Hair Loss: Principles of Diagnosis and Management of Alopecia
Hair Loss: Principles of Diagnosis and Management of Alopecia Jerry Shapiro, FRCPC Clinical Professor and Director of the UBC Hair Research and Treatment Centre Division of Dermatology University of British Columbia Vancouver Canada
Martin Dunitz
© 2002 Martin Dunitz Ltd, a member of the Taylor & Francis group First published in the United Kingdom in 2002 by Martin Dunitz Ltd, The Livery House, 7–9 Pratt Street, London NW1 0AE Tel: +44 (0) 20 7482 2202 Fax: +44 (0) 20 7267 0159 E-mail:
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Contents
Foreword Acknowledgements 1
2
3
Assessment of the patient with alopecia Alopecia areata: Pathogenesis, clinical features, diagnosis and practical management Androgenetic alopecia: Pathogenesis, clinical features and practical medical treatment
vii
4
Surgical management of androgenetic alopecia
121
5
Drug-induced alopecia
135
6
Telogen effluvium: acute and chronic
147
Cicatricial (scarring) alopecia
155
ix
1
7 19
Index
83
175
Foreword
Jerry Shapiro is a dedicated clinician/scientist who has devoted himself to all aspects pertaining to the hair follicle. He has written a unique text that will be invaluable for clinicians, researchers, and students of the hair follicle. This is an organized and rational guide for assessing and managing hair loss, which is set apart from others by the blending of rich clinical detail with the latest investigative research and theories of pathogenesis, all extensively referenced. It is a practical and personal approach that reflects Dr Shapiro’s long experience with hair problems both in the clinic and in the laboratory. His explicit recommendations about management are given, and where appropriate, he also includes the treatment
preferences of other hair experts. Complex issues are presented, such as immunological factors in alopecia areata, in clear terms for all readers. The illustrations are extensive, a collection of unique photographs and photomicrographs from his own collection. The text is exceptionally readable and complements the book’s systematic and inviting organization. Jerry Shapiro has accomplished an amazing single-authored, comprehensive text about hair that enriches the reader from bench to bedside. Vera H Price MD, FRCPC Professor of Clinical Dermatology School of Medicine University of California, San Francisco
Acknowledgements
There are certainly many individuals to thank in the making of this book. First and foremost, I am most indebted to my hair loss patients who have trusted me and given me the privilege of taking care of their hair. It continues to be an honor for me and I thank them for this. Next, I would like to thank certain individuals who have played an important part in my career. Dr Harvey Lui, who has, and continues to guide and nurture me in the field of dermatology. Dr William Stewart, who was the first individual to encourage me to take on the field of hair. Dr David McLean, whose advice, support and encouragement helped the University of British Columbia Hair Research and Treatment Centre flourish. Dr Vera Price, who has been my ‘’hair’’ mentor for over 15 years and has been an inspiration and role model. Dr Wilma Bergfeld, who allowed me to learn from her in Cleveland and from whom I continue to learn. My Hair Fellows: Dr Chantal Bolduc, Dr Shabnam Madani and Dr Olga Bernardo, who took time out of their busy lives to commit a year to studying hair with me. Each fellow has questioned, challenged and inspired me to learn so much more; they truly are very special people. My research associate, Dr Liren Tang, who continues to teach me the molecu-
lar biology and basic science of hair. Drs Magda Martinka and David Shum, who continue to enlighten me regarding the histopathology of the hair follicle. Nina MacDonald, my first Hair Clinic nurse, who was dedicated and helped shape the University of British Columbia Hair Clinic during its early years. Lucianna Zanet, my Hair Transplant nurse, who has guided me for the last 10 years with all her great surgical skills and great common sense approach to patients. I thank my editors, Charlotte Mossop and Robert Peden, whose time and efforts were absolutely essential in making this book possible. I would like to thank the University of British Columbia’s Division of Dermatology and the Vancouver General Hospital Skin Care Centre for providing the environment for me to work in the field of hair. I also would like to especially thank my family and friends who stood back and allowed me to take the weekends and evenings to finally accomplish this endeavor. Jerry Shapiro University of British Columbia Hair Research and Treatment Centre
1 Assessment of the patient with alopecia
Hair loss (alopecia) is a very common patient problem and often a significant source of patient distress. An accurate diagnosis can frequently be difficult. A rational, organized approach is crucial, as therapy is dictated by the appropriate diagnosis.1 The first task of the physician is to address the patients’ concerns fully, exploring the impact of alopecia on psychosocial well-being. Next, an organized diagnostic approach can assist the physician in the recognition of the characteristic differential features of each disorder and help to identify the cause of alopecia and guide therapeutic direction. Ancillary laboratory evaluation may sometimes be necessary to help confirm a diagnosis. Patients are most appreciative of a supportive diagnostic approach.
The hair follicle is divided into 4 parts: (Figures 1.1 and 1.2) 1. Bulb: consisting of dermal papilla and matrix intermixed with melanocytes (Figure 1.3) 2. Suprabulbar area from matrix to insertion of arrector pili muscle 3. Isthmus extending from insertion of arrector pili muscle to sebaceous gland 4. Infundibulum extending from sebaceous gland to the follicular orifice.
Basic trichologic anatomy and physiology In order to appreciate an organized diagnostic protocol for alopecia, it is important to review the basics of hair anatomy and physiology of the scalp. Knowledge of the hair cycle is essential in understanding the patho-physiology of hair diseases and the mechanism of action of the present therapeutic agents used to modulate hair growth.
Figure 1.1 Diagrammatic representation of hair anatomy: The hair follicle is divided into 4 parts: bulb, suprabulbar area, isthmus, and infundibulum.
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Hair Loss: principles of diagnosis and management of alopecia
Figure 1.2 (a) Histology of the hair follicle on longitudinal section showing dermal papilla (DP), matrix (M), inner root sheath (IRS), outer root sheath (ORS) and fibrous root sheath (FRS). (b) Two anagen follicles side by side at the level of fat. Note the melanocytes within the matrix providing pigment to the hair. (Courtesy of Dr Magdalena Martinka and Dr David Shum.)
The lower portion of the hair follicle consists of five major portions (1) dermal papilla; (2) matrix; (3) the hair shaft, consisting from inward to outward of medulla, cortex, and cuticle; (4) inner root sheath, consisting of inner root sheath cuticle, Huxley’s layer on the inside and Henle’s layer on the outside; and (5) the outer root sheath.
The base of the follicle is invaginated by the dermal papilla, which contains highly vascularized connective tissue (Figure 1.4). Dermal papilla fibroblasts are inherently different from non-follicular dermal fibroblasts. There is a large amount of acid-mucopolysaccharides within the dermal papilla, staining positively for Alcian blue and metachromatically for
Assessment of the patient with alopecia
3
Figure 1.3 (a) Close-up of longitudinal section of dermal papilla (DP), which is an invagination of the dermis into the matrix (M). The DP allows capillaries to gain entrance to the cells of the matrix. It is the signal transduction and communication between the DP and the matrix that determines how long a hair will grow and how thick a shaft will be produced. Melanocytes fill the matrix and produce the pigment of the hair. (b) Cross-section of the follicle at the level of the dermal papilla. (Courtesy of Dr Magdalena Martinka.)
toluidine blue. The ground substance consists of not only non-sulfated polysaccharides such as hyaluronic acid, but also sulfated mucopolysaccharides such as chondroitin sulfate. Alkaline phosphatase activity is also increased in the anagen phase. In persons with dark hair large amounts of melanin can be seen in the dermal hair papilla. The hair matrix has large vesicular nuclei and deeply basophilic cytoplasm. Dopa-positive melanocytes are interspersed between the basal cells of the matrix lying on top of the dermal papilla (Figures 1.2 and 1.3). Melanin, varying in quantity in accordance with the color of the hair, is produced in these melanocytes and incorporated into the future cells of the hair through phagocytosis of the distal portion of the dendritic melanocyte. Cells of the hair matrix differentiate into six different types of cells, each of which
Figure 1.4 The different layers of the hair follicle
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Hair Loss: principles of diagnosis and management of alopecia
Figure 1.5 (a) Cross-section and (b) longtitudinal sections of the follicle at the suprabulbar level. In the central portion of the follicle the matrix (M) is forming cortex, which is surrounded by the cuticle. This is subsequently invested by the cuticle of the inner root sheath (IRS), Huxley’s layer with trichohyaline granules, and the already keratinized Henle’s layer.The outer root sheath (ORS), hyaline membrance and fibrous root sheath (FRS) surround the whole structure. (courtesy of Dr David Shum.) keratinizes at a different level. The outer layer of the inner root sheath (IRS), Henle’s layer, keratinizes first, establishing a firm coat around the soft central portions of the follicle. The two apposed cuticles covering the inside portion of the IRS and the outside of the hair keratinize next, followed by Huxley’s layer. The hair cortex then follows, and the medulla is last (Figure 1.4). The hair medulla appears amorphous because of its only partial keratinization. It may not always be present. The hair cortex cells during upward growth from the matrix cells keratinize gradually by losing their nuclei and become filled with keratin fibrils. No keratohyaline granules (as in keratinizing epidermis) or trichohyaline granules (as in inner root sheath) are formed
during keratinization. Keratin of the cortex is hard keratin, in contrast to the inner root sheath or epidermis, which is soft keratin. The hair cuticle located peripheral to the hair cortex consists of overlapping cells arranged like shingles and pointing upward with their peripheral portions. The cells of the hair cuticle are tightly interlocked with the cells of the inner root sheath cuticle, resulting in the firm attachment of the hair to its inner root sheath. The hair and the inner root sheath move in unison upward. The inner root sheath is composed of three layers (Figures 1.4 and 1.5). None of these layers contain melanin, and all keratinize with trichohyalin granule formation. These granules stain eosinophilic, in contrast to the basophilic keratohyalin granules of the epidermis. The cuticle of the IRS consists of one layer of flattened overlapping cells that
Assessment of the patient with alopecia
point downward in the direction of the hair bulb. Since the cells of the hair cuticle point upward, these two types of cells interlock tightly. Trichohyalin granules are few in the IRS cuticle. Huxley’s layer is two cell layers thick and develops numerous trichohyalin granules (Figure 1.5). Henle’s layer, only one cell layer thick, already shows numerous trichohyalin granules as it emerges from the matrix. Just before the isthmus the IRS becomes fully keratinized (Figure 1.6). However, at the level of the isthmus the IRS disintegrates. The cells of the IRS do not contribute to the emerging hair, but serve as a hard molding scaffold up to the arrector pili muscle. The outer root sheath (ORS) extends from the matrix cells to the entrance of the sebaceous duct, where it changes into surface epidermis. The ORS is thinnest at the level of the hair bulb, gradually increases in thickness, and is thickest in the middle portion of the hair follicle, the isthmus. In its lower portion, below the isthmus, it is covered by IRS and does not undergo keratinization. The ORS has plentiful vacuolated cytoplasm owing to its plentiful glycogen. The point of insertion of the arrector pili muscle is referred to as the bulge area, and is the likely location of the first primordial cells (stem cells) of the hair follicle.2–7 Stem cells from the bulge area likely migrate to other portions of the hair follicle and differentiate into its differing layers. The isthmus is the segment that extends from the arrector pili muscle to the sebaceous gland duct entrance. There is no inner root sheath here. The ORS undergoes trichilemmal keratinization, producing large homogeneous keratinized cells without the formation of keratohyaline granules. The upper portion of the follicle above the entrance of the sebaceous duct is the infundibulum. It is lined by surface epidermis
5
Figure 1.6 Cross-section of the follicle just beneath the isthmus showing the eosinophilic completely keratinized inner root sheath (IRS) enclosing the hair shaft (HS). All of this is surrounded by outer root sheath, hyaline membrane and fibrous root sheath. Only anagen hairs have inner root sheaths. (Courtesy of Dr David Shum.)
undergoing keratinization with the formation of keratohyaline granules. The glassy or vitreous layer, which forms a homogeneous eosinophilic zone peripheral to the outer root sheath, is periodic acid Schiff-positive and diastase-resistant. It differs from usual basement membrane zone by being thicker. It is thickest around the lower third of the hair follicle. Peripheral to this vitreous layer lies the fibrous root sheath, which is composed of thick collagen bundles. This connective tissue sheath may contain considerable reproductive potential, as was recently shown by Reynolds et al.8 Melanosomes of the hair cortex are larger than those of the epidermis. They lie singly or within groups not within lysosomes. They are located usually in the interfibrillary matrix,
6
Hair Loss: principles of diagnosis and management of alopecia
within the cells, and only rarely in the intercellular space (Figure 1.7). Two types of melanin are present in mammalian hair, the black brown pigment eumelanin and the yellow red pheomelanin. Both are synthesized from tyrosine, which is converted to dopaquinone which can then undergo oxidative reactions to form either eumelanin or pheomelanin. In the eumelanin containing follicle, melanocytes contain ellipsoidal melanosomes with a lamellar internal structure (eumelanosomes) Pheomelanogenesis is associated with melanocyte-containing spherical melanosomes which have a less well defined internal structure containing granules or vesicles. In fire-red hair there are high levels of pheomelanosomes. In other hair colors, melanocytes have higher amounts of eumelanosomes. Dark hair contains more eumelanin and blond hair more pheomelanin. In white hair, melanocytes at the basal layer of the hair matrix are usually reduced in number or are absent. Melanocytes show degenerative changes, especially of melanosomes. The hair shafts only contain the detritus of melanin or no melanin at all. Unlike animals, where hair cycling is synchronous, on the human scalp there is an asynchronous mixture of hairs actively growing and resting. During the hair cycle, the middle and upper portions of the hair follicle are the permanent segment of the hair follicle, while the lower portion is non-permanent. (Figure 1.8). The growing or anagen hairs are anchored deeply within the subcutaneous fat (Figure 1.8) and cannot be pulled out easily. Hair fiber is produced during anagen at a rate of approximately 1 cm/month or 0.35 mm/day. The telogen hairs are located higher up in the dermis (Figures 1.8 and 1.10) and can be pulled out relatively easily. The normal scalp contains 100,000 hairs. Blonds
Figure 1.7 Melanosomes, either eumelanin or pheomelanin, during anagen are transferred from melanocytes to matrical cortex cells via dendritic ends.
tend to have more, at 120,000, and redheads less, at 80,000. The average number of hairs for a normal scalp is 250 per square cm or 1100 per square inch. There is ethnic variation, with fewer hairs per square cm in Blacks and Orientals. The scalp consists of almost 90% of hairs in anagen, 1% in catagen and 10% in telogen. Anagen may last up to 2–6 years, telogen 3 months, and catagen 3 weeks. This ratio is usually uniformly distributed over the entire scalp. In certain individuals, there is periodicity in the number of telogen hairs, with a maximal number in late summer. Increased hair shedding is usually noted in autumn. Decreased telogen hairs occur in December, January or February. Physiologic hair shedding of 100 hairs per day is usual on the average, with fluctuations over the year. The sizes of the hair shafts are important in determining a diagnosis. Vellus hairs or miniaturized vellus-like hairs of androgenetic alopecia (AGA) have a shaft diameter of less than
Assessment of the patient with alopecia
7
Figure 1.8 During the hair cycle, the middle and upper portions of the hair follicle are the permanent segments of the hair follicle, while the lower portion is non-permanent. (a) The growing or anagen hairs are anchored deeply within the subcutaneous fat and cannot be pulled out easily. The telogen hairs are located higher up in the dermis and can be pulled out relatively easily. The scalp consists of almost 90% hairs in anagen, 1% in catagen and 10% in telogen. Anagen may last up to 2–6 years, telogen 3 months, and catagen 3 weeks. This ratio is usually uniformly distributed over the entire scalp. The dermal papilla (DP) is pulled upward with each cycle, and during telogen is closely associated with the stem cells of the bulge area. Communication signals between dp and stem cells of the bulge probably determine the length of anagen and the matrix girth of the next hair cycle. (b) The newly formed anagen hair pushes out the previous telogen hair.
Figure 1.9 Vellus-like hairs are less than 0.03 mm in diameter and rarely grow more than 1–2 mm. Terminal hairs are coarse over 0.06 mm in diameter and can grow up to 3 feet. A true vellus hair does not have an attached arrector pili muscle. Only miniaturized vellus-like hairs of androgenetic alopecia have arrector pili muscle.
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Hair Loss: principles of diagnosis and management of alopecia
0.03 mm (Figures 1.9 and 1.11). Terminal hairs have a shaft diameter greater than 0.06 mm. One can induce hair growth promotion by increasing the number of anagen hairs per unit area and by increasing the duration of the anagen phase.
Patient approach Figure 1.10 Cross-section of telogen hair. A central starshaped area of trichilemmal keratin can be noted, surrounded by outer root sheath, hyaline membrane and fibrous root sheath. The lower portion of terminal telogen hairs is found higher up in the dermis, unlike terminal anagen hairs, whose bulbs are found in the area of subcutaneous fat. (Courtesy of Dr David Shum.)
There are many etiologic factors that cause clinical hair loss, or alopecia, including endocrine abnormalities, genetic predisposition, systemic illness, drugs, psychological abnormalities, diet, trauma, infections, autoimmunity, and structural hair defects. Because of the multiplicity of disorders that can result in hair loss, a thorough history and physical examination are important, and ancillary laboratory work-up may be necessary.
Figure 1.11 Small vellus-like hairs (V) in androgenetic alopecia, (a) Hair shafts are small ( 25 mg/day) may affect iron absorption adversely.31 At the University of British Columbia Hair Clinic our approach to CTE is: (1) Confirm the diagnosis with a 4 mm scalp biopsy with transverse sectioning (see Figure 6.3). (2) Make sure you have ruled out any underlying cause of telogen effuvium. (3) Top up ferritin levels to greater than 30 µg/1. The patient should be monitored every 4–6 months with repeat ferritin levels until they have reached this threshold level. (4) Topical minoxidil 5% solution twice daily. We have found that topical minoxidil solution is beneficial in maintaining hairs in anagen and increasing conversion of hairs from telogen to anagen. Patients must be warned that initially there may increased shedding with topical minoxidil solution, as one must temporarily shed more telogen hairs to increase the eventual percentage of anagen hairs. We feel that it is likely that topping up ferritin levels will maximize the hair growth potential of topical minoxidil in those menstruating women with low ferritins. However, further studies with double-blinded placebo controls analyzing the single and combinational benefits of supplemental iron and topical minoxidil solution for CTE are needed. CTE is usually reversible. However, in those women who have a genetic predisposition to androgenetic alopecia (AGA), CTE may unmask their AGA, and hair will not necessarily grow back to the same density as before.
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References 1. Headington J.T. Telogen effluvium. New concepts and review. Arch Dermatol, 1993; 129(3):356–63. 2. Fiedler V. Diffuse alopecia: telogen hair loss. In Disorders of hair growth, ed. E.Olsen, pp. 241–252. 1993, McGraw-Hill, Inc.: New York. 3. Yaar M., Karassik R.L., Schnipper L.E. and Gilchrest B.A. Effects of alpha and beta interferons on cultured human keratinocytes. J Invest Dermatol, 1985; 85(1):70–4. 4. Tabibzadeh, S.S., P.G. Satyaswaroop and P.N.Rao. Antiproliferative effect of interferon-gamma in human endometrial epithelial cells in vitro: potential local growth modulatory role in endometrium. J Clin Endocrinol Metab, 1988; 67(1):131–8. 5. Pecoraro V. The normal trichogram of pregnant women. In Advances of biology of the skin, ed. W.Montagna, p. 203. 1969, Pergamon Press: Oxford. 6. Lynfield Y. Effect of pregnancy on the human hair cycle. J Invest Dermatol, 1960; 35: 323–7. 7. Schiff B. Study of postpartum alopecia. Arch Dermatol, 1963; 87:609. 8. Skelton J. Post partum alopecia. J Obstet Gynecol, 1966; 94:125. 9. Rook A. Diffuse alopecia: Endocrine, metabolic and chemical influences on the follicular cycle. In Diseases of the hair and scalp, ed. A.Rook, pp. 136–66. 1991, Blackwell Scientific Publications: Oxford. 10. Rooth G. and S.Carlstrom. Therapeutic fasting. Acta Med Scand 1970; 187(6): 455–63. 11. Freinkel R.K. and N.Freinkel. Hair growth and alopecia in hypothyroidism. Arch Dermatol, 1972; 106(3):349–52. 12. Williams R. Thyroid and adrenal interrelations with special reference to hypotrichosis and axillairis in thyrotoxicosis. J Clin Endocrinol Metab, 1947; 7:52.
13. Rushton D.H., Ramsay I.D., James K.C., et al. Biochemical and trichological characterization of diffuse alopecia in women. Br J Dermatol, 1990; 123(2):187–97. 14. Hard S. Non-anemic iron deficiency as an etiologic factor in diffuse loss of hair of the scalp in women. Acta Derm Venereol, 1963; 43:562–9. 15. Camacho F. Alopecias due to telogen effluvium. In Trichology: diseases of the pilosebaeous follicle, ed. F.Camacho, pp. 403–9. 1997, Aula Medica Group SA: Madrid. 16. Thompson J.S. Alopecia after ileal pouchanal anastomosis. Dis Colon Rectum, 1989; 32(6):457–65. 17. Desai S.P. and E.R.Roaf. Telogen effluvium after anesthesia and surgery. Anesth Analg, 1984; 63(1):83–4. 18. Abel R. Post operative (pressure) alopecia. Arch Dermatol, 1960; 81:34. 19. Klein A.W., R.I.Rudolph and J.J.Leyden. Telogen effluvium as a sign of Hodgkin disease. Arch Dermatol, 1973; 108(5):702–3. 20. Lubach D. [Dermatological changes in patients receiving long-term hemodialysis]. Hautarzt, 1980; 31(2):82–5. 21. Scoggins R. Cutaneous manifestations of hyperlipidemia and uraemia. Postgrad Med 1967; 41:357. 22. Zaun H. Wachstumsstorungen der kopfhaare als folge von hepatopathien. Arch Klin Exp Derm, 1969; 235:386–93. 23. Schattner A. and Y.Shanon. Crohn’s ileocolitis presenting as chronic diffuse hair loss. J R Soc Med, 1989; 82(5):303–4. 24. Kligman A. Pathologic dynamics of human hair loss. Arch Dermatol, 1961; 83:175–98. 25. Dahlin P.A., J.George and J.C.Nerette. Telogen effluvium: hair loss after spinal cord injury. Arch Phys Med Rehabil, 1984; 65(8): 485–6. 26. Berg C. The unconscious significance of hair. 1951, London: George Allen & Unwin Ltd. 27. Guy W. Diffuse cyclic hair loss in women. Arch Dermatol, 1959; 81:83–5.
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28. Whiting D.A. Chronic telogen effluvium. Dermatol Clin, 1996; 14(4):723–31. 29. Whiting D.A. Chronic telogen effluvium: increased scalp hair shedding in middleaged women. J Am Acad Dermatol, 1996; 35(6): 899–906.
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30. Trueb R.M. [Idiopathic chronic telogen effluvium in the woman]. Hautarzt, 2000; 51(12):899–905. 31. Van Neste D.J. and D.H.Rushton. Hair problems in women. Clin Dermatol, 1997; 15(1):113–25.
7 Cicatricial (scarring) alopecias
Introduction Cicatricial (scarring) alopecia represents a diverse group of diseases characterized by lack of follicular ostia (Figure 7.1) and irreversible alopecia. The terms cicatricial and scarring are used interchangeably. A basic knowledge of follicular anatomy is important in the understanding of scarring alopecias, because the location of the inflammatory infiltrate is crucial in determining irreversibility of alopecia. Follicular stem cells are located in the bulge area where the arrector pili muscle inserts into the follicles. These cells migrate down into the
hair follicle, and subsequently differentiate into the various layers of the hair follicle. As the hair cycles through anagen, catagen, and telogen, there is a permanent upper portion of the hair follicle and a non-permanent lower portion, (see Chapter 1, Figure 1.8). When the inflammation is located deep, in the vicinity of the non-permanent portion, a scarring alopecia is unlikely to develop. If the inflammation is located within the permanent portion, particularly around the stem cells of the bulge area and the infundibulum, then a cicatrizing alopecia is more likely to occur. Follicles can be saved from irreversible damage if this peribulge infiltrate can be controlled. Scarring alopecias are true trichologic emergencies.
Classification
Figure 7.1 Lack of follicular ostia is the hallmark sign of scarring hair loss.
Classification schemes for cicatrizing alopecias have been based upon clinical, histological or proposed pathogenic criteria.1,2 Clinically, scarring alopecias are categorized as either inflammatory or non-inflammatory. The non-infectious inflammatory scarring alopecias include chronic cutaneous lupus erythematosus (CCLE), lichen planopilaris (LPP) and folliculitis decalvans (FD). CCLE and LPP are characterized by keratotic follicular papules, while FD presents with pus-
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Hair Loss: principles of diagnosis and management of alopecia
tules. The non-inflammatory scarring alopecias are pseudopelade of Brocq (PP) and follicular degeneration syndrome, developmental abnormalities, genetic disorders, and neoplastic infiltrates. A second scheme, based upon pathology, classifies the cicatrizing alopecias according to inflammatory infiltrate cell type: lymphocyte or neutrophil. The lymphocytic-mediated disorders include CCLE, LPP, and PP, while the neutrophilic mediated conditions include FD, dissecting cellulitis, and acne keloidalis. This pathologically based classification system assists the clinician both in therapeutic decision-making and in gaining a better patho-physiological understanding of these disorders. Scarring alopecias can also be classified as primary or secondary.3 Primary scarring alopecia is defined microscopically as preferential destruction of follicular epithelium and / or its associated adventitial dermis with relative sparing of the interfollicular reticular dermis. In primary scarring alopecias, the hair follicle is the primary target of destruction. CCLE, LPP, PP, and FD are primary alopecias. Secondary scarring alopecias result from events outside the follicular unit that impinge upon and eventually eradicate the follicle. In these cases, the hair follicle is simply an ‘innocent bystander’. Follicular destruction is not the primary event. Sarcoidosis and morphea are examples of secondary scarring alopecias. Sperling has coined the term central, centrifugal scarring alopecia (CCSA).4 This grouping includes pseudopelade, follicular degeneration syndrome, and folliculitis decalvans. These conditions are centered on the crown or vertex and progress in a roughly symmetrical pattern, with disease activity limited to the peripheral zone surrounding the alopecic zone.
The biopsy for cicatrizing alopecias A scalp biopsy is crucial in the diagnosis of a cicatrizing alopecia. First, a biopsy site is selected. This site should be representative of active disease (primary lesion), preferably with a positive pull test and a paucity of follicular orifices. A less cosmetically important site, such as the posterior scalp, is preferable. The area is marked with a red marker, and lidocane with epinephrine is infiltrated into the area. Ten minutes is then allowed to take advantage of the vasoconstrictive effect of the epinephrine. The hair in the biopsy site is clipped. The punch is placed parallel to the direction of the hairs and inserted to the depth of the bevel. The biopsy should include the subcutaneous fat, because this is the location of terminal anagen hair bulbs. Two 4 mm punch biopsies are performed. One is submitted for transverse sectioning and the other is divided in half and submitted for both direct immunofluorescence and longitudinal sectioning. Special stains, such as PAS and elastin, may also be requested. Pressure is then applied to the biopsy site with a cotton applicator that may be saturated with aluminium chloride. The biopsy site is then closed with a blue 4.0 nylon suture. The blue suture allows for easier recognition and differentiation from hair during suture removal 7 to 10 days later.
Lymphocytic-mediated cicatricial alopecias Clinical features The three most common lymphocytic-mediated cicatricizing alopecias are CCLE, LPP and PP.
Cicatricial (scarring) alopecias
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Figure 7.2 Chronic cutaneous lupus erythematosus of the scalp. (a) and (b). A 23-year-old female with painful erythematous atrophic plaques. (c). A 60-year-old female with frontal scalp involvement. (d). Follicular hyperkeratosis occurring centrally within a plaque of lupus erythematosus. CCLE accounts for 30 to 40% of patients with scarring alopecias and has a definite female predilection. Very few patients (< 10%) who present with CCLE ever progress to systemic LE. However, an ANA is recommended for all patients with CCLE. In a series of 86 patients with CCLE of a mean duration of 15.1 years, 35 per cent (30/86) had scarring alopecia.5 A published report6 of 89 patients with CCLE showed that 34% had scalp involve-
ment. More than half these patients had scalp involvement at the onset of the condition. In a smaller study by Callen, 7/17 patients (41%) with CCLE had cicatricial scalp involvement.7 In three out of the seven, the scalp was the most prominent finding.7 This common involvement of the scalp is intriguing, because the scalp is a relatively light-protected area. In 10% of patients with CCLE, scalp involvement may be the sole manifestation of LE.8 Age of
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onset of scalp CCLE is usually at between 20 and 60 years of age. Patients present with erythematous plaques of alopecia, atrophy, telangiectasia and follicular hyperkeratosis (Figure 7.2). Scalp lesions begin as erythematous papules or irregular small scaly plaques. These lesions slowly progress to large erythematous, edematous plaques. At this point patients may experience loss of hair. This initial alopecia induced by follicular inflammation is potentially reversible. A prominent thickened and adherent scale may develop, which when removed reveals keratinous plugs on its under-surface. These keratinous plugs are from the follicular openings, and represent follicular hyperkeratosis. Follicular hyperkeratosis is more active in the center of a plaque, a clue to help distinguish CCLE from LPP (Figure 7.2d). As the lesion expands, the central erythema fades and the surface flattens. Hypopigmentation and depigmentation begin to appear. Central atrophy and telangiectasia eventually become prominent, and scarring develops. With continued spread of the disease, large, white atrophic scarred alopecic plaques will predominate over their inflammatory precursors. There is also increased curliness of hairs in scarred areas, owing to torsional within the hair follicle. In addition, normal anagen hairs can easily be pulled out of the scalp, a characteristic feature of the scarring alopecias. The term lichen planopilaris was first introduced in 1895 by Pringle,9 who described the association of lichen planus with follicular keratotic lesions. In 1915, Graham-Little10 described folliculitis decalvans et atrophicans or follicular scalp lesions resulting in cicatricial alopecia associated with follicular keratotic lesions at other sites. These two presentations are now considered variants of lichen planus. A clinical triad of classic plaquetype lichen
planus, spinous or acuminate lesions, and alopecia of the scalp or other hairy areas has been described.11 It was felt 40 years ago that one had to have this triad to make a diagnosis of LPP. This view is limited, and fails to account for the majority of intermediate cases. There is a spectrum of LPP. Mehregan et al.12 showed that 50% of their series of 45 patients with scalp LPP had strictly scalp involvement only. Seven per cent had either axillary or groin involvement, 7% nail involvement, 27% mucous membrane involvement and 40% glabrous skin involvement. Clearly, patients with scalp lichen planus should be followed up to assess whether lichen planus develops elsewhere (Figures 7.3h, 7.3i and 7.3j). The whole skin surface, the oral mucosa and the nails must be examined. Of all patients who have lichen planus, a series of 807 patients showed that only 10 (< 1%) had scalp involvement.13 LPP accounts for 30–40% of scarring alopecias. It usually occurs between 30 and 70 years of age, and a female predominance (2:1) has been noted. LPP is usually an insidious process evolving over several years, with a predilection for areas of greater hair density, such as the occipital scalp in men with AGA (Figures 7.3b and 7.3c). Follicular hyperkeratosis is present at the periphery of the plaques, rather than centrally (Figures 7.3a), and ulcerations may even develop (Figure 7.3d). Pruritus and tenderness are often a prominent feature, and anagen hairs can be extracted with gentle hair-pulling. Lesions typical of lichen planus do not occur on the scalp. LPP may be very widespread, with its extent not clearly apparent unless the scalp is shaved (Figures 7.3e, 7.3f, 7.3g). Occasionally drugs such as gold14 or mepacrine (atabrine)15 can trigger scalp lichen planus and cause irreversible hair loss. Tufted folliculitis consisting of several hair shafts emerging from a single ostium can also
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Figure 7.3 Lichen planopilaris (LPP). (a) Follicular hyperkeratosis at the periphery of erythematous alopecic areas. (b) and (c) LPP affecting the spared areas of male androgenetic alopecia. (b) Showing active inflammation. (c) Burnt out LPP. (d) Ulcerative lesion of LPP of the scalp. (e) Extensive case of LPP at the back of the scalp.
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(f) and (g). Close-up after the head has been shaved, showing marked involvement of much of the scalp. (h), (i), (j). LPP in a 45-year-old male with scarring alopecia as well as acuminate lesions on the arms and lichen planus-like lesions in the groin. This fits well with GrahamLittle disease. (k). Tufting of hairs in LPP.
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Figure 7.4 Pseudopelade of Brocq (a). Scarring hair loss affecting central portion of the scalp. (b) A 5year-old with pseudopelade (Brocq). (c), (d), (e) An 8-year-old boy with scattered pseudopelade (Brocq).
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(f) and (g) PP progressing over 10 years in a 40-year-old male. (h) PP affecting the area spared by androgenetic alopecia. (i) PP affecting the area most affected by androgenetic alopecia and mimicking androgenetic alopecia. (j) pp affecting tne beard area.
Cicatricial (scarring) alopecias
occur in LPP (Figure 7.3k). Tufting is common as an endstage phenomenon in many scarring alopecias, and occurs because the infundibular epithelium of damaged follicles often heals so as to cause the formation of a common large infundibulum. This is known as polytrichia.16 There is a variant of LPP, post-menopausal frontal fibrosing alopecia.17–19 Kossard has described an entity occurring in postmenopausal women presenting with perifollicular erythema along the marginal hairline, producing a frontal fibrosing hair loss extending to the temporal and parietal hair margins. Eyebrow loss was described in 13/16 women.19 Histological findings were indistinguishable from LPP. In 1885, Brocq of Paris described what later became known as Pseudopelade19a. Pelade is the French word for alopecia areata (AA). Pseudopelade refers to ‘like alopecia areata but not alopecia areata’. In pseudopelade (Brocq), the follicular ostia are not present while in AA they are most certainly present. Brocq subsequently admitted that this term does confuse the Iiterature 19b,19c. Pseudopelade (Brocq) (which is referred to as PP in this text) is regarded by most as a condition in which destruction of follicles leading to permanent patchy baldness is not accompanied by any clinically evident inflammatory pathology. End-stage LPP or CCLE may mimic an early pseudopelade (Brocq) as discussed below. PP is an idiopathic disorder, usually of adulthood. However, PP in children has been described. This author has seen at least 3 cases in children under the age of 10 (Figures 7.4b-e). Braun-Falco et al. reported an incidence of 4/ 142 (4.35%) cases of PP under the age of 11 and nine patients (9.6%) in the age range of 11–20.20 PP presents with small, irregular, asymmetrical, ivory porcelain white patches devoid of follicular units. This has been classically described as ‘footprints in the snow’. There is
163
controversy as to whether PP is a distinct entity or is effectively the same as end-stage CCLE or LLP.21 Detailed studies by Braun-Falco et al.20,22 strongly support the idea that pseudopelade can exist as a distinct entity. His group described 94/142 (66.2%) patients with PP without any previous underlying condition. PP is usually asymptomatic and without inflammation. Occasionally there may be erythema and mild pruritus. The parietal and vertex areas of the scalp are primarily involved (Figures 7.4a and 7.4b). Occasionally PP may affect the beard area and not just the scalp (Figure 7.4j).23 The course is extremely variable. In the majority of cases, extension of the process takes place only very slowly (Figures 7.4f and 7.4g). The course is often protracted and prolonged. Indeed, after 15– 20 years the patient may still be able to arrange his/her hair to conceal the patches effectively. However, in some cases, extension occurs more rapidly, and exceptionally there may be almost total baldness after 2 to 3 years. Occasionally the pattern of hair loss of PP can mimic androgenetic alopecia as described by Zinkernagel et al.,24 and the diagnosis of PP may be missed (Figure 7.4i). As with other cicatrizing alopecias, anagen hairs are easily extracted. A form of central centrifugal scarring alopecia in African-Americans, also known as follicular degeneration syndrome (FDS), overlaps significantly with PP with marked non-inflammatory cicatricial alopecia on the top of the scalp in black patients.25,26 Although initially thought to be a consequence of hair-care practices, it is now believed to represent an idiopathic disorder unrelated to trauma or hair cosmetics. Sperling believes the main etiology for FDS is that the inner root sheath desquamates prematurely far below the level of the isthmus not only in alopecic areas but even in non-inflamed follicles or the clinically normal scalp of affected individuals (Figure 7.5).
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Figure 7.5 Central centrifugal scarring alopecia (follicular degeneration syndrome) in African-Americans. (a) Black female with significant alopecia. (b) Close-up showing obliteration of follicular ostia. (c) Black male with significant alopecia. (d) Close-up of patient illustrating lack of follicular ostia.
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Figure 7.6 Algorithm for diagnosis of major non-infectious scarring alopecias.
Some clinical pearls can be helpful in establishing a diagnosis (Figure 7.6). First, if follicular hyperkeratosis is present, a central localization tends to occur in CCLE, while a peripheral distribution is seen in LPP. Second, the most likely diagnosis is PP if the scarring alopecia is non-inflammatory. Finally, if pustules are present, then FD is the most likely diagnosis.
Pathology The histopathology of CCLE reveals follicular vacuolar interface changes, a superficial and deep perivascular and periadnexal lymphocytic infiltrate, loss of sebaceous epithelium, and fibrosis (Figure 7.7). Perifollicular inflammation is most severe at the level of the infundibulum, and inflammatory cells may invade the follicular epithelium. The presence of a focally thinned epidermis, a thickened basement membrane zone and an increased dermal mucin helps support the diagnosis of CCLE. Pigment incontinence is present. Direct immunofluorescence demonstrates granular deposits of C3 of IgG distributed along the dermal-epidermal junction.1
Figure 7.7 Pathology of lupus erythematosus showing peri-adnexal and perivascular lymphocytic infiltration with follicular hyperkeratosis.
The lymphocytic infiltrate of LPP is lichenoid, with a characteristic perifollicular interface dermatitis (Figure 7.8). Other features include loss of sebaceous epithelium and marked perifollicular lamellar fibrosis. Inflammation affects the upper portion of the follicle, but may extend down the length of the follicle. Pigment incontinence is present.
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Figure 7.8 (a), (b) and (c). Pathology of lichen planopilaris displaying the characteristic follicular lymphocytic interface dermatitis. (Courtesy of Dr Magdalena Martinka.)
Figure 7.9 Numerous hairs exiting from one infundibulum which clinically appears as polytrichia or tufted folliculitis. (Courtesy of Dr Magdalena Martinka.)
Perivascular and peri-eccrine infiltrates are usually not present, as in LE. There may also be tufted folliculitis in the upper portion of the epidermis (Figure 7.9). Direct immunofluorescence may demonstrate grouped globular IgM cytoid bodies in follicular epithelium. The pathology of PP depends on disease duration. In the early stages, a peri-infundibular lymphocytic infiltrate is present beneath a normal epidermis. As PP progresses, the epidermis becomes atrophic, rete ridges vanish, and sebaceous glands and hair follicles are obliterated. Pigment incontinence is less evident than in LE or LPP. The end stage of PP is characterized by marked scarring and the absence of an inflammatory infiltrate. Direct immunofluoresence is negative. Special staining techniques may help in establishing a diagnosis of a scarring alopecia. Elastin staining demonstrated normal or abundant elastic tissue in PP, while in LE and LPP the quantity of elastin is significantly dimin-
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Figure 7.10 Algorithm for pathological assessment of major noninfectious scarring alopecias.
7.10 dividing entities into lymphocytic- versus neutrophilic-mediated. Folliculitis decalvans is neutrophilic-mediated (Figure 7.11), and will be described below.
Differential diagnosis
Figure 7.11 Neutrophilic infiltrate in folliculitis decalvans. (Courtesy of Dr Magdalena Martinka.) ished.27 Periodic acid Schiff staining in LE will demonstrate a thickened basement membrane zone and alcian blue stain or colloidal iron stains will show increased dermal acid mucopolysaccharides. An algorithmic approach to the pathology of scarring alopecias is presented in Figure
Scalp psoriasis has the presence of follicular ostia and the lack of follicular plugging and atrophy. However, there are reported cases of scarring alopecia in severe scalp psoriasis.28 Inflammatory changes in the infundibular area of the follicle in psoriasis may disrupt follicular stem cells and result in scarring alopecia. Tinea capitis can be scarring, but again there is no follicular plugging or atrophy. A potassium hydroxide preparation and/or culture will help confirm the diagnosis. Keratoacanthomas and squamous cell carcinomas can mimic hypertrophic lupus erythematosus. The lymphocytic scarring alopecias can certainly be difficult to tell apart from each other. Early CCLE and LLP can look quite similar. In addition, the co-existence of LPP and CCLE
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Figure 7.12 Algorithmic approach to treatment of lymphocytic-mediated scarring alopecias.
has been reported.29 Differentiating clinical and histopathological features of lymphocytic scarring alopecias are discussed above and are summarized in Figures 7.6 and 7.10.
Treatment The treatment of scarring alopecia depends on three variables: diagnosis, patient age, and disease severity. The severity is determined by the rapidity of the progression of the condition, the degree of inflammation, the severity of symptoms, and the extent of scalp involvement. The goals of treatment are to arrest the cicatrizing process, decrease follicular inflammation and prevent further fibrosis. At the University of British Columbia Hair Clinic the therapeutic strategy for patients with lymphocytic-mediated scarring alopecias is based upon the extent of the alopecia: groups with less than 10% scalp involvement and those with more than 10% scalp involvement are treated differently. This is summarized in algorithmic form in Figure 7.12.
Figure 7.13 Injecting intralesional cortisone into the surrounding hairy areas of scarring alopecia. Triamcinolone 10 mg/ml, injected with a volume of 0.1 ml/injection for 20 injections, can halt further spread of the condition and reduce symptoms of itch and burning. Injections are performed once monthly.
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Figure 7.14 Lupus erythematosus: the patient from Figure 7.2c, showing marked improvement after 1 year of hydroxychloroquine 200 mg twice daily, monthly intralesional corticosteroid injections and topical superpotent corticosteroid ointment twice daily.
Figure 7.15 Lichen planopilaris: the patient from Figure 7.3d with previous ulcerative LPP improved markedly with hydroxychloroquine, intralesional corticosteroid and topical corticosteroid.
If there is less than 10% scalp involvement, double therapy with topical and intralesional corticosteriods is initiated. Intralesional corticosteroid, 2 ml of 10 mg per ml, is administered to scarring areas once every four weeks (Figure 7.13), and an ultra-potent topical corticosteroid is applied twice daily. If the patient is not responding within eight weeks to this double therapy, then hydroxychloroquine, 200 mg twice a day,30 is added for a minimum of six months (Figures 7.14 and 7.15). If the alopecia is very severe, rapidly progressive, inflamed, and symptomatic, then prednisone is added at 1 mg per kilogram per day and tapered over two months. The prednisone provides bridge therapy, because of a delay in the therapeutic effects of hydroxychloroquine. If there is more than 10% scalp involvement, triple therapy is immediately initiated with intralesional steroid, ultra-potent topical
corticosteroid and hydroxychloroquine. If the alopecia is rapidly progressive, very inflamed and symptomatic, then a systemic steroid is also administered for eight to twelve weeks. If improvement is not noted after six months, than other treatments can be attempted. Isotretinoin,31–33 at doses of 1 mg per kg per day, can be initiated and then tapered once improvement is detected. Dapsone (100 mg/day)34–37 and thalidomide (100 mg/day)38–40 are other alternatives. Again, therapy is tapered once improvement is acheived. A pull test is conducted with each visit, and therapy is continued for six to twenty-four months until the pull test is negative. When a pull test is negative for over two years and alopecia is clinically stable, then scalp reduction and/or hair transplantation are further options. Premature transplantation may actually aggravate the condition. Increasing the number of hairs, which can serve as a primary target in scarring
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Figure 7.16 Folliculitis decalvans in a 30-year-old male. (a) Marked erythema and folliculitis. (b) After 6 months of isotretinoin 1 mg/kg/day, showing much improvement.
Figure 7.17 Folliculitis decalvans in a 17-year-old female, showing hair shafts embedded within the skin.
Figure 7.18 Tufted folliculitis in dissecting cellulitis, most evident after the scalp has been shaved.
alopecias, may cause the patient to become more symptomatic with increased inflammation, pruritus or burning if the condition is remotely still active. The use of topical minoxidil is controversial. Although there are no controlled trials for
topical minoxidil solution for scarring alopecias, many clinicians feel that topical minoxidil, by retaining unaffected hairs in anagen for a longer period of time, enables the overall density to be better than that of untreated individuals.41
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Figure 7.19 (a). Dissecting cellulitis of the scalp with characteristic boggy cysts. (b). Close-up of boggy cysts.
Neutrophil-mediated cicatricial alopecias The neutrophil-mediated cicatricial alopecias, such as FD, are considered an abnormal immune response to the normal scalp flora. Patients present with round patches of alopecia with overlying erosion, scale or crust. Follicular-based pustules develop in successive crops (Figure 7.16). Hair shafts are occasionally embedded within the scalp (Figure 7.17) Tufted folliculitis is a feature frequently seen in FD (Figure 7.18).42 In the early stages, the pathology demonstrates a neutrophilic folliculitis (Figure 7.11); however, as the disease progresses, fibrosis is prominent.43,44 Dissecting cellulitis can present as a boggy cystic inflammatory process (Figure 7.19).
The therapeutic strategy for the neutrophilmediated cicatrizing alopecias is targeted at anti-staphylococcal therapy with systemic erythromycin, cephalosporins, cloxacillin, rifampin and fusidic acid. There is some evidence that a combination of rifampin 300 mg twice daily and clindamycin 300 mg twice daily for twelve weeks affords more benefit than single-agent therapy.43 Systemic fusidic acid may also have some benefit.44 Topical therapy can also be added, such as topical fusidic acid.44 For severe dissecting folliculitis, high-dose isotretinoin for a prolonged course is recommended.45–49 Patients may be so symptomatic with discomfort, itch and burning, that controlling the inflammation for these individuals is more important than salvaging the hair. Laser-assisted hair removal50 may help for this subset of patients.
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Conclusion The scarring alopecias are trichological emergencies. An accurate diagnosis is arrived at through a careful clinical and histo-pathological assessment. An aggressive multiplemodality therapeutic approach is often necessary to gain disease control.
References 1. Newton R.C., Hebert A.A., Freese T.W. and Solomon A.R. Scarring alopecia. Dermatol Clin, 1987; 5(3):603–18. 2. Headington J.T. Cicatricial alopecia. Dermatol Clin, 1996; 14(4):773–82. 3. Templeton S.F. and A.R.Solomon. Scarring alopecia: a classification based on microscopic criteria. J Cutan Pathol, 1994; 21(2):97–109. 4. Sperling L.C., A.R.Solomon and D.A. Whiting. A new look at scarring alopecia [editorial; comment]. Arch Dermatol, 2000; 136(2):235–42. 5. de Berker D., M.Dissaneyeka and S.Burge. The sequelae of chronic cutaneous lupus erythematosus. Lupus, 1992; 1(3):181–6. 6. Wilson C.L., Burge S.M., Dean D. and Dawber, R.P. Scarring alopecia in discoid lupus erythematosus. Br J Dermatol, 1992; 126(4):307–14. 7. Callen J.P. Systemic lupus erythematosus in patients with chronic cutaneous (discoid) lupus erythematosus. Clinical and laboratory findings in seventeen patients. J Am Acad Dermatol, 1985; 12(2 Pt 1):278–88. 8. Callen J.P. Chronic cutaneous lupus erythematosus. Clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol, 1982; 118(6):412–6. 9. Pringle J. Lichen pilaris spinulosus. Br J Dermatol, 1905; 17:77–102.
10. Little E. Folliculitis decalvans et atrophicans: Report of a case. Br J Dermatol, 1915; 27: 183–5. 11. Silver H. Follicular lichen planus (lichen planopilaris). Arch Dermatol Syph, 1953; 67: 346–54. 12. Mehregan D.A., H.M.Van Hale, and S.A. Muller. Lichen planopilaris: clinical and pathologic study of forty-five patients. J Am Acad Dermatol, 1992; 27(6 Pt 1):935–42. 13. Altman J. The variations and course of lichen planus. Arch Dermatol, 1961; 84:179. 14. Woods B. Lichen post-aurique. In Transactions of the St John’s Hospital Dermatological Society. 1968, London: The Society. 15. Feder A. Clinical observations of atypical lichen planus and related dermatoses due to atabrine toxicity. Ann Int Med, 1949; 31: 1078. 16. LoPresti P., C.M.Papa and A.M.Kligman. Hot comb alopecia. Arch Dermatol, 1968; 98(3):234–8. 17. Lee W.S., S.M.Hwang and S.K.Ahn. Frontal fibrosing alopecia in a postmenopausal woman. Cutis, 1997; 60(6):299–300. 18. Kossard S. Postmenopausal frontal fibrosing alopecia. Scarring alopecia in a pattern distribution [published erratum appears in Arch Dermatol 1994 Nov.; 130(11):1407]. Arch Dermatol, 1994; 130(6):770–4. 19. Kossard S., M.S.Lee and B.Wilkinson. Postmenopausal frontal fibrosing alopecia: a frontal variant of lichen planopilaris. J Am Acad Dermatol, 1997; 36(1):59–66. 19a. Brocq L.Alopecia, Journal of Cutaneous and Venereal Diseases 1885. 3:49. 19b. Brocq L. et al. Réchèrches sur 1’alopecie atrophiante, varieté psuedopelade. Annales de Dermatologie et de Syphiligraphie, 6, 1, 97, 209. 19c. Brocq L. Pseudopelade in Traite elementaire de dermatolgie Practique, Doin, Paris Vol. 2. P648. 20. Braun-Falco O., T.Bergner and G.P. Heilgemeir. [The Brocq pseudopelade—a disease picture or disease entity]. Hautarzt, 1989; 40(2):77–83.
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21. Dawber R. What is pseudopelade? Clin Exp Dermatol, 1992; 17(5):305–6. 22. Braun-Falco O., Imai S. and Schmoeckel C., et al. Pseudopelade of Brocq. Dermatologica 1986; 172(1):18–23. 23. Madani S., M.J.Trotter and J.Shapiro. Pseudopelade of Brocq in beard area. J Am Acad Dermatol, 2000; 42(5 Pt 2):895–6. 24. Zinkernagel M.S. and R.M.Trueb. Fibrosing alopecia in a pattern distribution: patterned lichen planopilaris or androgenetic alopecia with a lichenoid tissue reaction pattern? [see comments]. Arch Dermatol, 2000; 136(2): 205–11. 25. Sperling L.C. and P.Sau. The follicular degeneration syndrome in black patients. ‘Hot comb alopecia’ revisited and revised. Arch Dermatol, 1992; 128(1):68–74. 26. Sperling L.C., Skelton H.G. 3rd and Smith K.J., et al. Follicular degeneration syndrome in men. Arch Dermatol, 1994; 130(6):763–9. 27. Elston D.M., McCollough M.L., Warschaw K.E. and Bergfeld W.F. Elastic tissue in scars and alopecia. J Cutan Pathol, 2000; 27(3):147–52. 28. Wright A.L. and A.G. Messenger. Scarring alopecia in psoriasis. Acta Derm Venereol, 1990; 70(2):156–9. 29. Vanderhorst J. Mixed lichen planus-lupus erythematosus disease: A distinict entity: Clinical, histopathological and immunopathological studies in six patients. Clin Exp Dermatol, 1983; 8:631–40. 30. Bulengo-Ransby S.M. and J.T.Headington. Pseudopelade of Brocq in a child [see comments]. J Am Acad Dermatol, 1990; 23(5 Pt 1):944–5. 31. Shornick J.K., N.Formica and A.L.Parke. Isotretinoin for refractory lupus erythematosus. J Am Acad Dermatol, 1991; 24(1):49–52. 32. Vena G.A., C.Coviello and G.Angelini. [Use of oral isotretinoin in the treatment of cutaneous lupus erythematosus]. G Ital Dermatol Venereol, 1989; 124(6):311–15.
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33. Green S.G. and W.W.Piette. Successful treatment of hypertrophic lupus erythematosus with isotretinoin. J Am Acad Dermatol, 1987; 17(2 Pt 2):364–8. 34. Singh Y.N., Adya C.M., Verma K.K., et al. Dapsone in cutaneous lesions of SLE: an open study. J Assoc Physicians India, 1992; 40(11): 735–6. 35. Lindskov R. and F.Reymann. Dapsone in the treatment of cutaneous lupus erythematosus. Dermatologica, 1986; 172(4):214–7. 36. Rothe M.J. and F.A.Kerdel. Treatment of cutaneous lupus erythematosus. Lupus, 1992; 1(6):351–6. 37. Duna G.F. and J.M.Cash. Treatment of refractory cutaneous lupus erythematosus. Rheum Dis Clin North Am, 1995; 21(1): 99– 115. 38. Holm A.L., Bowers K.E., McMeekin T.O. and Gaspari A.A. Chronic cutaneous lupus erythematosus treated with thalidomide. Arch Dermatol, 1993; 129(12):1548–50. 39. Knop J., Bonsmann G., Happle R., et al. Thalidomide in the treatment of sixty cases of chronic discoid lupus erythematosus. Br J Dermatol, 1983; 108(4):461–6. 40. Hasper M.F. and A.H.Klokke. Thalidomide in the treatment of chronic discoid lupus erythematosus. Acta Derm Venereol, 1982; 62(4):321–4. 41. Dawber R. Update of minoxidil treatment of hair loss. In Hair and its disorders, biology, pathology, and management, ed. F.Camacho, pp. 167–76. 2000, London: Martin Dunitz Ltd. 42. Annessi G. Tufted folliculitis of the scalp: a distinctive clinicohistological variant of folliculitis decalvans [see comments]. Br J Dermatol, 1998; 138(5):799–805. 43. Powell J.J., R.P.Dawber and K.Gatter. Folliculitis decalvans including tufted folliculitis: clinical, histological and therapeutic findings. Br J Dermatol, 1999; 140(2):328–33. 44. Abeck D., H.C.Korting and O.Braun-Falco. Folliculitis decalvans. Long-lasting response to combined therapy with fusidic
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acid and zinc. Acta Derm Venereal, 1992; 72(2): 143–5. 45. Scerri L., H.C.Williams, and B.R.Allen. Dissecting cellulitis of the scalp: response to isotretinoin. Br J Dermatol, 1996; 134(6): 1105–8. 46. Plewig G., J.Nikolowski and H.H.Wolff. Action of isotretinoin in acne rosacea and gram-negative folliculitis. J Am Acad Dermatol, 1982; 6(4 Pt 2 Suppl): 766–85. 47. Shaffer N., R.C.Billick and H.Srolovitz. Perifolliculitis capitis abscedens et suffodiens. Resolution with combination therapy. Arch Dermatol, 1992; 128(10):1329–31.
48. Bachynsky T., O.M.Antonyshyn and J.B. Ross. Dissecting folliculitis of the scalp. A case report of combined treatment using tissue expansion, radical excision, and isotretinoin. J Dermatol Surg Oncol, 1992; 18(10):877–80. 49. Dubost-Brama A., Delaporte E., Alfandari S., et al. [Perifolliculitis capitis abscedens and suffidiens. Efficacy of isotretinoin]. Ann Dermatol Venereal, 1994; 121(4):328–30. 50. Chui C.T., Berger T.G., Price V.H. and Zachary C.B. Recalcitrant scarring follicular disorders treated by laser-assisted hair removal: a preliminary report. Dermatol Surg, 1999; 25(1):34–7.
Index Note: References to figures are indicated by ‘f’ and references to tables by ‘t’.
AA see alopecia areata acne 16, 47, 156 adrenoleukodystrophy, premature male AGA and 85 adriamycin (doxorubicin), alopecia and 137 AGA see androgenetic alopecia alkylating agents 138 alopecia assessment of patient with 1–18 causes of 10t DPCP treatment of 57f drug-induced 134–46 irreversible 155 reversible 139, 143 see also hair loss alopecia areata (AA) 9, 10, 16, 19–81, 163 AGA and 96–7 autoimmune disorders and 21 of beard 34, 36f clinical features of 28–36 cyclosporin in 66f cytokines and 24 differential diagnosis of 38–42, 40–1f Down’s syndrome and 20f, 21 emotional stress and 24 etiology of 19 extent of hair loss 30, 34f extracranial 35f genetic factors and 19–21 histopathology of 29f immunological factors and 21–4 intralesional corticosteroid injections for 44f nail changes and 39f nail dystrophy and 34, 39f neurological factors and 25 pathogenesis 23f pathology of 27–8 pattern of hair loss 30 prognosis of 36–7 systemic steroids and 46–7 telogen effluvium and 95–6 topical immunotherapy for 54–5f treatment of children with systemic steroids 47 treatment of 42–66
treatment plan 66–70 white hairs, vitiligo and 37f alopecia areata circumscripta 31–2f Alopecia Areata Investigational Assessment Guidelines 43 alopecia masking lotion 68 alopecia totalis (AT) 30, 34f, 42 alopecia universalis (AU) 30, 34f, 42 amitriptyline 143 amoxapine 143 ANA see antinuclear antibodies examination anagen effluvium 134, 136–8, 137f drug-induced 137t anagen (growing) hairs 6, 155 anagen phase, alkaline phosphatase activity and 3 anagen-telogen hair ratio 12, 27, 134 androgen blockade 102–4, 114 androgen receptor blockers (ARP inhibitors) 104–5 androgen receptor proteins (ARP) 85 androgenetic alopecia (AGA) 10t, 16, 83–119, 151, 158 differential diagnosis 38 history 9 iron deficiency and 148 miniaturization of hairs 27 surgical management of 121–33 treatment in men 109–12 treatment in women 108–9 vellus hairs in 6–8 in women 16, 88, 89f, 91f, 134 anemia, iron deficiency 16 anesthesias, telogen effluvium and prolonged 148 angiogenesis, tretinoin and 108 animal models, AA and non-AA 25–7 anthralin 43, 48, 49–51, 68, 69 anti-coagulants, hair loss and 139 anti-psychotics/anxiolytics 143 anti-thyroid drugs, telogen effluvium and 139 antidepressants, tricyclic/tetracyclic 143 antihypertensive agents 143 antinuclear antibodies (ANA) examination 16, 157 antitumor antibiotics 138 anxiety, telogen effluvium and acute 150
176
Index
arrector pili muscle 5, 98, 155 atherogenesis 88 autoeczematization 64 autoimmune diseases 21, 23 autoimmune polyglandular syndrome 21, 22 autoimmunity, clues for 21–4 baldness coronary heart disease and 87 drugs and 134 patterns in population 85 prostate cancer and 88 beard, alopecia areata of 34, 36f Beau’s lines 34 beta-blockers 143 betamethasone dipropionate 43, 48 biologic response modifiers 101, 105–8, 114 bitemporal recession 91, 151 bleomycin 137 body, alopecia areata of 34 body hair, thinning of 149 bulge area, stem cells of 5, 155 buspirone 143 busulfan 138 C3H/HeJ mice 25, 26 calcitonin gene-related peptide 25 captopril 143 carbamazepine, alopecia and 142–3 carbimazole 139 cardiovascular disease 87 carmustine 138 castling, DPCP and 52 catagen 134, 136, 155 catagen hairs 6, 27, 98 catagen-telogen hair ratio 101 cell-mediated immunity 22–4 cellulitis 156 central centrifugal scarring alopecia (CCSA) 156, 164f cephalosporins 171 chemotherapy 134 children anthralin and 49 hair loss in 9 systemic steroid treatment in 47 therapeutic modality choices for 69 topical therapies for 67 chlorambucil 137 chlormethamine 137 cholesterol-lowering agents 144
chondroitin sulfate 3 chromosome 8p 12 26 chronic cutaneous lupus erythematosus (CCLE) 155, 156, 157 histopathology of 165 vs LPP 158, 167 chronic telogen effluvium (CTE) 150, 151 cicatricial (scarring) alopecias 10t, 16, 17, 155–72 algorithm for diagnosis for 165f inflammatory 155 lymphocytic 167 pathology algorithm 167f cimetidine, alopecia induced by 136 circumscript alopecia 32f circumscript alopecia areata 38 clindamycin 171 clobetasol propionate 68 clofibrate 144 clonazepam 143 cloxacillin 171 colchicine 138 corticosteroids 43–7, 69 cortisone, injection of intralesional 168f coumarins 139 Cox proportional hazards model 87 Crohn’s disease 149 cyclophosphamide 137, 138 cyclosporin 65–6 cyproterone acetate (CPA) 101, 104–5, 108 cysts, boggy 171f cytarabine 137 cytochrome P450 aromatase enzyme 86 cytokines, alopecia areata and 24 cytomegalovirus (CMV) infection 24 cytosine arabinoside 138 cytostatic drugs 136–8 dacarbazine 138 dactinomycin 137 dapsone 169 daunorubicin 137 dehydroepiandrosterone sulfate (DHEAS) test 16, 98, 108 delayed anagen release (DAR) 138 delayed telogen release (DTR) 138 depression 9, 150 dermal acid mucopolysaccharides 167 dermographism, severe 64 despiramine 143 dexamethasone 43
Index
diabetes mellitus 22 dibromoketone 53 diffuse alopecia 16, 143, 148 diffuse alopecia areata 30, 33f diffuse cyclic hair loss, in women 150 dihydrotestosterone 85 dinitrochlorobenzene (DNCB) 51–2 diphenylcyclopropenone (DPCP) 26, 51, 52–64, delayed response 59f eczematous eruptions from 60–1 f pigmentary changes with 62f treatment of eyebrows with 60f unilateral treatment with 59f discoid lupus erythematosus (DLE) 10t, 16, 17 divalproex 142 dopaquinone 6 Down’s syndrome, alopecia areata and 20f, 21 doxepin 143 doxorubicin (adriamycin), alopecia and 137 drug-induced alopecia 134–46 anagen effluvium 137f, 145 lichenoid eruption of scalp 134 telogen effluvium 139t, 140t, 141t Dundee experimental bald rat (DEBR) 25 dyslipidemia 88 dysmorphobia 9 dystrophic anagen hairs, positive pull test 96 dystrophic hairs, counts of 12 dystrophy, checking for presence of 15 eczema, DPCP and 64 elastin staining 156, 166 eosinophils 27 epidermal growth factors (EGF) 105 erythema 163, 170f erythema multiforme 64 estrogen, AGA and 105 eumelanin 6 exclamation point hairs 32f eyebrows dermatography of 69 injection with triamcinolone 45f loss of 163 treatment with DPCP 64 facial edema 130 facial hypertrichosis 107 ferritin, levels of 98, 151 fever, alopecia and 147
177
finasteride 101, 102–4, 109, 133 hair transplants and 130 and minoxidil combination therapy 110 fluocinolone 43 fluorouracil 137 fluoxetine 143 follicular bundles, with miniaturized hairs 99f follicular degeneration syndrome (FDS) 156, 163, 164f follicular hyperkeratosis 58, 158, 165 follicular ostia 10, 88, 155 follicular scalp lesions 158 follicular stem-cell gene therapy 114 follicular stem-cells 155 folliculitis, tufted 166, 170f, 171 folliculitis decalvans (FD) 155, 156, 167, 170f, 171 fronto-parietal/fronto-temporal recession 90 fusidic acid 171 gastric parietal cell antibodies 22 gene replacement therapy 70 gold, hair loss and 158 graft hair preparation 126 Graham-Little disease 160f hair density and distribution of 10 dryness of 139 thinning of 86 hair anatomy 1–8 hair color, loss of 144 hair cortex 4, 5, 136 hair counts 13, 103 hair cycling, on human scalp 6 hair follicles 1–2 cellular components of 24 growth inhibitors 24 layers of 3f non-permanent and permanent segments 7 hair grafts, planting of 129 hair loss 9, 158 pattern in a family 95f prevention of 101, 113 severity of 148 see also alopecia hair matrix cell mitosis 136 hair removal, laser-assisted 171 hair shafts 2, 6 abnormalities of 15 quality of 10, 11f
178
Index
hair shedding 9, 12 abrupt diffuse 148f, 149f physiological 6 hair thinning 9, 89, 151 hair transplants 101, 108, 110, 121–2f, 169 complication of donor area 126 finasteride and 130 male 113f, 132f minoxidil and 130 multiple-bladed knife for 123f positioning of hairline 126–8 recipient area 126–30 removal of donor strips 124f hair weights, study of 103 hair-growth promoters 101 hair-specific antibodies 23 hairpieces 69, 101 hairs light-microscopic examination of 13–16 miniaturization of 27, 83 halcinonide 43 haloperidol 143 Henle’s layer 2, 4, 5 hen’s egg test 53 heparin 139 hepatic disease 149 hirsutism 16, 87, 108 Hodgkin’s disease 149 hormone modifiers 101, 102–5 Hox genes 26–7 human leukocyte antigens (HLA) 19–21 Huxley’s layer 2, 4, 5 hyaluronic acid 3 hydroxycarbamide 137 hydroxychloroquine 169 hydroxyurea 138 hyper-androgenism 16, 87, 98, 108 hyper-insulinemia 88 hyperpigmentation 64 hypertension 47, 88 hyperthryoidism 9 hypertrichosis 108 hypertrophic lupus erythematosus 167 hypo-proteinemia 147 hypopigmentation 64, 158 hypopituitarism 85 hypothyroidism 9, 136, 140, 148 iatrogenic hypothyroidism 139 ICAM-1 27
ichthyosis 144 ifosfamide 138 imipramine 143 immediate anagen release 138, 147 immediate telogen release 138 immunosuppressive therapy, responsiveness to 21 inflammatory bowel disease 149 infundibulum 1, 5, 155, 163 inner root sheath (IRS) 2, 4, 5 insulin-resistance-associated disorders 88 interferons 143 intracellular androgen metabolism, AGA and 85 intralesional corticosteroids 67, 69, 169 intramuscular corticosteroid therapy 47 iodine, telogen effluvium and 139 iron deficiency 16, 148 isotretinoin 169, 171 isthmus 1, 5 Kaplan-Meier survival analysis 53 keloids 125 keratin 4 keratinization, disturbed 136, 144 keratinocytes, abnormal 24 keratoacanthomas 167 keratotic follicular papules 155 leflunomide 26 lichen planopilaris (LPP) 155, 156, 158–63, 159– 60f, 169f cicatricial alopecia 10t pathology of 166f peripheral distribution 165 lichen planus 17, 22, 158 lichenoid eruption 136 lithium 140–2 Ludwig pattern, stages of 89 Ludwig Stage I pattern, in teenagers 95f Ludwig Stage III, women with 108 Ludwig Stages I–III 90f lupus erythematosus 22, 158, 169f chronic cutaneous scalp 157f luteinizing hormone-releasing hormone (LH-RH) 105 lymphadenopathy 62f, 64 lymphocytic-mediated cicatricial (scarring) alopecias 156–70 treatment algorithm 168f M phase drugs 138
Index
McKusick Mendelian Inheritance in Man (MIM) 83 Major Histocompatibility Complex (MHC) 19 malignant diseases 149 maprotiline 143 mechlormethamine 137 medulla 2, 4 melanin 3, 6 melanocytes 6, 24–5 melphalan 18, 138 men AGA treatment options 101 frontal hairline recession 89 vertex balding in 87 mepacrine (atabrine), hair loss and 158 6-mercaptopurine 138 mesenchymal-derived dermal papilla 86 methotrexate 137, 138 methylprednisolone 47 methylthiouracil 139 mice, hairless 26 micro-grafting 132 Microsporum canis 42 mini-grafting 132 miniaturized hairs 88, 93 minoxidil (Rogaine) 43, 47–8, 101, 105–8, 109 and hair transplants 130 hypertrichosis of the face and 107f topical 133, 170 use of betamethasone dipropionate and 48f monoamine oxide inhibitors 143 morphea 156 mouse teratogenicity test 53 myasthenia gravis 22 nail dystrophy, alopecia areata and 34, 37 National Alopecia Areata Foundation (NAAF) 19, 70 National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) 19 neutrophil-mediated cicatricial alopecias 171 nitrosoureas 138 non-cicatricial (non-scarring) alopecias 10f, 16, 17f non-inflammatory cicatrizing alopecias 155 nortriptyline 143 Norwood-Hamilton classification 92, 109 Norwood-Hamilton pattern 90, 94f Norwood-Hamilton Stage III 92f Norwood-Hamilton Stage III and IV 103 Norwood-Hamilton Stage VII 94f Norwood-Hamilton Stages IV–VI 93f
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obesity 47, 88 olanzapine 143 onychorrhexis 34 ophiasis 33f, 37, 58f ophiasis inversus (sisapho) 30, 33f oral contraceptives 143 oral cyclosporine 22 outer root sheath (ORS) 2, 5 papular atrichia 85 paroxetine 143 PAS stain 156 patchy alopecia areata 30, 33f, 42 patient, history of 9 patient expectations, therapy and 113–14 peri-infundibular lymphocytic infiltrate 166 perifollicular interface dermatitis 165 pernicious anemia 22 pheomelanin 6 photochemotherapy (PUVA) 64–5, 70 squaric acid dibutyl ester and 52 phototrichogram method 103 pigment incontinence 165 cis-platin 138 polymyalgia rheumatica 22 polytrichia 163 polytrichia folliculitis 166f post-menopausal frontal fibrosing alopecia 163 postpartum hair loss 138, 147 prednisolone, pulsed oral 47 pressure-induced alopecia (PIA) 38, 42 procarbazine 138 Propecia 102, 104 propylthiouracil 139 prostate cancer, AGA and incidents of 88 protriptyline 143 pruritus 158, 163 pseudopelade (PP) 38, 156, 161f, 163, 166 psycho-physical trauma 147 psychogenic pseudoeffluvium 151 psychopharmacologic medications 140–3 pull-tests 10, 11f, 93, 156, 169 pulse therapy, intravenous methylprednisolone 47 pustules 156 PUVA therapy see photochemotherapy pyrogens, endogenous 147 quail-chick model 86 5α-reductase 85
180
Index
renal failure 149 respiridone 143 reticular alopecia areata 30, 33f Retin-A 108 rifampin 171 Rogaine see Minoxidil S phase-specific drugs 138 SAHA (seborrhea, alopecia, hirsutism, acne) syndrome 87 Salmonella typhimurium 51 sarcoidosis 156 scalp cellulitis of 171f physiology of 1–8 scalp biopsies 14–15f, 16, 134, 151, 156 scalp irritation, minoxidil and 10 scalp lesions 158 scalp prostheses 68f scalp psoriasis 167 scalp reduction 169 scarring alopecia see cicatricial alopecia sebaceous epithelium, loss of 165 seborrheic dermatitis 100 serotonin reuptake inhibitors 143 sertraline 143 serum ferritin, evaluation of 16 sex hormone binding globulin (SHBG) 105 short-contact therapy 49 shortened anagen (SA) 138 sisapho 30, 33f skin diseases, alopecia and severe 136 Smyth chicken model 25 soriatane 144 spironolactone 101, 105, 108 squamous cell carcinomas 167 squaric acid dibutyl ester (SADBE) 26, 51, 52 steroid-metabolizing enzymes 85 steroids systemic 22, 46–7 topical, intralesional and systemic 43 stress alopecia areata and emotional 24 telogen effluvium and psychological 150 striae, systemic steroids and 47 substance P (SP) expression 24, 25 support groups 69 suprabulbar area 1, 4f syphilitic alopecia 27, 28 systemic diseases 136
systemic erythromycin 171 targeted follicular gene therapy 114 telangiectasia 158 telogen effluvium 9, 10t, 16, 96f, 142f acute and chronic 147–53 alopecia areata and 27, 28, 95 differential diagnosis 38, 134 drug-induced 139–44 pathology of 28 types of 138–9 in women 86 telogen hairs 6, 27, 98, 155 cross-section of 8f positive pull test 96 temporal triangular alopecia (TTA) 42 terminal-vellus hair ratio 27, 134 testosterone 85 thalidomide 169 thallium, hair loss and 144 thiotepa 137, 138 thyroid dysfunction 16 thyroid function assessment 140 thyroid influences 21, 148 thyroid screening 9 thyroid stimulating hormone test (TSH) 98 thyrotoxicosis 139, 140 tinea capitis 9, 10t, 38, 167 topical immunotherapy 43, 51–64, 69 topical ophthalmic beta-blockers 143 trachyonychia 34 traction alopecia 10t, 38 trazodone 143 tretinoin (all-trans-retinoic acid) 108 triamcinolone acetonide 45 triamcinolone hexacetonide 45 triangular temporal alopecia 38 trichodynia 151 trichogram/pluck test 12 trichologic anatomy 1–8 trichomalacia 28 trichotillomania 9, 27, 28, 38 triparanol 144 tufting, cicatricial alopecias and 163 tyrosine 6 ulcerative colitis 22 valproic acid (VPA) 142 vasopressin 138
Index
vellus hairs 6, 98, 99f vellus-like hairs 7f vertex pattern balding 87 vertex thinning 90 vinblastine 137, 138 vincristine 137, 138 vitiligo 63f, 64
women AGA in 88, 89f, 91f finasteride and 104 hair loss in 86 hair transplantation in 131–2 treatment of AGA in 101, 108–9 Woods light examination 42 zolpidem 143
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