Table 2.

Principal systemic treatment for atopic dermatitis

Treatment	Mechanism of action on AD	Adverse effects
Corticosteroids	Reduction of number and activity of lymphocites Reduction of inflammatory cytokines (IL-12 and INF- γ) Reduction of cyclooxygenase, platelet activating factor Vasoconstriction and reduction of small vessels permeability	Systemic effects: hypothalamic–pituitary–adrenal axis suppression, reduced linear growth in children, and bone density changes in adults Local effects: skin atrophy, bruising, telangiectasies, striae, steroid acne, hypertrichosis, tachyphylaxis, steroid resistance, worsening of underlying secondary infections
UVB-treatment	Suppression of Th2 chemokine production suggests that UVB exposure to the skin suppresses infiltration of Th2 cells to the epidermis	Skin erythema, skin burning, risk for skin malignancies
Cyclosporine	Inhibition of Il-2 production by blocking the function of the enzyme calcineurin (CaN)	Arterial hypertension, nephrotoxicity, and immunosuppression
Methotrexate	Inhibition of synthesis of purines and pirimidines required for cellular proliferation of lymphocytes	Anemia, thrombopenia, gastrointestinal dysfunction, and pneumonitis
Antihistamines	Inhibition of peripherical histamines receptors with reduction of vasodilatation and itching, inhibition of central histamines receptors with sedative effect, local anesthetic effect	Excessive sedation
Azathioprine	Inhibition of purine synthesis with consequent stop in synthesis of DNA, RNA, and proteins; it may also interfere with cellular metabolism and inhibit mitosis the proliferation of cells, especially leukocytes	Bone marrow suppression and oncogenic potential, gastrointestinal symptoms. Leukopenia or infection fever or chills, cough or hoarseness, lower back or side pain, painful or difficult urination, tiredness or weakness
Mycophenolate mofetil	Inhibition of inosine monophosphate dehydrogenase (IMPDH), with following de novo synthesis pathway of guanosine nucleotides (on which T and B lymphocytes are critically dependent for their proliferation)	Bone marrow suppression, peripheral edema, arrhythmia, artralgia
TNF-α inhibitors	Through inhibition of TNF-α, which has a great inflammatory activity, reduction in epidermal hyperplasia neoangiogenesis and itching	Increased risk of infection, especially reactivation of tuberculosis; increased risk of lymphoproliferative diseases, worsening of heart failure; local reactions