Alopecia areata in paediatric age group and its homoeopathic management : a litreture review

Dr Pooja S Hutagi

ABSTRACT
Alopecia areata (AA) is a common autoimmune disease marked by non-scarring patches of hair loss on the scalp and body. Alopecia areata is an organ-specific autoimmune disease that affects 0.15 percent of the population. Severity of Alopecia Tool (SALT) score for alopecia areata is used to assess the extent of AA. Although the course of AA is unpredictable, homoeopathy has effective medicines for treating AA based on individualisation.

Key Words : Alopecia areata, paediatrics, homoeopathy

INTRODUCTION
Alopecia areata (AA) is a common autoimmune illness characterized by non-scarring areas of hair loss on the scalp and body. AA is the third most prevalent skin disorder in children, and it is associated with lower health-related quality of life for both children and their parents. ¹

Alopecia can cause significant alterations in the psychological and emotional realms of affected patients, resulting in low self-esteem, feelings of vulnerability, and altered personal image. ⁴

EMBROLOGY AND NORMAL HAIR DEVELOPMENT
At birth, the full complement of hair follicles is present, and no new hair follicles form. Each follicle has the ability to produce three forms of hair: lanugo, vellus, and terminal. Lanugo hairs are neonatal nonpigmented, soft, fine hairs with no central medulla; vellus hairs are short, fine, lightly pigmented hairs found throughout the adult body; and terminal hairs are long, thick, strongly pigmented hairs found on the scalp and brows of adults and children, as well as the axillary and pubic areas of adults and the chest and facial areas of adult males.⁶

Human hair growth is cyclic. A scalp follicle undergoes 10–30 cycles in a lifetime. A new, distinct hair is produced during each anagen growth phase. Involution of the lower transient portion of  the follicle below the insertion of the arrector pili muscle occurs in catagen. The follicle appears to be dormant in telogen. Shedding of the dead hair from the follicle (exogen) occurs either late in telogen or early in anagen.

ALOPECIA AREATA
Alopecia areata is an organ-specific autoimmune disease, the                                        incidence of which is 0.15% of the population.It occurs in equal incidence in females and males.Forty to fifty percent of patients develop alopecia areata before the age of 21 years and 20% develop it after the age of 40. In 10–50% of patients there is a positive family history, and although it has been proposed that alopecia areata is an autosomal dominant trait with variable penetrance, it is more likely to be a multifactorial trait.Alopecia areata may be seen in association with atopic conditions and autoimmune diseases. There is also an increased frequency of alopecia areata in individuals with Down syndrome.⁶

PATHOPHYSIOLOGY
Two factors are known to be required for the development of alopecia areata: a genetic predisposition and a second triggering  event or cofactor. This secondary event is usually unidentified, but occasionally it may be a nonspecific febrile illness, pregnancy or a major life crisis. Anagen hair follicles do not normally express human leukocyte antigen (HLA) class I antigens, leading to a state of immune privilege. Aberrant expression of HLA class I antigens on the transient portion of the early anagen hair follicles possibly enables immune recognition of hair antigens by T lymphocytes. In response to cytokines released by the T lymphocytes, intercellular adhesion molecule (ICAM)-1 and HLA class II expression occurs  on the anagen hair bulbs, further enhancing the immunological attack on the hair. Following the follicular damage effected in anagen, the hairs prematurely enter telogen. The weakened hairs fracture off easily at the scalp surface, rapidly producing an area of alopecia. Alopecia areata is characterized by patchy or confluent hair loss that can occur on the scalp or any hair-bearing area of the body.⁶

A unique “bee-swarm pattern” of thick lymphocytic infiltrates is visible on histologic examination around the bulbar area of anagen hair follicles.⁵

THE HISTORY AND PHYSICAL EXAMINATION
Physical examination should evaluate all areas of the scalp in a systematic fashion. The scalp should be evaluated for localized or diffuse hair loss. The location of loss should be noted. Locations include periphery, occiput, vertex, temples, and parietal scalp. An evaluation should be performed for scale and redness of the scalp, which are signs of inflammation.³

A hair pull test is a simple tool all pediatricians can use because it requires no special instruments. The hair pull test involves gently pulling 20 to 60 hairs between the thumb and forefinger in multiple locations of the scalp. Anagen or growing hairs should remain rooted in place, whereas hairs in the telogen phase should come out easily. If 2 hairs come out on a hair pull of approximately 20 hairs, telogen is about 10%. Normal telogen is between 10% and 20%. It is important to ask patients about when they last washed their hair. Ideally, it is the day before the examination. If it was the same day, you should expect fewer hairs to be shed.Hairs from the pull test can be mounted and reviewed under microscope for hair shaft abnormalities as well as the phase of the cycle of the hair when practical.

CLINICAL APPEARANCE
AA manifests as a variety of clinical patterns. The most common pattern is the sudden appearance of smooth, bald, round patches on the scalp that are asymptomatic and very occasionally mildly pruritic. Within the patches, exclamation point hairs can be seen by the naked eye or by dermoscopy. These hairs are short hairs with dark, expanded tips that are markers of disease activity. Black dot hairs are hairs broken immediately at the surface of the scalp. The ophiasis pattern is a more extensive pattern of AA whereby hair is lost along the parietal scalp and the

occiput. This pattern has a less favorable prognosis. In rare cases, alopecia may be diffuse and look more like telogen effluvium. Some patients have total scalp hair loss (alopecia totalis), and some patients have total scalp and body hair loss (alopecia universalis). Only about 5% of patients who present with typical AA progress to alopecia totalis or universalis. As hairs grow, the hairs are often smaller in caliber and lighter in color. Hair color and diameter return with time. Nails may be involved, and many patients have pitting or vertical or longitudinal striations within the nails.³

Dermoscopic Findingof Alopecia²

Finding	Associated condition
Absence of follicular ostia	Destruction of follicle opening due to scarring alopecia
Fibrotic white dots	Fibrosis associated with scarring alopecia
Black dots	Broken hairs at the scalp surface – alopecia areata, tinea capitis
Yellow dots	Accumulation of sebum and keratin – alopecia areata
Exclamation points	Associated with alopecia areata and trichotillomania
Common hairs	Associated with tinea capitis
Medical and family history	Questions about past medical history and family history of alopecia (often undiagnosed) may assist diagnosis. In adolescent females, enquire about menarche. A diagnosis of telogen effluvium is often made when an inciting factor is identified (eg medical illnesses, stress, poor diet, medications)

SALT  Severity of Alopecia Tool
A tool for determining degree of hair loss based on the percentage of SSA involved on the top, back, and each side of the scalp  that is used in the assessment of the Severity of Alopecia Tool (SALT) score for alopecia areata (AA).⁷

PROGNOSIS
The course of AA is unpredictable. Hair loss and regrowth cycles can occur for years or for life. The prognosis is poorer if the age of onset is before puberty, there is a positive family history, hair loss is extensive, there is history of atopic dermatitis,  there is a history of long disease duration without regrowth, there are severe nail  changes, and/or patients have Down syndrome.

HOMOEOPATHIC MANAGEMENT

Name of  Repertory	Chapter-Rubric	No. of Medicines Listed with only names of first grade medicines
Schroyens F, Synthesis 9.0 8	HEAD – HAIR – baldness HEAD – HAIR – baldness – patches HEAD – HAIR – falling – spots, in HEAD – HAIR – falling – children in	(28) BAR-C. (19) (25)  FL-AC Nat mur
Murphy’s Repertory	Constitutions – HAIR, general, head and body – baldness, head Constitutions – HAIR, general, head and body – loss, of hair from head Ears – BALD, spot above	(18) BAR-C PH-AC SIL STANN (17) BAR-C. SIL (1) Phos
Boger C, Boenninghausen’s Repertory	HEAD – External – baldness	(8) BAR-C. LYC
VanZandvoort R, Complete Repertory, 2003	HEAD – HAIR – affections of – falling out, alopecia HEAD – HAIR – affections of – falling out, alopecia – spots, in, alopecia areata	(159) AUR. CARB-V. CARBN-S. FL-AC. GRAPH. KALI-C. KALI-S. LACH. LYC. NAT-M. NIT AC. PHOS. SEP. SIL. SULPH. THUJ (30) FL-AC
Oscar E. Boericke Repertory 9	SKIN- Alopecia HEAD-SCALP-HAIR-Falling out(Alopecia) MALE SEXUAL SYSTEM – Syphilis – Alopecia	(15) Ars, Fluor ac, Nat m, Phos ac, Phos, Pix. L, Sep (35) Alum., Ars., Fl. ac., Graph., Nat. m., Nit. ac., Phos. ac., Phos.., Selen.,Sep., Syph., Thallium., Vinca (14) Ars. Hep.. Lyc. Nit-ac. Phos
Clarke J.H. Clinical Repertory	B – baldness   A – alopecia	(5) Arn. Bar-c. Rosm. Sep. Thal (12) All-s. Asc-t. Bac. Cupr-s. Fl-ac. Jab. Lob. Ol-j. Pilo. Ust. Vesp. Vinc.

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Dr. Pooja S. Hutagi
MD Part I
Department of Paediatrics
Government Homoeopathic Medical College and Hospital, Bangalore-79.