|Year : 2006 | Volume
| Issue : 4 | Page : 253-255
Etiopathogenesis of seborrheic dermatitis
Emeritus Professor of Dermatology, LTM Medical College, Sion, Mumbai, India
R G Valia
51, Arcadia, Sir Bhalchandra Road, Dadar, Mumbai-400014
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Valia R G. Etiopathogenesis of seborrheic dermatitis. Indian J Dermatol Venereol Leprol 2006;72:253-5
Seborrheic dermatitis (SD) is a common inflammatory disorder of the skin, characterized by erythema covered with greasy-looking scales and seen over areas rich in sebaceous glands-namely, the scalp, face, chest, back and flexural areas. Though much remains to be learned, there is increasing understanding of the etiopathogenesis of seborrheic dermatitis. This should eventually lead to more effective management of the disease.
| Seborrhea|| |
Seborrheic dermatitis is not a disorder of sebaceous glands. Many normal young adults have an oily-looking skin but no SD. Moreover, the sebum secretion rate from the forehead of SD patients is normal. Though Parkinson's disease is associated with seborrhea and seborrheic dermatitis, its treatment with L-dopa reduces sebum secretion if it is in excess but has no effect if the sebum secretion is normal. It has been suggested that the increased sebum levels in patients of Parkinson's disease have permissive effect on the growth of Malassezia . It may be concluded that seborrhea may be a predisposing factor but is not the primary etiological factor for seborrheic dermatitis. This is supported by the fact that low-dose oral isotretinoin, a known sebostatic agent, given for several months, is useful in stubborn seborrheic dermatitis. However, the effects of isotretinoin on the regularization of disturbed keratinization may also be responsible for this improvement.
Newborns have high sebum production from active sebaceous glands due to their stimulation by circulating maternal androgens. Infantile seborrheic dermatitis (ISD) clears spontaneously within 3 to 4 weeks after birth and is attributed, albeit without much scientific support, to decreased levels of sebum production. Besides that, it is not established that ISD is the same condition as SD seen in adolescents and adults. Most infants with ISD become normal in adult life; only 7 of 88 ISD patients had persistent seborrheic dermatitis when reviewed 10 years later. Sometimes, typical ISD transforms into atopic dermatitis later. In two different studies, 19 and 27.5% of ISD patients, when reviewed 12 and 13 years later respectively, were diagnosed as having atopic dermatitis., This confusion is due to a clinical overlap between the two conditions, particularly in the early stages. Cohen concluded that ketoconazole is at least as effective at treating seborrheic dermatitis as steroid creams and may be better at preventing recurrences, providing a good alternative to steroid creams in infants.
| Pityrosporum ovale|| |
Schuster proposed that the organism Malassezia furfur or its yeast form, Pityrosporum ovale, plays an etiological role in SD. The organism is increased in number in SD and can be cultured from the lesions. Experimental infection with the organism causes the disease. Patients with dandruff have high antibody titers to Malassezia compared with controls. A good therapeutic response to antipityrosporal drugs proves the point. Improvement in the disease corresponds with a reduction in the number of Malassezia, while recolonization results in disease recurrence. In patients with pityriasis versicolor and pitysporum folliculitis, seborrheic dermatitis has been found in a higher percentage than expected.
Although correlation between yeast density and severity of SD has been reported, it is not certain that SD patients have higher Malassezia counts than controls. Also, some investigators have found no difference in the amount of Malassezia yeasts in lesional versus non-lesional skin of SD patients. Moreover, the response of SD to antifungal drugs like azoles and imidazoles may be due to their anti-inflammatory action.
| Skin lipids and inflammation|| |
How Malassezia yeasts initiate the inflammation of seborrheic dermatitis is not clear. They or their byproducts may cause inflammation by inducing cytokine production by keratinocytes or through involvement of Langerhans cells and T-lymphocyte activation. However, the occurrence of SD in early HIV infection, where the cell-mediated immunity is impaired, goes against the hypothesis that SD is mediated by T-lymphocyte activation by Pityrosporum ovale.
Another factor that may cause inflammation is the lipase activity of P. ovale, which generates inflammatory fatty acids from skin lipids. Though qualitative abnormalities in the composition of sebum have not been demonstrated in SD, mild abnormalities in the surface lipids could result from the ineffective keratinization that is often demonstrated histologically. In infants with active SD, levels of essential fatty acids 18:1W9 were increased and levels of 18:2W6 were decreased compared to healthy children. All deviant values became normal at the time of spontaneous remission, which can be explained by a transient impaired function of the enzyme d-6 saturase. In another study, SD patients had lower free fatty acids (FFAs) and raised triglycerides, whether they were HIV-positive or not.
| Immune dysfunction|| |
Though antimycotics 'clear' the condition with a reduction in the number of the organisms, recolonization and relapse occur on stopping treatment. This could be explained by an underlying immunological deficit. The increased prevalence of seborrheic dermatitis in HIV-positive patients also supports the hypothesis that seborrheic dermatitis has a strong immunological basis.
There may be a defective cell-mediated immune response to Pityrosporum ovale in patients with seborrheic dermatitis, although the evidence for this is incomplete and confusing.,,,, Though the relationship between seborrheic dermatitis and Malassezia yeasts is not yet completely understood, these studies support the postulation that strong skin colonization with P. ovale in seborrheic dermatitis is due to altered cell-mediated immunity and that the development of seborrheic dermatitis depends upon the way the patient's immune system reacts to antigens derived from P. ovale .
| Seborrheic dermatitis and AIDS|| |
The prevalence of SD in HIV-positive and AIDS patients is between 34% and 83% as opposed to 3% in the general population. Its incidence and severity are closely related to the stage of HIV infection and inversely correlate with the absolute CD4 and helper T cell counts. More severe, widespread disease in the HIV infected, with more erythematous, hyperkeratotic and psoriasiform lesions, has led to the suggestion that the clinical picture seen in HIV infection-AIDS should be termed as SD-like dermatitis of AIDS and should be regarded as a distinctive entity caused by immunological defects. As the disease becomes more advanced, the lesions spread and exacerbate, presumably due to the enhanced growth of yeasts secondary to immunosuppression.
| SD-like dermatitis|| |
Many drugs like auranofin, aurothioglucose, buspirone, chlorpromazine, cimetidine, ethionamide, gold, griseofulvin, haloperidol, interferon-a, lithium, methoxsalen, methyldopa, phenothiazines, psoralens, stanozolol, thiothixene and trioxsalen are known to induce a SD-like dermatitis by an unknown mechanism. Nutritional deficiencies, especially of riboflavin, pyridoxine, niacin, zinc and EFA, also cause a SD-like dermatitis by an unknown mechanism. The distinction between SD and SD-like conditions is not easy to make.
The cause of SD is yet to be resolved. Until then, the choice of therapy in SD will be between antimycotics, topical steroids, sebostatics or their combinations. The future may see more studies with topical immunomodulators or other nonsteroidal agents like metronidazole, whose mechanism of action is yet to be elucidated.
| References|| |
|1.||Burton JL, Pye RJ. Seborrhea is not a feature of seborrheic dermatitis. BMJ 1983;286:1169-971. [PUBMED] |
|2.||Binder RL, Jonelis FJ. Seborrheic dermatitis in neuroleptic-induced Parkinsonism. Arch Dermatol 1983;119:473-5. [PUBMED] |
|3.||Burton JL, Cartilidge M, Shuster S. Effect of L-dopa on the seborrhea of Parkinsonism. Br J Dermatol 1973;88:475-9. |
|4.||Plewig G, Jansen T. Seborrheic dermatitis. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick's Dermatology in general medicine. 6th ed. New York: McGraw-Hill; 2003. p. 1204. |
|5.||Henderson CA, Taylor J, Cunliffe WJ. Sebum excretion rates in mothers and neonates. Br J Dermatol 2000;142:110-1. [PUBMED] [FULLTEXT]|
|6.||Leung AK. Neonatal seborrheic dermatitis (letter). West J Med 1985;142:558-62. [PUBMED] |
|7.||Schechtman RC, Midgley G, Bingham JS, Hay RJ. Progress of seborrheic dermatitis. Br J Dermatol 1995;133:537-45. |
|8.||Neville EA, Finn OA. Psoriasiform napkin dermatitis: A follow-up study. Br J Dermatol 1975;92:279-85. [PUBMED] |
|9.||Podmore P, Burrows D, Eady DJ, Stanford CF. Seborrheic dermatitis: Disease entity or a clinical variant of atopic dermatitis? Br J Dermatol 1986;115:341-50. |
|10.||Cohen S. Should we treat infantile seborrheic dermatitis with topical antifungals or topical steroids? Arch Dis Child 2004;89:288-9. [PUBMED] [FULLTEXT]|
|11.||Schusten S, Blatchford N. Seborrheic dermatitis and dandruff - A fungal disease. Royal Soc Med Services 1988;132:1-54. |
|12.||Crespo EV, Delgado FV. Malassezia species in skin disease. Curr Opin Infect Dis 2002;15:133-42. |
|13.||Faergemann J, Fredriksson T. Tinea versicolor with reference to seborrheic dermatitis. Arch Dermatol 1979;115:966-8. [PUBMED] |
|14.||Back O, Faergemann J, Hornqvist R. Pityrosporum folliculitis: A common disease of the young and middle-aged. J Am Acad Dermatol 1985;12:56-61. [PUBMED] |
|15.||Heng MC, Henderson CL, Barker DC, Haberfelde G. Correlation of Pityrosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique. J Am Acad Dermatol 1990;23:82-6. [PUBMED] |
|16.||McGinley KJ, Leyden JJ, Marples RR, Kligman AM. Quantitative microbiology of the scalp in non-dandruff, dandruff and seborrhoeic dermatitis. J Invest Dermatol 1975;64:401-5. [PUBMED] |
|17.||Wattanbe S, Kano R, Sato H, Nakamura Y, Hasegawa A. The effect of Malassezia yeasts on cytokine production by human keratinocytes. J Invest Dermatol 2001;116:769-73. |
|18.||Bergbrant IM. Seborrheic dermatitis and pityrosporum yeasts. Curr Top Med Mycol 1995;6:95-112. [PUBMED] |
|19.||Pye RJ, Meyrick G, Burton JL. Skin surface in seborrheic dermatitis. Br J Dermatol 1977;97:12-4. |
|20.||Tolesson A, Frithz A, Berg A, Karlman G. Essential fatty acids in infantile seborrheic dermatitis. J Am Acad Dermatol 1993;28:957-61. |
|21.||Ostlers LS, Taylor CR, Harris DW, Rustin MH, Wright S, Johnson M. Surface lipids in HIV positive patients with and without seborrheic dermatitis. Br J Dermatol 1996;35:276-9. |
|22.||Bergbrant IM, Johansson S, Robbins D, Scheynius A, Faergemann J, Soderstrom T. An immunological study in patients with seborrheic dermatitis. Clin Exp Dermatol. 1991;16:331-8. [PUBMED] |
|23.||Parry ME, Sharpe GR. Seborrheic dermatitis is not caused by an altered immune response to Malassezia yeast. Br J Dermatol 1998;139:254-63. [PUBMED] [FULLTEXT]|
|24.||Wilker JR. Cell mediated deficiency in Pityrosporum orbiculare in patients with seborrheic dermatitis (abstract). J Invest Dermatol 1989;92:241-5. |
|25.||Neuber K, Kroger S, Gruseek E, Abeck D, Ring J. Effect of proliferation, immunoglobulin (IgA, IgG, IgM) synthesis and cytokine (IL2, IL10, IFN-a) production of peripheral blood mononuclear cells from seborrheic dermatitis. Arch Dermatol Res 1996;288:532-6. |
|26.||Faergemann J, Jones JC, Hettler O, Loria Y. Pityrosporum ovale (Malassezia furfur) as the causative agent of seborrheic dermatitis: New treatment options. Br J Dermatol 1996;134:12-5. [PUBMED] |
|27.||Berger RS, Stoner MF, Hobbs ER, Hayes TJ, Boswell RN. Cutaneous manifestations of human immunodeficiency virus exposure. J Am Acad Dermatol 1988;19:298-303. [PUBMED] |
|28.||Marino CT, McDonald E, Romano JF. Seborrheic dermatitis in acquired immunodeficiency syndrome. Cutis 1991;50:217-8. |
|29.||Kaplan MH, Sadick N, McNutt NS. Dermatologic findings and manifestations of acquired immunodeficiency syndrome (AIDS). J Am Acad Dermatol 1989;20:770-3. |
|30.||Selden S. Seborrheic dermatitis. http://www.emedicine.com/derm/topic396.htm Last updated: September 23, 2005. Last accessed: June 12, 2006. |
|31.||Patnaik R, Choudary TN, Shashikiran B. Nutrition and skin. In: Valia RG, Valia AR, editor. IADVL textbook and atlas of dermatology. 2nd edn. Bombay: Bhalani Publishing House, 1999. p. 974-1001. |
|32.||Cunha PR. Pimecrolimus cream 1% is effective in seborrheic dermatitis refractory to treatment with topical corticosteroids. Act Derm Venerol 2006;86:69-70. |
|33.||Siadat AH, Iraji F, Shahmoradi Z, Enshaieh S, Taheri A. The efficacy of 1% metronidazole gel in facial seborrheic dermatitis: A double blind study. Indian J Dermatol Venerol Leprol 2006;72:266-9. |
|This article has been cited by|
||The association of oxidative stress and disease activity in seborrheic dermatitis
| ||Selma Emre,Ahmet Metin,Duriye Deniz Demirseren,Gulsen Akoglu,Aynure Oztekin,Salim Neselioglu,Ozcan Erel |
| ||Archives of Dermatological Research. 2012; 304(9): 683 |
|[Pubmed] | [DOI]|
||Topical antifungal agents for seborrheic dermatitis: Systematic review and meta-analysis
| || Apasrawirote, W., Udompataikul, M., Rattanamongkolgul, S. |
| ||Journal of the Medical Association of Thailand. 2011; 94(6): 756-760 |
||New insights into HIV-1-primary skin disorders
| ||Cedeno-Laurent, F., Gámez-Flores, M., Mendez, N., Ancer-Rodríguez, J., Bryant, J.L., Gaspari, A.A., Trujillo, J.R. |
| ||Journal of the International AIDS Society. 2011; 14(1): 5 |
|| Seborrhoeic-like dermatitis | [Dermatoza o obrazie klinicznym przypominaja̧cym łojotokowe zapalenie skóry]
| ||Błaszkowski, M., Kaczorowska, A., Staszek, D., Kaszuba, A. |
| ||Postepy Dermatologii i Alergologii. 2010; 27(2): 101-105 |
||Is Demodex folliculorum an aetiological factor in seborrhoeic dermatitis?
| ||Y. Karincaoglu, B. Tepe, B. Kalayci, M. Atambay, M. Seyhan |
| ||Clinical and Experimental Dermatology. 2009; 34(8): e516-e520 |
|[Pubmed] | [DOI]|