Major progress has been achieved in our understanding of the pathophysiolog
y of different forms of chronic urticaria during the last years. Most impor
tant is the understanding of chronic urticaria as a symptom than as a disea
se. This symptom is the result of a malfunction of basophiles and/or mast c
ells resulting in an increased release of histamine and other inflammatory
mediators by these cells. The causes are quite different and include the re
lease of these agents by toxic events induced by specific drugs or other su
bstances known to be histamine releasers, allergic reactions which are in m
ost cases IgE-mediated and autoimmune reactions. This progress resulted als
o in new therapeutic options such as cyclosporin A, intravenous immunoglobu
lin, plasmaphereses, chloroquine, sulfones, calcium antagonists, although a
ntihistamines are still the first-line drugs in by far most cases of chroni
c urticaria. Therefore, the development of new antihistamines with less sid
e effects, such as the antihistamines of the "second generation" or the lat
est development leading to fexofenadin, descarboxyloratadine and levocetere
zine, compounds which establish a third generation of antihistamines in the
treatment of urticaria.