Alopecia Areata An Autoimmune Disease Biology Essay
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Alopecia areata can affect any hair-bearing area and can also involve nails. A peribulbar lymphocytic infiltrate in a 'swarm of bees' pattern is characteristic of the acute stage of the disease leading to a dystrophic anagen phase. There may also be increased psychiatric morbidity in patients with alopecia areata. Ikeda (2) classified alopecia areata into four types including the common type (81%), the atopic type (10%), the autoimmune type (5%) and the prehypertensive type (4%)
The course of the disease is unpredictable and the response to treatment is variable. The various treatment modalities used can be classified into topical and systemic therapies. The topical therapy includes intralesional corticosteroid, topical corticosteroids, minoxidil, anthralin and topical immunotherapy in the form of diphenylcyclopropenone (DPCP) and squaric acid dibutylester (SADBE). The systemic therapy includes systemic corticosteroids and photochemotherapy. Cyclosporine, methotrexate, sulphasalazine and biologics like etanercept, efalizumab, adalimumab and infliximab have been used with limited success. Intralesional corticosteroids are the treatment of choice for adults with less than 50% of scalp area involvement.
The sensitivity of picking up clinical response to treatment by a clinical examination is very variable and has interindividual variation. Dermoscopy is a noninvasive diagnostic tool which visualizes subtle patterns of skin lesions not normally visible to the unaided eye. It is performed by a hand held or a video dermoscope equipped with lenses that currently allow magnifications ranging from 10 to 1000, the images obtained can be visualized on a monitor and stored using specific software on a personal computer, to identify and compare changes over time.(3)
The characteristic features of alopecia areata on dermoscopy (4) are yellow dots, black dots, broken hair, vellus hair and tapering or exclamation mark hair. After therapy there is a decrease in the number of these characteristic findings. On the other hand, the presence of thin and unpigmented 'vellus hair' within the patch, and evidence of transformation of vellus hair into terminal hair, appearing as increased proximal shaft thickness and pigmentation, are characteristic of remitting disease and indicative of a response to treatment.
The present study is being undertaken to evaluate the efficacy of intralesional triamcinolone acetonide in the treatment of alopecia areata and to assess its local and systemic side effects. Dermoscopy has been used to identify signs of early clinical response to the chosen therapeutic regimen. The useful markers to assess the severity of alopecia areata on dermoscopy are the black dots, yellow dots, broken hairs or dystrophic hair, tapering or exclamation mark hair and short vellus hairs. Previous reports have suggested that the severity of alopecia areata is an important prognostic factor. Therefore, dermoscopic examination of patches of alopecia areata may provide predictors of the response to therapy and can also be utilized for monitoring response to any prescribed regimen.
Alopecia areata is an autoimmune disease of uncertain etiology that involves the hair follicle and sometimes the nail and is usually reversible. Although autoimmune, genetic and environmental factors have been implicated but the exact pathogenesis is yet to be elucidated.
Hippocrates first used the term alopecia which literally means 'fox's disease'. The characteristics of alopecia areata were first described by Cornelius Celsus in 30 A.D., who described two forms of alopecia. The first he described as complete baldness occurring in people of all ages. The second he called 'ophiasis', which literally means 'snake', due to the pattern in which the hair loss spreads across the scalp and also suggested that ophiasis was only seen in children. Alopecia areata is sometimes also referred to as 'area celsi' in tribute to Cornelius Celsus. Alopecia areata has been given many different names throughout history. However, the actual term 'alopecia areata' was first used by Sauvages in his "Nosologica Medica", published in 1760 in Lyons, France.
From the beginning of 19th century there was considerable debate about the cause of alopecia areata. Two main hypotheses were put forward, one based on parasitic infection by Gruby in 1843 and Radcliffe-Crocker in 1903 and the other based on a nervous disorder by Von Barensrung in 1858. The parasitic hypothesis drew support from the pattern in which alopecia developed -expanding slowly in size just as a local infection would. Even more significant were the apparent epidemics of alopecia areata reported to occur in institutions such as orphanages and schools. However, many attempts to isolate an infective organism and to transfer alopecia areata by inoculation failed.
The initiation of alopecia areata by a nervous disorder, known as the trophoneurotic, neurotrophic or neuropathic hypothesis, eventually gained the support of most dermatologists of the time. This vague hypothesis could be supported by the apparently frequent clinical observations of emotional or physical stress and trauma that were associated with the onset of alopecia areata and often reported in the medical journals of that time. Emotional stress and physical damage were believed to adversely affect hair follicles via the nervous system and Joseph in 1886 showed that patchy hair loss could apparently be induced by cutting nerves in the necks of cats (it was later suggested that the hair loss was actually due to the cats scratching themselves). The idea circulated among dermatologists for many years because it was very difficult to fundamentally prove or disprove that alopecia areata was a nervous disorder. The hypothesis is still supported by some dermatologists today.
One of the more unusual variations on the neuropathic origin of alopecia areata was put forward by Jacquet in 1902 who suggested that alopecia areata was initiated by sources of nerve irritation such as defective and diseased teeth. Jacquet's hypothesis was apparently confirmed by Decelle 1909, although Baily in 1910 showed dental disease to be equally frequent in people without alopecia areata. Eye strain was another suggested cause of alopecia areata by Kinnear 1939. With the start of the twentieth century, alopecia areata was known to be associated with disorders of the endocrine glands, particularly the thyroid. As such, some believed the underlying cause of alopecia areata was due to a hormone dysfunction. By the 1920's most dermatologists had abandoned the parasitic theory of alopecia areata and favoured variations on the trophoneurotic and endocrine theories - often combining the two.
Sufferers of alopecia areata were under extensive mental stress from fear that they would be suspected of having syphilis. Until the advent of antibiotics, syphilis was a widespread, contagious disease and it also often manifests itself by sudden, rapid loss of hair in well-defined patches, just like alopecia areata. Syphilis in the secondary stage can also affect finger nails. To further complicate the matter, some dermatologists suggested that alopecia areata could be found in increased association with syphilis - as distinct from the direct action of syphilis on hair follicles. Syphilis was believed to induce alopecia areata by the mental distress it created and its possible upset of the endocrine system. These clearly visible symptoms of syphilis were often confused with alopecia areata by the general population and resulted in social ostracism for the sufferer.
The early 20th century saw the development of another hypothesis of alopecia areata induction based on toxic agents. An unknown poison was believed to be introduced to the hair follicle via the blood system inducing hair loss. The sudden remission and relapse of alopecia areata and its action simultaneously over the body was believed to support the idea. Also in support, injection of thallium acetate (rat poison) was shown to induce alopecia areata like hair loss in some patients, with expression of exclamation mark hairs - a diagnostic feature of alopecia areata. However, the toxic origin of alopecia areata never gained widespread popularity against the neuropathic and endocrine hypothesis.
It is now widely believed that alopecia areata is an autoimmune disease. Even though studies more than 100 years old showed that alopecia areata affected hair follicles were invaded by inflammatory cells by Giovannini in 1891, the inflammatory autoimmune disease hypothesis did not become popular until the 1960's. The idea was first proposed by Rothman in a discussion of a paper by Van Scott in 1958.
Treatment of alopecia areata by intradermal corticosteroid injections has been practised for many years. Kalkoff and Macher in 1958 were the first to have reported a series using hydrocortisone. Thereafter, Orentreich et al in1960 and Gombinger and Malkinson in 1961 reported the use of prednisolone and triamcinolone, and Porter and Burton in 1971 used triamcinolone acetonide and hexacetonide. Moynahan and Bowyer in 1965 and Verbov and Abell in 1970 reported the initial use of jet injection apparatuses in a number of conditions including alopecia areata.(6)
Alopecia areata occurs worldwide and there is no racial or sex prelidiction. It is a common disease forming 0.7% to 3.8% of patients seen by dermatologists. (7) In the United States, alopecia areata was estimated to occur in 0.1% to 0.2% of the general population, with a lifetime risk of 1.7%.(1) Sixty percent patients present with their first patch below 20 years of age.(8) One study suggests that 85.5% of Asian patients with alopecia areata have disease onset before the age of 40 years.(9) The disease prevalence peaks between the second and the fourth decade of life. A family history is found in 5%-25% of patients.(10)
Natural history that includes the severity, course and prognosis is highly unpredictable and it can be said that 'the only thing predictable about its course and prognosis is that it is unpredictable'. With the available information at present the spontaneous remission rates have ranged from 34% to 80% within one year and 15% to 25% patients progress to total loss of scalp hair (alopecia totalis) or loss of the entire scalp and body hair (alopecia universalis), of which only 10% eventually recover. (11,12) It is a non-scarring alopecia and is reversible but it can be recurrent and abrupt and in long standing cases scarring can occur.
Alopecia areata is a chronic, autoimmune, organ specific disease, probably mediated by autoreactive T cells, which affect hair follicles and sometimes the nails. The increased frequency of other autoimmune diseases favours the above postulation. Hair follicle autoantibodies are also found although it is unlikely that these are involved in the pathogenesis of the disease.
Genetic factors: Most reports describe the prevalence of positive family history to be in the range of 10 to 20% but it is believed that some mild cases may be overlooked or concealed and hence the actual figure may be greater. Price and Colombe (13) found a family history of alopecia areata was more common in those who had a disease onset before the age of 30 years (37% compared with 7.1% in those with onset after 30 years). A study amongst monozygotic and dizygotic pairs found a concordance rate of 55% for monozygotic twins and no concordance amongst dizygotic twins.(14) The genetic basis of inheritance appears to be multifactorial and polygenic and not a simple Mendelian pattern.
The strongest associations have been with major histocompatibility complex (MHC), particularly the Class II alleles HLA-DQB1*0301 and HLA-DRB1*1104 and the association is linked to chromosome 6p and few susceptibility loci on chromosomes 10, 16 and 18. (15,16)
Atopy: Several studies have reported an association and also suggested an earlier age of onset and more severe disease in atopic individuals.(17,18)
Autoimmunity: A statistically significant association between alopecia areata and Hashimoto's thyroiditis, Addison's disease and pernicious anemia has been reported. It is also associated with other autoimmune diseases like vitiligo, lichen planus, Sjogren's syndrome, systemic lupus erythematosus, morphea, lichen sclerosus, pemphigus foliaceus, ulcerative colitis, myasthenia gravis, autoimmune haemolytic anemia, diabetes mellitus, autoimmune testicular and ovarian disease, Down's syndrome (in which other autoimmune disorders are common) and autoimmune polyendocrinopathy-candidiasis-ectodermal dysplasia syndrome (also called as autoimmune polyglandular syndrome-1) which is an autosomal recessive disorder in which there are mutations in autoimmune regulator gene.(19)
There is also evidence of circulating organ specific antibodies against thyroid, gastric parietal cell, adrenal tissue, smooth muscle, testis and the ovaries.
The cells in the lower part of hair follicle have low or absent expression of MHC proteins and the loss of this 'immune privilege' leading to induction of CD8+ T cell-mediated immunity against follicular melanocytes is hypothesized to be causative of alopecia areata. This explains the peribulbar lymphocytic infiltrate and also the sparing of white hair in the patch and hence leads to what is commonly called as the phenomena of "overnight greying."
Infection: Prior notion of alopecia areata being due to infection directly or due to a remote focus of infection has a long history and was very popular till the middle of 20th century. Skinner et al (20) reported finding mRNA for cytomegalovirus in alopecia areata lesions. Few reports of coexistence in husband and wife but many have refuted this and likened it to be a mere coincidence.
Stress: Is suggested to be an important precipitating factor and this also explains cures by sleep therapy, reassurance and suggestion therapy. Such patients may also have stress associated depression and the finding of elevated serotonin levels in such patients lends support to the theory.
It has been seen that there is aberrant expression of estrogen receptor -1 in the hair follicles of diseased mouse with alopecia areata. Corticotrophin releasing hormone (CRH) can induce mast cell differentiation from hair follicle mesenchyme and the CRH/receptor activity is seen to be high in alopecia areata skin.(21)
Diet: Iron deficiency has been postulated to modulate the hair loss in alopecia areata. The mechanism is by inhibiting the rate-limiting enzyme for DNA synthesis and hence it diminishes the proliferative capacity of hair follicle matrix cells.(22) It has also been seen that dietary soy intake increases the resistance to the development of alopecia areata. A study in a Japanese population living in Hawaii, where a Westernized non soy diet predominates, showed disproportionally higher alopecia areata incidence.(23)
Other factors that have been implicated include hormones, drugs, and vaccinations. These factors may increase or decrease susceptibility to the disease onset, pattern, severity, duration and response to treatment by modifying the physical and biochemical status of the immune system and hair follicles.(24)
Pathogenesis and pathology:
There are four key phases in the normal hair cycle which includes the anagen (growth) phase, the catagen (regression) phase, the telogen (resting) phase, and the exogen (controlled shedding phase). When the new hair cycle begins the old hair fiber is shed from the hair follicle in the exogen phase and hence this maintains the overall hair density of the scalp. If the exogen occurs before the anagen is renewed or there is a dystrophic anagen then this leads to a state called kenogen in which there is no hair fiber in the hair follicle.(24) Thus the patch of alopecia areata can be said to be in a state of kenogen. When the amount of inflammatory infiltrate around the hair follicle increases this can lead to miniaturization of the hair follicles and shortening of the hair cycle with rapid changes from anagen to telogen leading to the formation of 'nanogen' hair follicles which is an intermediate stage between terminal and vellus anagen.(25)
In the acute stage of the disease there is a "swarm of bees" infiltration of CD4+ and CD8+ lymphocytes into the peribulbar space of anagen stage hair follicles and some penetration of lymphocytes to intrafollicular locations which leads to a state of 'dystrophic anagen'. This disrupts the ability of the hair follicle to produce hair fibres of sufficient length and integrity and the expelled hair fiber is not replaced by a fiber that can produce adequate scalp coverage, hence leading to alopecia.(25) Hair follicles are smaller than normal and do not develop beyond the Anagen 3-4 stage, where the actual hair shaft begins to form and return prematurely to telogen.
As more and more hair follicle move to telogen phase the amount of inflammation decreases. At this stage most of the inflammation is localized to the papillary dermis around the miniaturized hair follicles. In all stages of the disease, there can also be a diffuse infiltration of eosinophils and mast cells into the disease affected skin. There is no inflammatory infiltrate which is seen around the isthmus of the hair follicle which is the site for the stem cells. Thus the pathological location of the disease process saves the stem cells from destruction and makes it a reversible and non-scarring alopecia. Trichocytes in the in the hair bulb matrix undergoing early cortical differentiation show vacuolar degeneration and are also the predominant cell types showing aberrant class I and II MHC expression.(10)
Ikeda's classification (2)
The atopic type (10%) begins during childhood or adolescence and progresses slowly over many years with individual patches lasting more than one year. Ophiasis and reticular patterns are common and the chances of developing total alopecia are very high (30-75%).
The autoimmune type (5%), affects the middle aged, runs a prolonged and led to alopecia totalis in 10%-50%.
The prehypertensive type (4%) occurred in young adults whose one or both parents were hypertensive progressed faster and led to total alopecia in 40%. Reticular pattern is common.
The common type (81%) is the prototype of the fast progressive form of disease that affects adults aged between 20-40 years. No associated conditions and individual patches last less than 6 months and there is spontaneous regrowth occuring within 3 years. Alopecia totalis may develop in 5%-15%.
Based on the pattern of alopecia:
Restricted to the scalp
Alopecia areata may begin at any age but the disease incidence peaks between 20-40 years of age and has an equal sex incidence. The characteristic initial lesion is a well circumscribed, totally bald smooth patch in which the skin appears slightly reddened. The disease is asymptomatic but few patients may complain of itching and burning prior to the onset of the lesions. During the active phase of the disease short easily extractable broken hairs are seen at the margins of the bald patches which are known as exclamation mark hairs and hair pull test is positive.(26)
Subsequent course is highly unpredictable. The initial patch may regrow hair or it may increase in size and new patches may appear after a variable interval. The succeeding patches may become confluent. In some cases the initial hair loss is diffuse and total scalp denudation has been reported in 48 hours. Regrowth is initially of fine vellus unpigmented hair and later these assume their normal thickness and pigmentation. It is possible that regrowth may occur in one region while alopecia is extending in another region.(10)
Alopecia areata may affect any hair bearing skin but the scalp is involved in 90% of patients. The eyebrows and eyelashes may be associated with hair loss elsewhere or may be the only site affected. The term alopecia totalis (AT) is used when complete loss of all scalp hair occurs and alopecia universalis (AU) when there is loss of all body hair. About 5% of patients progress to AT/AU. A new variant has been described by Sato-Kawamura et al (27) called as diffuse and total alopecia which has a favourable prognosis but has rapid progression and extensive involvement.
The disease process preferentially affects the pigmented hair and spares the white hair thus leading to the phenomena popularly known as the overnight greying of hair but this is a relative process as white hairs are also lost albeit less as compared to pigmented ones. Hair regrowth may be initially nonpigmented but later complete pigmentation occurs.
Nail involvement occurs in 10%-15% of patients in which the most characteristic feature is fine stippled pitting but sometimes there may also be trachyonychia, red or mottled lunulae, nail thinning and ridging, discoloration that includes longitudinally arranged punctate leuconychia, splitting, onychodystrophy and onycholysis may be seen.(26) Some studies have reported psychiatric diseases like mood disturbances and anxiety and ophthalmological findings like asymptomatic lens opacities and fundus changes.(28,29)
Poor prognostic indicators:(10)
Early age of onset
Extensive scalp involvement (>50% scalp)
Loss of eyebrows and eyelashes
Alopecia totalis or universalis
Patterns - ophiasis, sisaphio, reticular
Nail changes: Pits, onychodystrophy, onycholysis, anonychia
Associated systemic disorders: atopy, hypertension and connective tissue disease.
Associated genetic disorder: Down syndrome
Family history of alopecia areata
Macrophage migration inhibitory factor (MIF) -173*C gene
1. Trichogram/ hair pluck test:(30)
To perform the pluck test, hairs are taken from the specified sites on the fifth day after the last shampoo. The surrounding hairs are fixed with clips and 60-80 hairs are grasped with a hemostat covered with rubber. The hairs are plucked, twisting and lifting the hair shafts rapidly in the direction of immergence from the scalp. Hair shafts are then cut off 1cm above the root sheaths and roots are arranged side by side on a slide and then taped.
The anagen hair bulbs are seen as darkly pigmented triangular or delta-shaped bulbs with an angle to the hair shaft and there is presence of inner root sheath. The telogen hair is seen as less pigmented hair with club-shaped hair bulb and there is absence of inner root sheath. Anagen hairs are distinguished from the telogen hairs and anagen to telogen ratio is calculated.
Trichogram in alopecia areata reveals a mixed telogen-dystrophic pattern. Telogen hairs predominate in the slowly growing patches, whereas dystrophic anagen hair forms the majority in rapidly progressing disease.
2. Scalp biopsy:(10)
A peribulbar lymphocytic infiltrate in a "swarm of bees" pattern is characteristic of the acute stage of the disease, in which the number of follicles is normal and many are in catagen or telogen. In the later stages, only a few lymphocytes or eosinophils are present in fibrous tracts and in a peribulbar location. Many follicles in early anagen stage are observed in this late stage and the actual number of hair follicles may be reduced.
A dermoscope is a non-invasive diagnostic modality which can be used to visualize fine details of skin lesions and even subsurface skin lesions which are not visible to the naked eye. It is also called as skin surface microscope, epiluminescence microscope or an episcope. An advantage of their use is the storage of the results and their reproducibility. (3)
The history of dermoscopy:(31)
Skin surface microscopy began in Europe when in the year 1663, Kolhaus used a microscope for examining the small vessels in the nail fold. In 1878, Abbe described the use of immersion oil in light microscopy and this principle was transferred to skin surface microscopy by the German dermatologist, Unna, in 1893. He introduced the term ''diascopy'' and described the use of immersion oil and a glass spatula for the interpretation of lichen planus and for the evaluation of the infiltrate in lupus erythematosus.
The term "dermatoscopy" was introduced in 1920 by the German dermatologist Johann Saphier, when he used a used a new diagnostic tool which resembled a binocular microscope with a built-in light source. The term "dermoscopy" was introduced by Goldman from the United States when he used this new technique for the evaluation of pigmented lesions of the skin. In 1971, Rona MacKie had identified the advantage of surface microscopy for the improvement of preoperative diagnosis of pigmented skin lesions and for the differential diagnosis of benign versus malignant lesions. Dermoscopic patterns of pigmented skin lesions including melanoma were established and standardized in consensus conferences that were held in 1989 in Hamburg and 2001 in Rome.
Principle of dermoscopy: (3)
The basic principle is to transilluminate a lesion and then to study the same under a high magnification to visualize its subtle features. When light is incident on a skin surface it undergoes reflection, refraction, diffraction and absorption and the magnitude of each of these phenomena is influenced by physical properties of the skin. When light is reflected on a dry, scaly skin surface most of it is reflected back but when the same falls on a smooth, oily skin most of the light passes through it and reaches the deep dermis. Thus certain fluids are used to improve the translucency of the skin that includes oils (olive and mineral oil), liquid paraffin, glycerin and water. Hand-held dermoscope have the basic principles:
The refractive index of glass is almost similar to skin and when it is in contact with oil-applied skin, it further enhances the transillumination and hence visualization.
The application of a glass plate flattens the skin surface and provides an even surface for better examination.
Videodermoscopy represents evolution of dermoscopy and it is performed with video camera equipped with optic fibers and lenses that currently allow magnification ranging from 10X to 1000X, and images are visualized on a monitor and stored using specific software on personal computer.
Basic design of a dermoscope:(3)
The essential components include:
Achromatic lens: To achieve the desired magnification which ranges from 10X to 100X.
Inbuilt illuminating system: Various illuminating systems are used that include:
Halogen lamps emit yellow light which can alter the colour contrast of the lesions.
Light emitting diodes (LED): Used in Delta 20©, Dermlite©, provide high intensity and consume 70% less energy than the halogen lamps. The illumination provided can be adjusted by turning off a set of LEDs. Can also be designed to emit lights of different colors and hence wavelengths and this can help in better visualization of skin as the penetration of skin is directly proportional to its wavelength.
Power supply: By batteries eg. Lithium ion battery or using rechargeable handles.
The types of dermoscopy instruments that can be used include:
Instuments without image capturing facility.
Instuments with image capturing facility.
Instuments with image capturing facility and analytical ability.
It can be done either by the non-contact or the contact technique.
In the contact technique the glass plate of the dermoscope comes in contact with the fluid applied on the lesion whereas in the non-contact technique, there is no contact of the lens with the skin. The cross-polarized lens absorbs all scattered light and hence allows only light in one plane to pass through. The advantage of a non-contact technique is that there is no nosocomial infection but this is eclipsed by poor resolution and decreased illumination.
The contact plates used are made mostly of silicon glass and can be graduated for measuring the size of the lesion. These contact plates should be sterilized by using either 2% glutaraldehyde or methylated spirit. It can be used for the diagnosis of melanocytic nevi, melanoma, lichen planus, dermatofibroma, cicatricial alopecia, seborrheic keratosis and to calculate the follicular density in the donor area before follicular unit hair transplantation.
Dermoscopy of normal scalp:(32)
Dermoscopy of the scalp can be performed with or without interface solution, which is referred to as "dry dermoscopy". Dry dermoscopy is useful for observing tertiary structures of the skin, such as hairs, scaling and follicular hyperkeratosis. An interface solution (thermal water) is used to analyse follicular and interfollicular (vascular) patterns.
Dermoscopy of the normal scalp shows interfollicular simple red loops, and arborizing red lines, which represents the normal vascular patterns, and honeycomb pigmentation in sun exposed areas and in subjects with darker skin. Follicular units are easily identified and usually contain 1 to 4 hairs. In children, dermoscopy often shows 'dirty dots' corresponding to dust particles retained in the scalp. This feature is not observed in adolescents or adults as sebaceous secretions prevent particle deposition.
Dermoscopic findings in alopecia areata:
The characteristic findings are yellow dots, black dots, broken hair, tapering hairs corresponding to exclamation mark hair and regrowing vellus hair.
They are due to dilatation of the affected follicular infundibulum with keratinous material or sebum. (4) They vary in size, shape and colour. They may be round or polycyclic, yellow to pink.(33) They may be devoid of hair or contain miniaturized regrowing hair. They represent active and progressive disease. Although yellow dots are seen in androgenetic alopecia, female pattern of androgenetic alopecia, trichotillomania and discoid lupus erythematosus, the number of yellow dots is limited in these conditions as compared to alopecia areata, which shows numerous yellow dots and is its characteristic feature.(34)
The incidence of yellow dots reported in the study by Inui et al (4) was 191 of 300 patients and in the study by Mane et al it was 81.8%.(35) It is speculated that this may be the result of yellowish skin colour of Asian patients. Another possible reason may be the different devices used: a handheld dermoscope (DermLite® II pro) in the study by Inui et al vs. videodermoscopy and a handheld dermoscope by Ross et al (33) and only hand held dermoscope by Mane et al.(35)
They are remnants of exclamation hair and broken hair. They represent pigmented hairs broken or destroyed at the scalp level. They provide a sensitive marker of disease activity and disease severity.(4) The black dots of alopecia areata are characteristic of black haired individuals, including Asians, and these findings have not been used for the diagnosis of alopecia areata in white population. This feature may be attributed not only to hair colour but also to cuticle resistance. Takahashi et al (36) reported that Asian hair cuticles fall as large pieces while keeping their original shape under extension stress, whereas hair cuticles of white populations tend to collapse to form small fragments. They are also observed in dissecting cellulitis of scalp, tinea capitis, chemotherapy induced alopecia and trichotillomania.
Inui et al demonstrated black dots in 44.3% (133 out of 300) patients (4) whereas Mane et al demonstrated black dots in 67.7% (44 out of 66) patients.(35)
These result from hair regrowth either spontaneously or as a result of treatment. They can be seen by the dermoscope even when they are hardly perceived by the naked eye and hence shows the non-scarring nature of alopecia areata. Not only the pigmented short vellus hairs can be detected by dermoscopy, but also the white vellus hairs are easily seen. This shows the negative correlation of vellus hairs with the disease activity or severity of alopecia areata. This finding on follow up visits can be used to encourage patients to continue treatment.(4)
Broken/cadaverized hair/dystrophic hair:
They have fractured tips. They may be fractured before emergence from the scalp, known as cadaverized hair, or may appear as short twisted dystrophic hairs. Inui et al(4) demonstrated broken hair in 45.7% (137 out of 300) patients and in the study by Mane et al(35) demonstrated broken hair in 55.4% of patients. However the frequency of these was much higher 95% (19 out of 20) patients in another study of acute diffuse and total alopecia of female scalp.(27)
Tapering / exclamation mark hair:
They result from a truncated hair cycle consisting of premature telogen and dystrophic anagen and hence are fractured and short. These are indicative of an active disease process and are more commonly seen in the periphery of the lesion. They can also be seen in trichotillomania. Inui et al (4) demonstrated tapering hair in 31.7% (95 out of 300) patients and in the study by Mane et al,(35) tapering hairs were seen in 12.1% (8 of 66) patients.
These are hair of normal length that taper at the proximal end but not at the distal end. These hairs can be easily made to kink when pushed inward and this property was termed as coudability, which means an elbow effect. The premature rapid transition from anagen to catagen causes hair shaft narrowing at the follicles, reflecting a common pathomechanism of coudability hairs and exclamation hairs. Coudability hairs represent an early change of alopecia areata. The coudability score is based on the number of coudability hair (0= no coudability hair; 1= 1-3 coudability hair; 2= 4-9 coudability hair; 3= 10 or more coudability hair). Coudability hairs correlated positively with alopecia areata disease activity, hair-pull tests, short disease duration, black dots and exclamation-mark hairs, but negatively with short vellus hairs.
These are considered as sites of targeted follicular destruction i.e. fibrosis which are seen in cicatricial alopecia and long standing alopecia areata.(38)
Inui et al (4) in their study identified 3 useful markers to assess the severity of alopecia areata on dermoscopy, viz, the black dots, yellow dots, and short vellus hairs. Previous reports have suggested that the severity of alopecia areata is an important prognostic factor. Therefore, dermoscopic examination of patches of alopecia areata may provide predictors of the response to therapy and can also be utilized for monitoring response to any prescribed regimen.
Inui et al (4) also stated that the disease activity in their study was defined by the global estimation of scalp hairs. Pathognomonic hairs, such as black dots, tapering hairs and broken hairs, were seen even in improving cases, and a significant correlation was found between pathognomonic features and disease activity. Thus, in order to monitor the relationship between dermoscopic findings and disease activity, it is worthwhile identifying the activity of each lesion and investigating the correlation between the dermoscopic findings and activity in each lesion.
There are numerous treatments for alopecia areata that can lead to hair regrowth but none of them can alter disease course. There are few randomized controlled trials for various treatment options and no long term treatment outcomes except for contact immunotherapy. Thus counselling of the patient and informing him about the course and prognosis is very helpful and support groups can be really beneficial for the patients.
These are the treatment of choice for adults with less than 50% scalp area involvement and the use of triamcinolone acetinoide is preferred. The use of intralesional corticosteroids in alopecia areata was first described in 1958 with the use of hydrocortisone.(39) Porter and Burton (40) have shown that hair regrowth is possible in 64% and 97% with triamicinolone acetinoide and triamcinolone hexacetonide respectively. Concentrations ranging from 2.5 to 10 mg/ml may be used but 5mg/ml is preferred on the scalp and 2.5mg/ml over the eyebrows and face, with a maximum volume of 3 ml. The maximum dose per session was suggested to be 20 mg of triamcinolone acetonide.(41) Every 4 weeks triamicinolone acetinoide is injected intradermally with a 0.5-in long 26-gauge needle as multiple 0.1-mL injections at 1-cm intervals in the patch.(42) Adverse effects include transient atrophy and telangiectasia. Anaphylactic reaction to intralesional corticosteroid injection has been reported due to carboxymethylcellulose, a dispersant in corticosteroid preparation (43) and also to triamcinolone acetonide per se.(44) If no improvement occurs after 6 months then treatment should be stopped. This reduced efficacy in some patients is postulated to be due to a decreased expression of thioredoxin reductase 1 in the outer root sheath of the hair follicles. (45)
Topical mid potent steroids are the treatment of choice in children. Folliculitis, atrophy and telangiectasia are the observed side effects.
Used in a concentration of 5%, mainly as an adjuvant treatment to conventional therapy. Besides the usual mechanisms of vasodilatation, angiogenesis, and enhanced cell proliferation leading to hair regrowth, another mechanism postulated is its immunosuppressive effects. Price et al showed hair regrowth in 63.6% and 35.7% in the treated and placebo groups, respectively.(46) Contact dermatitis and hypertrichosis (facial hair growth) have been the reported adverse effects.
Used in a concentration of 0.5% to 1% as short contact therapy daily for 20 to 30 minutes. The contact time is gradually increased until a low grade irritation develops, which is important for Anthralin to produce a response. It acts by decreasing the expression of tumor necrosis factor-alfa (TNF-Î±) and -beta (TNFÎ²) in the treated areas. If there is no response by 3 months the treatment should be stopped as patient is unlikely to respond beyond that. Irritation, folliculitis, regional lymphadenopathy and staining of skin and clothes are the reported adverse effects.(42)
Contact sensitizers that have been used in the treatment of alopecia areata include dinitrochlorobenzene (DNCB), squaric acid dibutylester (SADBE), and
diphenylcyclopropenone (DPCP). DNCB is not used today because it is mutagenic. The treatment of choice for adults for more than 50% of scalp area involvement is Dipenylcyclopropenone (DPCP). Initial sensitization is by 2% concentration followed by weekly application of the lowest concentration that can cause irritation recognized as low grade erythema or mild pruritus on the treated area. If patient does not develop an allergic reaction to 2% DPCP then SADBE can be tried. The treatment needs to be stopped if there is no response after 6 months. The successful outcome of about 50% to 60% is seen with DPCP.(42)
Adverse effects reported include vesicular and bullous reactions, cervical & occipital lymphadenopathy, facial and scalp edema, contact urticaria, flu-like symptoms, erythema multiforme like reactions, and pigmentary disturbances (hyperpigmentation, hypopigmentation, dyschromia in-confetti, and even vitiligo). The mechanism of actions includes antigenic competition, perifollicular lymphocytes apoptosis, and changes in the peribulbar CD4/CD8 lymphocyte ratio.
These have been used in various forms such as daily, weekly mini pulses and monthly high dose pulse. The success rate varies between 30%-60% and a relapse rate of 25% at the end of 3 months of stopping therapy.(47) The adverse effects observed are hyperglycemia, osteoporosis, cataracts, immunosuppression, obesity, dysmenorrhea, acne, and Cushing's syndrome.
Systemic and topical psoralen plus ultraviolet A light (PUVA) phototherapy have been used with response rates ranging from 15%-70% in various studies. A high incidence of relapse rate coupled with a risk of skin malignancies makes it a less favoured option.(42)
Use of 308nm eximer laser twice weekly for a maximum duration of 24 months has shown hair regrowth in about 41.5% of patches in a study. Poor results were achieved in AT/AU patients.
It has been used as an adjunct with variable success.
Other systemic therapies that have been used include: (42)
Biologics- etanercept, efalizumab, adalimumab and infliximab.
Prostaglandin F2Î± analogues like Latanoprost.
Other topical therapies that have been used include: (42)
Calcineurin inhibitors like tacrolimus and pimecrolimus.
Studies pertaining to intralesional steroids in alopecia areata
Although intralesional corticosteroids have been used in the treatment of alopecia areata for about 50 years, no randomized controlled trials have been published as yet.(48)
Porter and Burton (40) in 1971 recruited 17 patients and showed that hair regrowth is possible in 64% and 97% of patients with triamcinolone acetinoide and triamcinolone hexacetonide (less soluble derivative of triamicinolone acetinoide) respectively, in patients of alopecia areata. The concentration of triamcinolone used was 10 mg/ml and a single injection was given at baseline. The patients were observed for a period of 36 weeks. It was also seen that both steroids produced a constant linear rate of growth of hair tuft, and that the effect of a single injection can persist for at least 9 months.
Abell and Munro (6) in 1973 recruited 84 patients with alopecia areata of varying degree (subtotal) and used a needleless injector (Porto-Jet) containing triamcinolone acetinoide at a concentration of 5 mg/ml as the treatment modality. The patients were examined for hair growth at 6 and 12 weeks after completion of treatment. Their study showed that hair regrowth was possible in 71% of patients with subtotal alopecia areata treated by triamcinolone acetinoide injections, three times given at weekly or 2-weekly intervals, and in 7% of control subjects injected with isotonic saline.
Frentz (49) in 1977 serially treated two groups of patients with subtotal to universal alopecia areata, 6 with intralesional triamcinolone acetonide suspension and 6 with contact irradiation by ultraviolet light from a high-pressure mercury-arc source with a quartz envelope (Kromayer lamp). The treatment was limited to one half of the scalp while the untreated half served as a control. Triamcinolone acetonide suspension given in 2 of the 6 treated patients (33%) showed a temporary stimulating effect on hair growth but later, hair growth inhibition was noted in 3 patients.
In an uncontrolled study by Kubeyinje et al (50) in 1994 of 62 Saudi Arabs with alopecia areata on monthly intralesional injection of triamcinolone acetonide, showed complete regrowth in 40 (63%) patients at 4 months. Regrowth was likely in young adults with few lesions (less than 5 patches), lesions of short durations (less than 1 month) and patches less than 3 cm in diameter. Regrowth was poor when associated with atopy (2 patients) and Mongolism (1 patient). Side effects of treatment were minimal and the drug was well tolerated.
Ferrando and Moreno-Arias (51) in 2000 used mesotherapy multi-injection round plate with five or seven 27 gauge, 4 cm long needles with a fixed distance of 15 mm between each of them containing triamcinolone acetonide, paramethasone acetate or betamethasone (acetate or disodium phosphate). Post injection, the area was massaged to evenly spread the steroid solution and this avoided atrophy of injection site. Pain and bleeding which were easily controlled were the most common adverse effects of this study. All the patients treated (50 patients and more than 200 treatment sessions), reported it to be less painful than conventional insulin syringe based injections and no case of atrophy was reported on follow up.
Chang et al (52) in 2009 recruited ten patients with extensive alopecia areata (50-99% of scalp area involved). Six out of ten patients (60%) responded to treatment with intralesional triamcinolone acetonide. In comparison to the non-responders, the responders tended to have exclamation mark hairs and a positive hair pull test at their initial physical examination, and exhibited improvement during the initial months of treatment. Complications were negligible, with mild reversible atrophy in three patients. The treatment was well tolerated and, in some patients, pain was minimized by use of a topical anesthetic agent applied under occlusion prior to the visit. Thus the study concluded that intralesional triamcinolone acetonide is a safe and effective treatment for patients with extensive alopecia areata. Patients with exclamation point hairs and a positive hair pull test may be more likely to respond.
Kuldeep et al (53) in 2011 randomly allocated 78 patients with localized patchy alopecia areata (<3 patches ), in 3 groups as group A (28), group B (25) and group C (25) and 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 next 12 weeks. Hair regrowth was calculated using "HRG Scale"; Scale I- (0-25%), Scale II-(26-50%), Scale III - (51-75%) and Scale IV- (75-100%).
Hair re-growth started by 3 weeks in group B (Scale I: P<0.03). 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 tacrolimus. Thus the study concluded that intralesional triamcinolone acetonide is the best, and that betamethasone valerate foam is better than tacrolimus in management of localized alopecia areata.
Studies pertaining to topical steroids in alopecia areata
Tosti et al (54) in 2006 treated 34 patients with moderate to severe alopecia areata in a randomized double-blind trial using a new clobetasol propionate 0.05% foam. Clobetasol foam and the corresponding placebo foam were applied twice a day for 5 days/week for 12 weeks. From weeks 13 to 24 each enrolled patient continued only with the treatment (both on the right and left site) that was judged to have a greater efficacy than that on the contralateral side. The primary outcome of the trial, was the hair regrowth rate, which was evaluated using a semiquantitative score RGS (regrowth score from 0: no regrowth, to 4: regrowth of >75%). At baseline the AGS (alopecia grading score) was 4.1 (range: 2-5). At baseline the AGS (alopecia grading score) was 4.1 (range: 2-5). At the end of 12 weeks, a RGS of 2 (hair regrowth of more than 25%) was observed in 42%, RGS of 3 to 4 (hair regrowth of 50-75%) in 7 patients (20%) and a RGS of 4 (hair regrowth of >75%) in 3 patients (9%) was observed in clobetasol foam treated sites. At the end of 24 weeks, 47% patients had a RGS of 2 and 8 patients (25%) had a RGS of 3. Folliculitis occurred in two patients.
Mancuso et al (55) treated 61 patients with mild to moderate alopecia areata (hair loss < 26%) with betamethasone valerate foam (BVF) formulation and betamethasone dipropionate lotion (BDL). Both treatments were applied to the affected areas twice a day for 12 consecutive weeks. The primary study outcome was to compare the hair regrowth rate. Efficacy was evaluated at weeks 8 and 12 and at follow up (week 20), using a hair regrowth score (RGS) with a scale ranging from 0 (regrowth < 10%) to 4 (regrowth > 75%). At week 20, the RGS was 3.1 ±1.5 and 1.8 ±1.6 in the BVF and BDL groups, respectively (P< 0.01). A RGS > 3 was observed in 61% of patients in the BVF group (19/31) in comparison with 27% (8/30) in the BDL group (P< 0.03). No serious adverse events were observed in both groups during the study.
This was a hospital based interventional study done in all patients with alopecia areata subject to the inclusion and exclusion criteria who attended the Dermatology OPD of JIPMER, Puducherry from March 2011 to May 2012, after obtaining clearance from the institute ethics committee.
The study group consisted of 60 consenting patients of alopecia areata, satisfying the inclusion and exclusion criteria.
The inclusion criteria included
1. Alopecia areata of scalp.
2. Age > 10 years.
3. Duration of disease < 1 year.
4. 1 to 3 patches of alopecia areata
5. < 50% scalp area involved.
6. Should not be on any modality of therapy for atleast 2-4 weeks.
The exclusion criteria included
1. Children < 10 years.
2. Pregnant women.
3. Lactating women.
4. History of steroid allergy.
5. Immunocompromised patients.
6. Patients having bleeding diathesis.
7. Patients having active scalp inflammation.
8. Patients receiving systemic steroids.
9. Any patient not willing to take part in the study.
HISTORY & EXAMINATION: A detailed history was elicited pertaining to the following parameters - demographic parameters, age of onset, duration of disease and other associated symptoms, treatment history of use of topical or systemic immunosuppressant or any other drugs, history of similar complaints in family members and presence of any associated comorbid condition such as personal or family history of hypertension, diabetes mellitus, hypothyroidism, atopy, autoimmune and connective tissue disorders. A thorough clinical examination and dermoscopic evaluation was done and a diagnosis of alopecia areata of scalp was made. The pattern of alopecia, site, size and number of patches was noted. Any associated loss of body hair and nail changes were also recorded. The baseline assessment of alopecia grading was performed using a 6-point scale score called as alopecia grading scores (AGS)(54,55): S0 = No alopecia, S1 = hair loss < 10%, S2 = hair loss 11- 25%, S3 = hair loss 26 -50%, S4 = hair loss 51-75% and S5 = hair loss > 75%. The disease activity (4) of alopecia areata was estimated as follows: progressive alopecia areata, an increase in total hair loss of more than 5%; stable alopecia areata, a change in total hair loss of less than 5%; remitting alopecia areata, a decrease in total hair loss of more than 5% over the month prior to presentation.
PROCEDURE: The patients were selected based on the clinical examination and the inclusion and exclusion criteria. A baseline digital camera photograph of the patch and dermoscopic parameters at centre of patch and at 3 O' clock position were recorded which included black dots, yellow dots, vellus hair, broken hair, tapering hair and pigmented hair. The 3 O' clock position was defined as that seen from front when patch is anterior to vertex and that from behind when patch is posterior to the vertex. Heine DELTA 20® dermatoscope was used for the study. The dermoscopic parameters for each patch were counted in the centre of the patch and at one representative field in the periphery designated as 3 O' Clock position and their number documented and a total for each patch calculated as summation of readings at centre and periphery.
Triamcinolone acetonide was injected in a concentration of 5 mg/ml (maximum volume, 3ml) with a 0.5 inch long, 30-gauge needle, fitted to an insulin syringe, as multiple 0.1 ml injection, intradermally in the patch, at 1 cm intervals. Injections were repeated every 4 weeks. Patients were followed up at 4 weeks interval and the response to intralesional triamicinolone acetonide on the regrowth of terminal hair seen clinically, was evaluated by using a 5-point semiquantitative score, regrowth scale (RGS) (54,55)with the scale ranging from 0 Score (regrowth < 10%), 1 Score (regrowth 11-25%), 2 Score (regrowth 26 -50%), 3 Score (regrowth 51-75%), 4 Score (regrowth â‰¥ 75%). The dermoscopic readings at the centre of the patch and at 3 O' clock position were documented for a maximum of 6 months.(45) The changes in the various dermoscopic parameters were looked for assessing the response to the prescribed therapeutic regimen. The presence of thin and unpigmented vellus hair within the patch, and transformation of vellus hair into terminal hair, appearing as increased proximal shaft thickness and pigmentation, is characteristic of remitting disease and hence indicators of a response to treatment as are the decrease in the number of black dots, yellow dots, broken hair and tapering hair. (4)
An early age of onset was defined as onset â‰¤20 years of age.
A significant change in dermoscopic parameters was defined as â‰¥75% reduction in number from baseline occuring in the total number of the following dermoscopic parameters i.e. yellow dots, black dots, broken hair and tapering hair.
Maximum dermoscopic change was defined as 100% reduction in number from baseline occuring in the total number of the following dermoscopic parameters i.e. yellow dots, black dots, broken hair and tapering hair.
Maximum clinical improvement was defined as â‰¥75% terminal hair regrowth seen clinically, a RGS score of 4.
The study also involved early identification of patients that developed various adverse effects due intralesional triamcinolone acetonide injections and their documentation at the observed number of weeks after starting treatment was done.
STATISTICAL ANALYSIS: The data collected was tabulated in Microsoft Excel worksheet and computerized analysis was performed using SPSS 17.0 (SPSS, Chicago, IL, USA). A descriptive statistical analysis was carried out for presenting the dermoscopic parameters and socio-demographical parameters. The outcome variables (clinical response and dermoscopic parameters) were assessed and quantified in each time point (every 4th week for a follow up of maximum 6 months). For comparison of means, one way ANOVA was used. Chi-square test (Ï‡2 test) was used to evaluate the association of outcome variables with the socioeconomic and demographic factors. In cases where any one of the cell value was less than five, Fischer's exact test was used. Correlations between the incidence of each dermoscopic finding and the disease activity were analysed using the Spearman rank-order correlation coefficient by rank test. All statistical analyses were carried out at 95% confidence interval and the P value <0.05 was considered as significant.
Alopecia areata is a disease characterized by non-scarring hair loss on the scalp or any hair-bearing surface.(54) A wide range of clinical presentations can occur, from a single patch of hair loss to complete loss of hair on the scalp (alopecia totalis) or the entire body (alopecia universalis). Particularly in severe or chronic cases, alopecia areata may cause considerable psychological and emotional distress for affected individuals. Strong direct and indirect evidence supports an autoimmune aetiology for alopecia areata. T lymphocytes are predominantly present in the peribulbar inflammatory infiltrate and are presumed to play a role in hair loss. Alopecia areata frequently occurs in association with other autoimmune diseases, such as thyroiditis and vitiligo. Autoantibodies to follicular components have been detected. Various therapeutic agents have been developed for the treatment of alopecia areata, but none is curative or preventive.(42) The aim of alopecia areata treatment is to suppress the activity of disease. The various treatment modalities can be classified into topical and systemic therapies. The topical therapy includes intralesional corticosteroid, topical corticosteroid, minoxidil, anthralin and topical immunotherapy in the form of diphenylcyclopropenone (DPCP) and squaric acid dibutylester (SADBE). The systemic therapy includes systemic corticosteroids and photochemotherapy. Cyclosporine, methotrexate, sulphasalazine and biologics have been used with limited success.
Intralesional glucocorticoid injection is the most common therapy for limited scalp involvement. To evaluate the efficacy of intralesional triamcinolone acetonide in the treatment of alopecia areata we enrolled 60 patients, attending the outpatient clinic with alopecia areata satisfying the inclusion and exclusion criteria and to assess its local and systemic side effects and also used dermoscopy to identify signs of early clinical response and adverse effects to the chosen therapeutic regimen.
National guidelines from British Association of Dermatologists, recommend intralesional corticosteroid therapy as the first line treatment for localized patchy alopecia areata, with approximate success rates of 60-75%. The use of intralesional corticosteroids in alopecia areata was first described in 1958 with the use of hydrocortisone. Concentrations ranging from 2.5 to 10 mg/ml may be used but 5mg/ml is preferred on the scalp and 2.5mg/ml over the eyebrows and face, with a maximum volume of 3 ml. The maximum dose per session was suggested to be 20 mg of triamcinolone acetonide. Every 4 weeks triamicinolone acetinoide is injected intradermally with a 0.5 inch long 26-gauge needle as multiple 0.1-mL injections at 1 cm intervals in the patch.(42)
Porter and Burton (40) recruited 17 patients and showed that hair regrowth is possible in 64% and 97% of patients with triamcinolone acetinoide and triamcinolone hexacetonide respectively, in patients of alopecia areata. The concentration of triamcinolone used was 10 mg/ml and a single injection was given at baseline. The patients were observed for a period of 36 weeks. It was also seen that both steroids produced a constant linear rate of growth of hair tuft, and that the effect of a single injection can persist for at least 9 months.
Abell and Munro (6) recruited 84 patients with alopecia areata of varying degree (subtotal) and used a needleless injector (Porto-Jet) containing triamcinolone acetinoide at a concentration of 5 mg/ml as the treatment modality. The patients were examined for hair growth at 6 and 12 weeks after completion of treatment. Their study showed that hair regrowth was possible in 71% of patients with subtotal alopecia areata treated by triamcinolone acetinoide injections, three injections given at weekly or 2-weekly intervals, and in 7% of control subjects injected with isotonic saline.
In an uncontrolled study by Kubeyinje et al (50) in 1994 of 62 Saudi Arabs with alopecia areata on monthly intralesional injection of triamcinolone acetonide, showed complete regrowth in 63% patients at 4 months. Regrowth was likely in young adults with few lesions (less than 5 patches), lesions of short durations (less than 1 month) and patches less than 3 cm in diameter. Regrowth was poor when associated with atopy (2 patients) and Mongolism (1 patient). Side effects of treatment were minimal and the drug was well tolerated.
Ferrando et al (51) used mesotherapy multi-injection round plate with five or seven 27 gauge, 4 cm long needles with a fixed distance of 15 mm between each of them containing triamcinolone acetonide, paramethasone acetate or betamethasone (acetate or disodium phosphate). Post injection, the area was massaged to evenly spread the steroid solution and this avoided atrophy of injection site. Pain and bleeding which were easily controlled were the most common adverse effects of this study. All the patients treated (50 patients and more than 200 treatment sessions), reported it to be less painful than conventional insulin syringe based injections and no case of atrophy was reported on follow up.
Chang et al (52) recruited 10 patients with extensive alopecia areata (50-99% of scalp area involved). Sixty percent patients responded to treatment with intralesional triamcinolone acetonide. Mild, reversible atrophy was seen in three patients. The study concluded that intralesional triamcinolone acetonide is a safe and effective treatment for patients with extensive alopecia areata and that the patients with exclamation point hairs and a positive hair pull test may be more likely to respond.
Kuldeep et al (53) randomly allocated 78 patients with localized patchy alopecia areata (<3 patches ), in 3 groups as group A (28), group B (25) and group C (25) and were prescribed topical betamethasone valerate foam twice daily, intralesional triamcinolone acetonide (10mg/ml) every 3 weeks and topical tacrolimus ointment 0.1% twice daily respectively for 12 weeks. They were followed for next 12 weeks. Hair regrowth started by 3 weeks in the intralesional triamcinolone acetonide group. At the end of 12 weeks follow up hair regrowth (>75%) was the best in the intralesional triamcinolone acetonide group (60%), followed by group A (53.6%) and lastly group C (0%) patients. Few patients reported mild pain and atrophy at injection sites. The study concluded that intralesional triamcinolone acetonide is the best, and that betamethasone valerate foam is better than tacrolimus in management of localized alopecia areata.
In our study, a total of 65 patients were recruited. Out of these 5 patients were lost to follow up and were excluded from the study. In the remaining 60 patients, a total of 70 patches (fifty one patients had one patch, only 8 patients had 2 patches and one patient had 3 patches) were treated with injections of intralesional triamcinolone acetonide in a concentration of 5 mg/ml at 4 weeks interval, till the patients achieved a RGS of 4. They were followed up once in 4 weeks for duration of 24 weeks. According to the surface area of scalp involved, 59 patients had S1 (<25% of scalp area involved) and a single patient had S2 (25-50% of scalp area involved). At baseline the mean alopecia grading score was 1.34 (ranging from 1 to 3 with a median of 1 and a S.D. of ±0.562). At the end of 4 weeks, the mean RGS was 0.97 ±1.02 which is nearly a regrowth of 11-25%. The mean RGS increased to 2.24 ± 1.08 at the end of 8 weeks which is nearly a regrowth of 26-50%. By the end of 12 weeks the mean RGS was 3.13 which is nearly a regrowth of 50-75%. Beyond 12 weeks there was a small rise in the mean RGS till it reached 24 weeks when it became 3.91± 0.28 which is nearly a regrowth of 75-100%.
At 4th week, 3 patients (5%) showed nearly complete recovery with a RGS of 4 (regrowth â‰¥ 75%) and hence received only a single intralesional triamicinolone injection and completed the study. By the end of 12th week, 28 patients (47%) showed nearly complete recovery with a RGS of 4 (regrowth â‰¥ 75%). At the end of the study period of 24 weeks, 57 patients (95%) of the patients showed nearly complete recovery with a RGS of 4 (regrowth â‰¥ 75%).
Most of the studies have been done with alopecia areata of subtotal to universal(6,51,52) severity. In our study we chose patients with minimal scalp surface area involvement mainly to assess the response to the patches dermoscopically along with assessing the response clinically. Thus our study population included 49 cases (85%) with hair loss <10% of scalp area. Only a single patient (1.7%) had hair loss >25% of scal
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