Interesting information I have not seen

[historybook]

This is a website I had come across, discussion about the T-Cell in the roll of Seb derm: http://www.emedicine.com/derm/topic396.htm

Background: Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. In addition to sebum, this dermatitis is linked to Malassezia, immunologic abnormalities, and activation of complement. It is commonly aggravated by changes in humidity, changes in seasons, trauma (eg, scratching), or emotional stress. The severity varies from mild dandruff to exfoliative erythroderma. Seborrheic dermatitis may worsen in Parkinson disease and in AIDS.


Pathophysiology: Seborrheic dermatitis is associated with normal levels of Malassezia but an abnormal immune response. Helper T cells, phytohemagglutinin and concanavalin stimulation, and antibody titers are depressed compared with those of control subjects. The contribution of Malassezia may come from its lipase activity—releasing inflammatory free fatty acids—and from its ability to activate the alternative complement pathway.


Frequency:


Internationally: The prevalence rate of seborrheic dermatitis is 3-5%, with a worldwide distribution. Dandruff, the mildest form of this dermatitis, is probably far more common and is present in an estimated 15-20% of the population.
Race: Seborrheic dermatitis occurs in persons of all races.

Sex: The condition is slightly worse in males than in females.

Age: The usual onset occurs with puberty.

It peaks at age 40 years and is less severe, but present, among older people.
In infants, it occurs as cradle cap or, uncommonly, as a flexural eruption or erythroderma.

History:

Intermittent, active phases manifest with burning, scaling, and itching, alternating with inactive periods. Activity is increased in winter and early spring, with remissions commonly occurring in summer.
Active phases may be complicated by secondary infection in the intertriginous areas and on the eyelids.
Candidal overgrowth is common in infantile napkin dermatitis. Such children may have a diaper dermatitis variant of seborrheic dermatitis or psoriasis.
Generalized seborrheic erythroderma is rare. It occurs more often in association with AIDS, congestive heart failure, Parkinson disease, and immunosuppression in premature infants.
Physical:

Scalp appearance varies from mild, patchy scaling to widespread, thick, adherent crusts. Plaques are rare. From the scalp, seborrheic dermatitis can spread onto the forehead, the posterior part of the neck, and the postauricular skin, as in psoriasis.
Skin lesions manifest as branny or greasy scaling over red, inflamed skin. Hypopigmentation is seen in blacks. Infectious eczematoid dermatitis, with oozing and crusting, suggests secondary infection. A seborrheic blepharitis may occur independently.
Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and the postauricular skin. An extension to submental skin can occur. Presternal or interscapular involvement is more common than nonscaling intertrigo of the umbilicus, axillae, inframammary and inguinal folds, perineum, or anogenital crease, which also may be present.
Two distinct truncal patterns can occasionally occur. An annular or geographic petaloid scaling is the most common. A rare pityriasiform variety can be seen on the trunk and the neck, with peripheral scaling around ovoid patches, mimicking pityriasis rosea.
Causes:

Malassezia organisms are probably not the cause but are a cofactor linked to a T-cell depression, increased sebum levels, and an activation of the alternative complement pathway. Persons prone to this dermatitis also may have a skin-barrier dysfunction.
Because seborrheic dermatitis is uncommon in preadolescent children, and tinea capitis is uncommon after adolescence, dandruff in a child is more likely to represent a fungal infection. A fungal culture should be completed for confirmation.
Various medications may flare or induce seborrheic dermatitis. These medications include auranofin, aurothioglucose, buspirone, chlorpromazine, cimetidine, ethionamide, gold, griseofulvin, haloperidol, interferon alfa, lithium, methoxsalen, methyldopa, phenothiazines, psoralens, stanozolol, thiothixene, and trioxsalen.

[kristina b]

Thanks for posting this, history book. So I suppose an "abnormal immune response" could refer to people with overactive immune systems - eg. a tendency to autoimmune conditions - as well as those with compromised immune systems?

Kristina