The history of pharmacology travels together to history of scientific method and the latest frontiers of pharmacology open a new world in the search of drugs. New technologies and continuing progress in the field of pharmacology has also changed radically the way of designing a new drug. In fact, modern drug discovery is based on deep knowledge of the disease and of both cellular and molecular mechanisms involved in its development. The purpose of this book was to give a new idea from the beginning of the pharmacology, starting from pharmacodynamic and reaching the new field of pharmacogenetic and ethnopharmacology.

Background: In most cases the cause of chronic urticaria (CU) remains unknown - chronic idiopathic urticaria (CIU). The most important mediator is histamin and antihistamines are the main drugs used. They alleviate pruritus and decrease the incidence of hives in most patients with CIU. However, all patients do not respond to this therapy and some of them benefit from therapy wilh antileukotrienes. Beside histamine, arachidonic acid metabolites - sulphidoleukotrienes (sLT) are also important mediators of allergic reactions.Their role in the evolution of CIU is not yet known. AimsČ In a prospective manner we tried to find out if the response of our patients with CLU to antileukotriene therapy correlates with sulphidoleukotriene (sLT) concentration in leukocite suspension after different stimulations oržand withbasophils activation Subject and methods: The data were obtained from patients we diagnosed and treated for CIU in the years 1999 and 2000. We selected those who had symptoms in spite of antihistamine treatment. In a double blind crossover manner those patients took antileukotriene (montelukast10 mg per day) or placebo. Efficacy was assessed by pruritus score, number of wheals per day and sleep interference. We defined a subgroup of very severe urticaria as at least 30% higher symptom score than the mean score of the whole group. We compared the ability of leukocites of patients and healthy controls to release sLT (ELISA assay) and portion of activated basophils (flow citomerty) through receptor dependent (anti-IgE, unti-FCeRI, C5a) and non-dependent (ionomycine) stimulation. (Abstract truncated at 2000 characters).