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1 nges may be implicated in the development of xerosis.
2 n in human immunodeficiency virus-associated xerosis.
3 skin diseases, such as atopic dermatitis and xerosis.
4 ution and/or hair depigmentation (18 [44%]), xerosis (8 [20%]), scrotal erythema/ulceration (6 [15%])
6 onic inflammatory phenotype characterized by xerosis and pruritic eczematous lesions; dermal infiltra
10 atures of human atopic dermatitis, including xerosis, conjunctivitis, inflammatory skin lesions, Stap
11 (psoriasiform eczema, 30.6%; eczema, 23.5%; xerosis cutis, 10.6%; palmoplantar pustulosis, 5.3%; pso
16 s afflicted by inflammatory skin diseases or xerosis/eczema that could be triggered or exacerbated by
17 (HR, 0.755; 95% CI, 0.635-0.897; P = .001), xerosis (HR, 0.626; 95% CI, 0.469-0.834; P = .001), nons
19 n of human immunodeficiency virus-associated xerosis patients (upper arm, n = 12; upper leg, n = 11)
20 sent results show that amoebae exposed to C. xerosis produce increased amounts of MIP133 and more sev
21 r receptor antagonists: papulopustular rash, xerosis, pruritus as well as hair, nail, and mucosal cha