Table 1.

Commonly used treatments for AD

Treatment	Mode of action	Benefits	Limitations/side effects	References
Emollients	Hydration, moisturizing	(↓) TEWL (↑) hydration	Not effective against Staphylococcusaureus colonization or AD severity reduction.	[23]
TCS	Immune cells blocking	(↓) proinflammatory cytokines	skin atrophy, hypothalamic–pituitary–adrenal axis alteration, rosacea	[28]
TCI	Calcineurin-dependent T- cell activation	(↓) proinflammatory cytokines	Burning, stinging and pruritus	[7], [29]
Phototherapy	NbUVB (311 nm)	Steroid-like effect	Erythema	[30], [31]
	UVA1 (340–400 nm)		Eczema, blisters, hyperpigmentation, skin aging
Cyclosporine A	Inhibits Th1 and Th2	(↓) inflammation (↓) pruritus	Nausea, headache, hypertension, renal impairment, chronic immunosuppression	[7], [32]
Azathioprine	TH cell proliferation inhibition	(↓) inflammation	Nausea, vomiting, diarrhea, bone marrow suppression	[33]
Infliximab	Antagonist against TNF-α	(↓) inflammation	Risk of infection	[34]
Omalizumab	Monoclonal antibody that blocks IgE function	(↓) IgE in serum	Slight differences against the placebo High cost	[35], [48]
Mepolizumab	IL-5 monoclonal antibody	(↓) eosinophil recruitment	No significant differences in AD	[11]
Dupilumab	Blocks IL-4 and IL-13 signaling	(↓) pruritus	No apparent adverse effects	[36]

AD, atopic dermatitis; TEWL, trans epidermal water loss; TCS, topical corticosteroids; TCI, topical calcineurin inhibitors; UV, ultraviolet light; NbUVB, narrowband UVB; IL, interleukin; TH, T helper cell; TNF-α, tumor necrosis factor-alpha.