Oral antihistamines act primarily by blocking activity
at the histamine H1 receptor, attenuating the allergic
response. However, in vitro studies have found that
these agents also directly inhibit the release from mast
cells and basophils of many of the proinflammatory
mediators that contribute to late-phase congestion.35–37
Moreover, antihistamines have been reported to inhibit
tumor necrosis factor-α– and nuclear factor κB–
dependent transcription and release of proinflammatory
cytokines by histamine H1, further supporting an
anti-inflammatory role for these agents.38