Alopecia: causes, diagnose, and treatment
Alopecia: Alopecia means loss of hair. There are two types of alopecia.
- Non-cicatricial alopecia
- Cicatricial alopecia
Etiology
The pathogenesis of AA is uncertain and following factors are incriminated:
- Immunological factors: AA is considered an immunological disease because of:
- Association of AA with other auto-immune diseases (auto-immune thyroid disease, pernicious anemia, vitiligo, and atopy)
- Cytokines produced by dermal papillae in lesions not only attract lymphocytes to perifollicular region but also stimulate them to multiply.
- As opposed to normal hairs, strong major histocompatibility complex (class 1 and class 2) immunoreactivity found in affected follicles.
3. Emotional factors: In some patients, AA is precipitated by emotional stress.
Epidemiology
- Prevalence: AA is a common type of alopecia.
- Gender: Both males and females are equally affected.
- Age: Can start at any age.
Clinical features
Morphology
- AA typically presents as a discoid patch of alopecia, which shows no scaling, papules, inflammation or atrophy.
- Presence of exclamation mark hair at the periphery of the lesion is pathognomonic.
- Some patients lose hair in a band-like pattern at the periphery of the scalp (ophiasis)
- Others lose all the hair from their scalp (alopecia totalis)
- While a few patients show loss of hair from whole body (alopecia universalis).
Associations
- Nails: Pitting and thinning of nail plate.These pits are fine unlike the course pits of psoriasis.
Course
- Single lesions usually recover within a few months. Regrowth begins at the centre of the lesion and initially the new hair is fine and gray, but gradually regains normal thickness and color.
- If the lesions recur or more lesions appear, the regrowth is slower. Recovery in some patches may occur along with progress of the disease in other areas.
- Early onset (childhood).
- Associated history of atopy.
- Widespread alopecia (alopecia totalis and universalis).
- Ophiasis.
Investigations
- Generally none needed.
- If suspected, rule out other autoimmune diseases.
Diagnosis
Dignosis is based on:
- Presence of noncicatricial patch of hair loss with no inflammation (scaling, erythema, and papulation).
- Presence of exclamation mark hair at the edge of the patch. Regrowth with gray hair, in centre of lesions.
- Commonly on scalp, sometimes beard, mustache, eyebrows, and eye lashes. Occasionally entire body.
- Nail changes.
Treatment
Few lesions
- <6 months duration: observe, as spontaneous regrowth frequent.
- >6 months duration: Topical therapy with steroids, minoxidil, PUVA/PUVA sol.
1. Oral steroids:
- May be used, but withdrawal often results in a relapse.
- Given as daily/ weekly doses. Weekly doses of steroid given as oral mini pulse (OMP), given as betamethasone initially 5 mg once or twice a week, then tapered gradually.
- Associated with side effects.
- Used in extensive lesions.
- Can be combined with oral steroids given as OMP in rapidly progressing and extensive lesions.
4. Cosmetic cover in the form of wigs for alopecia totalis.
Androgenic Alopecia (AGA)
Etiology
Basic pathology is miniaturization of hair follicles.
Genetic: Gene association studies have identified association of AGA with polymorphism of androgen receptor gene on X chromosome.
Hormonal:
- Males: Alopecia is distinctly androgen dependent. So does not develop in males castrated at puberty.
- Females: Most women diagnosed to have AGA do not have elevated circulating levels of androgens.
Clinical features
Males
- Terminal hair is replaced by fine vellus hair.
- Terminal hair is replaced by fine vellus hair.
- Hair loss in women may be diffuse often initially manifesting as widening of the central parting.
- Some patients develop the alopecia early in life while others develop alopecia later and the inheritance of the two conditions may be distinct.
- In women, features of hyperandrogenism may be present in the form of hirsutism, acne, and clitoromegaly.
- Always rule out Polycystic Ovary Disease (PCOD).
Investigations
- Males: No investigation is required.
- Females: Most women with AGA, do not have other evidence of virilization. However, full evaluation to rule out an androgen secreting pathology desirable if: 1.Hair loss sudden in onset, rapidly progressive and advanced. 2.AGA accompanied by menstrual disturbances, hirsutism, or recrudescence of acne.
Diagnosis
Males: AGA in males has a typical presentation.
Females: AGA in females should be differentiated from other causes of diffuse hair loss like chronic telogen effluvium.
Treatment
Men
Topical minoxidil (2-5%)
- Slows hair loss and may even stimulate growth of new hair.
- Hair growth is temporary because if medication is withdrawn the hair fall restarts. So it is important to ensure, before initiating therapy, that patient is motivated enough to apply minoxidil for life.
- Should be used cautiously in males.
- Finestride (1mg daily), a 5 alpha-dihydrotestosterone reductase inhibitor has been used successfully in males patients with minimal side effects.
- Surgical procedures are based on the principle of donor dominance.
- Attempts to relocate occipital hair over the alopecic scalp.
- techniques used are follicular unit transplantation and follicular unit extraction.
- Ordinary wigs are used. Or techniques to weave small wigs with the existing hairs have been used.
Women
Topical minoxidil (2-5%)
Systemic antiandrogens
- Antiandrogens like finestride, cyproterone acetate (with ethinyl estradiol), and spironolactone have been used with some success.
- More effective in women with evidence of hyperandrogenism.
- Since the alopecia is diffuse, surgical techniques are not helpful in females.
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