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Alopecia Areata & other autoimmune conditions
By Tony Pearce RN.
Specialist Trichologist, National Trichology Services
Autoimmune states are thought to be polygenic, i.e. there are multiple genetic factors to their susceptibility. There factors eventually interact with physiological &/or environmental issues to activate the condition. Some initiating triggers are:
- Sudden shock or protracted emotional/physiological stress. ‘Physiological stress’ may be an underlying disease that has begun to develop (eg: haemochromatosis).
- Viral or bacterial infection, vaccinations, or chemical substance not previously exposed to.
- Disordered liver detoxification pathways or gut function.
- Chronic infection (tooth abscess, chronic tonsillitis or sinusitis), or head trauma from accidents or contact sports such as rugby.
- Anaesthetised on an operating room table for extended periods of time for major surgery has caused ‘pressure lesions’ in predisposed people.
- Alopecia areata is frequently associated with other autoimmune problems such as autoimmune thyroiditis, vitiligo, lupus, rheumatoid arthritis, Sjogren’s syndrome, & psoriasis.
Different autoimmune conditions are also regularly seen within related members of extended families. These families are referred to as ‘atopic’, meaning that they have a genetically inherited hypersensitivity to certain foods, chemicals, and/or their general environment.
Autoimmune problems can involve any system, organ or tissue of our body, and the scalp is commonly affected. Conditions such as psoriasis may only involve the cells of the outer skin, leaving the hair relatively unscathed. Some may influence both, causing hair loss of a (sometimes) temporary nature – alopecia areata being one example. Still others ‘scar’ the skin – destroying hair follicles and other underlying skin appendages as they progress. These are collectively termed ‘cicatricial’ alopecias and include folliculitis decalvans, pseudopelade, lichen planus, and ‘lupus’ (discoid type). Permanent hair loss results from cicatricial alopecia.
Active Folliculitis Decalvans is accompanied by severe inflammatory reaction and pustular eruptions across the scalp. In susceptible people it’s thought their skin initiates an exaggerated immune response to the toxins of Staphylococcus Aureus bacteria. Medical practitioners will often prescribe topical and oral combinations of antibiotics to treat this form of scarring alopecia.
Studies reveal Vitamin D deficiency is associated with an increased risk of autoimmune conditions such as alopecia areata, vitiligo, psoriasis, & inflammatory bowel disease. These are collectively known as T-Helper 1 cytokine-mediated inflammatory disorders. Vitamin D alters gene response, to reduce T-Helper 1 (white blood cell) cytokine levels & activity.
Most autoimmune problems that affect the hair and scalp can be treated and at least stabilised by a variety of therapies, which are often best used in combination.
Alopecia areata (AA) usually presents as patchy, non-scarring circular or oval ‘bald spots’ which are well defined & appear suddenly. AA may involve the eyebrows/eyelashes, beard, or any other part of the body where hair grows. Nail involvement consisting of ‘pitting’, splitting, or longitudinal ridging is a common feature.
There are three clinical variants of AA:
- Alopecia areata (also termed ‘partialis’)
- Totalis – total loss of scalp & body hair from the head. Includes eyebrows, eyelashes, facial hair/beard.
- Universalis – total loss of body hair from the entire body. This is the most severe form of alopecia with the poorest prognosis.
- Three sub-groups of AA(partialis) are:
- ‘Ophiasis’ type “snakes” around the hairline margins at the bottom of the scalp.
- ‘Reticulate’ type most commonly starts at the back of the head, and leaves a patchwork of hair loss across the scalp. The surviving areas of hair resemble the "faun tails" of deer.
- ‘Diffuse' alopecia areata is often difficult to diagnose as it mimics diffuse or androgenic hair loss in women.
Genetic & Autoimmune Factors:
- Ten-forty percent of patients seen report a family history of alopecia areata.
- >40% have associated atopic features in their personal &/or family history.
- Diagnostic histology is lymphatic infiltration of activated CD+4 T lymphocytes in & around the hair follicles when the condition is active.
- Hair follicles are normally ‘immune response protected’ skin appendages. The consequences of AA result when the immune concessions against this tissue-specific autoimmune state are withdrawn.
- Pigmented hairs are most susceptible, whilst white (unpigmented) hairs are mostly unscathed. Exclamation point hairs (short, broken hairs) are a diagnostic feature of AA.
- >85% of patients will experience their first episode of alopecia before age 40. Males & females are affected equally,* whilst there is an increased incidence of alopecia areata in dark haired and Asian people.
*Research from the Mayo Clinic (Journal of Immunology, Nov.2004) illustrates that the male immune system is less reactive than the female, because testosterone slows & weakens T lymphocyte response. Though females are more susceptible to autoimmune disease (because of their lower levels of testosterone), a male’s immune response is blunted when faced with a similar threat because of their higher testosterone levels.
Current treatments for alopecia areata involve the use of ‘immunomodulators’ alone or in combination with biologic response modifiers such as Minoxidil topical solution in strengths of 6-15%. An immunomodulator suppresses or increases the body’s immune response either locally or systemically.
Corticosteroid injections, lotions or tablets, as well as contact sensitisers (Anthralin, DCP) are the common immunomodulators. Immunosuppressors such as ‘Protopic’ or systemic ‘Prograf’ (Tacrolimus) are used by some Dermatologists for the treatment of intractable alopecia and psoriasis.
L-tyrosine amino acid is an immunomodulation therapy that trichologists have used to successfully treat autoimmune diseases affecting the hair and scalp. Tyrosine helps raise the immunomodulation neuropeptides (IP) –produced by nerves in the skin – which modulate skin inflammation & are thought to provide the potential link between the brain & skin disease. There is evidence that a deficiency of one IP – calcitonin gene-related peptide (CGRP) may influence the onset and course of AA. Blood levels of CGRP in patients with active AA are 50% less than that of the population unaffected by AA.
Whilst Tyrosine is considered a very safe & versatile oral supplement, it’s contra-indicated in persons with a history of epilepsy. Migraine headache sufferers are advised to use caution as Tyrosine can induce headaches in some and relieve them in others.
Photo-biotherapy such as ‘soft/cold’ low level laser light (LLLT) is a strong vasodilator & moderates skin immune response by inducing changes in T-cell reaction. To be therapeutically effective these laser appliances should be classified ‘3A’; be in the wavelength vicinity of 660-780nm & with a power output of 60-400mW. LLLT is a non-UV light source.
*References for this article available on request.
About the Author: Tony Pearce RN is a specialist trichologist and a registered nurse. He is a founding member of the Society for Progressive Trichology. Tony has a clinical practice in Sutherland & Rozelle NSW. He is the Clinical Director for Trichology of Virginia/DC in the United States. In Australia Tony can be contacted on 02 9542 2700, or through his website at www.hairlossclinic.com.au
A qualified Trichologist has studied & successfully completed a recognised Trichology Educational Program.
© Anthony Pearce
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