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It has been suggested that this article be split into multiple articles.
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 an
inflammatory[2] 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 [hide]
1 Causes
1.1 Stress
1.2 Nutritional hypo- and
hyperalimentation
1.3 Fungal
1.4 Secondary to other medical
conditions
2 Symptoms
2.1 Hair loss
3 Treatments
3.1 Antifungal
3.2 Medications other than
antifungals
3.3 Phototherapy
3.4 Natural treatments
3.5 Supplements
3.6 Diet
3.7 Alternative treatments
4 See also
5 References
6 External links
[edit]
Causes
The cause of seborrhoeic dermatitis remains unknown, although a yeast
that often lives on the skin, Malassezia furfur, may play a role.[3]
[edit]
Fungal
Another example of seborrhoeic dermatitis on scalp
Alternatively, seborrhoeic dermatitis is believed to be an inflammatory
reaction related to a proliferation of a normal skin inhabitant, a yeast
called Malassezia (formerly known as Pityrosporum ovale). The main
species found in the scalp is Malassezia globosa. It produces toxic
substances that irritate the skin. Patients with seborrhoeic dermatitis
appear to have a reduced resistance to the yeast.[citation needed]
However, the colonization rate of affected skin may be lower than that
of unaffected skin.[7]
Malassezia growth is supported by saturated, not unsaturated fatty
acids. In all cases, pure, unsaturated FAs were unable to support
growth of M. globosa or M. furfur. Interestingly, growth of both species
was supported by saturated FAs. This is further evidenced by lard,
which is rich in saturated triglycerides. Implications for dandruff and
seborrheic dermatitis: Previously, it has been shown that: 1. 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. 2. In dandruff susceptible individuals pure OA,
an unsaturated FA and Malassezia metabolite, induces flaking in the
absence of Malassezia by direct effects on the host skin barrier. This
finding, that Malassezia require saturated, and not unsaturated FAs,
coupled with previous data, supports 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 and due to their non-uniform structure breach the
skin's barrier function. This barrier breach induces an irritation
response, leading to dandruff and seborrheic dermatitis.[8]
The widely present yeast, Malassezia furfur (formerly known as
Pityrosporum ovale), is involved,[9][10] as well as genetic,
environmental, hormonal, and immune-system factors.[11][12] The claim
that seborrhoeic dermatitis is an inflammatory response to the yeast has
not been proven.[13] Those afflicted with seborrhoeic dermatitis have an
unfavourable epidermic response to the infection, with the skin
becoming inflamed and flaking.
[edit]
Secondary to other medical conditions
The condition is one of the autonomic signs of Parkinson's disease.
Those with immunodeficiency (especially infection with HIV) and with
neurological disorders such as Parkinson's disease and stroke are
particularly prone to it.[14]
[edit]
Symptoms