salivary microbiota between CSU patients and healthy controls (HC). Twenty-three participants—13 patients with CSU and 10 HC were enrolled; salivary microbiota was determined by molecular approach targeting 16S ribosomal RNA. Terminal restriction fragment length polymorphism (T-RFLP) analysis was performed. Results: Alpha diversity of salivary microbiota in CSU patients was significantly reduced compared to HC, resulting in alteration of the community composition. Species richness determined via the Shannon index was significantly reduced in the CSU group. Conclusion: Dysbiosis of salivary microbiota may contribute to a dysregulated immune system in the development of CSU. To our knowledge, this was the first study that reported an alteration in salivary microbiota composition in CSU patients.