Lyn Guenther MD FRCPC

Professor of Dermatology, Western University, London ON, Canada

Conflict of interest:
Dr. Guenther has been a consultant, speaker and clinical researcher for Leo Pharma Inc. Dr. Guenther received an unrestricted educational grant from Leo Pharma to write the paper.


In 2018, Fucibet® was launched in Canada by Leo Pharma Inc. for the topical treatment of confirmed or suspected secondarily infected Staphylococcus aureus eczematous dermatoses, such as atopic dermatitis (AD), discoid eczema, stasis dermatitis, and seborrheic dermatitis.1 It is intended to be used for a maximum of 2 weeks. Safety in individuals greater than age 6 years has been established.1

It was first launched in 1992 in Europe in a different vehicle under the name of “Fucicort® cream”, then in 2007 in a lipid cream base as “Fucicort Lipid cream” in an effort to ameliorate dryness. Fucibets® has the same base as “Fucicort Lipid cream.” It contains 2% fusidic acid and 0.1% betamethasone 17-valerate, and the non-medicinal ingredients all-rac-α-tocopherol, cetostearyl alcohol, citric acid monohydrate, hypromellose, liquid paraffin, methyl parahydroxybenzoate, potassium sorbate, propyl parahydroxybenzoate, purified water, steareth-21 and white soft paraffin.


  • Up to ¼ of children2 and 10% of adults3 are affected by AD.
  • In contrast to the 3% colonization rate of S. aureus in healthy individuals, 70% of AD patients are colonized, with higher rates in severe disease.3
  • Disruption of the epidermal barrier, filaggrin mutations, lower antimicrobial peptide production and activation of the Th2 pathway in AD increase susceptibility to S. aureus infection. AD flares are preceded by microbial dysbiosis dominated by S. aureus.3
  • Secondary skin infection may present clinically as impetigo, pustulosis, folliculitis, abscesses and cellulitis.3

Treatment Management Options for Infected Eczematous Dermatoses

  • Mild localized skin infections are usually treated with a topical antibiotic, while more severe and widespread infections are treated with a course of systemic antibiotics such as an early-generation cephalosporin or amoxicillin-clavulanate.3
  • Antibiotics should only be given when there is clinical evidence of an infection; indiscriminate use may increase bacterial resistance.
  • It is important to realize that skin cultures in colonized patients may grow S. aureus even when patients are not clinically infected and that a culture may not be able to distinguish colonization from infection.

Treatment Rationale for Combination Fusidic Acid/Betamethasone Lipid Cream

  • The combination of the topical antibiotic fusidic acid, and topical steroid betamethasone valerate, allows for eradication of the secondary infection and improvement of dermatitis at the same time.
  • Fusidic acid cream and ointment have been marketed in Canada since 1985. Fusidic acid has high activity against methicillin-sensitive and methicillin-resistant S. aureus [minimum inhibitory concentration of 50% (MIC50) of Canadian isolates of 0.12 and MIC90 of 0.25], and low (<3%) resistance in Canadian hospitals.4
  • Up to 2.5% of topical fusidic acid can cross intact human skin within 30 minutes, with up to 10% penetrating into the stratum corneum.1 Fusidic acid also has high activity against Clostridium and Corynebacteria spp., and moderate in vitro activity against streptococci.5
  • Its unique structure limits cross-resistance to other antibiotics.4
  • It is associated with a very low incidence of hypersensitivity in contrast to other antibiotics such as neomycin.6
  • Topical steroids are standard anti-inflammatory therapy for AD.2 Steroids stimulate the production of a glycoprotein called lipocortin which results in inhibition of phospholipase A2 and inhibition of release of arachidonic acid and biosynthesis of prostaglandins and leukotrienes.7 They also cause direct repression of the NF-κB transcription factor, inhibit mRNA for proinflammatory genes including those for interleukin-1 (Il-1), Il-2, Il-6, TNF-α, Il-4 and inducible nitric oxide (iNOS), and promote transcription of anti-inflammatory genes such as Il-10.7
  • There is no evidence that treatment of infected dermatoses with topical steroids in addition to topical antibiotics allows for overgrowth of pathogens and masks clinical infection.

Supporting Evidence from Clinical Trials

  • In a study of 629 patients with clinically infected AD, two weeks treatment with twice daily Fucidin/betamethasone in the lipid base and original base resulted in comparable reduction in the total severity of score (TSS) of the eczematous lesions (82.9% and 82.7% respectively vs. 33.0% for vehicle) and successful bacteriological response (89.7% and 89.6% vs. 25.0% for vehicle). In 94.1% of patients with fusidic acid susceptible isolates, active treatment was successful in eradicating the organisms.8 There were fewer perilesional adverse drug reactions (primarily pruritus and skin burning) with the active agents vs. placebo. The onset of action was rapid with a reduction in TSS after the first week of treatment.
  • In a double-blind, 1 week left/right infected or potentially infected AD and contact dermatitis study involving 81 patients (55 adults and 26 children), 2% fusidic acid/0.1% betamethasone was marginally superior to 0.1% betamethasone, although the combination eliminated 67% of bacteria vs. 51% with steroid.9 In addition, there was a significant patient preference for the combination (32 vs. 14 vs. 35 with no preference p<0.05).
  • In two published studies6,10 the clinical and bacteriological efficacy of fusidic acid/betamethasone valerate cream and neomycin/betamethasone cream were similar.
  • In an open parallel, randomized comparison study involving 46 patients, fusidic acid/betamethasone produced similar clinical improvement to mupirocin ointment followed by betamethasone valerate cream twice daily for 2 weeks.11 In this study, there was no evidence that the fusidic acid/steroid combination increased resistance of S.aureus to fusidic acid.
  • A randomized, open study involving 99 adult and pediatric patients, showed that treatment with twice daily 2% fusidic acid/0.1% betamethasone was superior clinically to the fixed combination product containing 0.1% gentamicin/0.1% betamethasone [54% vs. 38% respectively “excellent” at day 2-4, and 74% vs. 55% respectively “excellent” after 7-12 days of treatment, p=0.03].12 In addition, there was a statistically significant greater reduction in the mean severity scores for individual symptoms with fusidic acid/betamethasone. Seventy-four percent on fusidic acid/betamethasone rated the treatment as excellent vs. 55% on gentamicin/betamethasone (p=0.08 not significant). Although there was greater clinical improvement with fusidic acid/betamethasone, there was no difference between the two treatments in eradication of pathogens and no tendency for selection of resistant skin bacteria.
  • It is therefore difficult to explain the superior efficacy of fusidic acid/betamethasone since they both contain the same steroid. Furthermore, in another study, there was no difference in the release of betamethasone from fusidic acid/betamethasone valerate lipid cream (Fucibet®) and gentamicin/betamethasone valerate cream (Valisone-G®), however, at day 7, fusidic acid/betamethasone lipid cream showed significantly higher skin hydration compared to gentamicin/betamethasone valerate cream (p<0.05).13 The fusidic acid/betamethasone lipid base was found to be more adhesive and less spreadable than that of gentamicin/betamethasone cream suggesting that the former may function as a film-forming product, retaining active ingredients in place for a longer time in contact with the skin surface.
  • The difference in efficacy in the study by Strategos may also be related to the bacteriological method which was only semi-quantitative.12 At the start of the study, there was a lower rate of resistance of isolated Staph aureus to fusidic acid (9%) vs. gentamicin (21%).12


Fusidic acid/betamethasone 17-valerate cream (Fucibet®) is a cosmetically acceptable, well tolerated cream which is hydrating and improves the TSS dermatitis score in secondarily infected dermatitis. In addition, it clears bacteria in infected dermatitis better than vehicle suggesting that improving the dermatitis with a steroid might be synergistic, perhaps through a reduction in bacterial load.


  1. Fucibet® Canadian Product monograph. April 12, 2018. Leo Pharma Inc. Thornhill, ON Canada.

  2. Guenther LC, Andriessen A, Lynde CW et al. J Drugs Dermatol. 2016 Dec 1;15(12):1485-94.

  3. Rangel SM, Paller AS. Clin Dermatol. 2018 Sep-Oct;36(5):641-647.

  4. Pfaller MA, Castanheira M, Sader HS, Jones RN. Int J Antimicrob Agents. 2010 Mar;35(3):282-7.

  5. Skov R, Frimodt-Møller N, Espersen F.  Diagn Microbiol Infect Dis. 2001 Jul;40(3):111-6.

  6. Javier PR, Oritz M, Torralba L, et al. Br J Clin Pract. 1986 Jun;40(6):235-8.

  7. Uva L, Miguel D, Pinheiro C, et al. Int. J Endocrinol. 2012; ;2012:561018.

  8. Schultz Larsen F, Simmonsen L, Melgaard A, et al. Acta Derm Venereol. 2007;87(1):62-8.

  9. Hjorth N, Schmidt H, Thomsen K. Pharmatherapeutica. 1985;4(2):126-31.

  10. Wilkinson JD, Leigh DA. Curr Ther Res. 1985;38:177-82.

  11. Ravenscroft JC, Layton AM, Eady EA, et al. Br J Dermatol. 2003 May;148(5):1010-7.

  12. Strategos J. Pharmatherapeutica. 1986;4(9):601-6.

  13. Molesini S, Urtro F, Cvetkovska AD, et al. Ther Deliv. 2018 Feb 1;9(3):177-84.