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PubMed2004

[Alopecia areata in animal models--new insights into pathogenesis and treatment of a T cell-mediated autoimmune disorder].

Alopecia areata is a common disease, but for ethical reasons it seems difficult to perform large-scale studies to elucidate the pathogenesis and to develop new therapeutic approaches in man. It is therefore helpful to develop appropriate animal models. The Dundee experimental bald rat (DEBR) and the C3H/HeJ mouse are well-established animal models for alopecia areata and can be used for the study of genetic aspects, pathogenesis and therapy of the disease. In C3H/HeJ mice alopecia areata can be experimentally induced by grafting lesional skin from an affected mouse to a histocompatible recipient which offers the possibility to study the influence of various factors on the development of the disease. Studies on the C3H/HeJ mouse and the DEBR have corroborated the concept that alopecia areata is a T-cell mediated autoimmune disease and various steps and aspects of the pathogenesis have been elucidated. Based on this knowledge new therapeutic options may be developed such as inhibition of lymphocyte-homing by an anti-CD44v10 antibody, or inhibition of costimulation by monoclonal antibodies. Therapeutic studies in the C3H/HeJ mouse and the DEBR suggest that alopecia areata can be treated by topical tacrolimus but treatment in humans may only be successful after development of an improved vehicle that facilitates penetration of tacrolimus down to the hair bulb. Current investigations in mice are designed to elucidate the mechanisms how contact sensitizers act in the treatment of alopecia areata, and this will hopefully lead to the development of more specific approaches based on the beneficial effect of contact sensitizers.

Alopecia Areata↗
PubMed1999

Association between alopecia and response to aggressive chemotherapy in patients with Hodgkin's disease.

The clinical significance and implications of absence of alopecia and/or neutropenia in patients treated with chemotherapy for malignant disease is unknown. We hypothesized that there is a common mechanism of resistance to the effects and the adverse effects of anticancer treatment, which may have clinical implications. To evaluate this hypothesis, we conducted a retrospective analysis of the charts of 17 consecutive patients with Hodgkin's disease who received at least 4 courses of combination chemotherapy (ABVD or MOPP/ABV). Twelve patients underwent complete alopecia while 5 patients retained their hair or had only minimal hair loss. The two groups had similar pretreatment characteristics. Ten (83%) of the patients with alopecia achieved complete remission as compared with 2 (40%) of the patients who retained their hair (P = 0.11). Also, patients without alopecia had fewer episodes of neutropenia (0% vs 33%, P = 0.02), delays of scheduled treatments (0% vs 66%, P = 0.02) or number of courses with dose reductions (20% vs 41%, P = 0.39). These differences shows a clear trend which did not reach statistical significance due to the small number of patients. We suggest that, in intensively treated patients with Hodgkin's disease, the absence of alopecia may predict a poor response to treatment. Also, patients without alopecia probably have fewer episodes of leukopenia, deferral of treatment courses or number of courses with dose reductions. We hypothesize that there is a common mechanism of resistance to cytotoxic agents that may prevent apoptotic death in both normal and malignant cells.

Adult↗
PubMed2001

Association of reversible alopecia with occupational topical exposure to common borax-containing solutions.

Boron is widely used in industrial materials, most frequently as the salt borax. Systemic exposure (eg, ingestion) to boron in boric acid been associated with reversible toxic alopecia among other manifestations. There is scant clinical literature on alopecia caused by topical exposure to boron. We observed a series of 3 patients in 2 workplaces who suffered reversible alopecia from cutaneous boron exposure. The scalp alopecia was global in 1 patient and patchy in 2 patients. Alopecia was completely reversed by elimination or reduction of exposure to boron-containing materials in all 3 patients. We conclude that occupational topical exposure to boron in solutions may cause reversible alopecia.

Adult↗
PubMed1999

Quantitative and ultrastructural analysis of inflammatory infiltrates in male pattern alopecia.

In order to determine whether lymphocytic inflammation around the lower infundibula in male pattern alopecia is incidental or a general phenomenon, we performed morphometric and ultrastructural analysis of inflammatory infiltrates in the transitional zones of the vertex and occipital hairy scalps of 19 patients with male pattern alopecia. Six normal subjects served as controls. The number of inflammatory infiltrates around the follicular infundibula of the alopecic vertices and non-alopecic occiputs of male pattern alopecia patients was significantly greater than the corresponding control value. The number of mast cells in the widened fibrous tracts in the vertices of male pattern alopecia patients was significantly greater than those in the adventitial fibrotic sheaths of control subjects and the non-alopecic occiputs of male pattern alopecia patients. These data support the idea that the inflammatory process may be, at least in part, responsible for the development of male pattern alopecia.

Adolescent↗
PubMed2006

Determination of the sildenafil effect on alopecia areata in childhood: An open-pilot comparison study.

BACKGROUND: Alopecia areata is an immunologically mediated cessation of hair growth primarily involving, but not limited to, the scalp. The treatment of alopecia areata involves promotion of hair growth (for instance with topical minoxidil application), immunosuppression (intralesional or systemic steroid therapy, phototherapy) or immunomodulation (anthralin, dinitrochlorobenzene, diphenylcyclopropenone, squaric acid dibutylester). All these medications have some disadvantages and difficulties for the treatment of children with alopecia areata. OBJECTIVE: To use an open-pilot study to assess the efficacy of topical 1% sildenafil in children diagnosed with alopecia areata. METHODS: Eight patients with (25% of scalp surface area involvement) alopecia areata who were refractory to previous topical treatments applied 1% sildenafil twice daily for 3 months. All the patients completed the study. RESULTS: Two patients experienced vellus-type hair growth and one patient had terminal hair growth. However, these outcomes were accepted as the spontaneous regression of the disease. CONCLUSION: We cannot recommend the use of topical 1% sildenafil for the treatment of alopecia areata without further evidence of its therapeutic benefit.

Adolescent↗
PubMed1998

A gene for universal congenital alopecia maps to chromosome 8p21-22.

Complete or partial congenital absence of hair (congenital alopecia) may occur either in isolation or with associated defects. The majority of families with isolated congenital alopecia has been reported to follow an autosomal-recessive mode of inheritance (MIM 203655). As yet, no gene has been linked to isolated congenital alopecia, nor has linkage been established to a specific region of the genome. In an attempt to map the gene for the autosomal recessive form of the disorder, we have performed genetic linkage analysis on a large inbred Pakistani family in which affected persons show complete absence of hair development (universal congenital alopecia). We have analyzed individuals of this family, using >175 microsatellite polymorphic markers of the human genome. A maximum LOD score of 7.90 at a recombination fraction of 0 has been obtained with locus D8S258. Haplotype analysis of recombination events localized the disease to a 15-cM region between marker loci D8S261 and D8S1771. We have thus mapped the gene for this hereditary form of isolated congenital alopecia to a locus on chromosome 8p21-22 (ALUNC [alopecia universalis congenitalis]). This will aid future identification of the responsible gene, which will be extremely useful for the understanding of the biochemistry of hair development.

Alopecia↗
PubMed1998

Cloning, genomic organization, alternative transcripts and mutational analysis of the gene responsible for autosomal recessive universal congenital alopecia.

Complete or partial congenital absence of hair (congenital alopecia) may occur isolated or with associated defects. The majority of families with isolated congenital alopecia has been reported to follow an autosomal recessive mode of inheritance (MIM 203655). We have previously mapped the gene for autosomal recessive congenital alopecia in a large inbred Pakistani family in which affected persons show complete absence of hair development (universal congenital alopecia) to a 15 cM region on chromosome 8p21-22. Here we report the cloning and characterization of the human homologue of the mouse hairless gene and show that it is located in the critical region on chromosome 8p21-22. Determining the exon-intron structure allowed detailed mutational analysis of DNA samples of patients with universal congenital alopecia. We detected a homozygous missense mutation in the Pakistani family and a homozygous splice donor mutation in a family from Oman. In addition, we show that the human hairless gene undergoes alternative splicing and that at least two isoforms generated by alternative usage of exon 17 are found in human tissues. Interestingly, the isoform containing exon 17 is the predominantly expressed isoform in all tissues but skin, where exclusive expression of the shorter isoform was observed. We speculate that this tissue-specific difference in the proportion of hairless transcripts lacking exon 17 sequences could contribute to the tissue-specific disease phenotype observed in individuals with isolated congenital alopecia.

Adult↗
PubMed2005

Expression of androgen receptor coactivator ARA70/ELE1 in androgenic alopecia.

BACKGROUND: Androgens have been implicated in androgenic alopecia as evidenced by the increased cutaneous expression of androgen receptor (AR), 5alpha-reductase, and decreased aromatase. Abnormalities of the AR-signal transduction pathway probably participate in the development of androgenic alopecia. ARA70/ELE1 is an AR coactivator with two isoforms, one full-length form (ARA70alpha/ELE1alpha), and an internally deleted form (ARA70beta/ELE1beta). We decided to examine the cutaneous expression of both isoforms in male androgenic alopecia. METHODS: Formalin-fixed, paraffin-embedded tissue sections from seven subjects with androgenic alopecia with matched punch biopsies from non-balding and balding areas were examined by in situ hybridization. RESULTS: Expression of at least one of the two probes for ARA70/ELE1 was present in all phases of the hair-growth cycle in all epithelial hair structures except for the inner root sheath. The dermal papilla and hair bulb expressed only the short (beta) but not the long (alpha) form of ARA70/ELE1. In situ labeling for ARA70beta/ELE1beta was weaker in the dermal papilla of balding recipient areas than those from donor ones. CONCLUSIONS: Our data further support that the hair growth is regulated by androgens. The differential expression pattern of ARA70/ELE1 suggests that this key androgen receptor coactivator is involved in androgenic alopecia. Lee P, Zhu C-C, Sadick NS, Diwan AH, Zhang PS, Liu JS, Prieto VG. Expression of androgen receptor coactivator ARA70/ELE1 in androgenic alopecia.

Alopecia↗
PubMed2004

Autoimmunity: alopecia areata.

Strong direct and indirect evidence supports an autoimmune etiology for alopecia areata. T lymphocytes that have been shown to be oligoclonal and autoreactive are predominantly present in the peribulbar inflammatory infiltrate. Alopecia areata frequently occurs in association with other autoimmune diseases, such as thyroiditis and vitiligo, and autoantibodies to follicular components have been detected. Finally, the use of immune modulating drugs, including corticosteroids and contact sensitizers such as dyphencyprone, can be beneficial in the management of this disease. Recent studies have demonstrated that alopecia areata scalp skin grafted onto nude mice with severe combined immunodeficiency grow hair and that infiltrating lymphocytes in the graft are lost. It is now also possible to induce alopecia areata in human scalp explants on these mice by injecting T lymphocytes with scalp homogenate. Neuropeptides produced by cutaneous nerves are known to modify immune reactivity and, in all likelihood, affect the alopecia areata process. Future studies may show that modulation of neuropeptide expression is associated with hair regrowth. Likewise, testing the efficacy of the newly developed immunomodulatory agents in patients with alopecia areata may lead to the introduction of novel therapies for this immune-mediated disease of the hair follicle.

Alopecia Areata↗
PubMed1986

Analysis of the relation between alopecia and resistance to 1,25-dihydroxyvitamin D.

Alopecia is a frequent feature in hereditary resistance to (1,25(OH)2D). We sought insight into this feature by analysing data from affected members of 30 kindreds. We assessed indices of mineral metabolism in one group with normal hair compared with a group with alopecia. Hereditary resistance to 1,25(OH)2D was diagnosed at an earlier age in alopecic patients (0.9 vs 3.3 years, P less than 0.05); this reflected late presentation of metabolic bone disease in some cases with normal hair and could not be attributed to early diagnosis resulting from the striking feature of alopecia. For untreated subjects, serum concentrations of calcium and 1,25(OH)2D were similar in both groups of patients. During calciferol therapy, however, the cases with alopecia showed lower serum calcium (1.9 vs 2.4 mmol/l, P less than 0.005), but higher serum 1,25(OH)2D (2900 v 340 pg/ml, P less than 0.005). Hair status did not predict the type of defect identified with cultured skin fibroblasts but did correlate with responsiveness of 25(OH)D 24-hydroxylase to 1,25(OH)2D3 in those cells. Cells from seven of eight kindreds with alopecia showed no 24-hydroxylase response to high doses of 1,25(OH)2D3 while cells from five of six kindreds with normal hair showed a 24-hydroxylase response to high doses of 1,25(OH)2D3. We conclude that in cases with hereditary resistance to 1,25(OH)2D alopecia reflects the more severe grades of this resistance based upon earlier age at time of diagnosis, lower potential for calcaemic response to calciferols, and lower potential for 24-hydroxylase response to 1,25(OH)2D3 by cultured skin fibroblasts.

Alopecia↗
PubMed2006

Enoxaparin-induced alopecia in patients with cerebral venous thrombosis.

OBJECTIVE: To report three cases of alopecia induced by the anticoagulant enoxaparin in cerebral venous thrombosis (CVT) patients. CASE SUMMARY: Three female patients were treated initially with direct intrasinus urokinase, and then followed by low-molecular-weight heparin (LMWH) enoxaparin at 1 mg/kg given subcutaneously twice daily for 3 weeks. It was switched to oral anticoagulant warfarin at 5 mg daily for another 6 months. Nearly 3 weeks after the initiation of anticoagulation, all of the three patients complained of excessive hair loss with large areas of patchy, non-scarring alopecia. Hair growth returned to normal within 1 month after the completion of enoxaparin. DISCUSSION: Unfractionated heparin remains the first-line treatment of CVT because of its efficacy, safety and feasibility. Alopecia has been reported as a side effect of LMWHs dalteparin and tinzaparin. The pattern of hair loss, telogen effluvium, involves the induction of the hair follicle into a resting phase without apparent pathologic implication. In addition, this article also reviewed other medications taken by the patients that are possibly associated with hair loss. CONCLUSION: From the review of literature, there is no report of alopecia caused by urokinase. Using the Naranjo ADR Probability Scale, a score of 6 suggests that enoxaparin was the probable cause of alopecia in our three patients. This report introduces evidence of alopecia as a probable side effect of enoxaparin, but stresses the efficacy and safety of LMWH. As this is not a life-threatening disorder, we hope to increase the awareness of pharmacists and clinicians to this relatively rare but important side effect.

Adult↗
PubMed2006

An overview on congenital alopecia in domestic animals.

Alopecia, that is, lack of hair in any quantity, is a frequent complaint of pet owners. Although mostly acquired, rare congenital forms of alopecia exist that are associated with abnormalities in hair follicle morphogenesis. Congenital alopecias can result in changes in quality or quantity of hair follicles and the hair fibres produced by them. They vary in terms of clinical presentation and mode of inheritance. Histopathology is usually needed in order to differentiate between a reduced number of otherwise normal hair follicles and qualitative hair follicle abnormalities. Although our understanding of the molecular mechanisms that drive hair follicle morphogenesis in mice and humans has significantly increased during the last decade, still very little is known about congenital alopecias in domestic animals. Because of their rarity and the general lack of knowledge about their pathophysiology, classification of congenital alopecias in domestic animals is still unsatisfactory. This article reviews hair follicle morphogenesis and its most important molecular mechanisms, and it discusses the various forms of congenital alopecia occurring in domestic animals that have been described in the literature, differentiating between hair follicle aplasia, hair follicle dysplasia (i.e. defects associated with hair follicle development and defects associated with hair shaft formation), and neuroectodermal dysplasias, the latter involving the hair follicle pigmentary system.

Alopecia↗
PubMed1994

Alopecia areata and increased prevalence of psychiatric disorders.

BACKGROUND: The relationship between psychiatric disorders and alopecia areata has not been well studied. Although previous reports have been unable to correlate psychiatric illness with hair loss, a recent study determined that 74% of patients with alopecia areata (AA) under evaluation had one or more lifetime psychiatric diagnoses. METHODS: Two hundred and ninety-four community-based patients with alopecia areata responded to a detailed questionnaire distributed by Help Alopecia International Research, Inc. The prevalence of psychiatric disorders was determined using diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders (DSM-IIIR). RESULTS: Major depression, generalized anxiety disorder, social phobia, and paranoid disorder were all present in patients with alopecia areata at rates significantly higher than in the general population. CONCLUSIONS: Alopecia areata patients are at a higher risk of developing psychiatric comorbidity during their clinical course.

Alopecia Areata↗
PubMedDate not supplied

Effects of psoralen-UV-A-Turban in alopecia areata.

BACKGROUND: Psoralen-UV-A (PUVA)-turban is a modification of PUVA-bath therapy used in alopecia areata. OBJECTIVE: The aim of this study was to assess the efficacy of PUVA-turban in different forms of alopecia areata. Twenty patients completed the study: nine with alopecia areata vulgaris and 11 with alopecia areata totalis or universalis. METHODS: 8-methoxypsoralen in a dilution of 0.0001% (1 mg/L) was administered to the scalp for 20 minutes using a cotton towel as a turban. The application was followed by UV-A radiation. Treatments were performed two or three times weekly. The cumulative doses ranged from 48.2-253.4 J/cm2, and single fractions ranged from 0.3-6.5 J/cm2. RESULTS: Hair regrowth was observed in 15 patients (total regrowth in six patients and partial regrowth in nine patients). Five patients did not respond to the therapy. CONCLUSIONS: PUVA-turban was significantly more effective in alopecia areata vulgaris than in alopecia areata totalis or universalis and proved to be a safe, well tolerated method without the systemic side effects of PUVA.

Administration, Topical↗
PubMed1993

Alopecia universalis in an HIV-positive patient: possible insight into pathogenesis.

Alopecia universalis, a variant of alopecia areata, is a disease of unknown etiology, though evidence for an autoimmune etiology continues to mount. We report an HIV-positive patient with altered T-lymphocyte subsets in whom alopecia universalis developed. A skin biopsy of the patient's scalp demonstrated a classic perifollicular lymphocytic infiltrate, and immunophenotyping of the same specimen revealed that the majority of the cells were CD4+ lymphocytes. During the active loss of hair, the patient's CD4/CD8 ratio was decreased. This ratio normalized during the period of regrowth. Our data suggest that systemic immune dysfunction, as seen in HIV infection, may be more important in mediating alopecia areata than localized immune responses. Given the proposed mechanism of alopecia areata developing in this patient, i.e. influx of CD4+ lymphocytes to the perifollicular regions of skin when the CD4/CD8 ratio is low, it is surprising that alopecia areata is not seen more commonly in patients with HIV infection.

Adult↗
PubMed2006

Coat condition, housing condition and measurement of faecal cortisol metabolites--a non-invasive study about alopecia in captive rhesus macaques (Macaca mulatta).

BACKGROUND: Previous studies have characterized alopecia in captive rhesus macaques (Macaca mulatta) by a mixed partial to complete alopecia in a bilateral symmetric pattern. METHODS: In this study, coat condition assessments were related to exogenous and endogenous factors in captive rhesus macaques under different housing conditions in order to identify disturbances in environmental factors controlling or influencing hair growth. Additionally, the degree of alopecia was investigated in relation to adrenal endocrine function as an indicator of social stress using faecal glucocorticoid measurements. RESULTS: Hair loss was found to vary with season and sex, was most pronounced in adult females during the winter and spring months. Generally, infants were not affected, but alopecia developed during adolescence. However, the housing system, available enclosure space and variations in group size and composition also appeared to influence coat condition. Levels of immunoreactive cortisol metabolites (11-oxoetiocholanolone) in faeces were significantly negatively correlated with alopecia, suggesting a relationship between hypothalamic-pituitary-adrenal (HPA) axis activity and hair loss in captive rhesus macaques. CONCLUSIONS: Although the present study demonstrates the influence of the HPA axis on coat condition, it is not known if hair loss is caused by abnormal behaviour or hormonal imbalances of the HPA axis itself. Our data suggest that alopecia in rhesus macaques is a highly complex multicausal disorder.

Aging↗
PubMed1990

Protection from chemotherapy-induced alopecia in a rat model.

Alopecia (hair loss) is among the most distressing side effects of cancer chemotherapy. Little progress has been made, however, in its prevention or treatment, partly because of the lack of suitable experimental model. In recent work on the treatment of myelogenous leukemia in the rat, the following observations were made: (i) treatment of 8-day-old rats with cytosine arabinoside consistently produced alopecia, and (ii) ImuVert, a biologic response modifier derived from the bacterium Serratia marcescens, uniformly produced complete protection against the alopecia. In subsequent experiments, both cyclophosphamide and doxorubicin also produced alopecia in this model, and the doxorubicin-induced alopecia was prevented by treatment with ImuVert. The potential relevance of these observations to chemotherapy-induced alopecia in the clinical setting should be examined.

Alopecia↗
PubMed1993

Scarring alopecia in neonates as a consequence of hypoxaemia-hypoperfusion.

Scarring alopecia is relatively uncommon in infants and children and rarely discussed in the paediatric literature. It does not appear to have been previously documented as a consequence of compromised oxygenation and blood supply in the neonatal population or as a complication of extracorporeal membrane oxygenation (ECMO) treatment. During a six month period, we observed five patients who presented to our neonatal intensive care unit with pressure ulcers that eventuated in scarring alopecia. The patients were all > or = 2500 g at birth, had some disruption of the cardiac circulation, were hypoxaemic and acidotic, and required vasopressor treatment. Institution of a positioning schedule and use of a thermostable Spenco gel pad during the subsequent six month period eliminated the presence of pressure ulceration and scarring alopecia in this at-risk population. Although scarring alopecia is a permanent condition, skin changes preceding its development in this setting are recognisable and follow a predictable pattern and time course, and should therefore allow for intervention at an earlier stage. Neonatal ECMO patients, as well as those who suffer hypoxaemia-hypoperfusion, but do not require circulatory bypass, appear to be at increased risk for development of the pressure ulcers that precede scarring alopecia. Paediatricians should consider this possibility and seek the appropriate historical information when confronted with a case of scarring alopecia after the neonatal period.

Acidosis↗