Central centrifugal cicatricial alopecia (CCCA; originally entitled follicular degeneration syndrome, or hot comb alopecia) was first described in African American women utilizing hot combs and/or strong chemical hair care products.
A 67 year old African American female was evaluated for the presence of alopecic areas occurring on the scalp vertex, and spreading centrifugally. The alopecic lesions appeared as diffuse patches, including atrophic small areas surrounding individual hair follicles.
Patients and Methods:
Skin biopsies for hematoxylin and eosin examination, as well as for direct immunofluorescence and immunohistochemistry analyses were performed.
hematoxylin and eosin staining demonstrated histopathologic findings of premature desquamation of the inner root sheath and eccentric thinning of the follicular epithelium, supporting the diagnosis of CCCA. Direct immunofluorescence revealed strong depositions of Complement/C3, fibrinogen and kappa light chains around the hair follicles. Immunohistochemistry demonstrated increased expressions of HLA-ABC (as in African American patients with insulin independent diabetes mellitus). We also detected positive p53, bcl-2 and MAC staining in the hair follicle areas.
Follicular degeneration syndrome may have an important immunological component previously not described, and multicolor immunofluorescence may be useful in establishing an early diagnosis.
Central centrifugal cicatricial alopecia; follicular degeneration syndrome; hot comb alopecia; survivin; p53; bcl-2; MAC; HLA-ABC; complement/C3
Hair loss is a very common complaint. Patients may describe increased shedding and diffuse or localized alopecia. The differential diagnosis of hair loss includes a number of disorders causing cicatricial or noncicatricial alopecias. This paper describes the clinical approaches and diagnostic tests that are useful in the evaluation of patients presenting with alopecia. It also reviews treatments for noncicatricial alopecias, including androgenetic alopecia, alopecia areata, and telogen effluvium, as well as cicatricial alopecias, including lichen planopilaris, its clinical variant frontal fibrosing alopecia, and discoid lupus erythematosus.
alopecia; evaluation; treatment
Scarring alopecias are classified into primary and secondary types according to the initial site of inflammation. In primary scarring alopecias, the hair follicle is the main target of destruction; the term secondary cicatricial alopecia implies that follicular destruction is not the primary pathologic event.
To review the histopathologic diagnoses of cases of cicatricial alopecia in order to classify them according to the North American Hair Research Society.
PATIENTS AND METHODS
Patients with biopsy specimens diagnosed as cicatricial alopecia seen from 2000 to 2005 at the Dermatologic Department of Hospital das Clinicas, São Paulo University Medical School had hematoxylin and eosin, Periodic acid-Schiff and Weigert stained slides reevaluated and sub-typed into different primary cicatricial alopecias.
Thirty-eight cases of primary cicatricial alopecias were reclassified as: chronic cutaneous lupus (17), lichen planus pilaris (4), pseudopelade of Brocq (12), folliculitis decalvans (3), dissecting folliculitis (1), and non-specific scarring alopecia (1). In our cases, the methods employed allowed an accurate diagnosis in 12 of 13 cases (92.3%) previously classified as non-specific cicatricial alopecias.
Even in the late, pauci or non-inflammatory phases, an approach with systematic evaluation of a constellation of criteria in routine hematoxylin and eosin stain, Periodic acid-Schiff and Weigert stain allowed for a more accurate diagnosis of cicatricial alopecias.
Cutaneous lupus erythematosus; Lichen planus pilaris; Pseudopelade of Brocq; Folliculitis decalvans; Dissecting folliculitis
Secondary cicatricial alopecia occurs as a result of destruction of hair follicles by scar tissue formed in the scalp and eyebrows. It is a permanent condition and regrowth of hairs in the area is not expected. The purpose of the study was to select the appropriate method for treating cicatricial alopecia. 24 patients were admitted to our hospital during the period from June 2006 to July 2007. They were suffering from acquired cicatricial alopecia affecting the scalp and the eyebrow. Their ages ranged from 6-48 years with mean age 26-25 years. They were treated surgically by total excision of the lesions with direct closure of the defect in ten cases, excision of alopecia with advancement flaps with the aid of scalp expanders in seven cases, scalp reduction through serial excision of alopecia in three cases and excision of alopecia and reconstruction of the defect by strip composite hair-bearing scalp grafts in four cases. Our results suggest there are three key factors that decide the surgical methods for treating alopecia: size, location and shape. We also discuss and evaluate the various techniques of reconstruction. Good results were obtained in 18 patients.
Alopecia; Secondary cicatricial; Scalp defects
Trichoscopy performed with a handheld dermoscope or a videodermoscope became an indispensable tool in differential diagnosis of hair and scalp diseases. Current research is focusing on trichoscopy of: 1) non-cicatricial alopecia, 2) cicatricial alopecia, 3) hair shaft disorders, and 4) inflammatory scalp diseases. This review summarizes current knowledge in these four fields of research. In all non-cicatricial alopecias presence of empty follicular openings is a common trichoscopy finding. In alopecia areata black dots and micro-exclamation mark hairs and tapered hairs correlate with disease activity, whereas yellow dots and vellus hairs correlate with disease severity. In androgenic alopecia trichoscopy shows hair shaft thickness heterogeneity, multiple thin and vellus hairs, yellow dots, perifollicular discoloration, and predominance of follicular units with only one hair. These features predominate in the frontal area. In all forms of cicatricial alopecia, trichoscopy shows milky-red or ivory-white areas lacking follicular openings. In classic lichen planopilaris trichoscopy shows perifollicular inflammation, tubular perifollicular scaling, elongated, concentric blood vessels and "classic white dots", which merge to form white areas. Frontal fibrosing alopecia shows mild perifollicular scaling. Folliculitis decalvans is characterized by tufted hairs, large follicular pustules with emerging hair shafts and perifollicular starburst pattern hyperplasia. In dissecting cellulitis characteristic findings are "3D" yellow dots imposed over dystrophic hairs, large, yellow amorphous areas and pinpoint white dots with a whitish halo. Trichoscopy is particularly useful to diagnose hair shaft abnormalities in trichorrhexis nodosa, trichorrhexis invaginata, monilethrix, pili torti, and pili annulati. The method may be also useful in diagnosing inflammatory scalp diseases. In discoid lupus erythematosus trichoscopy shows large arborizing vessels and large hyperkeratotic folliculilar yellow dots. Trichoscopy of scalp psoriasis shows regularly distributed twisted and lacelike blood vessels, whereas in seborroic dermatitis thin arborizing vessels may be observed. In tinea capitis trichoscopy shows comma, corkscrew and zigzag hairs. Examination tinea capitis may be facilitated by UV-light enhanced trichoscopy (UVET). In conclusion, trichoscopy is a non-invasive method which may be applied in differential diagnosis of most hair and scalp diseases.
alopecia; dermoscopy; hair; psoriasis; lichen planopilaris; lupus; seborheic dermatitis; trichoscopy; UV; videodermoscopy
Central centrifugal cicatricial alopecia is a common cause of progressive permanent apical alopecia. This unique form of alopecia includes entities previously know as “hot comb alopecia,” “follicular degeneration syndrome,” “pseudopelade” in African Americans and “central elliptical pseudopelade” in Caucasians. The etiology appears to be multifactorial and the condition occurs in all races.
Alopecia; central; centrifugal; cicatricial; pseudopelade
Cicatricial alopecias have a significant impact on the psychological status, quality of life, and social interaction of those suffering from it. Till date, limited or no data have been available regarding the psychosocial and quality of life aspects of cicatricial alopecias.
To assess the psychosocial impact of cicatricial alopecias.
Materials and Methods:
Thirty patients fulfilling the criteria for cicatricial alopecia irrespective of their age and sex were included in the study. Psychosocial assessment was carried out in 23 patients who were capable of responding to the questionnaire, using an adopted and suitably modified version of Women's Androgenetic Alopecia Quality of Life Questionnaire.
We observed that 73.9% of our patients with cicatricial alopecias had moderate to severe psychosocial impact due to their hair loss. Patients of younger age group and with inactive disease, suffered from greater psychosocial impact of the disease. Patients with slight hair loss also had considerable psychological distress. The chronicity of disease duration did not seem to reduce the psychosocial impact of the disease. Both married and unmarried patients suffered equally from the psychosocial impact of the disease.
The management of cicatricial alopecias needs a holistic approach. In addition to laying an emphasis on early diagnosis aided by clinco-pathological correlation, to prevent irreversible hair loss, the psychosocial impact of the disease should also be taken into consideration and addressed by the treating dermatologist.
Cicatricial alopecias; modified women's androgenetic alopecia quality of life questionnaire; psychosocial impact
Folliculitis et perifolliculitis capitis abscedens et suffodiens is a rare disease of unknown etiology. It is a suppurative process that involves the scalp, eventually resulting in extensive scarring and irreversible alopecia. The condition is also known as ‘acne necrotica miliaris’ or ‘Proprionibacterium’ folliculitis. Most often the disease affects men of African-American or African-Caribbean descent between 20 and 40 years of age. The clinical picture is determined by fluctuating painful fistule-forming conglomerates of abscesses in the region of the occipital scalp. The cause of scalp folliculitis is not well understood. It is generally considered to be an inflammatory reaction to components of the hair follicle, particularly the micro-organisms. These include: bacteria (especially Propionibacterium acnes, but in severe cases, also Staphylococcus aureus), Yeasts (Malassezia species) and mites (Demodex folliculorum). The initial histopathologic finding is an exclusively neutrophilic infiltration followed by a granulomatous infiltrate. The treatment of the disease is usually difficult and often disappointing. Successful treatment with isotretinoin 1 mg/kg body mass could be achieved only after regular systematic administration in the course of 3–4 months. Here we describe a patient with eruptive purulent form of the disease, which has been controlled with combination therapy: systemic antibiosis with metronidazole and clindamycin, dermatosurgical removal of single nodular formations, and isotretinoin 1 mg/kg body mass for 3–5 months.
Acne conglobata; Candida; isotretinoin; Spritzer; Hoffmann
Frontal fibrosing alopecia (FFA) is more common in postmenopausal women, but it can occur in younger women. Some authors consider FFA to be a distinct frontal variant of lichen planopilaris. From a clinical point of view, this relatively uncommon condition is characterized by progressive frontotemporal recession due to inflammatory destruction of hair follicles. Dermoscopy can be very useful, as the differential diagnosis between traction alopecia, alopecia areata, FFA and cicatricial marginal alopecia may be difficult. It is not clear whether or not treatment alters the natural history of the disease - the disease stabilized with time in most of the patients with or without continuing treatment. Here we report a case of a 50-year-old woman with FFA and discuss the relevance of dermoscopy in the differential diagnosis of this disease.
Alopecia; Dermoscopy; Menopausal; Lichen planopilaris
Dermoscopy has been established as an indispensable tool in the diagnosis and follow up of hair disorders. In alopecia areata, dermoscopy of active disease shows yellow dots, dystrophic hairs, as well as cadaverized (black dots) and exclamation mark hairs. Alopecia areata has been reported to occur equally among races, however, until date, there are no published data regarding dermoscopic findings in African-American patient.
We report a case of scalp dermoscopy of alopecia areata in an African-American patient that shows a diffuse honeycomb-like pigmented network, few yellow dots and white dots.
This case shows that skin color may affect dermoscopic findings in alopecia areata. In our African-American patient with alopecia areata dermoscopy showed a diffuse honeycomb-like pigmented network, which was previously considered characteristic for androgenic alopecia and white dots, which were considered characteristic for cicatricial alopecia. Further studies are needed to elucidate the presence of white dots in alopecia areata.
alopecia areata; dark skin; epiluminescence microscopy; hair loss; pigmented network; scalp; trichoscopy
Primary cicatricial or scarring alopecias (CA) are a group of inflammatory hair disorders of unknown pathogenesis characterized by the permanent destruction of the hair follicle. The current treatment options are ineffective in controlling disease progression largely because the molecular basis for CA is not understood. Microarray analysis of the lymphocytic CA, Lichen planopilaris (LPP), compared to normal scalp biopsies identified decreased expression of genes required for lipid metabolism and peroxisome biogenesis. Immunohistochemical analysis showed progressive loss of peroxisomes, proinflammatory lipid accumulation, and infiltration of inflammatory cells followed by destruction of the pilosebaceous unit. The expression of peroxisome proliferator-activated receptor (PPAR) γ, a transcription factor that regulates these processes, is significantly decreased in LPP. Specific agonists of PPARγ are effective in inducing peroxisomal and lipid metabolic gene expression in human keratinocytes. Finally, targeted deletion of PPARγ in follicular stem cells in mice causes a skin and hair phenotype that emulates scarring alopecia. These studies suggest that PPARγ is crucial for healthy pilosebaceous units and it is the loss of this function that triggers the pathogenesis of LPP. We propose that PPARγ-targeted therapy may represent a new strategy in the treatment of these disorders.
Primary cicatricial alopecias (PCAs), rare disorders that lead to permanent hair loss, have been poorly understood and are difficult to treat. Lichen planopilaris (LPP) is a prototypical PCA; patients often present with sudden onset of hair loss and clinically significant symptoms of itching, burning, and pain of the scalp. Examination reveals patchy alopecia or a more diffuse thinning of the scalp with characteristic perifollicular erythema and perifollicular scale at the margins of the areas of alopecia. Treatment typically includes use of anti-inflammatory medications; although symptomsmay improve, hair loss is often progressive.
We report a series of four patients who presented with complaints of diffuse non-scarring alopecia. They had similar clinical features of alopecia, hyperseborrhea, and distinct keratinaceous hair casts that encircled the hair shafts. Propionibacterium acnes was isolated from two of the patients’ scalp, and Gram-positive, Giemsa-positive bacteria were seen in the hair follicles in the scalp biopsy of one of the patients. The patients’ symptoms did not respond to standard treatment for seborrheic dermatitis, but responded to a course of systemic antibiotics targeting P. acnes. We propose a role for P. acnes colonization of the terminal hair follicles in the pathogenesis of hair casts, and possibly diffuse non-scarring alopecia. Possible mechanisms of pathogenesis are discussed with a literature review.
Hair casts; non-scarring alopecia; Propionibacterium acnes; systemic antibiotics
The appearance of hair plays an important role in people’s overall physical appearance and self-perception. With today’s increasing life-expectations, the desire to look youthful plays a bigger role than ever. The hair care industry has become aware of this and is delivering active products directed towards meeting this consumer demand. The discovery of pharmacological targets and the development of safe and effective drugs also indicate strategies of the drug industry for maintenance of healthy and beautiful hair. Hair aging comprises weathering of the hair shaft, decrease of melanocyte function, and decrease in hair production. The scalp is subject to intrinsic and extrinsic aging. Intrinsic factors are related to individual genetic and epigenetic mechanisms with interindividual variation: prototypes are familial premature graying, and androgenetic alopecia. Currently available pharmacologic treatment modalities with proven efficacy for treatment of androgenetic alopecia are topical minoxidil and oral finasteride. Extrinsic factors include ultraviolet radiation and air pollution. Experimental evidence supports the hypothesis that oxidative stress also plays a role in hair aging. Topical anti-aging compounds include photoprotectors and antioxidants. In the absence of another way to reverse hair graying, hair colorants remain the mainstay of recovering lost hair color. Topical liposome targeting for melanins, genes, and proteins selectively to hair follicles are currently under investigation.
hair weathering; graying; androgenetic alopecia; senescent alopecia; hair anti-aging
Alopecia areata (AAR) and androgenetic alopecia (AGA) are two major forms of alopecia based on altered hair growth condition. In general, the cell cycle is regulated by several mechanisms including the stem cell factor/c-kit signaling. To assess a role for stem cell activity in alopecia, we performed histopathological, immunohistochemical, and semiquantitative analyses of c-kit as well as Ki-67 in scalp biopsy specimens obtained from 14 patients with AAR, 18 patients with AGA, and 6 age-matched control subjects, using the specific antibodies. Formalin-fixed, paraffin-embedded skin sections were examined. Immunoreactivities for Ki-67 and c-kit were localized in keratinocytes and melanocytes in the outermost layer of hair follicles. The mean length of hair follicles was significantly shorter in the AAR and AGA groups than in the control group. The mean number of Ki-67-immunoreactive cells per follicle was significantly reduced in the AAR and AGA groups as compared with the control group. The mean number of c-kit-immunoreactive cells per follicle was significantly increased in the AAR and AGA groups as compared with the control group. Our results indicate that c-kit is upregulated in the hair follicle cells in these forms of alopecia, and suggest that the upregulation reflects a negative feedback mechanism in response to possible downregulation of the ligand stem cell factor.
alopecia; c-kit; histopathology; immunohistochemistry; semiquantitation
Atrichia with papular lesions (APL) is a rare autosomal recessive form of irreversible alopecia with onset at few months of age with papular keratin cysts over the body. It is associated with mutation in the Zinc finger domain of the human hairless gene on chromosome region 8p12. An eleven-year-old male presented with extensive alopecia starting at six months of age refractory to the treatment along with keratotic papules on the face and trunk. Biopsy from a papule showed mid-dermal keratin cysts and from the scalp showed few vellus follicles with no terminal hairs. The diagnosis of APL was made based upon the criteria proposed. Vitamin D-dependent rickets was ruled out as it has similar clinical presentation. Accurate diagnosis of APL is required to avoid unnecessary treatment to the patient as it is commonly misdiagnosed as alopecia universalis and treated with systemic steroids.
Alopecia universalis; atrichia; papular
Since the epochal work of Hamilton there has been general acceptance of the causal relationship of the male sex hormone, age and familial inheritance in development of male pattern baldness.
Some of the medicaments used in recent years may cause a diffuse loss of scalp hair. Alopecia that accompanies disease states is probably due to generalized toxemia and disturbances in metabolism. Sometimes male pattern baldness occurs in physiologic states, as exemplified by diffuse hair loss occasionally in the postpartum period.
Alopecia areata deserves a critical appraisal, since it may be evidence of underlying neuropsychotic states that need psychiatric diagnosis and treatment. The development of alopecia totalis or universalis in 50 per cent of the prepuberal cases of alopecia areata is of real significance, especially since so very few patients recover their normal scalp hair.
The conclusions reached by the authors of two articles reporting on 368 cases of alopecia areata, alopecia totalis and alopecia universalis that the evidence is overwhelming against the malfunction of the endocrine glands as the cause of alopecia areata must be considered real contributions to our understanding of this condition.
A few conditions simulate alopecia areata. Probably the ones which are seen most often are trichotillomania and patchy baldness caused by agents used in hair waving and straightening.
Our findings in 22 cases of alopecia areata of a persistent inflammatory perivascular and perifollicular infiltrate, massive plugging of the ostia, disappearance of robust hair follicles and diminution in total number of hair follicles and sometimes fibrosis are not necessarily diagnostic of alopecia areata but seem to be very definitely characteristic.
Treatment for alopecia areata is of little avail. At this time we do not recommend the general use of the corticosteroids despite the improvement of scalp appearance in the majority of instances in which the systemic administration of these hormones have been employed.
OBJECTIVE: To describe an organized diagnostic approach for both nonscarring and scarring alopecias to help family physicians establish an accurate in-office diagnosis. To explain when ancillary laboratory workup is necessary to confirm the diagnosis. QUALITY OF EVIDENCE: Current diagnostic and therapeutic interventions for hair loss are based on randomized controlled studies, uncontrolled studies, and case series. MEDLINE was searched from January 1966 to December 1998 with the MeSH words alopecia, hair, and alopecia areata. Articles were selected on the basis of experimental design, with priority given to the most current large multicentre controlled studies. Overall global evidence for therapeutic intervention for hair loss is quite strong. MAIN MESSAGE: The most common forms of nonscarring alopecias are androgenic alopecia, telogen effluvium, and alopecia areata. Other disorders include trichotillomania, traction alopecia, tinea capitis, and hair shaft abnormalities. Scarring alopecia is caused by trauma, infections, discoid lupus erythematosus, or lichen planus. Key to establishing an accurate diagnosis is a detailed history, including medication use, systemic illnesses, endocrine dysfunction, hair-care practices, and family history. All hair-bearing sites should be examined. A 4-mm punch biopsy of the scalp is useful, particularly to diagnose scarring alopecias. Once a diagnosis has been established, specific therapy can be initiated. CONCLUSIONS: Diagnosis and management of hair loss is an interesting challenge for family physicians. An organized approach to recognizing characteristic differential features of hair loss disorders is key to diagnosis and management.
Monilethrix is a heritable hair shaft defect characterized by localized or diffuse alopecia resulting from hair fragility over friction areas, predominantly the temporal and occipital regions, and follicular keratosis over the occipital region. However, it lacks macroscopic features that enable easy and rapid diagnosis in medical practice. Hair shaft microscopy is the basis for diagnosing monilethrix. We present a report of two Indian male siblings aged 24 and 21, who presented with thinning and hair loss from the scalp in male pattern distribution and multiple skin-colored follicular papules over the nape of the neck and bilateral forearms since childhood. Trichoscopy of scalp hair revealed characteristic uniform elliptical nodes and intermittent constrictions along with variation in hair shaft diameter, presence of few vellus hair and yellow dots, suggesting a diagnosis of monilethrix with early-onset androgenetic alopecia. Dermoscopy of the papules revealed multiple stubs of broken hair arising from them with a similar beaded appearance, suggesting a diagnosis of monilethrix. The diagnosis of monilethrix was confirmed with light microscopy and hair clipping. This report highlights the patterned distribution of hair loss in monilethrix probably due to the early unmasking of androgenetic alopecia and the use of trichoscopy as the diagnostic modality.
Androgenetic alopecia; hair shaft disorder; monilethrix; trichodermoscopy
Primary cicatricial alopecia (PCA) is a group of inflammatory hair disorders that cause scarring and permanent hair loss. Previous studies have implicated PPARγ, a transcription factor that integrates lipogenic and inflammatory signals, in the pathogenesis of PCA. However, it is unknown what triggers the inflammatory response in these disorders, whether the inflammation is a primary or secondary event in disease pathogenesis, and whether the inflammatory reaction reflects an autoimmune process. In this paper, we show that the cholesterol biosynthetic pathway is impaired in the skin and hair follicles of PCA patients. Treatment of hair follicle cells with BM15766, a cholesterol biosynthesis inhibitor, or 7-dehydrocholesterol (7-DHC), a sterol precursor, stimulates the expression of pro-inflammatory chemokine genes. Painting of mouse skin with 7-DHC or BM15766 inhibits hair growth, causes follicular plugging and induces the infiltration of inflammatory cells into the interfollicular dermis. Our results demonstrate that cholesterologenic changes within hair follicle cells trigger an innate immune response that is associated with the induction of toll-like receptor (TLR) and interferon (IFN) gene expression, and the recruitment of macrophages that surround the hair follicles and initiate their destruction. These findings reveal a previously unsuspected role for cholesterol precursors in PCA pathogenesis and identify a novel link between sterols and inflammation that may prove transformative in the diagnosis and treatment of these disorders.
Congenital alopecia includes a broad differential diagnosis and presents a diagnostic and therapeutic challenge for the physician. Congenital atrichia is a rare form of irreversible alopecia that is usually inherited as an autosomal recessive pattern. We report a 2-year-old male child presenting with total alopecia of scalp, eyebrows, eyelashes, and body hair since birth. The child had cardiac malposition with situs inversus of the viscera. Computed tomography of the chest and abdomen revealed median position of the heart with transposition of abdominal viscera. To our knowledge, this is the first case of congenital atrichia associated with situs inversus and mesocardia.
Congenital atrichia; mesocardia; situs inversus
Alopecia Areata (AA) is a “non-scarring” alopecia that has an autoimmune basis. Though clinically distinctive, problems arise in diagnosis depending on the temporal stage of the disease at presentation; some of them progress to scarring alopecia and predicting its prognosis is difficult. Histological changes depend on the disease stage and site of the biopsy.
To describe the spectrum of histologic features in AA.
Materials and Methods:
A prospective and retrospective study of H and E sections of all biopsies signed out as AA between 2001 and 2009 (20 cases) was undertaken.
The diagnosis was made on vertical sections in all cases. The total number of hair follicles ranged from 1 to 24 with an average of 7 and comprised mainly terminal follicles. Vellus follicles were scanty. Anagen to non-anagen ratio was 1:1.62. Miniaturization of follicles was noted in five (25%) cases. Peribulbar inflammation was seen in all the cases with a dominance of lymphocytes. Perifollicular fibrosis was noted in 12 (60%) and pigment casts in 5 (25%) cases. Scarring was seen in two cases. In these cases, a diagnosis of AA was rendered on the basis of even spacing of the fibrotic units and remnants of the catagenic basement membrane within the scars. The epidermis and interfollicular dermis were normal in all the cases.
The most consistent features of AA are an increase in non-anagen terminal follicles and peribulbar lymphocytic infiltrate. The etiology can be determined even in cases that have progressed to scarring.
Alopecia Areata; histopathology; non-scarring alopecia
Fewer than 45% of women go through life with a full head of hair. Female pattern hair loss is the commonest cause of hair loss in women and prevalence increases with advancing age. Affected women may experience psychological distress and impaired social functioning. In most cases the diagnosis can be made clinically and the condition treated medically. While many women using oral antiandrogens and topical minoxidil will regrow some hair, early diagnosis and initiation of treatment is desirable as these treatments are more effective at arresting progression of hair loss than stimulating regrowth. Adjunctive nonpharmacological treatment modalities such as counseling, cosmetic camouflage and hair transplantation are important measures for some patients. The histology of female pattern hair loss is identical to that of male androgenetic alopecia. While the clinical pattern of the hair loss differs between men, the response to oral antiandrogens suggests that female pattern hair loss is an androgen dependant condition, at least in the majority of cases. Female pattern hair loss is a chronic progressive condition. All treatments need to be continued to maintain the effect. An initial therapeutic response often takes 12 or even 24 months. Given this delay, monitoring for treatment effect through clinical photography or standardized clinical severity scales is helpful.
female pattern hair loss; androgenetic alopecia
Immune responses are largely regulated by cytokines secreted by activated T cells. Interactions among these cells are complex, and the interaction between two responses may alter the effect of either response alone. It is established that contact sensitization-induced inflammation can reverse hair loss due to alopecia areata. In parallel, the Renbök phenomenon demonstrates how two distinct autoimmune diseases, psoriasis and alopecia areata, interact to result in clinically active psoriasis suppressing alopecia areata.
We describe a patient with concurrent psoriasis and alopecia areata universalis with terminal hairs within plaques on his extremities, representing the only normal hair growth on his body. Adjacent biopsies confirmed our clinical suspicion of plaque psoriasis with normal hair follicles and alopecia areata universalis with a peribulbar lymphocytic infiltrate. Our patient’s psoriatic plaques cleared rapidly with nbUVB phototherapy but hair growth at the site was maintained. His scalp alopecia responded to squaric acid contact sensitization therapy.
Our patient represents a natural experiment in whom three distinct but overlapping immune responses favored psoriasis or contact dermatitis over alopecia areata. The precise mechanism responsible for these effects remains unclear; however, based on recent reports, we speculate that cytokine cross-regulation plays a role in competition among these distinct immune responses.
Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet, the mechanisms for decreased hair growth in this disorder are unclear. We show that prostaglandin D2 synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD2 levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor G protein (heterotrimeric guanine nucleotide)–coupled receptor 44 (GPR44), but not the PGD2 receptor 1 (PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD2 in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment.