Histamine and atopic eczema

Apart from increased production of immunoglobulin E antibodies and disturbed T-cell regulation, altered patterns of releasability of vasoactive mediators have been described in patients with atopic eczema. The best studied substance is histamine which is a classical inducer of pruritus in man. Elevated concentrations of histamine have been found in vivo in the skin and in the plasma of patients with atopic eczema especially during exacerbation of the disease. Similar findings have been described for other atopic diseases as extrinsic bronchial asthma. Histamine acts via characteristic receptors; symptoms as itch, wheal formation, mucus production, contraction of smooth muscle, tachycardia and hypotension are mediated via H1-receptors, while H2-effects include acid secretion in the stomach as well as the development of flush and itch reactions, blood pressure changes and cardiac arrhythmia. Of special interest is an inhibitory effect of histamine on lymphocyte reactions mediated via a H2-receptor. The existence of a new H3-receptor in the brain serving as autocrine feed-back inhibitor of histaminergic neurones has been established in the rat but not yet in man. In vitro an increased histamine releasability of peripheral leukocytes has been found after stimulation with a variety of different substances. The difference between patients with atopic eczema and normals is generally most pronounced after stimulation with anti-IgE. There is, however, a tendency towards an increased spontaneous histamine release compared to normals. The release reaction of histamine seems to occur more rapidly in atopics compared to normals. Among possible factors influencing histamine releasability the imbalance in the cyclic nucleotide system (increased response of cGMP to cholinergic stimulation and decreased response of cAMP to β-adrenergic stimulation) might play a pathogenetic role. Arachidonic acid metabolites known to regulate histamine release (PGE₂ inhibits histamine release while cyclooxygenase blockers enhance histamine release and lipoxygenase blockers inhibits histamine release) also may be of relevance. Histamine definitely is not the only relevant mediator substance in the pathophysiology of atopic eczema; it may, however, serve as a marker of mast cell and basophil activation. Clinical trials with various antihistamines have shown some therapeutic benefit in the management of atopic eczema patients. Future studies in the field of mediator research may lead to new therapeutic approaches for the treatment of atopic eczema.