Skin: immune-mediated disease – overview
Podcast: Skin: immune-mediated disease - overview
Mechanism of disease
- Immune-mediated skin diseases can be subdivided into primary or autoimmune, eg attack against self, or secondary, ie immunologic event that causes damage but it is not primarily directed against self.
- In autoimmune diseases either antibodies or activated lymphocytes develop. This could be due to cross-reactivity between a foreign antigen and a self-antigen or the exposure of self-antigens to the immune system that are normally not exposed.
- Additional possibilities for the development of an autoimmune disease include an inefficient suppressor T cell component and modification of antigens.
- Examples of autoimmune diseases include pemphigus complex Pemphigus foliaceus, bullous pemphigoid Skin: bullous pemphigoid, epidermolysis bullosa acquisita Skin: epidermolysis bullosa, lupus erythematosus Systemic lupus erythematosus-like syndrome.
Secondary immune-mediated disease
- In secondary immune-mediated diseases the antigen targeted is not a self-antigen and the immunological reaction aimed at the foreign antigen → tissue damage.
- Examples of immune-mediate disease include drug eruptions (eg erythema multiforme Erythema multiforme, toxic epidermal necrolysis), vasculitis Vasculitis, alopecia areata Hair: alopecia areata and amyloidosis Amyloidosis, purpura hemorrhagica Purpura hemorrhagica.
- Biopsy Dermatology: biopsy of primary lesions is very important in conjunction with detailed history and physical exam.
- Effort should be made to select primary lesions (papules, pustules, bullae, macules, wheals and more rarely nodules and plaques) and to biopsy affected patients before the initiation of glucocorticoids therapy and, possibly, after treatment of secondary infections.
- Cytology can be useful in some cases eg pemphigus foliaceus Pemphigus foliaceus.
- Hematology, biochemistry and urinalysis are indicated to assess systemic involvement.
- It consists in the identification, if at all possible, of the triggering factor or antigenic stimulation.
- If no external factor can be identified, then treatment is aimed at suppression of the aberrant immunologic response. That is accomplished with a combination of immunosuppressive doses of glucocorticoids Therapeutics: glucocorticoids and other steroid sparing agents, eg gold salts or azathioprine Therapeutics: skin. Doses are different depending on specific steroid used.
- In some cases, eg vasculitis Vasculitis , other immunomodulatory treatments can be considered such as pentoxifylline Therapeutics: skin.
- Monitoring depends on the condition treated and the treatment selected.
- Due to the potential of glucocorticoids to induce laminitis Foot: laminitis, monitoring of digital pulses and lameness should be done.
- CBC and chemistry should also be done in the event of immunosuppressive treatment to monitor for bone marrow suppression.
- Autoimmune disease or immune-mediated disease cannot be effectively prevented.
- In cases in which a triggering factor has been identified, re-challenge with such antigen should be avoided to minimize risk of relapse of the disease.
- Immune-mediated diseases can be costly due to the potential for life-long treatments.