Pathogenesis (disease development)
The exact cause of lichen sclerosus et atrophicus is unknown. Autoimmune processes, among others, are discussed, as is an infectious genesis (Borrelia, EBV, and wart infections).
The presence of associated autoimmune diseases (e.g., autoimmune thyroid diseases) is also discussed. However, specific autoantibodies cannot be detected in lichen sclerosus patients.
The development of lichen sclerosus (LS) may be triggered by the following factors:
Etiology (Causes)
Biographic causes
- Genetic burden is discussed (rare familial occurrence; association with HLA-B40, HLA-B44); approximately10% of patients with LS have blood relatives with the same disease
- Skin type – skin type I and II
- Hormonal factors – low estrogen production.
Behavioral causes
- Scratching/chafing effects due to too tight clothing.
- Overweight (BMI ≥ 25; obesity)
Disease-related causes
- Atopic eczema (neurodermatitis)
- Autoimmune diseases
- Diabetes mellitus
- Infections, for example with borrelia or streptococcus A
- Coronary artery disease (CAD; coronary artery disease).
Other triggering factors
- Irritation by urine – urinary incontinence (bladder weakness).
- Surgical scars
- Radiatio/radiation therapy
- Sexual abuse
- Local chronic trauma
- Medications:
- Carbamazepine
- Imatinib
- Oral contraception (contraceptives taken by mouth (“per os”)) with antiandrogenic partial effect.
