A. Sousa Basto


Atopic dermatitis is a chronic skin disease, recurrent, clinically characterized by the presence of inflammatory lesions in typical locations according to the patient’s age. This problem is highly pruriginous especially in the inflamed areas.

It’s frequently associated to other atopic conditions such as allergic rhinitis and asthma, and in many cases there’s a preexisting family precedent of atopy.

Dermatosis is multifactorial and results of an interaction of factors of genetic origin, structural alterations of the horny layer of the skin and modelating factors of intrinsic and environmental nature.

Atopic skin is therefore a genetically and structurally sensitive skin.

Among the factors of environmental nature that may exert an important action on the development and intensity of the clinical case one cam point out infectious agents, particularly Staphylococcus aureus (SA) 1.

Cutaneous colonization by SA in atopic skin quantifies 80 to 100%, whereas in non atopic skin it ranges from 5 to 30% 2.

Deficient mechanisms responseble for inflamatory response, like the reduced production of antimicrobian peptides, TLR dysfunction (toll-like receptors), and the permeability of the cutaneous layer 3, as well as adaptative immunity defects (Th2 polarity), can be pointed as the cause for agmented susceptibility to SA in atopic skin 4.

SA presence in affected and non affected skin has been associated with the severity of the affection 5.

About 30 to 60% of SA strains isolated in atopic dermatitis patients produce exotoxins with superantigenic characteristics, like enterotoxins A, B, C and D, as well as toxin -1 responsible for toxic shock syndrome. The presence of IgE antibodies reactive to this toxin has been related to the severity of the skin lesions 6.

IgE elevation on peripheric eosinophilia are Th2 polarity indicators, characteristic in atopic patients, suggesting that Th2 cytochines can favor SA colonization of the skin 2.

Staphylococcic superantigen identification and the accentuated SA colonization in moderate to severe cases of atopic dermatitis have produced a shift in ethiopathogenic concepts of the disease 7. SA would act not only as a primordial cause but as an important co-adjuvant factor for the outbreak and sustaining of this crisis.

All measures that aim to eliminate SA from affected and non affected skin exert an important preemptive effect in the prevention of cutaneous irritation.

Silver is highly effective against Gram + and Gram – bateria, as well as for several funguses, especially those of the Candida strain, responsible for the so called fold dermatitis or inthertrigo 8.

The use of silver impregnated clothing exerts a potent antibacterial action on SA, representing an important measure, both from a preemptive point of view as as a co-adjuvant of medical treatment 9 10 11.

The brown seaweed extract from the icy northern seas (Ascophyllum nodosum) with their anti-pruriginous and anti-inflammatory effect, when added to silver constitute a perfect symbiosis. The seaweed are extracted and treated with recurrence to natural processes with quemicals added.

Clothing impregnated with silver and seaweed extract is particularly suitable for sensitive and intolerant skin, namely atopic skin.

The antibacterial action of silver is also recommended in the prevention of skin infections in cases of obesity, diabetes, and imunodepression that constitute risk groups for these affections. The elimination of bacterial flora responsible for foul odors of the feet, due to their action on proteic components of sweat, in individuals with plantar hyperhydrosis is another of the uses for this metal.

Due to it’s potent antifungic action on Candida it can prevent fold dermatitis, inter and sub-mamarian infection, inter-buttock and genito-crural infection, when incorporated in bras and boxer shorts.

Both the silver and seaweed extract remain in the fabric fibers after washing and aren’t absorbed by the skin’s tegument, constituting an important prophylactic of inflammation and skin infection as they normalize both the bacterial and fungic flora of the skin.



(1) Lever R. Infection in atopic dermatitis. Dermatol Therapy 1996,1:32-37

(2) Breuer K, Haussler S, Kapp, Werfel T. Staphylococcus aureus: colonizing features and influence of an antibacterial treatment in adults with atopic dermatitis. Br J Dermatol 2002;147:55-61

(3) Alomar A. Dermatitis atópica y alteración de proteínas estruturales. Piel 2008;23,4:159-161

(4) Warner J.A., McGirt L.Y. and Beck L.A.. Biomarkers of Th2 polarity are predictive of staphylococcal colonization in subjects with atopic dermatitis. Br J. Dermatol 2009;160:183-185

(5) Gilani S.J., Gonzalez M., HusseinI et al. Staphylococcus aureus re-colonization in atopic dermatitis: beyond the skin. Clin Exp Dermatol 2005;30:10-13

(6) Breuer K., Wittman M., Bosche B et al. Severe atopic dermatitis is associated with sensitization to staphylococcal enterotoxin B (SEB) Allergy 2000;55:551-5

(7) Ribeiro D.P.N. e colaboradores. Prevalência da colonização por Staphylococcus aureus em pacientes com dermite atópica. Trab Soc Port Dermatol Venereol 2007;65,1:37-42