The EAACI/GA²LEN/EDF/WAO guideline for the definition, classification, diagnosis and management of urticaria.

This evidence- and consensus-based guideline was developed following the methods recommended by Cochrane and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group. The conference was held on 1 December 2016. It is a joint initiative of the Dermatology Section of the European Academy of Allergology and Clinical Immunology (EAACI), the EU-founded network of excellence, the Global Allergy and Asthma European Network (GA²LEN), the European Dermatology Forum (EDF) and the World Allergy Organization (WAO) with the participation of 48 delegates of 42 national and international societies. This guideline was acknowledged and accepted by the European Union of Medical Specialists (UEMS). Urticaria is a frequent, mast cell-driven disease, presenting with wheals, angioedema, or both. The lifetime prevalence for acute urticaria is approximately 20%. Chronic spontaneous urticaria and other chronic forms of urticaria are disabling, impair quality of life and affect performance at work and school. This guideline covers the definition and classification of urticaria, taking into account the recent progress in identifying its causes, eliciting factors and pathomechanisms. In addition, it outlines evidence-based diagnostic and therapeutic approaches for the different subtypes of urticaria.

[Sphingosine-1-phosphate signaling system and the innovative mechanism of action of fingolimod in treatment of multiple sclerosis: review of foreign literature].

Over the last years, sphingosine-1-phosphate signaling function (S1P) is thought to play a key role in the development of immunological and neurological components of multiple sclerosis (MS). Modulators of the S1P-system are highly effective in MS treatment. Fingolimod, a structural analogue of endogenous sphingosine, is a first generation drug of a new class of medications known as "modulators of sphingosine-1-phosphate receptors". The inhibition of S1P receptors by fingolimod in MS reduces the recirculation of autoreactive central memory T-cells and their infiltration of the CNS where they cause a damage that clinically reveals in the decrease in the number of MS exacerbations and less severe inflammatory brain changes in MRI.