the alopecias diagnosis and treatments: part 2

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10 Traumatic alopecia Pierre Bouhanna Traumatic alopecia is a hair loss essentially caused by physical trauma. Schematically there are three possible etiologies for these alopecia1: • Trichotillomania is a traction alopecia due to a compulsive disorder. Patients pull on and pluck hairs, often resulting in bizarre patterns of alopecia. In trichotillomania, the patient, with psychological disorders, will manipulate his or her hair, unconsciously or deliberately, but repeatedly, to cause more or less severe baldness. • Cosmetic alopecia is caused by the excessively strong or aggressive care and handling of hair. • Traumatic accident alopecia is easy to diagnosis. TRICHOTILLOMANIA Psychopathological aspects Trichotillomania is a tic of hair removal that occurs most often in boys under 6 years and in girls over 6 years (Figure 10.2).2–4 The most severe cases occur in women between adolescence and 40 years (Figure 10.3); in these instances, the psychological disorders are major. We will not deal here with some hair dysplasias (see Chapter 4) that are responsible for brittle hair or occipital alopecia in newborn children, which present at areas of friction (Figure 10.1). Figure 10.2 Trichotillomania in a 2-year-old child. Figure 10.1 Occipital alopecia of the newborn child. Figure 10.3 Circumscribed alopecia caused by trichotillomania located at the left half of the scalp in a young woman. (Note the angle and the rectilinear border.) 91 t he a lo pec ia s Figure 10.4 Circumscribed alopecia caused by trichotillomania located at the vertex in a young adult. (Note the angle and the rectilinear border.) Figure 10.5 Circumscribed alopecia caused by trichotillomania located at the vertex in an elderly woman. (Note the geometric contours.) Clinical aspects Alopecia appears as an area with a clear boundary (Figure 10.4). The skin surface is normal and nonsquamous. The manipulated hairs are broken at different lengths. The parietal region is the most frequently affected. In adults, the area of alopecia is often extensive, with short broken hairs. It can be localized to the vertex (Figure 10.5), appear unilaterally in the fronto-parietal– occipital region (Figures 10.3 and 10.6) or, exceptionally, be seen on the entire scalp. Tics of removing eyelashes, eyebrows, or other body hair (pubic or perianal) are exceptional. Diagnosis Histological aspects: The most constant element is that many hair orifices are empty. In addition, telogen hairs are absent or very few. Biopsy specimens from acute lesions of trichotillomania may demonstrate perifollicular hemorrhage and fractured fibers. Later stages of trichotillomania characteristically demonstrate the presence of normal follicles surrounded by empty follicles in a noninflammatory dermis. Numerous catagen follicles (characterized by numerous apoptotic cells and a wavy surrounding vitreous membrane) and pigment casts within the upper segments of the follicle may be noted. Trichoscopy5,6 (Figure 10.7) is useful to confirm the evidence of pulling. The scalp presents short, coiled, 92 Figure 10.6 Trichotillomania located in the parietaloccipital region in a 14-year-old boy. (Note the rectilinear or angular and geometric contours.) fractured hairs. The broken hair shafts show longitudinal splitting (see Chapter 3). Trichograms (1) show the almost exclusive presence of normal anagen hair (see Chapter 2). Differential diagnosis In children, a patch caused in trichotillomania may be confused with ringworm or alopecia areata. t r au mat ic a l opec ia Figure 10.7 Trichotillomania with erosion, black spots, hairs in “tulip” and hairs in “V.” (Courtesy of Dr. Y. Bourezane.) With ringworm, the skin surface is rough. Infected hair is recognized on examination by Wood lamp and by microscopic examination. In the case of alopecia areata, the presence of alopecia hair in “exclamation marks” is particularly evocative. Hair regrowth is fluffy and often clear or white, at first. In addition, abnormalities deriving from dystrophy of hair bulbs are visible on a trichogram. The major forms of trichotillomania in adults should be differentiated with a careful clinical examination and a trichogram from androgenetic alopecia localized to the vertex and which can be associated (Figure 10.8). Prognosis and treatment In children, the tic hair removal is almost always favorably resolved after raising the issues in the presence of the parents. In long-term cases of trichotillomania, permanent alopecia may occur. The prognosis is more difficult in the extended forms found in the adult (Figures 10.3 and 10.5), in that they deny they are responsible for the act and often refuse psychotherapy as a solution. COSMETIC ALOPECIA The requirements attributed to ethnic or religious customs or the social pressure exercised by fashion cause a variety of hair damage.7,8 Their diversity is directly proportional to the imaginative intensity of each individual (Figures 10.9a and b, 10.10a and b). Pathogenesis The pathogenesis of alopecia cosmetics may be attributed to Figure 10.8 Female androgenetic alopecia and traction alopecia. (Note the linear straight border.) • Breakage of hair secondary to manipulation of hair shafts, which have sometimes been weakened by chemical applications. • Repeated traction at the shaft o stiffen it. • Scarring alopecia induced by repeated pulling with preexisting inflammatory follicular lesions.9 Clinical aspects The essential elements of frontal traction alopecia are the presence of short broken hair, folliculitis lesions, and some small scar patches located on the frontotemporal edge (Figure 10.11). This clinical form often affects women making a tightly pulled “bun,” a “ponytail,” or even one or two big braids (Figure 10.9a and b). Note also that parietal bald patches are often observed in nurses due to traction on the hair by clips that keep their cap in place (Figure 10.12). The differential diagnosis is postmenopausal frontal fibrosing alopecia. • Alopecia due to the rollers. This process, used to “curl” hair deemed too stiff, causes bald patches surrounded by broken hair and a rash if used regularly or too frequently. • Alopecia due to wearing wigs braided to the remaining hair or attached by clips (Figure 10.13a 93 t he a lo pec ia s (a) (b) Figure 10.9 (a,b) Alopecia from frontotemporal traction occurring in women who regularly braid their hair. and b). The clinical aspect of alopecia secondary to wearing a hairpiece is similar to that described above. • Alopecia due to strong and repeated brushing. It will cause, among black patients whose hair is naturally weak (see Chapter 12), a recession of the frontotemporal line. (a) • Alopecia due to the use of straightening irons. Heat trauma causes a scarring alopecia gradually extending toward the vertex (Figure 10.14). • Alopecia due to repeated friction or massage. Massage or excessive and repeated friction can cause alopecia, such as repeated rubbing of the arms of glasses (Figure 10.15). (b) Figure 10.10 (a) Traumatic alopecia after the break dance practice, (b) the break dance. 94 t r au mat ic a l opec ia (a) (b) Figure 10.11 Frontotemporal alopecia after repeated hair straightening in a black patient. (Note the excess growth of vellus above the eyebrow after applying minoxidil lotion 2%.) Differential diagnosis The diagnosis is easily established by the results of a precise clinical examination, a trichoscopy examination, a trichogram evaluation, and eventually a biopsy. Figure 10.13 (a) Alopecia caused by traction from clips holding the hair in place. (b) Example of a small metal cylinder used to secure a prosthesis. Treatment The treatment is obviously related to the removal of the cause and prescription of cosmetic products (such as cream Figure 10.12 Temporoparietal alopecia in a woman after regularly wearing a cap. Figure 10.14 Almost complete scarring alopecia in a black woman who had been using hot hair-straightening irons for many years. 95 t he a lo pec ia s with karite) to decrease the possible underlying fragility of the hair shaft. It is not proved that the prescription of topical minoxidil encourages some regrowth because nearly all the hairs are in anagen phase, and it may increase the growth of vellus on the face of the female patient. TRAUMATIC ACCIDENT ALOPECIA Some traumatic accidents can cause nonscarring alopecia, for which the diagnosis of cause can be difficult; it is, most often, ischemia caused by prolonged or repeated compression of part of the scalp (Figure 10.15).7 This can occur, for example, from compression by forceps during childbirth (Figure 10.16) or during compression by repeated and prolonged wearing of a cap or orthodontic headgear (a head cap) by a child. (a) Figure 10.15 Temporal alopecia due to repeated rubbing and compression of the glasses arms. (b) Figure 10.16 Adult male patient with an occipital alopecia post-forceps. 96 Figure 10.17 (a) African patient after scalp burning with caustic soda. (b) Spontaneous healing without treatment. t r au mat ic a l opec ia TRAUMATIC THERMAL, CHEMICAL, AND ISCHEMIC ALOPECIA A variety of chemical (corrosive) and physical agents can cause permanent alopecia of the scalp. In general, any thermal, physical, or chemical injury sufficient to cause scalp necrosis can produce a permanent alopecia. In the acute stage, necrosis with crusting, an adherent eschar, or ulceration may be present (Figure 10.17a and b). Later, the scalp heals by reparative fibrosis. The result is usually an atrophic alopecic patch. Ischemic necrosis of the scalp produces a similar clinical picture. Ischemic scalp necrosis may be seen after prolonged anesthesia. The necrosis generally involves the occipital scalp and represents a pressure phenomenon. Ischemic necrosis may also occur as a result of vasoconstriction related to the infusion of pharmacologic agents such as vasopressin. RADIATION Radiation injury may cause transient nonscarring alopecia (epilating dose). Higher doses9 produce permanent alopecia with scarring. Histological changes in anagen (a) (b) Figure 10.18 (a) Bitemporal cicatricial alopecia after radiotherapy for brain tumor, and (b) correction after one hair transplant session. 97 t he a lo pec ia s hair follicles can be noted as early as 4 days following radiation. Similar effects are noted with x-rays and electron beam radiation. The earliest change is thinning of the hair bulb, especially in the area of the matrix. Two or 3 weeks following irradiation, hairs with tapered shafts are apparent. The number of follicles showing radiation effects is roughly proportional to the dose of radiation. The definitive treatment is the scar excision or, better, a hair transplant restoration (Figure 10.18a and b). CONCLUSION Traction alopecia and trichotillomania are types of physical trauma that can lead to alopecia. Traction alopecia is seen most commonly in black females. Trichotillomania is a traction alopecia related to a compulsive disorder. In the long term, permanent alopecia may occur. REFERENCES 1. Rook A, Dawber R. Diseases of the Hair and Scalp. Oxford, UK: Blackwell Scientific P blications; 1982. 98 2. Camacho F, Montagna W. Trichologie-maladies du follicule pilosébacé. Madrid, Spain: Grupo Aula Médica SA; 1997. 3. Olsen EA. Disorders of Hair Growth—Diagnosis and Treatment. New York, NY: McGraw-Hill; 1997. 4. Bouhanna P. Alopécies traumatiques. In: Bouhanna P, Reygagne P, ed. Pathologie du cheveu et du cuir chevelu. Paris, France: Masson; 1999:145–152. 5. Tosti A, Miteva M, Torres F, Vincenzi C, Romanelli P. Hair casts are a dermoscopic clue for the diagnosis of traction alopecia. Br J Dermatol. 2010;163:1353–1355. 6. Tosti A. Dermascopy of Hair and Scalp Disorders. London: Informa Healthcare; 2007. 7. Bouhanna P. Les alopécies traumatiques, une triple orientation diagnostique. In: Bouhanna P, ed. Les alopécies—de la clinique au traitement. Collection Guide Pratique de Dermatologie. Paris, France: Med’Com;2004. 8. Ferrando J. Alopecias: Guia de diagnostico y tratamiento. Barcelona, Spain: Pulso; 2000. 9. Camacho FM, Tosti A. Montagna tercera Edicion— Tricologia Enfermedades del foliculo pilosabaceo. Madrid, Spain: Biblioteca Aula Medica Editions; 2014. 11 Management of acquired primary cicatricial alopecia Salvador Villablanca and Juan Ferrando INTRODUCTION Human hair involves aspects of self-image, identity, ­ethnicity, and health, among other attributes. This is why it is no surprise that diseases that cause alopecia can cause altered self-perception and psychosocial interactions.1 Alopecia can be classified as cicatricial (or scarring) and noncicatricial. In turn, cicatricial alopecia (CA) is subdivided into primary cicatricial alopecia (PCA) and secondary cicatricial alopecia (SCA). The PCAs represent a rare and heterogeneous group of diseases, clinically characterized by the absence of follicular ostium and histologically by the replacement of hair follicle structures by fibrous tissue making the alopecia irreversible. From a physiopathological point of view, the scar is the end point of reparative fibrosis with permanent destruction of the preexisting tissue.2–4 In PCA the hair follicle is the main target of the inflammatory process, as evidenced microscopically as a preferential destruction of follicular epithelium and/or adventitial dermis associated with relative preservation of interfollicular reticular dermis.5,6 In secondary CA, the destruction of the hair follicle is not the primary pathological event. It results from nonfollicular damage that eventually destroys the follicle. In these cases, the permanent follicular scarring develops when the involved pathological process is close to the follicular unit. Exogenous factors such as trauma (burns, radiation, and traction) and infiltrative and inflammatory endogenous processes (sarcoidosis, pemphigus vulgaris, and scleroderma) may result in secondary scarring alopecia 2,4,7 (Table 11.1). Primary CA may become a true clinical challenge due to the limited knowledge of the natural history of the disease. Many do not have a known cause. Clinical findings often have limited useful data for the diagnosis, because of overlapping findings and lack of specific signs. This sometimes makes it difficult to distinguish between the different conditions. Also, the clinical and histological characteristics can change over time, finally resulting in most cases in hair replacement with scarring tissue. EPIDEMIOLOGY The epidemiology of PCA in the general population is unknown. Two retrospective studies in hair research institutions estimated prevalence between 3.2% and 7.3%.2,3 In a recent survey performed in the United Kingdom, the estimated incidence of PCA was 6.96 per 1000 new general dermatology referrals per year, which is equivalent to about 9.6 new cases per clinician per year.8 The ratio between PCA and SCA is estimated at 1:15, and the ratio between neutrophilic and lymphocytic PCA is 1:4.3 Between 30% and 40% of patients with PCA in a hair research institution are cataloged as pseudopelade (or Table 11.1 Causes of Secondary Cicatricial Alopecia Physical/ chemical agents • Chemical burns • Insect bites • Mechanical trauma, traction, compression or laceration • Radiation dermatitis • Thermal burns Dermal granulomatous infiltrations (infectious origin) • • • • • Fungic infections Protozoa Tuberculosis Syphilis Viral infections Dermal granulomatous infiltrations (noninfectious) • • • • Necrobiosis lipoidica Sarcoidosis Amyloidosis Actinic granuloma Sclerosing disorders • • • • Lichen sclerosus et atrophicus Morphea Scleroderma Sclerotic porphyria cutanea tarda Neoplastic infiltrations • • • • • • • • Basal cell carcinoma Squamous cell carcinoma Dermatofibrosarcoma protuberans Lymphoma Malignant melanoma Metastasic carcinoma Adnexal Tumor etc. Inherited and congenital disorders • Aplasia cutis, eccrine hamartoma, incontinencia pigmenti, keratosis pilaris spinulosa decalvans, neurofibromatosis, chondrodysplasia punctata, polyostotic fibrous dysplasia, cutis verticis gyrata, Darier disease, epidermal nevi, epidermolisis bullosa, hair follicle hamartoma, hypotrichosis congenita, ichthyosis (sex-linked recessive), porokeratosis of Mibelli 99 t he a lo pec ia s nonspecific cicatricial alopecia).2 This means that onethird of cases have no specific diagnosis, becoming a true diagnostic and therapeutic “desert” for both dermatologists and patients. The diagnosis of PCA is not a purely academic exercise, because early treatment of the inflammatory component may prevent the progression of primary scarring alopecia, and the secondary fibrosis that gives the alopecia its irreversibility. Within the PCA with predominantly lymphocytic infiltrate, the most frequent condition varies depending on the different series. First and second places in frequency are always disputed between lichen planopilaris (and its variants) and cutaneous discoid lupus erythematosus, followed by pseudopelade of Brocq (PB).2,3,9 This difference may be influenced by a discrepancy in the clinicopathological diagnostic criteria between authors, especially in regard to the classical PB (an entity in constant discussion). Among the causes of PCA with an initially neutrophilic infiltrate, we should consider folliculitis decalvans (FD) as the most common form (10% of al PCA), unlike perifolliculitis abscedens et suffodiens capitis (less than 5% of PCA).10 ETHIOLOGY There is a paucity of data in the literature regarding the origin of PCA. In most of the literature, histopathology revealed the presence of inflammation affecting the upper portion of the hair, which would explain the irreversibility of the process, because at this location, stem cells are housed. This place called the protuberance or bulge is located in the infundibulum, where the hair erector muscle inserts. In some situations, the trigger of this inflammatory response is the result of an antigenic stimulation of Langerhans cells that are located in the pilosebaceous unit. Examples of a possible antigenic stimuli would be ultraviolet radiation in the case of lupus erythematosus, certain medications in the case of lichen planopilaris, and Staphylococcus aureus in the case of folliculitis decalvans. With the new knowledge in respect to its origin, it is known that there is a loss of immune protection of bulge stem cells,5,11 a dysfunction in the ability of self-perpetuation of stem cells, increased autoimmune activity enhanced by pro-inflammatory cytokines, and predisposing genetic and environmental factors.12–14 Recent data also suggest association with an altered lipid metabolism and development of the PCA, where a sebaceous gland dysfunction could play an important role in their pathogenesis. Independent of the initial event, the obliteration or permanent functional impairment of the critical elements for the reconstitution of the follicle results in permanent alopecia.15–19 CLASSIFICATION Currently there are several classifications for PCA, but the most accepted is the one proposed by the North American Hair Research Society (NAHRS).20 This classification divides the PCA into two groups according to the 100 Table 11.2 Proposed NAHRS Working Classification of Primary Cicatricial Alopecia Lymphocytic Neutrophilic Mixed Chronic cutaneous lupus erythematosus Lichen planopilaris Classic lichen planus Frontal fibrosing alopecia Graham-Little syndrome Classic pseudopelade (Brocq) Central centrifugal cicatricial alopecia Alopecia mucinosa, Keratosis follicularis spinulosa decalvans Folliculitis decalvans Dissecting cellulitis/folliculitis (perifolliculitis capitis abscedens et suffodiens) Folliculitis (acne) keloidalis Folliculitis (acne) necrotica Erosive pustular dermatosis Nonspecifi Source: Adapted from Tan E, Martinka M, Ball N et al., J Am Acad Dermatol. 2004;50:25–32. type of predominant inflammatory cell infiltrate (lymphocytic and neutrophilic), a concept that had been previously suggested by other authors, but was improved by this working group, adding two more subgroups: mixed and nonspecific (Table 11.2). Although there have been debates about whether this classification is satisfactory, it gives us a practical and reasonable view for basic and clinical research. CLINICAL PATTERNS OF PRESENTATION There is a big clinical and histopathological overlap between different entities of PCA. There are some forms of PCA whose existence per se is discussed, and among them is the pseudopelade of Brocq. In daily practice we observe two major clinical patterns of presentations of scarring alopecia, the first correspond to patients with multiple irregular patches of scarring alopecia (Figure 11.1) on the scalp, and the second pattern correspond to patients with a central patch (Figure 11.2) surrounded by several smaller patches of scarring alopecia (“cicatricial satellitosis”). Both types of clinical presentations are final stages of cutaneous processes that previously had affected hair follicles (evi­ denced or not), finishing with these residual and non­ specific features that do not allow us to elucidate the etio­pathogenic origin of it. We call these two classic patterns of scarring alopecia presentation a “footprints in the snow” pattern for the first and “big patch” pattern for the second. If we look at other forms of clinical presentation of scarring alopecia, there are other characteristic patterns that could be called specific patterns: marginal pattern (frontal fibrosing alopecia, and tractional alopecia),
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