Atopic eczema (atopic dermatitis or childhood eczema) is a big problem worldwide. The skin of people with atopic eczema often contains high numbers of a bacterium called Staphylococcus aureus (S. aureus).
Sometimes S. aureus results in an obvious secondary infection. Even when the eczema does not look infected S. aureus may still play a part in promoting skin inflammation. As a result, lots of eczema treatments have been developed to reduce S. aureus, including antibiotics taken by mouth, washing with antibacterial soaps or antibiotics combined with other eczema treatments. We undertook a systematic review on this topic as it is not clear which treatments offer any clinical benefit and because there is some concern that their widespread use may promote bacterial resistance.
Our review included 21 randomised controlled trials involving 1018 participants covering a range of anti-staphylococcal treatments: oral antibiotics (3 trials), antibacterial soaps (1 trial), topical steroids combined with antibacterials (10 trials), antibacterial bath additives (2 trials), topical antiseptic/antibiotics creams (4 trials) and silver impregnated textiles (1 trial). Generally, the quality of the reported studies was poor, and many were too small to identify important differences even if they existed. None of the trials showed any clear benefit in terms of short-term eczema control for any of the interventions tested, although several interventions were associated with decreased numbers of S. aureus on the skin. There was no clear evidence that widely used topical steroid/antibiotic combinations were any better than the topical steroids used alone. Adverse effects like irritation were especially poorly reported and only one study reported on the emergence of resistant bacterial strains in the group treated with oral antibiotics. Only one small inconclusive study evaluated people with clinically infected eczema.
Care should be taken in interpreting the above studies as failure to show benefit in a series of small, poorly reported studies does not mean that the anti-staphylococcal interventions could not be helpful in eczema. It is clinical common sense to treat overtly infected eczema with oral antibiotics, and that practice should continue until good evidence suggests otherwise. However, given that none of the other studies showed clear clinical benefit for anti-staphylococcal interventions in non-infected eczema, their continued use should be questioned in such situations. More studies should be done to look at the long-term possible benefits and harms of such interventions in preventing flares of atopic eczema.
We failed to find clear evidence of benefit for antimicrobial interventions for people with atopic eczema, despite their widespread use. This does not necessarily mean they do not work because the studies were small and poorly reported. Further large studies with long-term outcomes and clearly defined participants are urgently required.
Staphylococcus aureus can cause secondary infection in atopic eczema, and it may promote inflammation in eczema that does not look infected. Many antimicrobial products exist for eczema, but it is unclear if they work or if they promote bacterial resistance.
To assess the effects of interventions to reduce Staphylococcus aureus for treating infected or uninfected atopic eczema.
We searched the Cochrane Skin Group Specialised Register (March 2008), the Cochrane Central Register of Controlled Trials (Cochrane Library Issue 1, 2008), MEDLINE (OVID) (from 2002 to March 2008), EMBASE (OVID) (from 2002 to March 2008), Ongoing trials registers (March 2008). References from trials and reviews were searched, pharmaceutical companies were contacted for unpublished trials. There were no language restrictions.
Randomised controlled trials (RCTs) of people with atopic eczema who have been treated with a product intended to reduce S. aureus on the skin.
Two people independently performed the study selection, data abstraction and quality assessment.
We included 21 studies (1018 participants) covering 7 treatment categories. Most studies were poorly reported and study differences limited pooling of results. Adverse effects were especially poorly reported, and only one study reported the emergence of resistant bacterial strains following oral antibiotics. Oral antibiotics were not associated with benefit in non-infected (2 trials, 66 participants) or infected eczema (1 trial, 33 participants). We did not find any benefit for antibacterial soaps (1 trial, 50 participants), or antibacterial bath additives (2 trials, 41 participants), or topical antibiotics/antiseptics (4 studies, 95 participants). Adding antibiotics to topical corticosteroids reduced numbers of Staphylococcus aureus in 4 trials (302 participants), but there was no evidence of any clinical benefit in 9 trials involving 677 participants: betamethasone plus neomycin vs clobetasol (MD 1.2; 95% CI 0.25, 2.15), prednicarbate plus antimicrobial vs prednicarbate (RR 0.64; 95% CI 0.25, 1.68), or betamethasone valerate plus gentamicin vs betamethasone (RR 0.31; 95% CI 0.07, 1.35). One trial (30 participants) showed no significant improvement in eczema for those using silver textiles (RR 2.67; 95% CI 0.98, 7.22), despite using 10 times the amount of topical steroids.