PROTOCOL FOR M.D.

(DERMATOLOGY,
VENEREOLOGY AND LEPROSY ) THESIS
COMPARATIVE STUDY OF COMBINATION OF INTRALESIONAL
TRIAMCINOLONE AND DERMAROLLER VERSUS
INTRALESIONAL TRIAMCINOLONE IN THE TREATMENT OF
ALOPECIA AREATA

NAME OF CANDIDATE : DR. AKSHAY MEENA

DEPARTMENT OF DERMATOLOGY
JNMC, AMU, ALIGARH

SUPERVISOR : DR. MOHAMMAD ADIL

DEPARTMENT OF DERMATOLOGY
JNMC, AMU, ALIGARH

PLACE OF STUDY : DEPARTMENT OF DERMATOLOGY

JNMC, AMU, ALIGARH

DATE OF BOS : 24-1-2024

DURATION OF STUDY : 2 years

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 INTRODUCTION

Alopecia areata is an autoimmune disorder that results in unpredictable hair loss. It is characterised
by autoreactive T cells around the hair follicles that release pro-inflammatory cytokines and
adversely affect the anagen hair follicle cycle.The condition is believed to result from immune
responses against the anagen hair follicle due to the collapse of immune privilege at that site .
Alopecia areata is most often asymptomatic, characterised by the sudden loss of hair at defined
areas of the body without atrophy. It can occur at any hairy area, but the scalp is the most common
site accounting for approximately 90% of cases seen in the dermatology clinic.The hair loss is
usually visible as a round or oval patch with characteristic ‘exclamation point’ hairs, short hairs
tapering towards their base . Re-growing depigmented hairs may also be seen at the edge of the
alopecia lesion
Clinically, alopecia areata can be classified into three common types .
Patchy alopecia areata, in which there is a single or multiple patches of hair loss, accounts for about
90% of alopecia areata cases. The skin at the site of the lesion looks normal with no scales, redness,
induration or hardness.
Alopecia totalis is characterised by the loss of all scalp hair, while alopecia universalis describes
the total loss of body hair including from the scalp. Five percent of alopecia areata patients progress
to alopecia totalis or alopecia universalis. Again, the skin at the lesion site usually looks normal in
both these clinical types. Other less common presentations of hair loss can be observed. For
example, ophiasis is a well-defined pattern of alopecia areata when the hair loss is localised to the
lower back and sides of the head . Ophiasis inversus is a rare form characterised by hair loss in the
frontal parieto-temporal region of the scalp in a band-like distribution. Sisaipho is another rare form
of alopecia areata with hair loss over the scalp but not around the periphery Nail Abnormalities
may occur in one or all of the nails of patients with alopecia areata.Nail pitting with longitudinal
rows is the commonest changes and nail abnormalities are strongly associated with the severity and
extent of hair loss.
The diagnostic histopathological feature of alopecia areata is an intrafollicular and perifollicular
infiltration of T lymphocytes, Langerhans cells and macrophages ,referred to as a ‘swarm of bees’.
Alopecia areata produces marked cosmetic disability and extensive psychological morbidity.
Diagnosis is simple but treatment is challenging and time consuming. Though various modalities
are available for the treatment of alopecia areata, assessment of the efficacy of a treatment must be
considered with care because the condition is highly unpredictable in presentation, evolution, and
response to treatment

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 AIM AND OBJECTIVES

AIM-
To compare the therapeutic efficacy of combination of intralesional triamcinolone and
dermaroller versus intralesional triamcinolone injection in treatment of alopecia aerata

OBJECTIVES-

PRIMARY-
to compare the decrease in SALT score after treatment.
SECONDARY-
to compare the DLQI and adverse effects.

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 REVIEW OF LITERATURE

DEFINITION-
Alopecia areata (AA) is a common,chronic , autoimmune, nonscarring, organ-specific disease
manifesting as patchy hair loss (1,2)

EPIDEMIOLOGY-
Currently, the global prevalence of AA is approximately 0.1%, with a lifetime incidence of around
2% [3]. Most literature suggests that there is no significant difference in incidence rates between
males and females. Some studies have suggested a higher incidence in females, but this may be due
to greater awareness and attention to hair loss and subsequent treatment in females, while the
incidence also varies across different countries [4]. AA can occur at any age, but the most common
age range is between 30 and 40 years old, with some differences in diagnosis age between males
and females. Males are more likely to be diagnosed in childhood, while females are more likely to
present during puberty [5]. Recent research on AA in children has indicated that it is the third most
common skin disease manifestation in children. Between 2010 and 2017, over 140,000 children in
the United States were diagnosed with AA, with a prevalence rate of approximately 0.23% and the
highest incidence in the 11–12-year age group. In addition, it was found that the number of new
cases of AA in children is increasing each year [6].

ETIOPATHOGENESIS-

AA is a complex autoimmune disease with multiple etiological factors. The disease is associated
with genetic, environmental, infectious, and immune system abnormalities [7]. Immune system
dysfunction is one of the main causes of AA pathogenesis, with abnormal T and B lymphocytes in
AA patients secreting cytokines and autoantibodies that attack hair follicle cells, leading to hair
loss. These immune cells release cytokines, such as interferon-γ and tumor necrosis factor, when
they enter the hair follicle and then induce apoptosis of hair follicle cells [7]. Furthermore, AA is an
autoimmune disorder characterized by immune-mediated hair loss, and the currently acknowledged
pathogenesis primarily revolves around the disruption of immune privilege. Immune privilege refers
to the phenomenon where specific tissues or regions exert inhibitory effects on the immune system
to protect themselves from immune attacks. This privileged state is observed in certain tissues or
organs, such as the eyes, testes, and placenta. Mechanisms underlying immune privilege include
reduced antigen presentation, immune cell death, or the release of immunosuppressive molecules.
Disruption of immune privilege can result in immune system attacks on these tissues, leading to
diseases or autoimmune reactions [8]. Under normal circumstances, hair follicles are recognized as
immune-privileged sites by the body’s immune system, remaining unaffected. However, in
individuals with AA, the immune system erroneously perceives the hair follicles as exogenous
entities, instigating an immune response that results in hair loss. In addition, autoantibodies bind to
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antigens on the surface of hair follicle cells, forming immune complexes that further damage hair
follicle cells. Immune system abnormalities in AA patients may also be related to other autoimmune
diseases. For example, a study in 2021 found a higher incidence of thyroid dysfunction in AA
patients compared to the general population, and when AA patients have thyroid dysfunction, the
disease severity may be increased [9]. Thyroid disease is an autoimmune disease caused by immune
system abnormalities, suggesting that AA may share similar pathogenesis with other autoimmune
diseases. Another important factor is genetics. Studies have shown that the risk of AA in families of
AA patients is several times higher than that in the general population, and about 10% of family
members are diagnosed with AA [10]. Several genetic factors associated with AA have been
identified, including the HLA gene cluster on chromosome 6. Specific HLA gene variants, such
as HLA-DQB1 and HLA-DRB1, are closely related to AA, whereas other non-HLA gene variants,
such as TLR7, IL-2/IL-21, and IL-23R, are also associated with AA [11]. These studies indicate
that genetic factors play an important role in the occurrence and development of AA. The
pathogenesis of AA is complex, involving multiple cells, molecules, and pathological processes.
Despite many related studies on the genetic level, unfortunately, the disease mechanism of AA is
not fully understood.

CLINICAL FEATURES-

The characteristic lesion of AA is commonly a round or oval, totally bald, smooth patch involving
the scalp or any hair bearing area on body. The hair loss is usually asymptomatic in most cases, but
some patients complain of parasthesias with mild to moderate pruritis , tenderness, burning
sensation or pain before the appearance of patches

Clinical classification of AA

1.Based on pattern 2. Based on extent 3. Based on area

Patchy type AA circumscripta AA of the scalp

Reticular type. AA subtotalis AA of eyelashes
Ophiasis type AA totalis AA of eyebrows
Sisaipho type AA universalis AA of beard
Diffuse type Diffuse AA AA of body hair
Perinevoid type AA incognito AA of nail

Alopecia areata – The most commonly used term covers all forms of the disease
Alopecia partialis – Defines specific patchy hair loss
Alopecia totalis – Involves100 % loss of scalp hair
Alopecia universalis – When all body and scalp hairs are lost
Alopecia areata barbae – AA lesion of beard
Alopecia areata ophiasis – A special band like pattern of AA , which winds
along the occipital hair line extending toward the temples ( oophiasis – Greek for snake)

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Diffuse AA –A term occasionally used for an alopecia areata where there is generalized thinning of
hair of scalp.
Reticular alopecia areata- Multiple active, stable or re growing patches, which may merge to form
mosaic or reticular pattern.
Sisaipho AA- Opposite of ophiasis where hairs are lost centrally and spared at the margins of scalp.
It may mimic androgenetic alopecia.
AA Incognito – First described by Rebora in 1987. Extremely acute onset with subsequent diffuse
hair loss that occurs within few weeks.
Perinevoid AA – An unusual and rare form with patches around a nevus.

Ikeda classification of AA

Based on the associated conditions and on the course of the disease

1. Atopic type (10%): Begins in early life and mostly (30-75%) progresses
to AT.
2. Autoimmune type (5%): Seen in middle-aged , runs prolonged course.
Associated with autoimmune diseases, diabetes mellitus, peptic ulcer and
progresses to AT in 10-50%.
3. Pre hypertensive type(4%): Occurs in young adults whose one or both
parents were hypertensive and progress fastly to AT in 40% of cases.
4. Common type(81%): Mostly affects adults aged 20-40 years and AT
develops in 5-15% of cases.
A frequent feature of an AA patch is ‘exclamation mark’ hair that may be present at its margin.
Exclamation mark hair denotes the broken short hairs that taper proximally. At the margins the
normal looking hair may be easily extracted. This pull test when positive may indicate very active
disease.
A hand lens shows that at the margin, the free ends are splayed, giving frayed appearance. Even the
apparently normal terminal hair, found within the patches, may show one or more constrictions in
their shaft.Shuster has described the coudablity sign to (differentiate diffuse AA from other diffuse
alopecia) in AA, a normal looking hair kinks when forced inwards or bents, the kink being situated
5-10mms above the surface.An intriguing feature of AA is sparing of white hairs. It appears
preferentially to affect pigmented hair, so that non pigmented hair is spared. The white hairs
although less susceptible are not immune to the disease.
The re growth of hair may be
• Fine and un pigmented hair initially
• Gradually gains in caliber and color
• Heterochromia of hair
• Hair growth starts in center, extends peripherally
• May remain un pigmented for a long time- leading to poliosisRe growth and extension may occur
simultaneously in different regions of the scalp

ASSOCIATED CLINICAL SIGNS

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NAIL INVOLVEMENT
Nail involvement may be associated with AA. The reported incidence of nail changes range from
10 to 66%. Changes may be seen in one ,several or all nails. The dystrophy may precede or coincide
with AA and may also occur after resolution of AA , some authors speculate the possibility of
‘Twenty nail dystrophy sine alopecia’
The commonest nail change is superficial,uniform minute pits arrange regularly along and across
the nail giving a ‘Scotch Plaid’ effect or coalescing into ripples.
Other changes include ,
• Trachyonychia or rough nails(longitudinal striation resulting in sand
appearance)
• Red or mottled lunula
• Nail thinning and ridging
• Beau’s lines (grooves through the nails matching that of the lunula margin)
• Onychorrhexis (Superficial splitting of nail extending to the free edge)
• Onychomeadesis (Onycholysis with loss of nails),
• Koilonychia punctate or transverse leuconychia
• Dystrophy
• splitting

EYE CHANGES

Keratoconus and cataract are the most common eye changes reported in
association with AA. Other reported eye changes include Horner’s syndrome, ectopia of the pupil,
iris atrophy or tortuosity of the fundal vessels.

ASSOCIATIONS

Thyroid autoimmunity,Vitiligo,Atopy,Down syndrome,Addison disease

,Autosomal recessive autoimmune polyglandular syndrome(APS- I),Pernicious
anemia,Lupus,Celiac disease,Ulcerative colitis,Multiple sclerosis,Psychological disturbances

INVESTIGATIONS

Diagnosis is based mainly on the clinical appearances. AA is characterized

by non scarring smooth bald patches. Histology can be used to corroborate the diagnosis.
Trichogram reveals a mixed telogen dystrophic pattern. Telogen hairs
predominate in the slowly progressing patches, whereas dystrophic anagen hairs form the majority
in rapidly progressing disease.
Presence of exclamatory mark hairs at periphery, positive hair pull test (>6 hairs), daily hair count
(>100 hairs), hair pluck test (more telogen hairs) and dermoscopy (black dots,yellow dots,
brokenhair, and tapering hair) suggest active disease

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TRICHOSCOPY

Trichoscopy is a non-invasive method of hair and scalp evaluation. The test may be performed with
the use of a handheld dermoscope or a videodermoscope. Trichoscopy findings in Alopecia Areata
o Yellow dots (hyperkeratotic plugs)
o Micro-exclamation mark hairs
o Black dots (destroyed hairs in the hair follicle opening)
o Miniaturized nanogen hairs

HISTOPATHOLOGY

The histopathological findings varies with duration of the disease. Ideal biopsy should include two
4 mm punch including the subcutaneous fat. One specimen is processed with vertical sectioning and
other with horizontal sectioning. If only a single specimen is planned, horizontal sections will give a
better view . A horizontally-sectioned scalp biopsy in addition confirming the diagnosis of AA also
provides information about the possible regrowth. The ideal site for biopsy is at the advancing
border of hair loss. This helps to view the follicles at different levels in dermis to quantify the hair
follicle density, diameter, and to assess the proportion of hair follicles in various stages. A mean
count of less than 1follicle/mm 2 usually indicates less chances of regrowth.

ACUTE STAGE - Peribulbar and intra bulbar lymphocytic inflammatory infiltrate around anagen
follicles, resembling 'swarm of bees,' is characteristic. The lymphocytic infiltrate are mainly found
around the hair matrix and dermal papilla sparing the bulge area, causing follicular edema, cellular
necrosis, micro vesiculation, and pigment incontinence. A dense lymphocytic inflammation can
cause weakening of the hair shaft resulting in a trichorrhexis nodosa-like fracture, leading to the
exclamation mark hairs.

SUB ACUTE STAGE - High proportion of catagen/telogen hair follicles are seen.

CHRONIC STAGE - Follicular miniaturization with variable inflammatory infiltrate are seen in
papillary dermis. The terminal to vellus hair ratio is decreased
to 1:1 in contrast to 7:1 in normal population. Androgenetic alopecia also shows follicular
miniaturization, but more number of telogen hairs with decreased anagen to telogen ratio may be a
clue towards AA. Immunofluorescence studies shows deposits of C3, IgG and IgM on the basement
membrane in the inferior part of hair follicle.
RECOVERY STAGE - The number of terminal anagen hairs increase and there is a lack of
inflammation.

SALT SCORE

Severity of AA can be measured by SALT((severity of alopecia tool) score, developed by the

National Alopecia Areata Foundation working committee.

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SALT score is useful to find out the quantitative assessment of scalp hair loss. The entire scalp was
divided into 4 parts based on the surface area, top (40% - 0.4), posterior (24% - 0.24), right side
(18% - 0.18), and left side of scalp (18% - 0.18). Percentage of hair loss in each area is determined
independently and is multiplied by the percentage of scalp covered in that area of the scalp, and
summing the products of each area will give the SALT score. For example, the hair loss is 40%,
30%, 20% and 10% in top, back and right and left side respectively, then the SALT score can be
calculated as- (40 × 0.4) + (30 × 0.24) + (20 × 0.18) + (10 × 0.18) =16 + 7.2 + 3.6 + 1.8 = 28.6.
SALT score is easily reproducible and validated. However, it does not include hair pigmentation,
body hair, and nail involvement.

DIFFERENTIAL DIAGNOSIS
AA has to be differentiated from the from the following conditions

1. Telogen effluvium - Here the hair loss is generalised over the entire scalp, where as in AA it is
usually patchy .The hairs that are shed are either in telogen or dystrophic anagen in AA, but are
predominantly in telogen in telogen effluvium.
2. Androgenetic alopecia-It typically involves the fronto temporal region and the vertex
3. Trichotillomania-Patches of alopecia with twisted broken hairs are noticed.
4. Secondary syphilis –It is a moth eaten alopecia with positive serological investigation
5. Alopecia neoplastica-There may be history of malignancies like carcinoma breast or others .The
affected skin is slightly indurated and erythematous. A biopsy clinches the diagnosis.
6. Congenital triangular alopecia- Characterised by a triangular area overlying the frontotemporal
suture just inside the anterior hair line with its base directed forward which is completely bald or
covered or by sparse vellus hair.
7. Tinea capitis- The patches of baldness of have irregular borders and broken bits may be seen
within the patch. Examination of hair root with 40%KOH reveals fungal elements.
8. Others – Congenital hypotrichosis, Ectodermal dysplasis, Loose anagen hair , Cicatricial
alopecia, Tractional alopecia

COURSE OF AA

The progress of AA is unpredictable. The initial patch may regrow within a few months or further
patches may appear after interval of 3 to 6 weeks and further patches may appear in a cyclical
fashion at varying intervals. A succession of discrete patches may rapidly become confluent by the
diffuse loss of remaining hair. In some cases the initial hair loss is diffuse and total denudation of
scalp has been reported. Diffuse hair loss also may occur over a part or whole of the scalp without
the development of bald patches. Kling miller has showed that white hairs are spared initially by the
disease process. Patients with sudden diffuse onset of AA would appear to ‘go white” over the
course of a few days. Re-growth is often at first fine and unpigmented but usually the hair gradually
resume its normal calibre and colour. Persistent depigmented hair regrowth from the site of AA has
also been reported.

TREATMENT

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Early recognition and intervention involving topical and or intralesional therapy
can provide patient with comforting reassurance about eventual recovery. An unpredicatable course
and heterogeneity of the disease leads to varying results being obtained with the same therapy. The
various modalities can be classified as follows,

1. Topical therapy
2. Systemic therapy
3. Others

TOPICAL THERAPY INCLUDES

1. Immunosuppresants- Topical corticosteroids with or without occlusion, intralesional steroids,

nitrogen mustard.
2. Non specific irritants- Anthralin, Phenol, Salicylic acid, sulphur , oil of cade, cantharidin, croton
oil, tretinoin
3. Contact sensitizer- Dinitrocholrobenzene ,Squaric acid dibutylester (SADBE) and diphencyprone
4. Photochemotherapy
5. Cryotherapy
6. Lasertherapy - excimer laser(308nm), pulsed infrared diode laser(904nm)

SYSTEMIC THERAPY

1. Immunosuppresants - corticosteroids, cyclosporine

2. Immunomodulators - alefacept
3. Photochemotherapy -whole body PUVA
4. Miscellaneous - Sulfasalazine, IVIg

OTHERS
1. Psychotherapy – hypnotherapy, systemic desensitization
2.Supportive therapy – Dermatography( tattooing) , hair pieces or wigs
3. Investigational therapy – Recombinanthuman bone morphognic protein ,
intralesional candida antigen

TOPICAL CORTICOSTEROIDS
Corticosteroids because of their anti-inflammatory action have been used
widely in the management of alopecia areata. Topical corticosteroids (TCs) are the most common
treatment for AA in patients who cannot receive ICs, with potent steroids such as betamethasone
dipropionate 0.05% cream, lotion, or ointment being used in both adults and children[12]

INTRALESIONAL CORTICOSTEROIDS
Intralesional corticosteroids (ICs) are the first-line treatment for small- to medium-sized areas of
alopecia areata (AA) in adults, with Triamcinolone acetonide injection at concentrations of 2.5–10

9
mg/mL is commonly used. The main side effects of ICs are pitting atrophy and injection pain,
which typically improve within a few months[11]

MINOXIDIL
Minoxidil, a vasodilator, has been found to be a safe and effective treatment for AA when used
locally in combination with other therapies. Studies have shown that low-dose minoxidil (0.25 to 5
mg daily to twice daily) is a safe and successful treatment for androgenetic alopecia and AA [13]

SYSTEMIC STEROID
Systemic corticosteroids are also a common treatment, typically using an initial dose of oral
prednisolone 0.5 mg/kg for a six-week course. However, long-term treatment may carry systemic
side effects such as weight gain and risk of osteoporosis and a higher risk of relapse after
discontinuation[12]

CYCLOSPORINE
Cyclosporine is also a commonly used treatment, and it is often used in combination with other
therapies. A systematic review by Joanna et al. [15] suggested that using cyclosporine in
combination with systemic corticosteroids was more effective than using cyclosporine alone.

METHOTREXATE
Methotrexate (MTX) is often used as monotherapy or adjuvant therapy for AA. A 2018 study found
that combination therapy had a higher complete remission rate compared to monotherapy, but some
patients experienced relapse after dose reduction [14]

FUTURE THERAPEUTIC OPTIONS

In recent years, there has been a growing interest in emerging therapies for alopecia areata (AA),
among which JAK inhibitors have received considerable attention. While further research is needed
to establish the long-term safety of JAK inhibitors, several studies have already demonstrated their
efficacy in treating AA [16]. Baricitinib, an orally administered Janus kinase 1 (JAK1) and JAK2
inhibitor, has been shown in phase 3 trials to effectively treat severe AA in adults without causing
significant adverse effects [17]

Astha arora et al (2022) carried out prospective randomized comparative study in 60 patients of
AA restricted to scalp not requiring systemic treatment randomly divided into two equal groups.
Group 1 patients underwent microneedling with local application of injectable TA and Group 2
patients were given injectable TA intradermally for a total of three sessions at 3 weeks interval.A
mean regrowth of 66.36% in Group 1 and 69.75% in Group 2 at week 9 was seen which was
comparative with no significant statistical difference between the two groups (P = 0.664). Thirteen
patients achieved 100% regrowth at week 9 in Group 1 and 16 patients achieved 50%-99%
regrowth in Group 2.
In this study, injectable TA used intralesionally and topically with microneedling had nearly similar
efficacy in causing regrowth of hair with microneedling resulting in a more uniform but less dense
regrowth of hair with lesser adverse effects.
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Mai Mohamed Omar et al (2022) carried out comparative study between topical application of
triamcinolone acetonide after fractional carbon dioxide laser versus microneedling in the treatment
of resistant alopecia areata.thirty patients were randomly divided into two groups of 15 patients
each: the Laser group received fractional CO2 laser treatment followed by topical application of
triamcinolone acetonide, and the MN group received dermapen treatment followed by topical
application of triamcinolone acetonide. In our study, we found no statistically significant difference
between the studied groups before and after treatment, except for black dot, which is higher in the
MN group than in the laser group (46.7% vs. 13.3%). There is a statistically significant difference
between the studied groups in terms of treatment response at the first follow-up, with 13.3% of the
laser group seeing terminal hair regrowth compared to 0 in the MN group after 12 weeks.
Regarding the degree of improvement, there was no statistically significant difference between the
laser group and the MN group. The use of fractional CO2 laser and MN for transepidermal drug
delivery (TED) allowed for more uniform drug distribution. There was no significant difference
between the two treatment methods in terms of their high effectiveness in the treatment of resistant
AA.

Sandeep Kaur et al (2015) carried out comparative study of Intralesional Triamcinolone Acetonide
Injection, Narrow Band Ultraviolet B, and their Combination in Alopecia areata. fourty patients (28
males and 12 females) with at least three patches of hair loss were enrolled after obtaining written
informed consent. Patches were subdivided as follows: Patch 1 was injected with triamcinolone
acetonide 2.5 mg/ml (total of three injections) at 3 weeks interval. Patch 2 - NBUVB was given
twice a week for a total of 12 weeks. Patch 3 - combination of injection and NBUVB. Therapeutic
response was recorded as regrowth of terminal hair (G0 to G4).At the end of treatment and follow-
up, that is,
at week 12, more than 50% of hair regrowth was evident in 27 (67.5%) patients with intralesional
steroid; 7 (17.5%) with NBUVB; and 25 (62.5%) patients with their combination. This difference in
the clinical response was statistically significant.intralesional steroid is more effective than NBUVB
and their combination is not synergistic in terms of the clinical response in AA.

Jihan M Muhaidat et al ( 2020) carried out randomized Comparison of Topical Betamethasone

Valerate Foam, Intralesional Triamcinolone Acetonide and Tacrolimus Ointment in Management of
Localized Alopecia Areata.105 patients of localized AA were initially registered but 27 were drop
out. So, 78 patients allocated at random in group A (28), B (25) and C (25) were prescribed topical
betamethasone valerate foam (0.1%) twice daily, intralesional triamcinolone acetonide (10mg/ml)
every 3 weeks and tacrolimus ointment (0.1%) twice daily, respectively, for 12 weeks. They were
followed for next12 weeks. Hair re-growth was calculated using “HRG Scale”; scale I- (0-25%), S
II-(26-50%), S III - (51-75%) and S IV- (75-100%).Hair re-growth started by 3 weeks in group B
(Scale I: P<0.03), turned satisfactory at 6 weeks in group A and B (Scale I: P<0.005, Scale IV:
P<0.001)), good at 9 weeks (Scale I: P<0.0005, Scale IV: P<0.00015), and better by 12 weeks of
treatment (Scale I: P<0.000021, Scale IV: P<0.000009) in both A and B groups. At the end of 12
weeks follow-up hair re-growth (>75%, HRG IV) was the best in group B (15 of 25, 60%),
followed by A (15 of 28, 53.6%) and lastly group-C (Nil of 25, 0%) patients. Few patients reported
mild pain and atrophy at injection sites, pruritus and burning with betamethasone valerate foam and

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tacrolimus.Intralesional triamcinolone acetonide is the best, betamethasone valerate foam is better
than tacrolimus in management of localized AA.

RATIONALE OF STUDY- Dermaroller has been proposed as a viable alternative to treatment of

AA. Earlier ILS were mainstay of treatment but ils lead to steroid induced atrophy and the injection
can be often painful,dermaroller on the other hand prevents these adverse effects and additionally
will provide uniform delivery of topical agents to larger area as well. It is also not a very costly or
technically challenging procedure and there are practically no particular concerns regarding this
procedure when compared to conventional ils.this study is crucial as we need to do establish that the
benefits are reproducible in both gender and sustained over longer periods of time.

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 MATERIAL AND METHOD

STUDY SETTING

The study will be conducted in the Outpatient department of Dermatology, JNMCH, AMU, Aligarh
, Uttar Pradesh.

STUDY POPULATION

All patients of AA following inclusion and exclusion criteria’s attending Outpatient Department of
JNMCH

STUDY DESIGN

This unblinded prospective Randomised Control Trial will be conducted on patients of AA

STUDY DURATION

The duration of study will be of 2 years.

SAMPLING

Sampling size-

Sampling methods-

After a detailed written informed consent, patients of AA will be enrolled into study according to
sample size. They will be randomised into two groups, Group A and Group B. Randomisation will
be done using “box and chit” method, in which chits with group A mark and chits with group B
mark will be placed in a box. Each patient will take one chit and will be allocated accordingly in the
respective group mentioned over the chit.

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INCLUSION CRITERIA
1.Patient giving consent for therapy.
2.Patient in the age group of >18 years
3.Patients having only scalp involvement
4. Patients who had no treatment either topical or systemic in the past 3
months.
EXCLUSION CRITERIA
1.Patient of age <18 years
2. Pregnant and lactating women.
3. Local/systemic Infection.
4. Any serious systemic illness or immunosuppressive disorders.
5.Patient not giving the consent
6.Patient with alopecia universalis , totalis
7.Patients with oophiasis and sisaipho pattern

ETHICAL CLEARANCE
The ethical clearance from the Institutional Ethical Committee of JNMCH, AMU, Aligarh will be
obtained for the same

INTERVENTION
All the patient of AA fulfilling the inclusion criteria will be given therapy according to the group
allocated after randomisation.

GROUP A
Group a patients treated with microneedling using a derma roller having
192 needles of 1.5-mm length each followed by topical application of
triamcinolone acetonide. Triamcinolone acetonide in concentration of 10
mg/ml (0.1 ml containing 1 mg of triamcinolone) was applied on each
lesion twice, before and after performing dermaroller. Under aseptic
precautions, the dermaroller was moved on the scalp patches diagonally,
vertically and horizontally 4 to 5 times in each direction after applying
triamcinolone acetonide. This created pin point bleeding which was taken
as an end point, following which triamcinolone was applied topically. No
anaesthesia was used as the procedure was relatively painless. A total of
three sessions were done for both patients at 3 weeks interval.
GROUP B
Patients were given injectable TA intradermally with disposable insulin
syringe.

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STUDY PLAN

A detailed history regarding the name, age, sex, address, contact number, marital status, occupation,
duration of disease, drug history and concomitant disease will be taken. Physical examination for
evidence of infections at local sites will be done.

History and examination

A detailed history of each patient will be taken and recorded in proforma designed for study
regarding demographic data of patients (name, age, sex, education, occupation, marital status,
residence), mode of onset, progression, duration,Family History .Examination of the patient
including general physical examination, vitals, systemic examination and cutaneous examination
will be done. Photographs of the affected region will be taken with a good quality camera.

STUDY TOOL

Patient will be assessed by observer at baseline and at the end of 3rd , 6th , 9th , 12th , 15th weeks
during the study period.All the immediate and late adverse effects will be evaluated after each
treatment session.

FOLLOW UP
Patient will be followed up at the end of 3rd, 6th, 9th, 12th and 15th weeks to assess the compliance
and to examine the patient to evaluate efficacy and safety.

STATISTICAL ANALYSIS

All the data will be tabulated and statistically analysed. Qualitative data will be described using
number and percentage. Quantitative data will be described using mean and standard deviation
(SD). Chi-square test and unpaired t-test will be applied at appropriate places. P-value less than 0.05
will be considered significant.

15
 REFERENCES

1 Gilhar A, Etzioni A, Paus R. Alopecia areata. N Engl J Med. 2012;366:1515–25.

2.Hon KL, Leung AK. Alopecia areata. Recent Pat Inflamm Allergy Drug Discov. 2011;5:98–107.
3. Rencz F., Gulácsi L., Péntek M., Wikonkál N., Baji P., Brodszky V. Alopecia areata and health-
related quality of life: A systematic review and meta-analysis. Br. J. Dermatol. 2016;175:561–571.
doi: 10.1111/bjd.14497.
4. Darwin E., Hirt P.A., Fertig R., Doliner B., Delcanto G., Jimenez J.J. Alopecia Areata: Review of
Epidemiology, Clinical Features, Pathogenesis, and New Treatment Options. Int. J. Trichol.
2018;10:51–60. doi: 10.4103/ijt.ijt_99_17.
5. Villasante Fricke A.C., Miteva M. Epidemiology and burden of alopecia areata: A systematic
review. Clin. Cosmet. Investig. Dermatol. 2015;8:397–403. doi: 10.2147/ccid.S53985.
6. Afford R., Leung A.K.C., Lam J.M. Pediatric Alopecia Areata. Curr. Pediatr. Rev. 2021;17:45–
54. doi: 10.2174/1573396316666200430084825.
7.Simakou T., Butcher J.P., Reid S., Henriquez F.L. Alopecia areata: A multifactorial autoimmune
condition. J. Autoimmun. 2019;98:74–85. doi: 10.1016/j.jaut.2018.12.001.
8.Bertolini M., McElwee K., Gilhar A., Bulfone-Paus S., Paus R. Hair follicle immune privilege
and its collapse in alopecia areata. Exp. Dermatol. 2020;29:703–725. doi: 10.1111/exd.14155.
9.Naik P.P., Farrukh S.N. Association between alopecia areata and thyroid dysfunction. Postgrad.
Med. 2021;133:895–898. doi: 10.1080/00325481.2021.1974689.
10.Blaumeiser B., van der Goot I., Fimmers R., Hanneken S., Ritzmann S., Seymons K., Betz R.C.,
Ruzicka T., Wienker T.F., De Weert J., et al. Familial aggregation of alopecia areata. J. Am. Acad.
Dermatol. 2006;54:627–632. doi: 10.1016/j.jaad.2005.12.007
11.Zhou C., Li X., Wang C., Zhang J. Alopecia Areata: An Update on Etiopathogenesis, Diagnosis,
and Management. Clin. Rev. Allergy Immunol. 2021;61:403–423. doi: 10.1007/s12016-021-08883-
0.
12. Strazzulla L.C., Wang E.H.C., Avila L., Lo Sicco K., Brinster N., Christiano A.M., Shapiro J.
Alopecia areata: An appraisal of new treatment approaches and overview of current therapies. J.
Am. Acad. Dermatol. 2018;78:15–24. doi: 10.1016/j.jaad.2017.04.1142.
13. Sharma A.N., Michelle L., Juhasz M., Muller Ramos P., Atanaskova Mesinkovska N. Low-dose
oral minoxidil as treatment for non-scarring alopecia: A systematic review. Int. J. Dermatol.
2020;59:1013–1019. doi: 10.1111/ijd.14933.
14. Phan K., Ramachandran V., Sebaratnam D.F. Methotrexate for alopecia areata: A systematic
review and meta-analysis. J. Am. Acad. Dermatol. 2019;80:120–127.e122.
doi: 10.1016/j.jaad.2018.06.064.
15Nowaczyk J., Makowska K., Rakowska A., Sikora M., Rudnicka L. Cyclosporine With and
Without Systemic Corticosteroids in Treatment of Alopecia Areata: A Systematic Review.
Dermatol. Ther. 2020;10:387–399. doi: 10.1007/s13555-020-00370-2
16. Zheng C., Tosti A. Alopecia Areata: New Treatment Options Including Janus Kinase Inhibitors.
Dermatol. Clin. 2021;39:407–415. doi: 10.1016/j.det.2021.03.005.
17 King B., Ohyama M., Kwon O., Zlotogorski A., Ko J., Mesinkovska N.A., Hordinsky M.,
Dutronc Y., Wu W.S., McCollam J., et al. Two Phase 3 Trials of Baricitinib for Alopecia Areata. N.
Engl. J. Med. 2022;386:1687–1699. doi: 10.1056/NEJMoa2110343.

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17
 THESIS PROFORMA
COMPARATIVE STUDY OF COMBINATION OF INTRALESIONAL
TRIAMCINOLONE AND DERMAROLLER VERSUS INTRALESIONAL
TRIAMCINOLONE IN THE TREATMENT OF ALOPECIA AREATA

S.NO.:

NAME:

DATE:

S/O:

AGE/SEX:

EDUCATION:

OCCUPATION:

ADDRESS:

PHONE NO.:

CLINICAL HISTORY
18
 • Chief complaints

• Duration and progression

• Past history

• Treatment history

• Personal history

• Family history

19
CLINICAL EXAMINATION

• General examination

• Systemic examination

• Cutaneous examination

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 INFORMED CONSENT

I.................................................S/o/D/o...........................................................
R/o................................................ give my consent for the study which will include intralesional
injection of steroid and/or dermaroller. All the steps and benefits of the procedure have been
explained to me. All my questions have been answered by the treating doctor up to my satisfaction.

PATIENT’S NAME/ PARENT’S NAME/ GUARDIAN’S NAME:

ADDRESS:

SIGNATURE:

WITNESS:

1.

2.

DATE:

21