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Seborrhoeic dermatitis
Classification and external resources
ICD-10 L21.
ICD-9 690
DiseasesDB 11911
MedlinePlus 000963
eMedicine derm/396
MeSH D012628

Seborrhoeic dermatitis (also Seborrheic dermatitis AmE, seborrhea) (also known as "Seborrheic eczema"[1]) is a skin disorder affecting the scalp, face, and trunk causing scaly, flaky, itchy, red skin. It particularly affects the sebum-gland rich areas of skin.

Contents

Causes

The cause of seborrhoeic dermatitis remains unknown,[citation needed] although many factors have been implicated. The widely present yeast, Malassezia furfur (formerly known as Pityrosporum ovale), is involved,[2][3] as well as genetic, environmental, hormonal, and immune-system factors.[4][5] The claim that seborrhoeic dermatitis is an inflammatory response to the yeast has not been proven.[6] Those afflicted with seborrhoeic dermatitis have an unfavourable epidermic response to the infection, with the skin becoming inflamed and flaking.

Acute form of seborrhoeic dermatitis on scalp
Another example of seborrhoeic dermatitis on scalp
Another example of seborrhoeic dermatitis on scalp

In children, excessive vitamin A intake can cause seborrhoeic dermatitis.[7] Lack of biotin,[8] pyridoxine (vitamin B6)[8][9] and riboflavin (vitamin B2)[8] may also be a cause.

In adolescents and adults, seborrhoeic dermatitis usually presents as scalp scaling (dandruff) or as mild to marked erythema of the nasolabial fold during times of stress or sleep deprivation.[8] The condition is one of the autonomic signs of Parkinson's disease.

Hair loss

Side effects to inflammation may include temporary hair loss. If severe outbreaks are untreated for extended intervals, permanent hair loss may result, because of damage to hair follicles.

Treatments

Among dermatologist-recommended treatments are shampoos, cleansers or any topical containing coal tar, salicylic acid, sulfur, ciclopiroxolamine, ketoconazole, selenium sulfide, zinc pyrithione, climbazole, or Piroctone olamine.[8] For severe disease, keratolytics such as salicylic acid or coal tar preparations may be used to remove dense scale. Topical terbinafine solution (1%) has also been shown to be effective in the treatment of scalp seborrhoea,[10] as may lotions containing alpha hydroxy acids or corticosteroids (such as fluocinolone acetonide). Pimecrolimus topical lotion is also sometimes prescribed. It is recommended that suffers of this condition always wash their hands before touching their face or head, thoroughly clean spectacles or sunglasses, especially nose supports and arms (using isopropyl alcohol)on a regular basis, and use Nizoral ointment as per instructions on the tube. This approach has proven effective against chronic, long-term seborrhoeic dermatitis of the face.

Topical application of a water-soluble ointment containing 50 mg of Vitamin B6 per gram of ointment has been used as an effective treatment.[11]

Several nutritional supplements are recommended including: 3 mg twice per day of biotin, [11] vitamin B complex,[11] 20-30 mg per day of zinc,[11] and 1 tbsp per day of flaxseed oil.[11]

Chronic treatment with topical corticosteroids may lead to permanent skin changes, such as atrophy and telangiectasia.[12][13]

UV-A and UV-B light inhibit the growth of M. furfur,[14] although caution should be taken to avoid sun damage.

Also used to reduce itching: daily use of isopropyl rubbing alcohol and hydrogen peroxide.

Other suggested treatments include using an air humidifier, as well as a gentle moisturizer.[citation needed] Applying milk of magnesia may help clear up seborrheic dermatitis; one may apply on the face while showering and rinse off at the end of the shower.[15]

As a last resort in refractory disease, sebosuppressive agents such as isotretinoin (Accutane) may be used to reduce sebaceous gland activity. However, isotretinoin has potentially serious side effects and few patients with seborrhea are appropriate candidates for therapy. The most devastating side effect is teratogenicity, but other serious side effects include hyperlipidemia, neutropenia, anemia and hepatitis. Mucocutaneous adverse effects include cheilitis, xerosis, conjunctivitis, urethritis and hair loss. Long-term use has been associated with the development of diffuse idiopathic skeletal hyperostosis (DISH). This agent must be used cautiously and only by physicians who are well versed in all of its adverse effects.

A more practical approach to the refractory patient may be to first try different combinations of the usual agents: a dandruff shampoo, an antifungal agent and a topical steroid. If this fails, short-term use of a more potent topical steroid in a "pulse fashion" may put some refractory patients into remission and actually decrease the total steroid exposure. Therapeutic choices for pulse therapy may include a nonfluorinated class III steroid such as mometasone furoate (Elocon) or an extra-potent class I or class II topical steroid such as clobetasol propionate (Temovate) or fluocinonide (Lidex). The class III topical steroid should be tried first, but if the condition remains unresponsive, the clinician may then choose to use a class I agent. These more potent agents may be applied once or twice per day, even on the face, but must be stopped after two weeks because of the increased frequency of side effects. If the patient responds before the two-week limit, the agent should be stopped immediately. Adjuvant therapy including use of a dandruff shampoo, an antifungal agent, or both, is essential during the "pulse" period and should be continued as maintenance therapy after each pulse.

Most corticosteroids are available as solutions, lotions, creams and ointments. Which vehicle to use is often determined by the patient and the treatment site. Lotions and creams are frequently used on all areas of the face and body, whereas solutions and ointments are more commonly used on the scalp. In general, application of a scalp solution is preferred by white and Asian patients but may be too drying for black patients. Ointments may be a better option. The vehicle affects the potency of a topical steroid. In most circumstances, the same steroid in an ointment is more potent than the steroid in a cream, which, in turn, is more potent than the same chemical in a lotion.[4]

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Plant-based treatments

The World Health Organization mentions Aloe vera gel as a yet to be scientifically proven traditional medicine treatment for Seborrhoeic dermatitis.[16]

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See also

References

  1. ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0721629210.
  2. ^ Hay R, Graham-Brown R (1997). "Dandruff and seborrheic dermatitis: causes and management". Clin Exp Dermatol 22 (1): 3–6. doi:10.1046/j.1365-2230.1997.d01-231.x. PMID 9330043. 
  3. ^ Nowicki R (2006). "[Modern management of dandruff]" (in Polish). Pol Merkur Lekarski 20 (115): 121–4. PMID 16617752. 
  4. ^ a b Johnson BA, Nunley JR (May 2000). "Treatment of seborrheic dermatitis". American Family Physician 61 (9): 2703–10, 2713–4. PMID 10821151. http://www.aafp.org/afp/20000501/2703.html. Retrieved 2009-11-20. 
  5. ^ Janniger C, Schwartz R (1995). "Seborrheic dermatitis". Am Fam Physician 52 (1): 149–55, 159–60. PMID 7604759. 
  6. ^ Parry M, Sharpe G (1998). "Seborrheic dermatitis is not caused by an altered immune response to Malassezia yeast". Br J Dermatol 139 (2): 254–63. doi:10.1046/j.1365-2133.1998.02362.x. PMID 9767239. 
  7. ^ MedlinePlus Encyclopedia Hypervitaminosis A
  8. ^ a b c d e Schwartz RA, Janusz CA, Janniger CK (2006). "Seborrheic dermatitis: an overview". Am Fam Physician 74 (1): 125–30. PMID 16848386. http://www.aafp.org/afp/20060701/125.html. 
  9. ^ Nutritional Neuropathy at eMedicine
  10. ^ Faergemann J, Jones J, Hettler O, Loria Y (1996). "Pityrosporum ovale (Malassezia furfur) as the causative agent of seborrheic dermatitis: new treatment options". Br J Dermatol 134 Suppl 46: 12–5: discussion 38. doi:10.1111/j.1365-2133.1996.tb15652.x. PMID 8763461. 
  11. ^ a b c d e Murray, Michael; Pizzorno, Joseph (1997). "Encyclopedia of Natural Medicine" (Revised 2nd Edition) Three Rivers Press. ISBN 0761511571
  12. ^ Smith J, Wehr R, Chalker D (1976). "Corticosteroid-induced cutaneous atrophy and telangiectasia. Experimental production associated with weight loss in rats". Arch Dermatol 112 (8): 1115–7. doi:10.1001/archderm.112.8.1115. PMID 952530. 
  13. ^ Scheinfeld N (2005). "Seborrheic dermatitis". Skinmed 4 (1): 49–50. doi:10.1111/j.1540-9740.2005.03961.x. PMID 15654167. http://www.medscape.com/viewarticle/499706. 
  14. ^ Wikler J, Janssen N, Bruynzeel D, Nieboer C (1990). "The effect of UV-light on pityrosporum yeasts: ultrastructural changes and inhibition of growth". Acta Derm Venereol 70 (1): 69–71. PMID 1967880. 
  15. ^ Graedon, Joe; Graedon, Teresa (2008-04-17). "The People's Pharmacy". Atlanta Journal Constitution Evening Edge (Atlanta Journal Constitution): pp. 15. 
  16. ^ "WHO Monographs on Selected Medicinal Plants - Volume 1: Aloe Vera Gel". World Health Organization. http://www.who.int/medicinedocs/en/d/Js2200e.6. Retrieved 2008-03-18. 
  17. ^ Matthias Augustin: 6.46 Stiefmütterchen In: Phytotherapie bei Hauterkrankungen, S.226-227; Elsevier, Urban & Fischer 2004. ISBN 9783437561207 Volltext
  18. ^ S. Meyer, T. Vogt, M. Landthaler, S. Karrer: Einsatz von Phytopharmaka in der Dermatologie - Indikationen, Therapiehinweise und Nebenwirkungen In: Der Hautarzt 05/2005, S. 494, Springer Medizin Verlag. Zusammenfassung und Volltext

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