Atopic diathesis is a predisposition to develop hay fever, allergic rhinitis, bronchial asthma, urticaria, and / or atopic dermatitis. The atopic person has a predilection to produce regain antibodies in abnormally large amounts. The regain response to allergens is preponderant in such individuals and this is responsible for the type 1st (IgE- mediated) hypersensitivity manifestations. Atopic dermatitis (AD) an expression of atopic diathesis, in an abnormally reacting skin, may manifest in form of eczema/ dermatitis. Intense pruritus being its hallmark, it usually has its onset between 2 to 6 months. It may pursue a chronic course with varied morpholgy and localization. It passes through infantile, childhood, and adult phases. Remissions and relapses are cardinal. Spontaneous resolution is frequent, at times; however, its relics are evident as stigma. A number of confirmed and putative activators are responsible for triggerng atopic dermatitis. These are stress, aeroallergens like mites, molds, yeast, human dander, foods, irritants, viruses and staphylococci.The initial event in the pathogenesis of atopic dermatitis is the release of mediators from the skin mast cells. Various factors have been implicated for it.• Serum levels of IgE are elevated in approximately 80 percent of patients and correlate with the disease activity.• Neuropeptides such as substance P stimulate histamine release from skin mast cells and may link the central nervous system to cutaneous inflammatory cells.• Abnormal cyclic nucleotide metabolism.The levels of cyclic adenosine monophosphate (cAMP) in stimulated leukocytes are reduced. This results from excessive hydrolysis by cAMP phosphodiesterase (PDE). The reduced levels of cAMP may be responsible for the hyperreleasebility of mediators of inflammation. Histamine released via these mechanism interferes with cell mediated immunity through inhibition of H2 receptor bearing lymphocytes.Alternatively or in addition, IgE immune complexes inhibit cell mediated immunity by blocking lymphocyte proliferation response to antigens. The resulting defective cell mediated immunity allows enhanced IgE production. Thus a vicious circle is established and cell mediated immunity is depressed and enhanced IgE production dominates the immune mechanism in atopic dermatitis is the manisfestation of IgE mediated late phase reaction, which are mediated by histamine and characterized by perivascular leukocytic infiltrate.Abnormalities of other secondary messenger systems, including abnormalties of protein kinase C activity and of inositol activation have been observed in atopic subjects. These may be a consequence of downregulation of second messenger systems because of chronic exposure to low levels of inflammatory mediators, but these may themselves be responsible for permitting further mediator release.These abnormalties offer a biochemical explanation for increased type 1st mediated immunity and diminished cell mediated immunity.The atopic subjects also show altered vascular response to histamine, serotonin, cholinergic, and sympathomimetic agents. The vascular abnormalities manifest as;• Pallor• Low finger temperature• Pronounced vasoconstriction on exposure to cold• White dermographism• A reduced reaction to histamine• White reaction to nicotinic acid esters• Delayed blanch with acetylcholine