Seborrhoeic dermatitis

Seborrheic dermatitis
Synonyms Seborrhoea, sebopsoriasis, seborrhoeic eczema, pityriasis capitis[1]
An example of seborrhoeic dermatitis between the nose and mouth
Specialty Dermatology
Symptoms Itchy, flaking, greasy, red, and inflamed skin[2]
Duration Long term[2]
Causes Genetic and environmental factors[2]
Risk factors Stress, winter, poor immune function, Parkinson disease, epilepsy, Down syndrome[2]
Diagnostic method Based on symptoms[2]
Differential diagnosis Psoriasis, atopic dermatitis, tinea capitis, rosacea, systemic lupus erythematosus[2]
Medication Antifungal cream, anti-inflammatory agents, coal tar, phototherapy[2]
Frequency ~2% (adults), ~40% (babies)[2]

Seborrhoeic dermatitis, also known as seborrhoea, is a long-term skin disorder.[2] Symptoms include red, scaly, greasy, itchy, and inflamed skin.[2] Areas of the skin rich in oil-producing glands are often affected including the scalp, face, and chest.[2] It can result in social or self-esteem problems.[2] In babies, when the scalp is primarily involved, it is called cradle cap.[2] Dandruff is a milder form of the condition, without associated inflammation.[2]

The cause is unclear but believed to involve a number of genetic and environmental factors.[2] Risk factors include poor immune function, Parkinson disease, epilepsy, and Down syndrome.[2] The condition may worsen with stress or during the winter.[2] It is not a result of poor hygiene.[3] Diagnosis is typically based on the symptoms.[2]

The typical treatment is antifungal cream and anti-inflammatory agents.[2] Specifically ketoconazole or ciclopirox are effective.[4] It is unclear if other antifungals, such as miconazole, are equally effective as they have been poorly studied.[4] Other options may include coal tar and phototherapy.[2]

The condition is most common in those around the age of 50, during puberty, and among those less than three months old.[2] In adults about 2% of people are affected.[2] Males are more often affected than females.[2] Up to 40% of babies may be affected to some degree.[2]

Signs and symptoms

Seborrhoeic dermatitis on scalp
Acute form of seborrhoeic dermatitis on scalp

Seborrhoeic dermatitis' symptoms appear gradually, and usually the first signs are flaky skin and scalp.[5] Symptoms occur most commonly anywhere on the skin of the scalp, behind the ears, on the face, and in areas where the skin folds. Flakes may be yellow, white or grayish.[6] Redness and flaking may also occur on the skin near the eyelashes, on the forehead, around the sides of the nose, on the chest, and on the upper back.

In more severe cases, yellowish to reddish scaly pimples appear along the hairline, behind the ears, in the ear canal, on the eyebrows, on the bridge of the nose, around the nose, on the chest, and on the upper back.[7]

Commonly, patients experience mild redness, scaly skin lesions and in some cases hair loss.[8] Other symptoms include patchy scaling or thick crusts on the scalp, red, greasy skin covered with flaky white or yellow scales, itching, soreness and yellow or white scales that may attach to the hair shaft.[9]

Seborrhoeic dermatitis can occur in infants younger than three months and it causes a thick, oily, yellowish crust around the hairline and on the scalp. Itching is not common among infants. Frequently, a stubborn diaper rash accompanies the scalp rash.[7] Usually, when it occurs in infants the condition resolves itself within days and with no treatment.

In adults, symptoms of seborrhoeic dermatitis may last from a few weeks, to years. Many patients experience alternating periods of inflammation. The condition is referred to a specialist when self-care has proven unsuccessful.

Causes

The specific causes are not known.[10] Current theories for the cause of the disease include a weakened immune system, the lack of specific nutrients or issues with the nervous system.[11]

Fungal

Seborrhoeic dermatitis may involve an inflammatory reaction to a proliferation of a form of the yeast Malassezia,[12][13] though this has not been proven.[14]

The main species of yeast found on the scalp of those with the condition is Malassezia globosa, others being Malassezia furfur (formerly known as Pityrosporum ovale) and Malassezia restricta. It has been suggested that the yeast produces toxic substances that irritate and inflame the skin. Patients with seborrhoeic dermatitis appear to have a reduced resistance to the yeast. However, the colonization rate of affected skin may be lower than that of unaffected skin.[15]

Only saturated fatty acids (FAs) have been shown to support Malassezia growth. It has also been shown that while number density of M. globosa and M. restricta do not directly correlate to dandruff presence or severity, removal correlates directly with amelioration of flaking. Furthermore, in dandruff-susceptible individuals pure oleic acid, an unsaturated FA and Malassezia metabolite, induces flaking in the absence of Malassezia by direct effects on the host skin barrier. These findings support the following hypothesis:

Malassezia hydrolyze human sebum, releasing a mixture of saturated and unsaturated fatty acids. They take up the required saturated FAs, leaving behind unsaturated FAs. The unsaturated FAs penetrate the stratum corneum. Because of their non-uniform structure, they breach the skin's barrier function. This barrier breach induces an irritation response, leading to dandruff and seborrhoeic dermatitis.[16]

Others

Genetic, environmental, hormonal, and immune-system factors can impact seborrhoeic dermatitis outbreaks.[17][18] Seborrhoeic dermatitis may be aggravated by illness, psychological stress, fatigue, sleep deprivation, change of season and reduced general health.[19] In children and babies, excessive vitamin A intake [20] or issues with delta-6 desaturase enzymes [19] have been correlated with increased risk. Seborrhoeic dermatitis-like eruptions are also associated with vitamin B6 deficiency.[21] Those with immunodeficiency (especially infection with HIV) and with neurological disorders such as Parkinson's disease (for which the condition is an autonomic sign) and stroke are particularly prone to it.[22]

Management

Medications

A number of medications are able to control seborrhoeic dermatitis including: certain antifungals, topical corticosteroids, and keratolytics such as topical urea, as well as antiandrogens and antihistamines.[1]

Antifungals

Daily use of an over-the-counter or prescription anti-fungal shampoo may help those with recurrent episodes. The topical antifungal medications ketoconazole and ciclopirox have the best evidence.[4] It is unclear if other antifungals are equally effective as this has not been studied.[4] Another potential option is natural and artificial UV radiation since it can curb the growth of Malassezia yeast [23]

Antiandrogens

Seborrhoea is recognized as an androgen-sensitive condition – that is, it is caused or aggravated by androgen sex hormones such as testosterone and dihydrotestosterone – and is a common symptom of hyperandrogenism (e.g., that seen in polycystic ovary syndrome).[24][25] In addition, seborrhoea, as well as acne, are commonly associated with puberty due to the steep increase of androgen levels at that time.[26]

In accordance with the involvement of androgens in seborrhoea, antiandrogens, such as cyproterone acetate,[27] spironolactone,[28] and flutamide,[29][30] are highly effective in alleviating the condition.[24][31] As such, they are used in the treatment of seborrhoea,[24][31] particularly severe cases.[32] While beneficial in seborrhoea, effectiveness may vary with different antiandrogens; for instance, spironolactone (which is regarded as a relatively weak antiandrogen) has been found to produce a 50% improvement after three months of treatment, whereas flutamide has been found to result in an 80% improvement within three months.[24][30] Cyproterone acetate is similarly more potent and effective than spironolactone, and results in considerable improvement or disappearance of acne and seborrhoea in 90% of patients within three months.[33]

Systemic antiandrogen therapy should only be used to treat seborrhoea in women, and never in men, as these drugs can result in feminization (e.g., gynecomastia), sexual dysfunction, and infertility in males.[34][35] In addition, antiandrogens theoretically have the potential to feminize male fetuses in pregnant women, and for this reason, should always be combined with effective contraception in sexually active women who can or may become pregnant.[33]

Antihistamines

Antihistamines are used primarily to reduce itching, if present. However, research studies suggest that some antihistamines have anti-inflammatory properties.[36]

Anti-inflammatory treatments

Topical steroids have been shown to be effective in short-term treatment of serborrhoeic dermatitis, and is as effective or more effective than azole treatment. There is also evidence for the effectiveness of calcineurin inhibitors and lithium salt treatment. [37]

Other treatments

  • Coal tar can be effective, but, although no significant increased risk of cancer in human treatment with coal tar shampoos has been found,[38] caution is advised since coal tar is carcinogenic in animals, and heavy human occupational exposures do increase cancer risks.
  • Pimecrolimus topical cream immunosuppressant[39]
  • Prednisone — an oral immunosuppressive treatment that has been used in short courses as a last resort due to its potential side effects.[40]
  • Isotretinoin — As a last resort in refractory disease, sebosuppressive agent isotretinoin may be used to reduce sebaceous gland activity. However, isotretinoin has potentially serious side effects and few patients with seborrhoea are appropriate candidates for therapy.[40]

Phototherapy

Some recommend photodynamic therapy using UV-A and UV-B laser or red and blue LED light to inhibit the growth of Malassezia fungus and reduce seborrhoeic inflammation.[41][42][43]

Epidemiology

Seborrhoea affects 1 to 5% of the general population.[1][44][45] It is slightly more common in men, but affected women tend to have more severe symptoms.[45] The condition usually recurs throughout a person's lifetime.[46] Seborrhoea can occur in any age group[46] but usually starts at puberty and peaks in incidence at around 40 years of age.[47] It can reportedly affect as many as 31% of older people.[45] Severity is worse in dry climates.[46]

See also

References

  1. 1 2 3 Dessinioti, C.; Katsambas, A. (2013). "Seborrheic dermatitis: etiology, risk factors, and treatments: facts and controversies". Clin Dermatol. 31 (4): 343–51. doi:10.1016/j.clindermatol.2013.01.001. PMID 23806151.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Borda, Luis (2015). "Seborrheic Dermatitis and Dandruff: A Comprehensive Review". Journal of Clinical and Investigative Dermatology. 3 (2). doi:10.13188/2373-1044.1000019.
  3. ↑ "Seborrheic dermatitis". American Academy of Dermatology. Archived from the original on 21 October 2017. Retrieved 20 October 2017.
  4. 1 2 3 4 Okokon, EO; Verbeek, JH; Ruotsalainen, JH; Ojo, OA; Bakhoya, VN (28 April 2015). "Topical antifungals for seborrhoeic dermatitis". The Cochrane Database of Systematic Reviews. 4: CD008138. doi:10.1002/14651858.CD008138.pub3. PMC 4448221. PMID 25933684.
  5. ↑ "Dermatitis Seborrheic Treatment". Archived from the original on 2010-06-02. Retrieved June 11, 2010.
  6. ↑ "Seborrheic Dermatitis". Archived from the original on June 15, 2010. Retrieved June 11, 2010.
  7. 1 2 "Dermatitis". Archived from the original on September 25, 2011. Retrieved June 11, 2010.
  8. ↑ "What is Seborrheic Dermatitis?". Archived from the original on April 20, 2010. Retrieved June 11, 2010.
  9. ↑ "Symptoms". Archived from the original on May 26, 2010. Retrieved June 11, 2010.
  10. ↑ Dessinioti, C; Katsambas, A (Jul–Aug 2013). "Seborrheic dermatitis: etiology, risk factors, and treatments: facts and controversies". Clinics in dermatology. 31 (4): 343–51. doi:10.1016/j.clindermatol.2013.01.001. PMID 23806151.
  11. ↑ Zieve, David. "Seborrheic Dermatits". A.D.A.M., Inc. Archived from the original on 2016-05-08.
  12. ↑ Hay, R.J.; Graham-Brown, R.A.C. (1997). "Dandruff and seborrhoeic dermatitis: causes and management". Clinical and Experimental Dermatology. 22 (1): 3–6. doi:10.1046/j.1365-2230.1997.d01-231.x. PMID 9330043.
  13. ↑ Nowicki R (January 2006). "[Modern management of dandruff]". Polski Merkuriusz Lekarski (in Polish). 20 (115): 121–4. PMID 16617752.
  14. ↑ Parry, ME; Sharpe, GR (1998). "Seborrhoeic dermatitis is not caused by an altered immune response to Malassezia yeast". British Journal of Dermatology. 139 (2): 254–63. doi:10.1046/j.1365-2133.1998.02362.x. PMID 9767239.
  15. ↑ "Treatment of Seborrheic Dermatitis". Archived from the original on July 6, 2010. Retrieved September 10, 2010.
  16. ↑ "P&G Beauty & Grooming | Role of Lipid Metabolism in Seborrheic Dermatitis (Dandruff)". Pgbeautygroomingscience.com. Archived from the original on 2013-01-31. Retrieved 2013-01-26.
  17. ↑ Johnson, Betty Anne; Nunley, Julia R. (May 2000). "Treatment of seborrheic dermatitis". American Family Physician. 61 (9): 2703–10, 2713–4. PMID 10821151. Archived from the original on 2010-07-06.
  18. ↑ Janniger CK, Schwartz RA (July 1995). "Seborrheic dermatitis". American Family Physician. 52 (1): 149–55, 159–60. PMID 7604759.
  19. 1 2 Schwartz, Robert A.; Janusz, Christopher A.; Janniger, Camila K. (July 2006). "Seborrheic dermatitis: an overview". American Family Physician. 74 (1): 125–30. PMID 16848386.
  20. ↑ MedlinePlus Encyclopedia Hypervitaminosis A
  21. ↑ Alamgir, A.N.M. (2018). Therapeutic Use of Medicinal Plants and their Extracts: Volume 2: Phytochemistry and Bioactive Compounds. Springer. p. 435. ISBN 3319923870.
  22. ↑ "Seborrhoeic dermatitis and dandruff (seborrheic eczema). DermNet NZ". . DermNet NZ. 2012-03-20. Archived from the original on 2012-06-15. Retrieved 2012-06-10.
  23. ↑ Wikler, JR.; Janssen N.; Bruynzeel DP.; Nieboer C. (1990). "The effect of UV-light on pityrosporum yeasts: ultrastructural changes and inhibition of growth". Acta dermato-venereologica. Stockholm. 70 (1): 69–71. PMID 1967880.
  24. 1 2 3 4 Singh, Shankar; Gauthier, Sylvain; Labrie, Fernand (2000). "Androgen Receptor Antagonists (Antiandrogens) Structure-Activity Relationships". Current Medicinal Chemistry. 7 (2): 211–247. doi:10.2174/0929867003375371. ISSN 0929-8673. PMID 10637363.
  25. ↑ Zouboulis, Christos C.; Degitz, Klaus (2004). "Androgen action on human skin – from basic research to clinical significance". Experimental Dermatology. 13 (s4): 5–10. doi:10.1111/j.1600-0625.2004.00255.x. ISSN 0906-6705. PMID 15507105.
  26. ↑ De Groot LJ, Beck-Peccoz P, Chrousos G, Dungan K, Grossman A, Hershman JM, Koch C, McLachlan R, New M, Rebar R, Singer F, Vinik A, Weickert MO, Handelsman DJ. "Androgen Physiology, Pharmacology and Abuse". PMID 25905231.
  27. ↑ Kenneth L. Becker (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 1004–. ISBN 978-0-7817-1750-2. Archived from the original on 2013-06-02.
  28. ↑ G. Plewig; A.M. Kligman (6 December 2012). ACNE and ROSACEA. Springer Science & Business Media. pp. 66, 685, 687. ISBN 978-3-642-59715-2. Archived from the original on 19 March 2017.
  29. ↑ NADIR R. FARID; Evanthia Diamanti-Kandarakis (27 February 2009). Diagnosis and Management of Polycystic Ovary Syndrome. Springer Science & Business Media. pp. 240–. ISBN 978-0-387-09718-3. Archived from the original on 19 March 2017.
  30. 1 2 Bentham Science Publishers (September 1999). Current Pharmaceutical Design. Bentham Science Publishers. pp. 717–.
  31. 1 2 Mutschler; Hartmut Derendorf (1995). Drug Actions: Basic Principles and Theraputic Aspects. CRC Press. pp. 304–. ISBN 978-0-8493-7774-7. Archived from the original on 2017-11-05.
  32. ↑ Joseph T. DiPiro; Robert L. Talbert; Gary C. Yee; Gary R. Matzke; Barbara G. Wells; L. Michael Posey (6 July 2008). Pharmacotherapy: A Pathophysiologic Approach. McGraw Hill Professional. p. 1598. ISBN 978-0-07-164325-2. Archived from the original on 19 March 2017.
  33. 1 2 A. Hughes; S. H. Hasan; G. W. Oertel; H. E. Voss; F. Bahner; F. Neumann; H. Steinbeck; K.-J. Gräf; J. Brotherton; H. J. Horn; R. K. Wagner (27 November 2013). Androgens II and Antiandrogens / Androgene II und Antiandrogene. Springer Science & Business Media. pp. 351, 516. ISBN 978-3-642-80859-3. Archived from the original on 19 March 2017.
  34. ↑ Larry E. Millikan (19 April 2016). Drug Therapy in Dermatology. CRC Press. pp. 295–. ISBN 978-0-203-90831-0. Archived from the original on 29 July 2017.
  35. ↑ Sara Brenner (13 December 2013). The Clinical Nanomedicine Handbook. CRC Press. pp. 97–. ISBN 978-1-4398-3478-7. Archived from the original on 5 November 2017.
  36. ↑ Grob, JJ; Castelain, M.; Richard, MA; Bonniol, JP; Beraud, V.; Adhoute, H.; Guillou, N.; Bonerandi, JJ (1998). "Antiinflammatory properties of cetirizine in a human contact dermatitis model. Clinical evaluation of patch tests is not hampered by antihistamines". Acta Dermato-Venereologica. 78 (3): 194–7. doi:10.1080/000155598441512.
  37. ↑ Kastarinen, Helena; Oksanen, Tuija; Okokon, Enembe O; Kiviniemi, Vesa V; Airola, Kristiina; Jyrkkä, Johanna; Oravilahti, Tuomas; Rannanheimo, Piia K; Verbeek, Jos H (2014-05-19). "Topical anti-inflammatory agents for seborrhoeic dermatitis of the face or scalp". Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD009446.pub2. ISSN 1465-1858.
  38. ↑ Roelofzen JH, Aben KK, Oldenhof UT, et al. (April 2010). "No increased risk of cancer after coal tar treatment in patients with psoriasis or eczema". J. Invest. Dermatol. 130 (4): 953–61. doi:10.1038/jid.2009.389. PMID 20016499.
  39. ↑ Firooz, A.; Solhpour, A; Gorouhi, F; Daneshpazhooh, M; Balighi, K; Farsinejad, K; Rashighi-Firoozabadi, M; Dowlati, Y (2006). "Pimecrolimus Cream, 1%, vs Hydrocortisone Acetate Cream, 1%, in the Treatment of Facial Seborrheic Dermatitis: A Randomized, Investigator-Blind, Clinical Trial". Archives of Dermatology. 142 (8): 1066–1067. doi:10.1001/archderm.142.8.1066. PMID 16924062.
  40. 1 2 Gupta, AK; Richardson, M; Paquet, M (January 2014). "Systematic review of oral treatments for seborrheic dermatitis". Journal of the European Academy of Dermatology and Venereology : JEADV. 28 (1): 16–26. doi:10.1111/jdv.12197. PMID 23802806.
  41. ↑ Wikler JR, Janssen N, Bruynzeel DP, Nieboer C (1990). "The effect of UV-light on pityrosporum yeasts: ultrastructural changes and inhibition of growth". Acta Dermato-venereologica. 70 (1): 69–71. PMID 1967880.
  42. ↑ Calzavara-Pinton PG, Venturini M, Sala R (2005). "A comprehensive overview of photodynamic therapy in the treatment of superficial fungal infections of the skin". Photochem Photobiol. 78 (1): 1–6. doi:10.1016/j.jphotobiol.2004.06.006. PMID 15629243.
  43. ↑ "Antibacterial photodynamic therapy in dermatology – Photochemical & Photobiological Sciences (RSC Publishing)". rsc.org.
  44. ↑ Mark A. Goldstein; Myrna Chandler Goldstein; Larry P. Credit (17 March 2009). Your Best Medicine: From Conventional and Complementary Medicine--Expert-Endorsed Therapeutic Solutions to Relieve Symptoms and Speed Healing. Rodale. pp. 462–. ISBN 978-1-60529-656-2. Archived from the original on 5 November 2017.
  45. 1 2 3 Miranda A. Farage; Kenneth W. Miller; Howard I. Maibach (2 December 2009). Textbook of Aging Skin. Springer Science & Business Media. pp. 534–. ISBN 978-3-540-89655-5. Archived from the original on 5 November 2017.
  46. 1 2 3 Jeanette Jacknin (2001). Smart Medicine for Your Skin: A Comprehensive Guide to Understanding Conventional and Alternative Therapies to Heal Common Skin Problems. Penguin. pp. 271–. ISBN 978-1-58333-098-2. Archived from the original on 2017-11-05.
  47. ↑ Ooi ET, Tidman MJ (2014). "Improving the management of seborrhoeic dermatitis". Practitioner. 258 (1768): 23–6, 3. PMID 24689165.
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