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Published on 1 September 2005

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Advances in seborrhoeic dermatitis treatment

teaser

Dimitris Rigopoulos
MD
Associate Professor of Dermatology

Stamatis Gregoriou
MD
Clinical Fellow
University of Athens
Dermatology Academic Department
“A Sygros” Hospital
University of Athens
Athens
Greece
E:drigop@hol.gr

Seborrhoeic dermatitis is a common dermatological disorder with a prevalence of 2–5%. Clinically, it presents with inflammation and desquamation in lipid-rich areas of the skin such as the face, chest and scalp. Dandruff, which affects 5–10% of the population, is considered to be the mildest form of seborrhoeic dermatitis. Considerable amounts of money are spent each year on ­therapeutic agents in an attempt to eliminate the problem.(1)

Although it is generally accepted that Malassezia yeasts are associated with seborrhoeic dermatitis, most of the evidence comes from the efficacy of anti‑fungal drugs. The mechanism by which the yeast causes the dermatosis is not clear. Studies have shown that Malassezia stimulates cytokine production by human keratinocytes.(2) The lipase enzyme produced by Malassezia has also been suggested to split tri­glycerides into irritant fatty acids, which induce scaling or release of arachidonic acid.(3) Investigators have also proposed that impaired cell immunity may facilitate fungal survival in the skin.(4) Increased incidence of seborrhoeic dermatitis has been documented in HIV/AIDS patients and patients with neurological disorders such as Parkinson’s disease, multiple sclerosis and depression.(5) Several traditional treatments of seborrhoeic dermatitis are currently being used.

Nonspecific agents
Selenium sulphide,(6) propylene glycol,(7) sulphur and tar-containing compounds(8) have been successfully used, with efficacy attributed to their keratolytic ­properties. Lithium has also been used,(9) with efficacy attributed to inhibition of the fatty acid production (necessary for Malassezia proliferation) and to anti-inflammatory properties.

Topical corticosteroids
In the past, intermediate- and high-potency corticosteroids(10) have been used in the treatment of ­seborrhoeic dermatitis, due to their anti-inflammatory properties. When adverse long-term effects on the adrenal cortex and on the skin became apparent, interest shifted to low-potency drugs such as hydro­cortisone 1%,(11) with excellent results.

Topical antifungals
This drug type includes zinc pyrithione,(12) which has both keratolytic and antifungal properties, and ­­­­topical azoles such as bifonazole,(13) miconazole(14) and ­ketoconazole.(15)

New topical treatments for seborrhoeic dermatitis
The success of ketoconazole in the treatment of seborrhoeic dermatitis has fuelled interest in the efficacy of new antifungal agents.

Fluconazole
Fluconazole is an azole derivative commonly used for dermatoses caused by Malassezia spp. A recent open trial reported complete recovery or improvement in all patients with seborrhoeic dermatitis using ­­­­fluconazole 2% shampoo twice weekly for two weeks. All cultures for Malassezia spp were negative at the end of the treatment.(16)

Metronidazole
The efficacy of metronidazole remains controversial. Although one double-blind, randomised study found that metronidazole gel 1% applied twice daily for eight weeks was more effective than placebo in the treatment of seborrhoeic dermatitis,(17) another double-blind trial evaluating metronidazole gel 0.75% applied at the same frequency showed no superiority over placebo.(18)

Ciclopirox olamine
Ciclopirox olamine has a broad spectrum of anti­fungal action, in addition to anti-inflammatory properties. A recent trial demonstrated that ciclopirox olamine 1% cream was as effective as ketoconazole 2% foaming gel in the treatment of facial seborrhoeic dermatitis.(19)

Terbinafine
Terbinafine is a fungicidal allylamine. A solution of terbinafine 1% has been successfully used in the treatment of seborrhoeic dermatitis.(20)

Topical immunomodulators
Topical immunomodulators such as tacrolimus and pimecrolimus are a new class of medications that have been used in the treatment of seborrhoeic dermatitis. They are potent and lack the adverse events associated with the long-term use of topical corticosteroids.

Topical tacrolimus ointment 0.1% was proven to be effective in the treatment of seborrhoeic dermatitis in an open-label study. The effect is attributed to the anti-inflammatory and antifungal properties of the drug, which have been demonstrated in vitro against Malassezia spp.(21)

In a randomised, open-label study, ­pimecrolimus cream 1% was found to be as effective as beta­methasone valerate in controlling the symptoms of seborrhoeic dermatitis, with fewer relapses and no rebounds.(22)

Other topical therapies: natural therapies
In vitro, cinnamic acid reduces the growth of Malassezia spp; therefore, mild formulations may prove to have therapeutic use.(23) A recent report has shown that 90% of honey diluted in warm water could be used in the treatment of seborrhoeic dermatitis.(24) Dandruff has been successfully treated with 5% tea tree oil shampoo.(25) Topical mud treatment has also been suggested to represent an alternative to the treatment of seborrhoeic dermatitis.(26)

Systemic treatments for seborrhoeic dermatitis
Oral treatments may be considered in patients refractory to topical treatment or when seborrhoeic ­dermatitis is extremely widespread.

Ketoconazole
Oral ketoconazole 200mg daily for four weeks is an effective treatment of ­seborrhoeic dermatitis of the scalp and body. However, use of oral ketoconazole for more than four weeks has been associated with an increased possibility of side-effects.(27)

Itraconazole
Itraconazole 200mg daily is effective in the treatment of seborrhoeic dermatitis and lacks the marked ­hepatotoxicity associated with ketoconazole.(28)

Terbinafine
Oral terbinafine, although ineffective in the treatment of pityriasis versicolor, may be effective against seborrhoeic dermatitis when administersd at a dose of 250mg/day for four weeks.(29)

UVB (TL-01) phototherapy
Ultraviolet B (UVB) phototherapy has been reported to produce excellent results in the treatment of ­seborrhoeic dermatitis.30

Prophylaxis
Seborrhoeic dermatitis is a chronic, recurring, inflammatory skin disorder. Consequently, attention should be given to the long-term control of the disorder. The ideal treatment agent should offer reduced relapses, increased tolerability and long-term safety, thus ensuring high rates of patient compliance. Ketoconazole shampoo for the scalp and ­ketoconazole or ­miconazole cream for skin eruption seem to be the preferred drugs in the prophylactic treatment of seborrhoeic dermatitis. The new topical immunomodulators tacrolimus and ­pimecrolimus might prove a good alternative prophylactic treatment, provided that their long-term safety is confirmed.

Conclusion
Topical antifungal agents remain the mainstay of therapy in seborrhoeic dermatitis. Their advantages include good efficacy and tolerability, as well as low cost. Tacrolimus and pimecrolimus might be considered as second-line treatment, because they offer symptom control as fast as that of corticosteroids and lack the latter’s long-term adverse effects.

References

  1. Dermatology 2004;208:89-93.
  2. J Invest Dermatol 2001;116:769-73.
  3. Drugs 1991;41:178-84.
  4. J Med Vet Mycol 1994;32 Suppl 1:367-78.
  5. Clin Dermatol 2003;21:417-25.
  6. J Pharm Sci 1969;58:1279-80.
  7. Cutis 1988;42:69-71.
  8. J Int Med Res 1981;9:152-6.
  9. Psychiatr J Univ Ott 1983;8;27-9.
  10. Curr Ther Res Clin Exp 1972;14:35-8.
  11. J Am Acad Dermatol 1988;19:850-3.
  12. Br J Dermatol 1985;112:415-22.
  13. Acta Derm Venereol 1992;72:454-5.
  14. Br J Dermatol 1986;114:695-700.
  15. Br J Dermatol 1987;116:217-21.
  16. Int J Dermatol 1994;33:136-7.
  17. Dermatology 2001;202:35-7.
  18. Int J Dermatol 2003;42:632-5.
  19. Dermatology 2003;206:233-40.
  20. Br J Dermatol 1996;134 Suppl 46:12-5.
  21. Br J Dermatol 2003;148:1242-4.
  22. Br J Dermatol 2004;151:1071-5.
  23. Dermatology 2000;201:332-6.
  24. Eur J Med Res 2001;6:306-8.
  25. J Am Acad Dermatol 2002;47:852-5.
  26. J Eur Acad Dermatol Venereol 2004;18:372-4.
  27. Br J Dermatol 1984;111:603-9.
  28. G Ital Dermatol Venereol 2002;137:1-7.
  29. Br J Dermatol 2001;144:854-7.
  30. Br J Dermatol 2000;143:964-8.


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