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Wang, Eddy Hsi Chun. "The pathogenesis of alopecia areata." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/51360.
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The development of a hair loss disease, alopecia areata (AA), is believed to be associated with the initiation of an autoimmune response triggered by the activation of cytotoxic T-cells (CTLs) by unidentified autoantigen epitopes. The long-term sequelae of AA also have not received investigation beyond clinical observations. I hypothesized that CTLs in AA can be activated by autoantigen epitopes derived from hair follicle (HF) cells and activated CTLs may affect the viability of HF keratinocytes. Furthermore, I hypothesized the development of AA can have adverse effects on heart health and induce apoptosis of cardiomyocytes mediated in part by stress hormones. To test these hypotheses, I stimulated AA human peripheral blood mononuclear cells (PBMCs) and mouse LNCs with HF autoantigen epitope peptides. I showed that trichohyalin (TCHH) peptides induced higher frequencies of AA PBMC activation and led to keratinocyte apoptosis, while cytokeratin 16 (KRT16) peptides activate more AA mouse LNCs; both indicating the importance of keratinocyte autoantigens in AA pathogenesis. We showed that AA mice displayed significantly heavier hearts and collagen deposition in hearts compared to controls. Exposure of heart tissues to stress hormone adrenocorticotrophic hormone (ACTH) resulted in differential expression of interleukin-18 (Il18) genes and increased secretion of cardiac disease marker cardic troponin-I (cTnI). AA patients showed highest levels of cTnI compared to androgenetic alopecia (AGA) and no-hair-loss (NHL) groups. Culturing of cardiomyocytes with plasma from AA subjects with higher levels of cTnI also resulted in higher levels of apoptosis compared to cultures with plasma expressing low levels of cTnI; suggesting presence of harmful factors in the plasma. Additionally, to prove AA is a cell-mediated disease, we established a new mouse model of AA via injecting naïve C3H/HeJ mice with cultured LNCs isolated from spontaneously affected AA mice. In conclusion, AA pathogenesis is associated with higher frequencies of PBMC or LNC activation upon keratinocyte antigen epitope challenge and AA development resulted in changes in gene expression and heart morphology in mice and heart tissue remodeling markers in humans.Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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Wendel, Caroline. "Kortikosteroider som behandling mot Alopecia Areata." Thesis, University of Kalmar, School of Pure and Applied Natural Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:hik:diva-287.
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Alopecia areata (AA) betyder fläckvis håravfall och uppstår vanligen på huvudet men även på kroppen. Det är en harmlös, reversibel, organ-specifik, autoimmun hudsjukdom som drabbar hårfolliklarna. Den autoimmuna reaktionen förmedlas av T-lymfocyter som angriper hårfolliklarna och hämmar hårväxt. Det årliga incidenstalet för både kvinnor och män är 20,2 per 100 000 personer och 1,7 % av befolkningen riskerar att drabbas någon gång under livet. Även om genetiskt anlag och miljöfaktorer, såsom emotionell stress, graviditet och tillfälliga infektioner kan utlösa sjukdomen så är den exakta orsaken fortfarande okänd. De behandlingar som finns mot AA påverkar inte den autoimmuna processen som orsakar alopecin utan syftet med dessa är att stimulera hårfolliklarna och dämpa sjukdomens aktivitet. Kortikosteroider används vid behandling mot AA, men kan ge svåra biverkningar vid långvarig behandling. De olika administrationsformer av kortikosteroider som används mot AA är främst lokala och systemiska, men även intralesionella.
Målet med denna litteraturstudie var att undersöka om kortikosteroider har någon effekt mot AA. Samtliga studier visade att kortikosteroider har effekt mot AA, men att risken för återfall är stor. Tre av de fem studierna visade att behandlingen gav bättre resultat hos de patienterna med mindre svår AA, kort duration och första episoden av sjukdomen. Dåliga prognostiska faktorer visade sig vara omfattande AA, lång duration, atopi, nagelinvolvering och flera episoder av sjukdomen.
En studie visade att patienter med plurifocal AA svarar bättre på behandlingen än patienter med ophiasic AA, AA totalis och AA universalis. I samtliga studier fick patienterna biverkningar av behandlingen med dessa var inte så allvarliga att patienterna fick avbryta behandlingen. Slutsatsen av detta arbete är att kortikosteroider har effekt mot AA, men att risken för återfall är stor.
2008:F3
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Olsen, E. A., M. K. Hordinsky, V. H. Price, J. L. Roberts, J. Shapiro, D. Canfield, M. Duvic, et al. "Alopecia areata investigational assessment guidelines ¿ part ii." American Academy of Dermatology, 2004. http://hdl.handle.net/10454/4042.
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noAlopecia areata is an immunologically mediated disease characterized by extreme variability not only in the time of initial onset of hair loss but in the duration, extent and pattern of hair loss during any given episode of active loss. These variables, as well as the unpredictable nature of spontaneous regrowth and lack of a uniform response to various therapies, has made clinical trials in alopecia areata difficult to plan and implement. In fact, there are currently no drugs FDA-approved specifically for the indication of alopecia areata. To help facilitate well-controlled clinical trials for alopecia areata, this National Alopecia Areata Foundation (NAAF) sponsored subgroup of investigators/clinicians experienced in clinical trials and/or in the clinical care of patients with alopecia areata has outlined some general principles and potential endpoints for clinical studies in alopecia areata. These guidelines build on the Alopecia Areata Investigational Assessment Guidelines published in 1991 which established baseline clinical staging and background information important to gather on any alopecia areata patient involved in clinical research.
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Funabashi, Marcia Yuri. "Alopecia areata no caso Flora: uma investigação psicopatológica." Pontifícia Universidade Católica de São Paulo, 2006. https://tede2.pucsp.br/handle/handle/15477.
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A investigação psicanalítica das manifestações somáticas levanta o enigma acerca da sua causalidade psíquica ao apostar na associação entre as vicissitudes destas doenças e questões da subjetividade. O tema desta dissertação retoma este impasse a partir da construção psicopatológica no caso Flora. Flora procura análise com a demanda de um saber sobre a alopecia areata universal, manifestação somática que rompeu com a sua lógica, deixando-a num completo desamparo. Ao tecer uma construção simbólica em torno da doença, Flora vai nos revelando a especificidade deste fenômeno. O conteúdo desta dissertação é uma mostra possível de um trabalho de elaboração em busca da palavra representativa do vivido na clínica. A construção metapsicológica resultante desta trajetória segue o pensamento da psicopatologia fundamental, sendo um produto de inúmeras reformulações promovidas pela escuta clínica e pelo constante diálogo com a teoria freudiana, de seus contemporâneos e com o discurso médico. Ao longo deste percurso de pesquisa, o estudo sobre a topologia lacaniana produziu um sentido na vivência clínica, ao sustentar que o corpo se estrutura a partir da articulação dos registros real, simbólico e imaginário, estabelecendo uma lógica precisa. Sendo assim, encontramos neste pensamento um eixo teórico para a compreensão da alopecia areata no caso Flora, através da investigação da estrutura presente nesta manifestação somática. A fim de alcançarmos uma maior compreensão acerca desta topologia de Lacan, realizamos uma releitura da metapsicologia freudiana, buscando resgatar idéias que deram subsídios para a proposta lacaniana. Com isso, juntamente com o retorno a Freud, avançamos com a posição de Lacan
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Hamed, Nagy. "Investigating the mechanisms underlying the pathogenesis of alopecia areata." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/20611/.
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Brand, Anna Maria [Verfasser]. "Vitamin-D-Status bei Alopecia areata : eine Metaanalyse / Anna Maria Brand." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1225740967/34.
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West, Emma Kuliana. "Bald truths : living and coming to terms with alopecia areata hair loss." Thesis, University of Essex, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537953.
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This research set out to enhance our understanding of what it means to live with hair loss diagnosed as alopecia areata (AA), exploring how individuals adapted over time. This was achieved through depth interview with 33 persons (19 women; 14 men) living with various levels of hair loss severity and duration. There is a growing body of quantitative evidence indicating that the condition can be emotionally, psychologically and socially devastating. This investigation explored the issue qualitatively, directly from the perspectives of those affected, so as to gain a fuller perspective on negative outcomes for men and women. Results revealed how a great deal of uncertainty accompanied the early AA career and much effort was invested as individuals attempted to make sense of their experiences and exert control over the condition. As hair loss worsened and physical appearance became increasingly `different', questions of identity and self came to the fore, causing those affected to feel that the essence of their personhood was under threat. Over time some adapted more successfully than others, although those most zealous in their efforts to keep it hidden from others undoubtedly led the most restricted lives. Both men and women expressed negative feelings about their hair loss, particularly from the head and around the eyes. However, there were also clear gender differences in meanings according to hair loss in particular body areas. Moreover, women invested more in `normalising' their appearance. I have argued that simplistic assumptions regarding the heightened threat for women undermine the gravity for men and contribute towards the difficulty many men experience in seeking and gaining support. This research represents a preliminary step towards a fuller understanding of the experience of living with AA. It is anticipated that these findings will enable professionals to improve the planning and delivery of health care for A. A.
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Iorizzo, Matilde <1975>. "The role of scalp dermoscopy in the diagnosis of alopecia areata incognita." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/1065/1/Tesi_Iorizzo_Matilde.pdf.
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Iorizzo, Matilde <1975>. "The role of scalp dermoscopy in the diagnosis of alopecia areata incognita." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/1065/.
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Styring, Nicola. "Examining the predictive utility of the theory of cognitive adaptation in relation to alopecia areata." Thesis, University of Sheffield, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434455.
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Singh, Vibhuti [Verfasser], and M. [Akademischer Betreuer] Zöller. "Attending persistent T cell activation in alopecia areata : A therapeutic option / Vibhuti Singh. Betreuer: M. Zöller." Karlsruhe : KIT-Bibliothek, 2011. http://d-nb.info/1014279712/34.
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Fick, Louis Jean. "The role of stress in the pathogenesis of Alopecia Areata: an objective assessment via hair cortisol level." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29387.
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BACKGROUND The pathogenesis of alopecia areata (AA) is poorly understood and multifactorial. There seems to be a strong belief, but conflicting evidence that stress causes or exacerbates AA. Hair cortisol measurement has been proven to be a reliable biological marker for cumulative prior stress. This measurement has up to date not been used in AA cases and may provide convincing evidence in the debate of stress and AA. OBJECTIVES: The primary aim of this project was to determine whether stress triggers onset of hair loss (OOHL) in AA by analysing the relationship between hair cortisol concentrations (HCCs) pre-OOHL in cases vs controls. Three secondary objectives were identified: • To determine whether there is a difference in HCC of lesional skin versus perilesional skin in cases. • To determine whether there is a correlation between disease activity (as determined by the hair pull test) and HCC. • To determine whether validated stress questionnaires correlate with HCC.
METHODS
A case control study was performed. Fourteen patients, fulfilling the inclusion criteria were recruited from the GSH and RXH outpatient departments. For each case consent was obtained, a data sheet was filled out, stress questionnaire(s) and two strands of hair, one lesional and one peri-lesional, were collected. Next, 14 healthy controls were recruited from whom a hair strand each was collected. On the hair samples, the position of onset of hair loss (OOHL) was determined by measuring one centimetre per month after OOHL, from the proximal (scalp near) end. Then three sections of three centimetres each were cut, two distally (representing the six-month period before OOHL) and one proximally (representing the three months post OOHL). In six of these cases a fourth or “current” section was obtained. This represented the section on the scalp and thus reflected current stress by measuring the most recent HCC. Next, the HCC’s of these sections were measured using the Salivary ELISA Cortisol kit©. An additional 44 cases, not meeting the inclusion criteria, were recruited for acquisition of additional stress questionnaires and data sheets.
RESULTS
HCC’s on average were higher in cases than in controls (before, during and after OOHL). The difference in HCC’s, however, was not statistically significant. There was no statistical difference between HCC’s in lesional and peri-lesional scalp samples. Distal section HCC’s were the highest. HCC’s correlated positively with disease activity, but was nonsignificant. There was no statistically significant relationship between HCC’s and stress questionnaires.
CONCLUSIONS: Although the result was not statistically significant, likely due to small sample size, stress as measured by HCC may trigger OOHL in AA. HCC does not play a role in whether an area of the scalp is affected or not. Disease activity may be cause for stress. A larger study is warranted to validate these findings.
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Johnsson, Eleonor. "Vilken effekt har olika typer av immunsuppressiv behandling vid de autoimmuna hudsjukdomarna alopecia areata och vitiligo? : En litteraturstudie." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-82498.
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Bakgrund: Människans försvar mot omvärlden och patogena mikrober består av ett väl utvecklat immunsystem innehållande det medfödda immunsystemet, innate, som inte förändras nämnbart över tid samt det adaptiva immunsystemet som skapar minnesceller efter immunrespons på peptidantigen. Det medfödda immunsystemets receptorer binder främmande strukturer och agerar snabbt genom att skapa inflammatorisk respons. Människans adaptiva immunsystem har celler som tar upp, bryter ned och via major histocompatibility complex (MHC) presenterar peptidantigen för T-celler. T-celler behöver flera stimuleringsvägar för att starta immunrespons. Immunsystemets celler kontrolleras så immunologisk tolerans upprätthålls. Autoimmunitet orsakas troligen av genetisk känslighet där den genetiska dispostitionen inte kan upprätthålla immunologisk tolerans vid trauma. Alopecia areata och vitiligo är de enda kända autoimmuna hudsjukdomarna som inte är antikroppsmedierade. Sjukdomarna drabbar 1 – 2 % av befolkningen. Hårfolliklar attackeras av autoreaktiva T-celler vid alopecia areata vilket ger håravfall. Vitiligo ger depigmenterade hudområden orsakat av autoreaktiva T-celler som förstört melanocyter. Sjukdomarna behandlas med immunsuppressiva läkemedel lokalt på huden eller systemiskt. Syfte: Examensarbetet syftade till att erhålla en djupare kunskap rörande likheter och skillnader i mekanism mellan de autoimmuna hudsjukdomarna alopecia areata och vitiligo samt undersöka och besvara frågeställningen vilken effekt olika typer av immunsuppressiv behandling har vid dessa sjukdomar. Metod: Examensarbetet är en litteraturstudie som baseras på sex stycken vetenskapliga artiklar framsökta ur databasen PubMed genom flera sökningar. Sökningarna avgränsades genom användande av bl.a. sökorden alopecia areata, vitiligo, treatment, tacrolimus och janus kinase. Resultat: Studie 1 och 2 utvärderar systemisk puls-behandling med glukokortikoider. Patienterna i studie 1 hade alopecia areata med omfattande håravfall och behandlingsrespons sågs hos många patienter. Vitiligo-patienterna i studie 2 uppvisade minskad sjukdomsaktivitet vilket ses i färre nya lesioner samt repigmenterade lesioner, dock ses ingen repigmentering hos en del patienter. Studie 3 och 4 utvärderar lokal behandling med takrolimus-salva. Patienter med vitiligo i studie 3 fick viss repigmentering av lesionerna och patienterna med alopecia areata i studie 4 fick delvis håråterväxt. Effekten av oralt administrerade januskinas-hämmare utvärderas i studie 5 och 6. Studie 5 visar att många patienter med alopecia areata fått mycket håråterväxt vid behandlingens slut och studie 6 påvisar behandlingsrespons hos hälften av vitiligo-patienterna där repigmentering främst ses på hudområden exponerade för solljus. Slutsats: Litteraturstudien visar att olika typer av immunsuppressiv behandling kan lindra sjukdoms-utbrott samt förkorta sjukdomstid vid de autoimmuna hudsjukdomarna alopecia areata och vitiligo. Immunologiskt sett har sjukdomarna liknande sjukdomsmekanismer genom inflammatorisk respons som ger aktivering av autoreaktiva T-celler. Behandlingsresistensförekommer och därför behövs fortsatt forskning kring sjukdomsmekanismer och nya läkemedel.Humans are depending on a functional immune system that provides defense against microbes and other things in our environment that can harm us. The skin is the largest and the heaviest of our organs. It’s important to have a barrier between the inner functions of the body and the world outside. The innate immune system specificities are recognition of microbes and damage. The adaptive immune system includes B and T cells which develops from stem cells in the bone marrow. The mature B and T cells are tested for self-tolerance before they are released. Having a functional immune system needs immunologic cells with immunologic tolerance. Immunologic tolerance demand B and T cells to know the difference between self antigens and pathogens. Autoimmunity is probably caused by genetic susceptibility under influence of trauma such as local tissue injury and infection. The trauma cause imbalance in the immune system and gives an autoimmune response with activated T cells reacting on self antigens. Autoimmune diseases can be systemic or organ specific and different mechanisms cause the damage of tissue. Diseases caused by autoimmunity tend to be chronic, self-perpetuating and progressive. Alopecia areata and vitiligo are autoimmune skin diseases which gives hair loss and depigmentation. Hair loss in alopecia areata is caused by autoimmune T cells attacking hair follicles and depigmentation in vitiligo is caused by destruction of melanocytes by autoimmune T cells. The diseases can’t be cured but immunosuppressive therapy can reduce disease activity and give faster recovery. The aim of this literature study was to get a deeper knowledge about the autoimmune skin diseases alopecia areata and vitiligo, and evaluate the efficiency of different immunosuppressive therapies used against alopecia areata and vitiligo. Found six scientific articles from the database PubMed through several searches. The searches were delimited by use of the keywords alopecia areata, vitiligo, treatment, tacrolimus and janus kinase. Studies 1 and 2 evaluate systemic pulse management with glucocorticoids. The patients in study 1 had alopecia areata with extensive hair loss and treatment reactions were seen in many patients. Vitiligo patients in study 2 show reduced disease activity as seen in fewer lesions as well as repigmented lesions, however, no repigmentation seen in some patients. Studies 3 and 4 evaluate local treatment with tacrolimus ointment. Patients with vitiligo in study 3 received some repigmentation of the lesions and the patients with alopecia areata in study 4 received partial hair regrowth. The effect of orally administered janus kinase inhibitors is evaluated in studies 5 and 6. Study 5 shows that many patients with alopecia have received a lot of hair regrowth at the end of treatment and study 6 shows treatment response in half of vitiligo patients where repigmentation is mainly seen in sunlight exposed areas. The literature study shows that different types of immunosuppressive treatment can relieve disease outbreaks and shorten disease in autoimmune skin diseases alopecia areata and vitiligo. Immunologically the diseases have similar disease mechanisms through inflammatory responses that provide activation of autoreactive T cells. Conclusion of this smallscale literature study is the need for further research on mechanisms of the diseases and research on therapies because therapy resistance is seen in both diseases although many patients responded to the immunosuppressive therapies.
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Barekatain, Armin. "Disease mechanisms in the C3H/HeJ Mouse Model of Alopecia." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/4063.
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Alopecia areata (AA) is a chronic inflammatory disease of hair follicles manifesting as
patchy areas of hair loss on the scalp and body. Development of AA is associated with
pen- and intra-follicular inflammation of anagen stage hair follicles, primarily by CD4+
and CD8+ cells. We hypothesized that if cell-mediated cytotoxicy against hair follicles is
to be a component of the hair loss disease mechanism, increased expression of genes and
products typical of cytotoxic cells, as well as increased apoptosis activity within affected
hair follicles, would be expected to occur in the lesional skin compared to the normal
skin. Furthermore, we studied gene expression levels of multiple cytokines and
characteristic chemokines, using the C3FI/HeJ mouse model of AA. mRNA expression
levels of granzyme A, granzyme B, perform Fas, Fas ligand, TNF-cL, TNF-aRl and R2,
TRAIL, TRAILR, TRAMP, Thi-, Th2-, and Th17-associated cytokines, as well as
multiple chemokines were compared between the skin, draining lymph nodes, thymus
and spleens of normal and AA-affected mice using quantitative reverse transcriptase
PCR. FasL, granzyme A, granzyme B, pro- and anti-inflammatory cytokines were all
highly up-regulated in the skin of AA-affected mice. Immunohistochemical studies of the
skin revealed that, although greater numbers of granzyme B and FasL expressing cells
were present in AA affected skin, the cells were morphologically diffusely distributed
and not exclusively located within the focal pen- and intrafollicular infiltrate. The
majority of these cells were further characterized as mast cells, which were also found in
substantially greater numbers in the skin of mice with AA compared to their normal
haired controls. Almost no perform expressing cells were identified in AA affected
mouse skin and TUNEL staining suggested relatively limited apoptosis activity in hair
follicle keratinocytes. In conclusion, while granzymes and FasL may play important roles
in disease development, the profiles and patterns of expression are not consistent with
direct cell-mediated cytotoxic action against the follicular epithelium in chronic mouse
AA. Potentially, hair growth inhibiting cytokines may play a more dominant role in AA
development than previously thought. Furthermore, mast cells, with their increased
presence around hair follicles in the AA affected mouse skin and their ability to express
granzyme B and FasL, are suggested as potential key players in the pathogenesis of AA.
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Erb, Ulrike [Verfasser], and A. [Akademischer Betreuer] Cato. "Autoimmunerkrankungen erfordern eine kombinierte Therapie aus Toleranzinduktion und Immunsuppression - Modelluntersuchung bei der Alopecia Areata / Ulrike Erb. Betreuer: A. Cato." Karlsruhe : KIT-Bibliothek, 2014. http://d-nb.info/1058625519/34.
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Santiago, Gabriela Andrade. "Presença de comorbidades como fator agravante de alopecia areata em crianças e adolescentes de 0 a 19 anos de idade no Hospital Universitário de Brasília." reponame:Repositório Institucional da UnB, 2011. http://repositorio.unb.br/handle/10482/9041.
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Alopecia areata é uma afecção crônica não cicatricial dos folículos pilosos, caracterizada por perda localizada ou difusa de cabelos ou pelos. Considerada doença autoimune mediada por células T, órgão-específica, onde uma infiltração linfocítica dos folículos pilosos resulta em ruptura de cabelos anágenos, ocasionando alopecia não inflamatória. Pode ocorrer em qualquer área corporal, sendo mais frequente em couro cabeludo e barba. Objetivos: O objetivo principal desta pesquisa foi investigar a presença de comorbidades e sua relação como fator agravante de alopecia areata. O objetivo secundário foi avaliar os aspectos epidemiológicos da alopecia areata, estudar a prevalência de alterações ungueais e a prevalência dos antecedentes pessoais e familiares de atopia nos pacientes participantes do estudo. Material e métodos: Desenvolveu-se o estudo com 30 pacientes portadores de Alopecia Areata, atendidas no Serviço de Dermatologia do Hospital Universitário de Brasília. Para elaboração dos testes foi utilizado o pacote estatístico SPSS, Statistical Package for the Social Sciences, versão 15.0, e para testar a associação entre as variáveis utilizou-se o teste exato de Fisher, agregado ao método computacional de Monte Carlo. Foi considerado significante valor inferior a 0,05. Resultados: A maior prevalência de AA encontra-se na faixa etária de crianças de 6 a 7 anos de idade (23,3%), sendo 18 pacientes do sexo feminino (60%) e 12 do sexo masculino (40%). Dos 30 pacientes avaliados, dez (33,3%) tinham antecedentes pessoais de atopia e 12 (40%) tinham alguma patologia concomitante. Destes, 7 (58%) pacientes tinham classificação S1 (<25% perda capilar); 2 (17%) tinham classificação S2 (25-49% perda capilar); 2 (17%) com classificação S4 (75-99% perda capilar) e 1 (8%) com classificação S5 (100% perda capilar). Conclusão: Associação com comorbidades não foi significativa para a gravidade da alopecia areata. _______________________________________________________________________________ ABSTRACT
Alopecia areata is a chronic non-scarring hair follicles, characterized by localized or diffuse hair loss disease. Considered an autoimmune disease mediated by T cells, organ-specific, where a lymphocytic infiltration of hair follicles results in disruption of anagen hair, causing non-inflammatory alopecia. It can occur in any body area, was more frequent in the scalp and beard. Objectives: The main objective of this research was to investigate the presence of comorbidities and their relationship as an aggravating factor for alopecia areata. The secondary objective was to evaluate the epidemiological aspects of alopecia areata, to study the prevalence of nail changes and the prevalence of personal and family history of atopy in the study participants. Methods: We developed the study with 30 patients with Alopecia Areata, served in the Department of Dermatology in the University Hospital of Brasilia. For preparation of tests, we used the SPSS statistical package, Statistical Package for the Social Sciences, version 15.0, and to test the association between the variables used the Fisher exact test, added to the computational method of Monte Carlo. Was considered significant below 0.05. Results: The higher prevalence of AA is in the age group of children 6-7 years old (23.3%), 18 female patients (60%) and 12 males (40%). Of the 30 patients evaluated, ten patients (33,3%) had as a personal history of atopy and 12 (40%) had some concomitant disease. Of these, 7 (58%) patients were rated S1 (<25% hair loss), 2 (17%) were rated S2 (25-49% hair loss), 2 (17%) were rated S4 (75-99% loss capillary) and 1 (8%) were rated S5 (100% hair loss). Conclusion: Association with comorbidities was not significant for the severity of alopecia areata.
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West, Emma. "Coping with hair loss : a content analysis exploring the support options available to women with alopecia areata in the UK /." St. Lucia, Qld.,, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17348.pdf.
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Bertolini, Marta [Verfasser]. "Abnormal interactions between perifollicular mast cells and CD8+ T-cells may contribute to the pathogenesis of alopecia areata / Marta Bertolini." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2015. http://d-nb.info/1066401799/34.
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Jagielska, Dagny [Verfasser]. "Die Folgeuntersuchung der genomweiten Assoziationsstudie zeigt IL13 und KIAA0350 als neue Suszeptibilitätsloci mit genomweiter Signifikanz bei Alopecia areata / Dagny Jagielska." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1047097478/34.
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Kuhn, Jennifer [Verfasser], Peter [Akademischer Betreuer] Nürnberg, and Angelika [Akademischer Betreuer] Nögel. "Molecular Genetics of Alopecia Areata in Dundee Experimental Bald Rats and in Humans / Jennifer Kuhn. Gutachter: Peter Nürnberg ; Angelika Nögel." Köln : Universitäts- und Stadtbibliothek Köln, 2011. http://d-nb.info/1038065410/34.
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Kolivras, Athanassios. "Immunohistochemistry in the histopathological diagnosis of primary scalp alopecia." Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/238160.
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Primary scalp alopecia is classically divided into cicatricial (scarring) and non-cicatricial (non-scarring). Challenging cases are assessed with a scalp biopsy. The use of both horizontal and vertical sections (HoVert sections) has dramatically improved the accuracy of histopathological diagnosis. In this work, we have used immunostaining to address diagnostic difficulties, which persist despite all currently available tools. We performed an immunostain panel (CD3, CD4, CD8 and CD20) in order to distinguish pattern hair loss from alopecia aerate in cases which do not have the usual peribulbar lymphocytic infiltrate and showed that CD3+ T-lymphocytes within the empty fibrous follicular tracts favor a diagnosis of alopecia areata. We performed CD123 in order to distinguish lichen planopilaris from alopecia lupus erythematosus in cases with only a superficial lymphocytic infiltrate and an uninvolved interfollicular epidermis and showed that clusters of CD123+ plasmacytoid dendritic cells favor a diagnosis of lupus erythematosus. We performed cytokeratin 15 in order to assess whether the loss of the follicular bulge stem cells has diagnostic value in cicatricial alopecia and demonstrated that the loss of cytokeratin 15+ bulge stem cells is identified in lichen planopilaris, frontal fibrosing alopecia, and lupus erythematous, so cytokeratin 15 has no diagnostic value. We have attempted to integrate the new concepts and our findings into the traditional classifications of alopecia and proposed a new diagnostic algorithm. In conclusion, immunostaining combined with HoVert grossing advances the accuracy of histopathological diagnosis of primary scalp alopecia.L’alopécie primitive du cuir chevelu est habituellement classée en cicatricielle et non-cicatricielle. Dans les cas difficiles, la biopsie du cuir chevelu peut aider au diagnostic. L’utilisation de coupes, à la fois verticales et horizontales sur le même spécimen (technique HoVert), a radicalement amélioré le diagnostic histopathologique. Dans ce travail, nous avons utilisé l’immunohistochimie pour évaluer les difficultés diagnostiques qui persistent malgré tous les outils actuels. Nous avons utilisé les CD3, CD4, CD8 et CD20 pour différencier l’alopécie androgénique de la pelade dépourvue de l’infiltrat lymphocytaire péribulbaire habituel et nous avons démontré que la présence de lymphocytes CD3+ dans les travées folliculaires fibreuses est en faveur de la pelade. Nous avons utilisé le CD123 pour différencier le lichen plan pilaire du lupus érythémateux alopécie avec infiltrat lymphocytaire superficiel et sans atteinte de l’épiderme interfolliculaire et nous avons démontré que la présence d’amas de cellules dendritiques plasmacytoïdes CD123+ est en faveur du lupus érythémateux. Nous avons utilisé la cytokératine 15 pour évaluer si la perte des cellules souches du bulge a une valeur diagnostique dans l’alopécie cicatricielle et nous avons démontré que cette perte s’observait de manière identique dans le lichen plan pilaire, l’alopécie frontale fibrosante comme dans le lupus érythémateux et n’avait donc aucune valeur diagnostique. Nous avons tenté d’intégrer les nouveaux concepts et nos données dans les classifications traditionnelles des alopécies et nous avons élaboré un nouvel algorithme diagnostique. L’association des immunomarquages avec la technique HoVert ouvre de nouvelles perspectives dans le diagnostic histopathologique des alopécies primaires du cuir chevelu.
Doctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
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Leung, Man Ching. "Identification of human hair follicle antigens targeted in the presumptive autoimmune hair follicle disorder Alopecia Areata and their potential functional relevance In Vitro. Methods development for isolation and identification of Alopecia Areata-relevant human hair follicle antigens using a proteomics approach and their functional assessment using an Ex Vivo hair follicle organ culture model." Thesis, University of Bradford, 2008. http://hdl.handle.net/10454/4330.
Full textAbstract:
Alopecia areata (AA) is a putative autoimmune hair loss disorder. It mainly affects the scalp hair but can also involve body hair, and can also affect the nail and the eye. While there are may be several lines of evidence to support the autoimmune basis of AA, there is still very little information on the hair follicle autoantigen(s) involved in its pathogenesis. In this project, serum antibodies (AA=10, control=10) were used to immunoprecipitate AA-relevant target antigens from normal human scalp hair follicle extracts. These immunoprecipitates were analysed by LC-MALDI-TOF/TOF mass spectrometry for target protein identification. This part of the project involved substantial methods development. Trichohyalin was immunoprecipitated by all AA sera, but by only 5 normal sera. Importantly, the mean Mascot scores of the AA group was significantly higher than the normal group (p=0.005). Keratin 16 was also identified from immunoprecipitates as another potential AA-relevant target antigen. Functional studies by ex vivo whole hair follicle organ culture using commercial antibodies to trichohyalin and keratin 16 significantly inhibited hair fibre elongation compared to controls. Indirect immunofluorescence studies revealed that AA sera contained higher immunoreactivity against normal human scalp anagen hair follicles compared to normal sera. Immunoreactivities were mainly in the outer root sheath and inner root sheath, and less so to the medulla and hair bulb matrix. Double immunofluorescence studies of AA and normal serum with anti-trichohyalin antibody (AE15) revealed co-localisation of 9 of the AA sera antibodies with trichohyalin in the inner root sheath (mostly in Henle's, less in Huxley's/inner root sheath cuticle), but only weakly in 3 normal sera. This study supports the involvement of an antibody response to anagen-specific hair follicles antigens in AA. Moreover, there may be some evidence that these antibodies may have a pathogenic role.
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Hennewig, Ulrike [Verfasser]. "Assoziation von Helicobacter pylori und Alopecia areata unter spezieller Betrachtung von unspezifischen Antikörpern gegen Helicobacter pylori und spezifischen Antikörpern gegen dessen CagA-Protein / Ulrike Hennewig." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2004. http://d-nb.info/1021567973/34.
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Rasche, Florian [Verfasser], and Henning [Gutachter] Hamm. "Retrospektive Analyse von Wirksamkeit, Sicherheit, prognostischen Parametern und Faktoren der Lebensqualität bei der topischen Immuntherapie der Alopecia areata mit Diphenylcyclopropenon / Florian Rasche ; Gutachter: Henning Hamm." Würzburg : Universität Würzburg, 2021. http://d-nb.info/1241965595/34.
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Holmes, Kasie. "Her-Storicizing Baldness: Situating Women's Experiences with Baldness from Skin and Hair Disorders." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5241.
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A general goal to my study was to promote an inclusive approach to baldness by sharing and centering women's experiences with baldness from skin and hair conditions, such as autoimmune alopecia areata conditions and monilethrix. Specifically, a main goal of my study was to her-storicize the lived experiences of women who are bald from skin and hair conditions by examining medical and cultural discourses surrounding these conditions, femininity, and female baldness. Additionally, my study considers strategies of accommodation and resistance that bald women perform in a given context, space, or time. For instance, I consider the ways participants manage their conditions and baldness within certain contexts. To achieve these goals, I interviewed four women who are bald from alopecia areata, alopecia totalis, alopecia universalis, and monilethrix by using an interactive approach to the interviews. Once the interviews were completed, I used interpretative phenomenological analysis to extract themes across the four interviews. Based on the analysis, I organized the findings into two overarching themes that include (a) navigating the feminine ideal and (b) negotiating the assumptions of illness and female baldness. In these themes, I discuss how participants' experiences demonstrate the significance of accommodating and/or resisting hegemonic notions of femininity and illness.
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Stöckli, Lachner Yvette Daniela. "Systemische Kortikosteroide (Solu-Medrol®)in der Behandlung der Alopezia areata /." Bern : [s.n.], 2005. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Craveiro, Ana Pedro Cunha. "Alopecia Areata." Master's thesis, 2017. http://hdl.handle.net/10400.6/8027.
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A Alopecia Areata constitui uma condição clínica auto-imune, multifatorial, de etiologia desconhecida, responsável por perda capilar não-cicatricial. Afeta crianças e adultos, sem preferência racial ou por género e tem um curso imprevisível, que, na grande maioria das vezes, não é modificado pelos tratamentos atuais. Estudos mostram que pacientes com Alopecia Areata possuem maior risco de ansiedade, atopia, vitiligo, patologia da tiróide e outras condições auto-imunes.
Contudo, a carência de estudos aleatorizados e controlados sobre a doença, aliada às inúmeras interrogações que lhe estão associadas, têm contribuído para que a abordagem da Alopecia Areata continue a ser um desafio.
A corticoterapia tem sido a modalidade de tratamento mais usada, mas o seu espetro de atuação parece redutor nalgumas formas da doença. Por outro lado, e apesar do seu grave impacto psicológico, a Alopecia Areata não comporta consequências diretas na saúde geral, pelo que esperar por uma eventual remissão espontânea poderá ser uma opção sensata nalguns casos. Desta forma, o presente trabalho visa conhecer as caraterísticas epidemiológicas e clínicas da Alopecia Areata, comorbilidades frequentemente associadas e principais limitações das atuais possibilidades terapêuticas. Igualmente com este intuito, e como forma de aproximar o racional teórico da prática clínica, é apresentado um resumo organizado de casos clínicos de Alopecia Areata diagnosticados e acompanhados no serviço de Dermatologia do Centro Hospitalar Cova da Beira, entre 2014 e 2016.Alopecia areata is an autoimmune condition of multifactorial and unknown etiology which causes nonscarring air loss. It affects both children and adults, with no gender prevalence and as an unpredictable outcome which, in the majority of cases, is not affected by the available therapies. Several studies have shown that patients who suffer from this condition have a greater risk of anxiety disorders, atopy, vitiligo, thyroid pathology and other autoimmune conditions. The approach to Alopecia areata has remained a challenge due to the lack of randomized and controlled studies together with the innumerous doubts still associated with this disease. Corticotherapy has been the most used kind of therapy but limited success has been achieved in some forms of the disease. On the other hand, and despite its psychological burning, Alopecia areata does not carry direct health consequences and to only observe the progression of the illness, as the problem often spontaneously regresses, seems to be a reasonable and wise option in some cases. The current review aims to provide knowledge about the epidemiology, clinical features, usually associated clinical conditions and the state of art therapies of Alopecia Areata. It is also presented a set of clinical cases dating from 2014 to 2016 and collected from Centro Hospital Cova da Beira Dermatology Department with the intention of bringing theoretical and practical concepts together.
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Petukhova, Lynn Meredith. "The Genetic Architecture of Alopecia Areata." Thesis, 2013. https://doi.org/10.7916/D8SJ1SVS.
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Alopecia areata (AA) is the most prevalent autoimmune disease in the US. With An estimated lifetime risk of 1.7%, it affects both genders with similar frequencies and people of all ages. AA affects more individuals than most other autoimmune diseases combined, and yet despite its prevalence, there is an enormous unmet medical need, in part due to the dearth of information about the underlying pathogenesis. In AA, autoimmunity arises against the hair follicles in the skin, which causes hair loss associated with an aberrant accumulation of immune-response cells around the affected hair follicles. Evidence supporting a genetic basis for AA stems from multiple lines of research, including increased risk of disease in first degree relatives, twin studies, and more recently, our initial family-based linkage study and genome wide association study (GWAS) in a cohort of unrelated individuals. Importantly, our GWAS identified a set of 16 statistically independent risk haplotypes across 8 loci, implicating specific genes that increase risk of AA, all of which have been validated. Genome wide genetic studies can provide critical insight into disease mechanisms, especially when little is known about the underlying causes of disease. In this study, I use complementary gene mapping methods, performing one study in a cohort of families and a second study in a cohort of unrelated cases and controls. Using these two approaches, I obtain new evidence about the genetic influences on AA. Our family cohort contains statistically significant evidence for linkage at a new locus, on chromosome 2q36.1-q37.3 (LOD=4.17) and family-based tests of association implicate 47 genes. I then conducted a GWAS that expanded our initial cohort with the addition of 800 cases and obtained statistically significant evidence for a new locus at chromosome 16p13.13 (p=4.6x10-7). This region has been implicated in several other autoimmune diseases and contains several genes that are known to be involved with immune processes. Taken together, these two studies demonstrate the presence of both rare and common variants are contributing to AA etiology and support emerging evidence that suggests the genetic architecture of common complex diseases involves both rare and common variants.
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"Genetic and Environmental Determinants of Alopecia Areata." Thesis, 2020. https://doi.org/10.7916/d8-7wzy-zr95.
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Alopecia Areata (AA) is a highly prevalent autoimmune disease in the US with a lifetime risk of 2.1%. In AA, autoimmunity develops against the hair follicles, which leads to infiltration of immune cells around affected follicles. Among genetic risk factors in complex autoimmune diseases, variants cluster in genes regulating the immune response, as well as the target organ. AA is believed to result from both genetic and environmental factors. To identify underlying genetic drivers in AA, we analyzed AA risk genes using various sequencing techniques and analysis methods to identify causal variants and placed them in functionally relevant contexts using innovative mapping techniques.
To address the role of variants in immune function, we studied the Interleukin-2 Receptor Alpha (IL2RA), which we identified as a significant locus to study genetic factors underlying immune function from our AA GWAS studies (p=1.74*10-12)11. IL2RA plays a crucial role in regulating immune tolerance and controlling activity of regulatory T cells (Treg)13. We identified significant causal variants in the IL2RA region associated with AA using GWAS, targeted resequencing, and custom capture exome sequencing approaches. We validated the expression of these variants in immune cell cluster tissue types in silico, and specifically in CD4+ T cells. The variant rs3118740 increases AA susceptibility for carriers of the C allele. Such allele specific effects could lead to a perturbation of Treg function, for example, one study in T1D where patients with the rs3118470 risk variant have Treg with IL-2 signaling defects14. These studies demonstrated that identifying causal variants may lead to an improved understating of Treg function and risk of autoimmunity in AA.
Next, to study genetic susceptibility in the target organ in AA, the hair follicle (HF), the second candidate GWAS susceptibility gene we studied was peroxiredoxin 5 (PRDX5) (p= of 8.7*10-14), which is also a GWAS gene in Crohn’s disease, sarcoidosis, and psoriasis15,16. PRDX5 is a member of the family of antioxidant enzymes that are crucial for regulating oxidative stress. Our lab performed whole exome sequencing in 849 AA patients, together with selected custom capture regions of genomic sequencing. Using a test of variant enrichment, we identified variants in PRDX5 that were significant in both our GWAS and exome studies, and thus represented likely candidate causal variants. Using Bayesian fine mapping, we identified a GWAS and exome sequencing variant, rs574087, that was significantly enriched in both, and is predicted to be a causal variant in keratinocytes and melanocytes. To functionally validate PRDX5, we immunostained healthy human HF and AA affected HF, and found that PRDX5 is upregulated AA human HF. PRDX5 is expressed in cultured melanocytes by immunostaining, which is consistent with melanocytes exhibiting high levels of oxidative stress. We postulated that PRDX5 may be involved in protection from oxidative stress, and that its dysregulation may contribute to autoimmunity.
Finally, along with genetic predisposition, environmental triggers such as the microbiome have emerged as potential factors contributing to pathologic immune responses in autoimmune diseases. To determine the role of the microbiome in AA pathobiology, we performed 16S rRNA sequencing of skin swabs, hair follicles, and stool samples from a cohort of 34 AA patients and 12 healthy controls (HCs). Unexpectedly, we found evidence of striking gut dysbiosis, consisting of over-representation of Firmicutes and under-representation of Bacteroides in the gut microbiome of AA patients compared with healthy subjects, but no significant differences in skin or hair follicle (HF) microbiome composition. To investigate the role of the gut microbiome in AA development in vivo, we depleted the gut microbiome in C3H/HeJ mice and found that the mice were largely protected from AA developing. These data revealed a requirement for gut microbiota in the onset of murine AA. Taken together with recent reports in the literature of reversal of AA in several patients following fecal microbiota transplant (FMT)17,18, our findings suggest that restoring homeostasis of the gut microbiome may represent an effective new treatment modality in the management of AA.
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Broadley, David, and Kevin J. McElwee. "A "hair-raising" history of alopecia areata." 2020. http://hdl.handle.net/10454/17672.
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YesA 3500‐year‐old papyrus from ancient Egypt provides a list of treatments for many diseases including “bite hair loss,” most likely alopecia areata (AA). The treatment of AA remained largely unchanged for over 1500 years. In 30 CE, Celsus described AA presenting as scalp alopecia in spots or the “windings of a snake” and suggested treatment with caustic compounds and scarification. The first “modern” description of AA came in 1813, though treatment still largely employed caustic agents. From the mid‐19th century onwards, various hypotheses of AA development were put forward including infectious microbes (1843), nerve defects (1858), physical trauma and psychological stress (1881), focal inflammation (1891), diseased teeth (1902), toxins (1912) and endocrine disorders (1913). The 1950s brought new treatment developments with the first use of corticosteroid compounds (1952), and the first suggestion that AA was an autoimmune disease (1958). Research progressively shifted towards identifying hair follicle‐specific autoantibodies (1995). The potential role of lymphocytes in AA was made implicit with immunohistological studies (1980s). However, studies confirming their functional role were not published until the development of rodent models (1990s). Genetic studies, particularly genome‐wide association studies, have now come to the forefront and open up a new era of AA investigation (2000s). Today, AA research is actively focused on genetics, the microbiome, dietary modulators, the role of atopy, immune cell types in AA pathogenesis, primary antigenic targets, mechanisms by which immune cells influence hair growth, and of course the development of new treatments based on these discoveries.
Alopecia UK.
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"Alopecia Areata no Caso Flora: Uma Investigação Psicopatológica." Tese, Biblioteca Digital da PUC-SP, 2006. http://www.sapientia.pucsp.br//tde_busca/arquivo.php?codArquivo=2501.
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Zhang, X., and Kevin J. McElwee. "Allergy promotes alopecia areata in a subset of patients." 2019. http://hdl.handle.net/10454/17535.
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YesIn this commentary, we focus on allergy as a facilitating factor in the pathogenesis of alopecia areata (AA). From previous studies on AA, it is well known that subsets of patients can have one or more of; seasonal relapse, comorbid atopic rhinitis, asthma and dermatitis, lesion infiltrating eosinophils and plasma cells, high levels of total IgE, specific IgE for house dust mites (HDMs), and/or disrupted skin barrier function by the evaluation of filaggrin. Allergy and AA share a similar genetic background; both contributing to an immune reaction imbalance. Furthermore, adjunctive treatment with antihistamines, or desensitization for HDM, can reduce the severity of alopecia in atopic AA patients. Therefore, allergies may contribute to the onset and relapse of AA. Identification of an allergic or atopic immune component in AA patient subsets may indicate adjunctive treatment intervention measures against allergies should be taken which may improve the success of conventional AA treatment.
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Kang, H., W.-Y. Wu, M. Yu, J. Shapiro, and Kevin J. McElwee. "Increased expression of TLR7 and TLR9 in alopecia areata." 2019. http://hdl.handle.net/10454/17531.
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YesAlopecia areata (AA) is thought to be an autoimmune process. In other autoimmune diseases, the innate immune system and Toll‐like receptors (TLRs) can play a significant role. Expression of TLR7, TLR9 and associated inducible genes was evaluated by quantitative PCR in peripheral blood mononuclear cells (PBMCs) from 10 healthy individuals and 19 AA patients, categorized according to disease duration, activity and hair loss extent. Microdissected scalp biopsies from five patients and four controls were also assessed by quantitative PCR and immunohistology. TLR9 was significantly upregulated 2.37 fold in AA PBMCs. Notably, TLR9 was most significantly upregulated in patients with active AA, as shown by a positive hair pull test, compared to stable AA patients. In hair follicle bulbs from AA patients, IFNG and TLR7 exhibited statistically significant 3.85 and 2.70 fold increases in mRNA, respectively. Immunohistology revealed TLR7 present in lesional follicles, while TLR9 positive cells were primarily observed peri‐bulbar to AA affected hair follicles. The increased expression of TLR7 and TLR9 suggest components of the innate immune system may be active in AA pathogenesis.
National Alopecia Areata Foundation; Canadian Dermatology Foundation; Michael Smith Foundation for Health Research, Grant/Award Number: CI‐SCH‐00480(06‐1); Canadian Institutes of Health Research, Grant/Award Number: MOP‐167368 and MSH‐192593‐140450
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Todorova, Antonia [Verfasser]. "Die Wirksamkeit von Diphenylcyclopropenone (DCP) bei der Alopecia areata = Effectivity of topical Diphenylcyclopropenone (DCP)-Therapy in the treatment of Alopecia areata / Antonia Todorova." 2007. http://d-nb.info/98806801X/34.
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Leung, Man Ching, Chris W. Sutton, D. A. Fenton, and Desmond J. Tobin. "Trichohyalin is a potential major autoantigen in human alopecia areata." 2010. http://hdl.handle.net/10454/6066.
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Several lines of evidence support an autoimmune basis for alopecia areata (AA), a common putative autoimmune hair loss disorder. However, definitive support is lacking largely because the identity of hair follicle (HF) autoantigen(s) involved in its pathogenesis remains unknown. Here, we isolated AA-reactive HF-specific antigens from normal human scalp anagen HF extracts by immunoprecipitation using serum antibodies from 10 AA patients. Samples were analyzed by LC-MALDI-TOF/TOF mass spectrometry, which indicated strong reactivity to the hair growth phase-specific structural protein trichohyalin in all AA sera. Keratin 16 (K16) was also identified as another potential AA-relevant target HF antigen. Double immunofluorescence studies using AA (and control sera) together with a monoclonal antibody to trichohyalin revealed that AA sera contained immunoreactivity that colocalized with trichohyalin in the growth phase-specific inner root sheath of HF. Furthermore, a partial colocalization of AA serum reactivity with anti-K16 antibody was observed in the outer root sheath of the HF. In summary, this study supports the involvement of an immune response to anagen-specific HFs antigens in AA and specifically suggests that an immune response to trichohyalin and K16 may have a role in the pathogenesis of the enigmatic disorder.
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Erjavec, Stephanie O'Toole. "Utilizing functional genomics approaches to characterize risk genes in alopecia areata." Thesis, 2020. https://doi.org/10.7916/d8-m28r-hx51.
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Understanding the genetic architecture of complex disorders is important for identifying disease mechanisms and potential molecular targets for therapeutic interventions. Genetic diseases are broadly classified as either Mendelian (monogenic) diseases or complex (polygenic) diseases. Common, polygenic disorders result from inheritance of multiple common variants with low penetrance. In contrast, monogenic, Mendelian disorders are caused by rare variants with high penetrance at a single genetic locus. However, an increasing number of studies support a role for rare variants of moderate effect size in complex diseases. As a result, genetic approaches previously utilized for discovering rare variants in Mendelian diseases, such as next generation sequencing, can now effectively be applied to complex diseases to define the contribution of both rare and common variants to the genetic burden of polygenic traits and diseases.
Alopecia Areata (AA) is a complex autoimmune disease characterized by non-scarring hair loss that is due to a combination of both enviornmental and genetic factors. Our previous Genome-wide Association Study (GWAS) identified at least 14 genetic regions contributing to AA disease susceptibility. Although useful in identifying disease-associated loci and surrounding linkage disequilibrium (LD) blocks, GWAS is not sufficiently granular to 1) elucidate causal (association-driving) variants; and 2) discover rare risk variants. This level of resolution can only be achieved by deep sequencing followed by functional validation of variants.
The goal of this thesis was to address these challenges in AA using two genetic approaches that have not been previously utilized in the context of this disease. In Chapter 2, I performed a hypothesis-driven analysis of common variants in a GWAS-associated locus using targeted genomic sequencing. In Chapter 3, I utilized whole exome sequencing (WES) in an unbiased approach to assess rare variant contribution in AA disease risk. To conduct these analyses simultaneously, we designed a whole exome sequencing (WES) chip that also included custom capture of 24 Mb of genomic regions covering the 14 genetic loci previously identified using GWAS. I applied these two sequencing approaches in a large AA patient cohort and identified potentially causal variants in several genes. To interrogate the consequences of these variants, I performed functional analyses to determine the effects of disease-causing variants on the target organ of AA attack, the hair follicle (HF).
In Chapter 2, I report on the use of targeted genomic sequencing to interrogate the coding and non-coding regions surrounding a previously implicated GWAS locus. This approach provided fine mapping of coding and non-coding common variants in regions that may be contributing to disease risk. In this thesis, I focused on the effect of genetic perturbations on the end-organ HF, and consequentially prioritized my functional analysis using two criteria: 1) genes expressed in the (HF) and; 2) GWAS regions that were not previously implicated in other autoimmune diseases. One of the regions that satisfied these criteria harbored the Syntaxin 17 (STX17) gene, which encodes a SNARE protein involved in autophagy and mitochondrial fission. Targeted genomic sequencing of the STX17 region in 849 AA cases identified 35 non-coding and 0 coding variants in high LD with the GWAS SNP. Thirty-three variants were significantly enriched in cases compared to controls, and the remaining two were nominally significant. Thirty-two of the significantly associated AA variants were confirmed to be AA skin eQTLs that downregulated expression of STX17 in affected scalp skin of AA patients. Downstream analyses incorporated in silico and functional cell assays that uncovered a novel autophagy-independent role for STX17 in melanocyte biology. I discovered that a reduction of STX17 expression was associated with an accumulation of a melanocyte-specific antigen and increased immunogenicity, as seen by CD8+ T cell infiltrates in the skin of AA patients with low levels of STX17 expression. I used a targeted sequencing approach to successfully identify candidate causal variants driving the GWAS association at the STX17 locus, and propose a novel mechanism underlying STX17-dependent melanocyte perturbation and AA disease.
In the second section of this thesis, we used the WES feature of the chip to assess the genetic contribution of rare variation in AA, in a genome-wide and unbiased manner. WES data and gene-level burden analyses of 18,653 genes in 849 AA patients was compared to 15,640 controls to identify rare variants associated with AA. Unexpectedly, this analysis identified one gene, encoding a hair-specific keratin, Keratin 82 (KRT82) that harbored significantly more rare damaging mutations in AA cases compared to controls (p=2.68E-06). Eleven rare damaging mutations were found in 51 AA patients in the heterozygous state (6.01%) compared to 2.58% controls. These variants resided in evolutionary conserved amino acid residues, and nine out of the eleven mutations were located in established disease-causing domains in keratin proteins. I determined that KRT82 expression was absent or largely reduced in AA hair follicles, including the bulb region, the site of AA immune attack. Moreover, AA patients with damaging variants and reduced KRT82 expression had increased perifollicular CD8+ T cell infiltrates in comparison to control HFs with intact KRT82 expression remaining. I proposed that damaging mutations in the coding regions of KRT82 resulted in loss of functional protein, thereby weakening the protective HF cuticle and predisposing the HF to immune attack.
In summary, I used two genetic approaches (targeted genomic sequencing and WES) to identify common (Chapter 2) and rare variants (Chapter 3) with novel contributions to the complex genetic architecture of AA. I focused my functional studies on genes expressed in the target HF, with the goal of defining the role of unidentified, variant-mediated end-organ disruption in the predisposition of AA patient HFs to aberrant autoimmune attack. Up to now, most efforts in AA mechanistic studies have focused on the aberrant immune response. The work in my thesis uncovered novel roles for perturbations in the HF itself as a participating factor in AA disease risk.
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Zhang, X., Y. Ye, Z. Zhu, Y. Yang, H. Cao, Kevin J. McElwee, and Y. Ling. "Sequential cyclic changes of hair roots revealed by dermoscopy demonstrate a progressive mechanism of diffuse alopecia areata over time." 2018. http://hdl.handle.net/10454/17237.
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YesBACKGROUND: Diffuse alopecia areata (DAA) often leads to a complete hair shedding within a few months. OBJECTIVE: To explore features and mechanisms underlying DAA. MATERIALS AND METHODS: Scalp and hair root dermoscopy were conducted on 23 DAA patients throughout the disease process, 20 patchy Alopecia areata patients, 23 acute telogen effluvium (ATE) patients and 10 normal controls. Histopathology was also evaluated. RESULTS: We found almost all hair roots were anagen in early stage DAA in 18 patients (18/23, 78.3%) within the first 4-8 weeks after hair loss onset. Anagen effluvium (~4 weeks) was followed by catagen (~4 weeks) and then telogen/exogen (~8 weeks) effluvium with overlap. Hair root and proximal hair shaft depigmentation was more prominent in later DAA disease stages. Black dots, exclamation mark hairs and inconsistent thickness of hair shafts were found more often in early than later DAA (Ps < 0.01). Early DAA histopathology revealed more prominent inflammation and hair follicle regression than that observed in the later stages. Patchy alopecia areata patients showed mixed anagen, catagen and telogen hair roots while ATE patients showed increased exogen and mildly decreased hair root pigmentation. CONCLUSION: Sequential cyclic staging of shed hairs in DAA indicates the insult may be hair-cycle specific. We suggest that DAA is initially an anagen effluvium disease involving an intense inflammatory insult, later progressing to a brief catagen effluvium, and then to telogen effluvium with premature exogen, in later stages of DAA.
This study was supported by the following grants to Xingqi Zhang: National Natural Science Foundation of China (81573066); Natural Science Foundation of Guangdong Province (2014A030313098).
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Rasche, Florian. "Retrospektive Analyse von Wirksamkeit, Sicherheit, prognostischen Parametern und Faktoren der Lebensqualität bei der topischen Immuntherapie der Alopecia areata mit Diphenylcyclopropenon." Doctoral thesis, 2021. https://doi.org/10.25972/OPUS-24454.
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Diese retrospektive Analyse untersucht die Behandlung von Patienten mit Alopecia areata in der Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie der Universitätsklinik Würzburg mit Diphenylcyclopropenon und beleuchtet Faktoren der durch die Behandlung beeinflussten LebensqualitätThis study evaluates the efficacy of the treatment of alopecia areata in the dermatology department of the university clinic in Würzburg, Germany and shows prognostic factors that may be detrimental in regards to a positive outcome. Furthermore, the influence of the therapy's side-effects on everyday life are shown
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Tobin, Desmond J. "Alopecia areata and vitiligo - partners in crime or a case of false alibis." 2014. http://hdl.handle.net/10454/7067.
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NoIt has long been appreciated in science that correlation does not imply causation. However, with any logical fallacy, simply spotting that the reasoning behind an argument is faulty does not imply that the resulting conclusion is false. Thus, I begin the tricky business of exploring the basis upon which researchers and clinicians are often tempted to conclude that two medical conditions (here alopecia areata and vitiligo), with some striking resemblances, are in fact related. This is relevant, particularly if assumptions of shared aetiology (and to some extent shared pathomechanism) encourage a common strategy to finding a treatment or cure.
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Jalili, R. B., R. T. Kilani, Y. Li, M. Khosravi-maharlooie, L. Nabai, E. H. C. Wang, Kevin J. McElwee, and A. Ghahary. "Fibroblast cell-based therapy prevents induction of alopecia areata in an experimental model." 2018. http://hdl.handle.net/10454/16554.
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YesAlopecia areata (AA) is an autoimmune hair loss disease with infiltration of proinflammatory cells into hair follicles. Current therapeutic regimens are unsatisfactory mainly because of the potential for side effects and/or limited efficacy. Here we report that cultured, transduced fibroblasts, which express the immunomodulatory molecule indoleamine 2,3-dioxygenase (IDO), can be applied to prevent hair loss in an experimental AA model. A single intraperitoneal (IP) injection of IDO-expressing primary dermal fibroblasts was given to C3H/HeJ mice at the time of AA induction. While 60–70% of mice that received either control fibroblasts or vehicle injections developed extensive AA, none of the IDO-expressing fibroblast-treated mice showed new hair loss up to 20 weeks post injection. IDO cell therapy significantly reduced infiltration of CD4+ and CD8+ T cells into hair follicles and resulted in decreased expression of TNF-α, IFN-γ and IL-17 in the skin. Skin draining lymph nodes of IDO fibroblast-treated mice were significantly smaller, with more CD4+ CD25+ FoxP3+ regulatory T cells and fewer Th17 cells than those of control fibroblast and vehicle-injected mice. These findings indicate that IP injected IDO-expressing dermal fibroblasts can control inflammation and thereby prevent AA hair loss.
Canadian Institutes of Health Researches (Funding Reference Number: 134214 and 136945).
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Abdel, Kader Gassan. "Alopecia areata und Vitiligo Untersuchungen zur Epidemiologie und Relevanz klinisch chemischer und immunserologischer Laboruntersuchungen /." 2004. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014192264&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
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Wang, E. H. C., L. Santos, X. Y. Li, A. Tran, S. S. Y. Kim, K. Woo, J. Shapiro, and Kevin J. McElwee. "Alopecia areata is associated with increased expression of heart disease biomarker cardiac troponin I." 2018. http://hdl.handle.net/10454/16565.
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YesThe development of androgenetic alopecia is associated with a risk of developing cardiovascular diseases, but the association of alopecia areata with cardiovascular diseases in humans is largely unexplored. We measured the plasma level of two common cardiovascular disease markers, cardiac troponin I and Creactive protein, in alopecia areata and androgenetic alopecia-affected subjects. Also, we investigated the possible presence of pro-apoptotic factors in the plasma of hair loss subjects. The mean plasma cardiac troponin I level was highest in alopecia areata subjects, moderately higher in androgenetic alopecia subjects, and lowest in subjects without hair loss (p < 0.05). Alopecia areata subjects not receiving treatments had highest levels of cardiac troponin I (p < 0.05). Alopecia areata plasma samples with high cardiac troponin I levels also induced significantly higher rates of cardiomyocyte apoptosis in cell culture assays. The results suggest the potential for increased heart remodelling. Close monitoring of cardiovascular health in alopecia areata subjects, as well as subsets of androgenetic alopecia patients, may be appropriate.
Canadian Institutes of Health Research (CIHR; MOP-82927). EW is the recipient of a Banting Postdoctoral Fellowship (SAC-92845).
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Gong, Y., Y. Zhao, X. Zhang, S. Qi, S. Li, Y. Ye, J. Yang, S. Caulloo, Kevin J. McElwee, and X. Zhang. "Serum level of IL-4 predicts response to topical immunotherapy with diphenylcyclopropenone in alopecia areata." 2018. http://hdl.handle.net/10454/17236.
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YesBackground: This study investigated predictors of response to topical diphenylyclopropenone (DPCP) immunotherapy in patients with alopecia areata (AA). Objective: To identify predictors of response, or resistance, to treatment for AA through clinical observations and serum tests. Methods: Eighty four AA patients were treated with DPCP. Serum cytokine levels were measured in 33 AA patients pre- and post-treatment, and in 18 healthy controls, using ELISA assays. Results: Of patients, 56.1% responded to DPCP with satisfactory hair regrowth; the response rate was negatively correlated with hair loss extent. Before DPCP treatment, higher serum IFN-γ and IL-12 cytokine levels were observed in AA patients compared to healthy controls. Non-responders to DPCP had significantly elevated serum IL-4 pre-treatment (3.07 fold higher) and lower IL-12 levels compared with responders. After DPCP treatment, non-responders had persistently high IL-4, increased IL-12, negligible decrease in IFN-γ and decreased IL-10. Post-treatment DPCP responders exhibited significantly decreased IFN-γ and IL-12, and increased IL-4 and IL-10. Development of adverse side-effects was significantly associated with higher pre-treatment serum IgE levels. Limitations: A small number of subjects were evaluated. Conclusions: Potentially, elevated pre-treatment serum levels of IL-4 and IL-12 can be used as unfavorable and favorable predictors of DPCP therapeutic effect, respectively. In addition, pre-treatment elevated serum total IgE may predict increased risk for severe adverse side-effects to DPCP application. Whether serum cytokine expression levels can be used as predictors of response to other forms of treatment is unknown, but it may warrant investigation in the development of personalized treatments for AA.
This work is supported by the National Natural Science Foundation of China (81573066) and Natural Science Foundation of Guangdong Province (2014A030313098) to Xingqi Zhang.
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McElwee, Kevin J., and A. Tosti. "New developments in hair research." 2020. http://hdl.handle.net/10454/17750.
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YesThis article is an editorial for the special focus theme issue on “hair research” published by the Experimental Dermatology journal. Here we introduce the articles from the special issue and pose a few questions. The full list of publications for the hair research special issue is available on the Journal’s web site. Many of the articles can be viewed free of charge on the web site. This is for; Experimental Dermatology, Volume 29, Number 3, published March 2020.
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Toksoy, Atiye. "Die Expression von Chemokinen bei entzündlichen Reaktionen der Haut." Doctoral thesis, 2008. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-34692.
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Für das Verständnis der Pathogenese entzündlicher Hauterkrankungen ist die Zusammensetzung des zellulären Entzündungsinfiltrates und die Verteilung der Entzündungszellen von wesentlicher Bedeutung. In Anbetracht der chemotaktischen Funktion der Chemokine liegt die Annahme nahe, dass das zelluläre Infiltrationsmuster in entzündlichen Hauterkrankungen das Expressionsmuster von Chemokinen und umgekehrt widerspiegelt. Die Infiltrationsroute der Leukozyten in die Haut erfolgt immer vom Lumen dermaler Gefäße in das dermale Milieu und ggf. weiter in das epidermale Kompartiment (sog. Epidermotropismus). Die Migration inflammatorischer Zellen über die Grenzen unterschiedlicher Hautkompartimente hinweg ist einzigartig und präsentiert ein ideales Modell, um die chemotaktischen Cytokin- bzw. Chemokinfunktionen zu evaluieren. Anhand verschiedener ausgewählter Hautdermatosen (Wundheilung, Psoriasis, Alopecia areata) wurden die unterschiedlichen Expressionsmuster einer Auswahl von Chemokinen untersucht. Dabei nehmen Chemokine, die von Endothelzellen exprimiert bzw. sezerniert werden, eine zentrale Rolle ein, da sie eine „Pförtnerfunktion“ ausführen. Diese Funktion ist entscheidend bei der Rekrutierung und Akkumulation der für das Erkrankungsbild und bei reparativen Vorgängen der Wundheilung spezifischen Leukozytensubpopulation ins dermale bzw. epidermale GewebeThe composition of the cellular inflammatory infiltrates and the distribution of inflammatory cells is essential for the understanding of the pathogenesis of inflammatory skin diseases. In view of the chemotactic function of chemokines we assume that the cellular infiltration pattern in inflammatory skin diseases reflects the expression patterns of chemokines and vice versa. The route of leukocyte infiltration into the skin is always directed from the lumen of dermal vessels in the dermal milieu and in some cases further into the epidermal compartment (so-called epidermotropism). The migration of inflammatory cells across the borders of different skin compartments is unique and represents an ideal model to evaluate the chemotactic function of cytokines or chemokines. In various representative dermatoses (wound healing, psoriasis, alopecia areata) we investigated the different expression patterns of selected chemokines. Chemokines, expressed or secreted by endothelial cells, play an important role because they exert a "gatekeeper function". This is crucial in the recruitment and accumulation pattern of the disease and repair processes of wound-specific leukocyte subpopulation, which invade the dermal and epidermal compartment
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Tobin, Desmond J. "The cell biology of human hair follicle pigmentation." 2010. http://hdl.handle.net/10454/7456.
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noAlthough we have made significant progress in understanding the regulation of the UVR-exposed epidermal-melanin unit, we know relatively little about how human hair follicle pigmentation is regulated. Progress has been hampered by gaps in our knowledge of the hair growth cycle’s controls, to which hair pigmentation appears tightly coupled. However, pigment cell researchers may have overly focused on the follicular melanocytes of the nocturnal and UVR-shy mouse as a proxy for human epidermal melanocytes. Here, I emphasize the epidermis-follicular melanocyte pluralism of human skin, as research models for vitiligo, alopecia areata and melanoma, personal care/cosmetics innovation. Further motivation could be in finding answers to why hair follicle and epidermal pigmentary units remain broadly distinct? Why melanomas tend to originate from epidermal rather than follicular melanocytes? Why multiple follicular melanocyte sub-populations exist? Why follicular melanocytes are more sensitive to aging influences? In this perspective, I attempt to raise the status of the human hair follicle melanocyte and highlight some species-specific issues involved which the general reader of the pigmentation literature (with its substantial mouse-based data) may not fully appreciate.
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Stockmeier, Markus [Verfasser]. "Topische Immuntherapie mit Diphenylcyclopropenon bei verschiedenen Typen der Alopecia areata : Assoziation zu klinischen Parametern und einem funktionellen Genpolymorphismus des Interleukin-6-Promotors / vorgelegt von Markus Stockmeier." 2004. http://d-nb.info/977599213/34.
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