Seborrheic Dermatitis
Basics
Basics
Basics
DESCRIPTION
DESCRIPTION
DESCRIPTION
- Seborrheic dermatitis (SD) is a common, multifactorial skin disease influenced by both host and environmental factors.
- Involves sebaceous areas of the body
- Including the scalp, face, back, chest, and intertriginous areas
- Characterized by greasy, yellow, scaly erythematous lesions
- Usually a self-limited condition in infants but can be a chronic, relapsing condition in adolescents and adults
EPIDEMIOLOGY
EPIDEMIOLOGY
EPIDEMIOLOGY
- Trimodal distribution: infants, adolescents, and adults >50 years of age
- Highest prevalence between 2 weeks and 3 months of life
- Affects approximately 10% of the general population and up to 70% of infants in the first 3 months of life
- No sex predilection in infants; however, in adolescents and adults, males are affected more commonly than females.
- Seasonal pattern: Prevalence of disease increases in winter months.
- Strong association between Malassezia species, a common commensal organism, and SD
RISK-FACTORS
RISK-FACTORS
RISK-FACTORS
- There are no known genetic factors that contribute to disease.
- Hormonal effects: exposure to maternal estrogen in infancy and surge of androgens in puberty
- Use of neuroleptic medications
- Immunocompromised status
- Impaired cellular immunity may contribute to pathogenesis of disease.
- Prevalence of SD in immunocompromised patients is significantly higher than in general population.
GENERAL-PREVENTION
GENERAL-PREVENTION
GENERAL-PREVENTION
There are no known preventive measures.
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
- Unknown, but suspected role of sebum, Malassezia, and inflammatory factors
- Androgens stimulate sebaceous glands, causing production of more sebum.
- Malassezia
- A lipophilic yeast that is normally found in sebum-rich areas of the skin
- Can break down skin sebum lipids, producing potentially inflammatory fatty acids
- In response to the inflammatory fatty acids, keratinocytes produce proinflammatory cytokines.
ETIOLOGY
ETIOLOGY
ETIOLOGY
Not completely known, although it is hypothesized that yeast, androgens, and the local host immune response play a role in SD development.
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