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PubMed2005

Alopecia areata: a tissue specific autoimmune disease of the hair follicle.

The goal of this review is to introduce the immunologic community to alopecia areata as a model system for the study of tissue directed autoimmune disease. Alopecia areata is marked by autoimmune assault on the hair follicle resulting in hair loss. It is linked to HLA-DQ3 and evidence suggests it is mediated by T-lymphocytes with a TH1 cytokine profile. Hair follicles are an immune protected site with deficient MHC expression. Evidence is presented suggesting that alopecia areata results from loss of immune privilege with presentation of autoantigens. Alopecia areata is one of the most common human autoimmune conditions, with a lifetime risk of approximately 1.7%. Study of alopecia areata in humans is facilitated by the accessibility of scalp for biopsy. It is possible to transfer the condition with lesional human lymphocytes in a human scalp graft/SCID mouse model. There are also spontaneous animal models which share the features of the human condition. For these reasons, alopecia areata is a powerful model for study of the induction and pathogenesis of tissue directed autoimmune disease.

Alopecia Areata↗
PubMed2006

The non-synonymous C1858T substitution in the PTPN22 gene is associated with susceptibility to the severe forms of alopecia areata.

Alopecia areata is an acquired hair loss disorder resulting from an immunologically- mediated attack on hair follicles and autoimmunity may play a part in its pathogenesis. The non-synonymous C1858T substitution in the PTPN22 gene, which encodes lymphoid protein tyrosine phosphatase, has been shown to be associated with susceptibility to autoimmune disorders. In this study, the objective was to ascertain whether or not the disease-associated 1858T (W620) allele was associated with alopecia areata. For this, the allelic distribution of the PTPN22 C1858T alleles was determined in 196 English patients with alopecia areata and 507 healthy subjects in a case control study using a restriction fragment length polymorphism-polymerase chain reaction (PCR-RFLP) genotyping method. The results indicated that the frequency of the 1858T allele did not differ significantly between the alopecia areata patient group and the control cohort: of 392 alopecia areata alleles, 41 (10.5%) encoded the W620 variant compared to 86 of 1014 (8.5%) control alleles. However, in patients with severe disease, 25/168 (14.9%) alleles were 1858T and this frequency differed from that in the control group (P = 0.0127; OR, 95% CI = 1.89, 1.17 - 3.05). These results suggest that the non-synonymous C1858T substitution in the PTPN22 gene may have an influence on the severity of alopecia areata and provide further evidence for autoimmunity as an aetiological factor in this disorder.

Adolescent↗
PubMed2005

Frontal fibrosing alopecia in postmenopausal women.

BACKGROUND: Frontal fibrosing alopecia is a variety of cicatricial alopecia characterized by a band of frontal/frontoparietal hair recession and marked decrease or a complete loss of the eyebrows, typically observed in women who are postmenopausal. OBJECTIVE: The purpose of this study was to report clinical and histopathologic findings and results of treatment in a group of women affected by the disease. METHOD: A total of 14 women with alopecia of the frontal hairline were evaluated from June 2000 through July 2003 in our outpatient consultation for hair disorders. RESULTS: Clinical examination revealed a band of symmetric recession of the frontoparietal hairline extending to the preauricular areas associated with loss of follicular orifices, mild skin atrophy, and perifollicular erythema at the scalp margin. In all, 9 patients also had partial or total loss of the eyebrows. The histologic features of the scalp specimens were similar in all our patients with a reduction of the number of hair follicles, and a high number of intermediate and velluslike follicles. Intemediate and velluslike follicles were more commonly affected than terminal follicles by the lymphocytic inflammatory infiltrate and perifollicular fibrosis. CONCLUSION: Frontal fibrosing alopecia is a cicatricial alopecia that follows destruction of hair follicles by an inflammatory lymphocytic infiltrate that is localized around the upper portion of the hair follicle. It differs from lichen planopilaris because the lymphocytic infiltrate and fibrosis affect selectively the intermediate and the velluslike follicles of the frontal margin and eyebrows. The reason for this selective involvement is still unknown. Frontal fibrosing alopecia may represent a variety of lichen planopilaris with selective involvement of certain androgen-dependent areas. The affected follicles may have typical biologic markers that could explain the clinical and histologic features found in the disease. It is interesting to note that some of the patients treated with finasteride (2.5 mg/d) showed an arrest in the progression of the disease. Even if there is no proof for a hormonal basis of the disease, the effectiveness of finasteride in some patients may indicate that androgens might be partially responsible of the pathogenesis of the disease.

Aged↗
PubMed2004

Autoantibodies to DFS70/LEDGF are increased in alopecia areata patients.

Alopecia areata (AA) has been suspected to be an autoimmune disease, although there is no distinct evidence, we investigated the relationship between AA and autoantibodies against dense fine speckles 70 kDa (DFS70) in 111 patients with alopecia and 105 healthy controls. The sera from 59 out of 111 (53%) Japanese alopecia patients were positive for anti-nuclear antibody (ANA), as compared to the sera of 16 out of 105 (15%) healthy controls (p < 0.001). Twenty percent (22/111) of the alopecia patients were shown to be positive for the prevalence of anti-DFS70 antibodies, as compared to 8% (8/105) of the healthy controls (p < 0.01). IgG subclass analysis by ELISA showed that IgG1 and IgG2-anti-DFS70 antibodies were dominant in alopecia patients. The DFS70 gene expression in the hair structures was clearly detected in both those with and those without the anti-DFS70 antibody by RT-PCR. Immunohistochemical techniques showed that the DFS70 was localized predominantly in the outer root sheath (ORS) cells. The elevated anti-DFS70 antibodies in alopecia patients and the localization of the DFS70 in the ORS suggest that autoantibodies against the DFS70 are related to the etiology in a certain population of AA.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Anti-alopecia mechanisms of soymetide-4, an immunostimulating peptide derived from soy beta-conglycinin.

Previously, we found that orally administered soymetide-4 (MITL), an immunostimulating peptide derived from soybean beta-conglycinin alpha' subunit, suppressed alopecia induced by the anti-cancer drug etoposide in neonatal rats. Soymetide-4 has weak affinity for N-formyl-methionyl-leucyl-phenylalanine (fMLP) receptor. fMLP showed an anti-alopecia effect after intraperitoneal administration, though it was inactive after oral administration. Anti-alopecia effect of fMLP was blocked by pyrilamine or cimetidine, antagonists for histamine H1 or H2 receptor, respectively. However, the anti-alopecia effect of soymetide-4 was not inhibited by the histamine antagonists but by indomethacin, an inhibitor of cyclooxygenase (COX), or AH-23848B, an antagonist of the EP4 receptor for PGE2. Anti-alopecia effect of soymetide-4 was also blocked by pyrrolidine dithiocarbamate, an inhibitor of nuclear factor-kappaB (NF-kappaB). These results suggest that PGE2, which is produced after activation of COX by soymetide-4, might suppress apoptosis of hair matrix cells and etoposide-induced alopecia by activating NF-kappaB.

Adjuvants, Immunologic↗
PubMed2006

The histopathology of noncicatricial alopecia.

During the past 2 decades, the use of transverse sections in the evaluation of scalp biopsy specimens has led to a better understanding of the histopathologic changes in both cicatricial and noncicatricial alopecia. However, the technique has provided the most significant gains in the study of the latter type of alopecia, where evaluation of follicle density and follicular dynamics are integral to accurate diagnosis. This report reviews the histopathologic findings of four common types of noncicatricial alopecia: androgenetic alopecia, telogen effluvium, alopecia areata, and trichotillomania/chronic traction alopecia.

Alopecia↗
PubMed2006

The histopathology of primary cicatricial alopecia.

Alopecia typically is divided into cicatricial (scarring) and noncicatricial (nonscarring) forms. "Scarring" alopecia implies that follicular epithelium has been replaced by connective tissue and is therefore an irreversible process. In contrast, nonscarring alopecia is potentially reversible as follicular epithelia remain intact. Classification of cicatricial alopecia can be confusing and controversial as most disorders demonstrate overlapping clinical and histologic features. Herein, we present an overview of the histologic assessment of cicatricial alopecia, including an algorithmic approach to the evaluation of biopsy specimens from patients with scarring alopecia.

Alopecia↗
PubMed2006

Medical treatment of noncicatricial alopecia.

Androgenetic alopecia, alopecia areata, and telogen effluvium are the primary nonscarring alopecias found in clinical practice. Androgenetic alopecia is considered to be the most common form of human alopecia and is postulated to affect more than 50% of men by age 50. Alopecia areata affects up to 2% of the U.S. population. Telogen effluvium frequently occurs after major life events, such as a severe illness, childbirth, or high fever, and may be associated with the use of certain medications or iron deficiency, particularly in women. The focus of this review is on the medical treatment of these common hair loss conditions.

Alopecia↗
PubMed1997

Postmenopausal frontal fibrosing alopecia: a frontal variant of lichen planopilaris.

BACKGROUND: Lichen planopilaris usually produces multifocal areas of scarring alopecia. Recently, a condition in postmenopausal women characterized by progressive frontal hairline recession associated with scarring has been described. OBJECTIVE: Our purpose was to study the clinical and histopathologic features and results of treatment in a group of women with the frontal variant of lichen planopilaris and to compare the immunohistochemical profile of scalp biopsy specimens from this subset with that found in the multifocal variant of lichen planopilaris. METHOD: The clinical data as well as the histopathologic findings in 16 women with frontal fibrosing alopecia were collated. The immunohistochemical profile of six scalp biopsy specimens from the frontal hairline were compared with six specimens from women with multifocal lichen planopilaris. RESULTS: In addition to the progressive frontal fibrosing alopecia in all 16 women, total loss or a marked decrease of the eyebrows was observed in 13. No evidence of lichen planus was observed at other sites. In one patient multifocal areas of lichen planopilaris developed in the scalp. The frontal fibrosing alopecia was slowly progressive but has stabilized in five patients. Biopsy specimens from the frontal hairline showed histologic changes identical to lichen planopilaris. Immunophenotyping failed to reveal any significant differences between the frontal and multifocal variants. No effective treatments emerged although oral steroids and antimalarials may temporarily slow the course. Hormone replacement therapy did not appear to influence the course of the alopecia. CONCLUSION: Progressive frontal fibrosing alopecia is a clinically distinct variant of lichen planopilaris that affects in particular elderly women and frequently involves the eyebrows. The basis for this lichenoid tissue reaction targeting frontal scalp follicles and eyebrows is unknown.

Administration, Oral↗
PubMed2001

[Is alopecia areata a psychosomatic disease?].

INTRODUCTION: Destruction of hair follicles by lymphocytes induces alopecia aerata. Hence, immunological mechanisms are involved in this disease, as for numerous dermatoses. Nonetheless, alopecia aerata appears to be a psychosomatic disease. Is there any contradiction? CURRENT KNOWLEDGE AND KEY POINTS: Alopecia aerata often occurs after stress, particularly during mourning. Psychiatric disorders are more frequent in patients with alopecia than in healthy subjects. But these disorders might be secondary to the visible hair disease. Psychopathological mechanisms need to be clarified but alexithymia seems to be the key for understanding how stress could induce hair loss. In the skin (and the scalp) all functions are narrowly controlled by nerve fibers. Among these functions are hair growth and immunity. Immune cells and hair follicle cells possess receptors for neurotransmitters, which are synthesized by neuronal endings. When activated, these receptors are able to modulate cell properties. The same phenomena are described with stress-induced hormones. In alopecia aerata, like in numerous other diseases, psychosomatics and immunology are not opposed because immune cells are controlled by the nervous system through neurotransmitters. FUTURE PROSPECTS AND PROJECTS: Research needs to be thorough in both the fields of psychology and neurobiology. Psychotherapies or psychotropes appear to be useful in the treatment of alopecia aerata.

Alopecia Areata↗
PubMed2000

Prevention of chemotherapy-induced alopecia using an effective scalp cooling system.

Alopecia is a distressing side-effect of cancer treatment. Taxanes (TX), anthracyclines (ANR) and etoposide (ET) have been consistently associated with significant alopecia. We studied an effective scalp cooling system, the Penguin Cold Cap system, for the prevention of chemotherapy-induced alopecia in 70 patients receiving chemotherapy, including one of the following major alopecia-causing agents: Group A, TX-based regimes (without ANR); Group B, TX+ANR; Group C, ANR-based regimes (without TX); Group D, ET-based regimes. Protection from hair loss was achieved by maintaining scalp temperatures below 15 degrees C before, during and after chemotherapy by frequent changing of the caps. Assessment was carried out using a grading system from 0 to 4. Grades 0-2 were considered as satisfactory hair protection, whilst Grades 3-4 were considered failures. 57 patients were evaluable for assessment. An overall 81% protection was achieved. In groups C and D 11 of 12 patients (92%) had no alopecia, whilst 30 of 34 patients (88%) treated with taxanes had adequate hair protection. In Group B, 4 of 11 patients (36%) had adequate hair protection. The system was well tolerated and is a very effective method for protection from hair loss caused by TX, ANR and ET. Our results are comparable with and, in most cases, better than those reported in other studies using various alopecia preventive methods.

Adult↗
PubMed1998

Novel agents for the treatment of alopecia.

Recent approval in the United States of two new products, Propecia (Merck Co, Rahway, NJ) and Rogaine Extra Strength 5% (Pharmacia & UpJohn Co, Kalamazoo, MI), indicated in men to promote scalp hair growth, have added a new dimension to treatment options offered by physicians in treating androgenetic alopecia (AGA). The search for new and effective agents to treat many different hair loss problems has been intensified by the increase in hair biology research taking place worldwide, from university academic institutions to the pharmaceutical companies. All have a desire to profit from marketing such drugs that have been termed, "cosmeceuticals". Millions of men and women of every race suffer from various forms of alopecia, the most common being AGA where the target tissue active androgen, 5 alpha-dihydrotestosterone (DHT) aggravates genetically programmed scalp hair follicles that results in short, fine, miniaturized hairs. Currently available to treat alopecia are drugs indicated for other disease processes because no other agents are accessible; some have severe side-effects and many are minimally effective. These prescription drugs were not originally indicated for alopecia and have not been adequately tested in controlled clinical trials to assess for efficacy, safety, and toxicity. These agents continue to be used clinically to treat patients with various forms of alopecia. As a result, a variety of new agents are emerging in the patient application process to gain protection and approval specifically for various forms of alopecia. This report reviews the most recently approved products, some of the more promising compounds in clinical trial development, as well as those in the over-the-counter (OTC) "natural" treatments category.

Alopecia↗
PubMed2002

Relationship between irreversible alopecia and exposure to cyclophosphamide, thiotepa and carboplatin (CTC) in high-dose chemotherapy.

Reversible alopecia is a commonly observed, important and distressing complication of chemotherapy. Permanent alopecia, however, is rare after standard-dose therapy, but has occasionally been observed after high-dose chemotherapy with cyclophosphamide, thiotepa and carboplatin (CTC). We evaluated the relationships between total exposure to these three compounds and their different metabolites in the high-dose CTC regimen, and the subsequent development of irreversible alopecia. Twenty-four patients received two or three courses of high-dose CTC, each followed by peripheral blood progenitor cell transplantation. Plasma levels of cyclophosphamide, its active metabolite 4-hydroxycyclophosphamide, thiotepa, its active metabolite tepa, and carboplatin were determined, and the area-under-the-plasma concentration-versus-time curves (AUC) of the compounds were calculated. Eight of the 24 patients included in the study developed permanent alopecia, while seven had normal hair regrowth and nine patients developed incomplete and/or thin hair regrowth. The carboplatin AUC and the summed AUC of thiotepa and tepa were both significantly associated with increasing irreversibility of hair loss. These results suggest that high exposure to carboplatin and the sum of the thiotepa and tepa exposure may lead to the development of permanent alopecia. This knowledge could guide therapeutic drug monitoring in order to prevent the occurrence of permanent alopecia and thereby improve the patients' quality of life.

Adolescent↗
PubMed2001

Melanocyte-associated T cell epitopes can function as autoantigens for transfer of alopecia areata to human scalp explants on Prkdc(scid) mice.

Alopecia areata is a tissue restricted autoimmune condition affecting the hair follicle, resulting in hair loss. The goal of this study was to test the hypothesis that the autoantigen of alopecia areata is melanocyte associated. Potential autoantigens were tested in the human scalp explant/Prkd(scid) CB-17 mouse transfer system. Scalp T cells from lesional (bald) alopecia areata scalp were cultured with antigen-presenting cells, and antigen, along with interleukin-2. The T cells were then injected into autologous lesional scalp grafts on SCID mice, and hair regrowth was measured. Hair follicle homogenate was used as an autoantigen control. T cells cultured with melanoma homogenate induced statistically significant reduction in hair growth (p <0.01 by ANOVA). HLA-A2-restricted melanocyte peptide epitopes were then tested with lesional scalp T cells from HLA-A2-positive alopecia areata patients. Melanocyte-peptide-activated T cells significantly reduced the number of hairs regrowing in two experiments with six patients (p <0.001 by ANOVA). Injected scalp grafts showed histologic and immunochemical changes of alopecia areata. The most consistent peptide autoantigens were the Gp100-derived G9-209 and G9-280 peptides, as well as MART-1 (27-35). Melanocyte peptide epitopes can function as autoantigens for alopecia areata. Multiple peptides were recognized, suggesting epitope spreading.

Adult↗
PubMed2003

Alopecia areata susceptibility in rodent models.

With our current view of alopecia areata as an autoimmune disease, it is probable that disease development in an individual is dependent on multiple genetic and environmental factors interacting in a complex system. Rodent models afford the opportunity to investigate alopecia areata development and to define the significance of the different factors involved. Recently, rodent model characterization has been conducted using flow cytometry, microarray analysis, and functional studies. From these a pattern of events in alopecia areata development has emerged. Although the preliminary activation events for the onset of alopecia areata remain unknown, the response of the immune system is characterized by antigen presentation and costimulation of lymphocytes in the lymph nodes and skin, a deficiency of CD4+/CD25+ regulatory cells, and an action of activated lymphocytes on hair follicles via Fas/FasL signaling and cytokines. Thus, onset of disease may require appropriate (or inappropriate) expression of stimulatory antigens within the hair follicle, the breakdown of the putative hair follicle immune privilege, the presentation of antigens to the immune system, a failure of immune system regulation, and the ability of the activated immune system to disrupt anagen-stage hair follicles. Once the sequence of events is initiated, it may become a self-perpetuating cycle, with epitope spreading leading to a wider range of targets in chronic alopecia areata. Rodent model studies have provided significant insight into alopecia areata, but much more remains to be explained about the mechanisms of disease development.

Alopecia Areata↗
PubMed2003

Genetic linkage studies in alopecia areata.

Alopecia areata affects approximately 4.6 million individuals in the United States alone. It is typified by patchy hair loss on the scalp that can progress to cover the entire scalp (alopecia totalis) and eventually the entire body (alopecia universalis). Despite the high incidence of this condition, its genetic basis is largely unknown. It is now generally accepted, however, that it fits the paradigm of a complex trait, in which a combination of genetic and environmental factors results in the final phenotype. Genetic studies have been limited thus far to association analyses, which suggest that a permissive HLA status may potentiate the development of alopecia areata. A systematic screen for identifying the primary genetic mechanisms underlying this disorder has never before been undertaken, however. Here we discuss our approach to the identification of susceptibility genes for alopecia areata. In particular, we recently initiated a comprehensive genetic analysis by performing a genome-wide scan in a collection of alopecia families with multiple affected family members. There are currently a number of examples of complex diseases of the skin, such as psoriasis and atopic dermatitis, in which genetic studies are being undertaken that substantiate the timeliness of this approach. We anticipate that these studies will lead to the identification of the susceptibility genes and provide a foundation for understanding how they interact with each other and with other variables, such as the immune system and environmental factors.

Alopecia Areata↗
PubMed2003

Therapy of alopecia areata: on the cusp and in the future.

Over the past decade, basic research has established alopecia areata as a T cell-mediated autoimmune disease and has clarified many of its genetic, cellular, and molecular aspects. Perifollicular and intrafollicular mononuclear cell infiltrates directed at anagen hair bulbs are characteristic and striking histologic features in early alopecia areata. The inflammatory infiltrate is composed predominantly of activated CD4+ and CD8+ T cells, together with macrophages and Langerhans cells. The initiation phase of alopecia areata is mediated by type 1 cytokines, including interleukin-2, interferon-gamma, and tumor necrosis factor-alpha. Like other diseases with a strong autoimmune component, alopecia areata has associated with it specific human leukocyte antigens, which determine susceptibility, severity, chronicity, and resistance. New topical immunomodulating drugs and biologic therapies that have been developed, or that are in development, for the treatment of other immune-mediated inflammatory skin diseases will likely be effective in alopecia areata as well. The present discussion addresses the treatment of alopecia areata within the framework of these new modalities.

Adjuvants, Immunologic↗
PubMed2000

HLA in alopecia areata.

BACKGROUND: The aim of this study was to investigate the human leukocyte antigen (HLA) characteristics of Turkish alopecia areata patients, and the correlation of the HLA profile with age of onset, severity and duration of the disease, presence of ophiasis, and family history. METHODS: A total of 88 patients with alopecia areata, alopecia totalis, or alopecia universalis were compared with 100 healthy controls. HLA typing was performed by the Terasaki microlymphocytotoxicity method. RESULTS: The frequency of HLA-A1, HLA-B62(15), HLA-DQ1, and HLA-DQ3 was significantly higher in patients than in controls. HLA-DR16 was significantly less common in patients than in the control group, and we concluded that this allele might have a protective role for alopecia areata. Juvenile onset and severe involvement were related with HLA-Cw7 and HLA-DR1, respectively. The HLA profile was independent of the existence of long-standing disease, presence of ophiasis, and a positive family history. CONCLUSIONS: In HLA-alopecia areata association, ethnic differences may play a role.

Adolescent↗