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4 Haartalgdruesen SS 09.Pdf Klinik für Dermatologie und Allergologie Philipps-Universität Marburg Seminarreihe Dermatologie Erkrankungen der Anhangsgebilde: - Haare insbes. Alopezien - Talgdrüsen insbes. Acne, Rosacea, Rhinophym SS – 2009 Haarzyklus Anagen = Wachstumsphase 3 - 6 Jahre 1/3 mm /d Katagen = Übergangsphase wenige Tage Telogen = Ruhephase 2 - 4 Monate 100 Kolbenhaare /d Haarerkrankungen Begriffsdefinitionen Hypotrichose, Atrichie Î angeborene Verringerung der Haardichte / vollständigesFehlen der Haare Haarerkrankungen Begriffsdefinitionen Hypotrichose, Atrichie Î angeborene Verringerung der Haardichte / vollständigesFehlen der Haare Effluvium Î Haarausfall (d.h. der Vorgang) Anageneffluvium Î während der Wachstumsphase Telogeneffluvium Î während der Ruhephase (Kolbenhaare) Haarerkrankungen Begriffsdefinitionen Hypotrichose, Atrichie Î angeborene Verringerung der Haardichte / vollständigesFehlen der Haare Effluvium Î Haarausfall (d.h. der Vorgang) Anageneffluvium Î während der Wachstumsphase Telogeneffluvium Î während der Ruhephase (Kolbenhaare) Alopezie Î erworbener Verlust der Behaarung (d.h. der Zustand) Alopezie ● diffuse Alopezie: - gleichmäßiger Befall - Musterbildung ("patterned") ● umschriebene Alopezien - herdförmig Alopezie ● vernarbend: irreversibel ● nichtvernarbend: oft reversibel Nichtvernarbende Alopezie, Beispiele ● Androgenetische Alopezie ● Alopecia areata ● Chemisch / medikamentös - Schwermetalle: Thallium, Arsen, Blei etc. - Thyreostatika: Thiouracil, Carbamizol - Antikoagulanzien: Cumarin, Heparin - Retinoide - Zytostatika - u.a.: Lipidsenker, ß-Blocker, ACE-Hemmer etc. ● traumatische Alopezie (oft vernarbend) - Trichotillomanie (nicht vernarbend) ● extreme Mangelzustände (Fe, Zn, Protein, sehr selten!) ● endokrin (Postpartal, Schilddrüse, endokrin akt. Tumoren) ● Infektionen (meist vernarbend), z.B.Lues II Vernarbende Alopezie, Beispiele ● physikalische Schäden ● Neoplasien ● Infektionen - Furunkel, Karbunkel - Lues - tiefe Trichophytie -Zoster etc. ● Autoimmundermatosen - Lupus erythematosus chronicus discoides - Sklerodermie - Lichen ruber planopilaris ● weitere Dermatosen Pseudopelade Brocq, Folliculitis decalvans Androgenetische Alopezie ● häufigste Alopezie: - mind. 80% der Männer - 60% d. Frauen bis 60. Lj. ● polygen determinierte Androgen- empfindlichkeit der Follikel ● Androgene erhöhen Telogenrate Î Vellushaarfollikel ● keine "Krankheit" aber oft hoher Leidensdruck ● große genetisch determinierte Schwankungen d. Schweregrads Androgenetische Alopezie Telogenrate erhöht Androgenetische Alopezie Pathogenese ● genetisch determinierte Androgenempfindlichkeit ● praktisch immer normale Androgenlevel Androgenbedingte Hemmung der Adenylatzyklase → intrazelluläre cAMP-Konz. ↓ → Miniaturisierung des Haarfollikels ● Telogenrate Ç, regressive Metamorphose, Vellushaare ● absolute Anzahl d. Haarfollikel bleibt unverändert Androgenetische Alopezie nicht völlig gleichmäßig diffus, sondern in Mustern (pattern) Grund: 3 Typen von Haarfollikeln bzgl. Hormoneinfluß ● androgenempfindlich: frontal / parietal ● androgenabhängig: Bart- /Schambehaarung, Körperhaare ● androgenunabhängig: Brauen, Wimpern, okzipital (relativ) Klinik der androgenetischen Alopezie männliches Muster (male pattern) männliches Muster der androgenetischen Alopezie Stadieneinteilung nach Hamilton / Norwood ... geht's noch genauer? Stadieneinteilung nach Hamilton / Norwood ... geht's noch genauer? Î Voilà! weibliches Muster der androgenetischen Alopezie (female pattern) Stadieneinteilung nach Ludwig N.B.: manchmal wird bei Männern das weibliche und bei Frauen das männliche Muster beobachtet! Androgenetischen Alopezie der Frau ● starke psychische Belastung ● aber: oft Mißverhältnis zwischen eher diskretem Befund und Leidensdruck Î Dysmorphophobie, "Nihilopezie" Diagnostik bei Androgenetischer Alopezie ● Klinik ● Familienanamnese: wird oft heftig negiert Î Fehleinschätzung! (Großeltern?) optional: ● Trichogramm: okzipital versus triangulär / parietal Î Telogenrate > 25% im androgensensitiven Areal Î meist verzichtbar ● Hormonanalysen? Serumandrogene meist normal! bei Frauen manchmal sinnvoll, bei - Zyklusstörungen, Hirsutismus: V.a. PCO etc. Î freies Testosteron, DHEAS, Prolaktin, SHBG - Schwitzen, Tachykardie, Diarrhoe, Gewichtsänderung Î TSH Grundsätzliches zur Therapie der Androgenetischen Alopezie ● Aufklärung! Therapieziel: Progressionsstop frühester Erfolgszeitpunkt: nach 3 Monaten ● Haarewaschen: zu seltenes (!) Waschen begünstigt seborrhoisches Kopfekzem (Pityrosporon) Ekzem triggert Effluvium Th.: antimykotische Shampoos ● kosmetische Manipulation: Färben, Tönen, Dauerwelle Î erlaubt, wenn kein Kopfekzem entsteht ● Zug auf Haar vermeiden (Haarknoten, langer Zopf etc.) Î cave Traktionsalopezie ● Diät? - Eisenmangel erhöht Androgensensitivität - Proteinmangel z.B. bei "crash"-Diät - Zink-/Biotinmangel? praktisch nie! (außer z.B. Anorexia nervosa) Therapie der androgenetischen Alopezie bei Männern Hemmung der 5α-Reductase durch Finasterid Systemische Therapie bei Männern: Finasterid 1mg /d p.o. Therapie der Androgenetischen Alopezie bei Männern ● Finasterid (effektivste Behandlung): 1mg p.o./d ca. 50 €/Monat ● externe Tinkturen: - Minoxidil 5%-Lsg. (Aktivator des ATP-abh. Kaliumkanals) 2x tgl. 1 ml ca. 23 €/Monat -17α-Estradiol (keine hormonelle Wirkung, fragliche Effektivität) ● Haartransplantationen (z.B. micrografts) ● Haarteil, Perücke Therapie der Androgenetischen Alopezie bei Frauen ● orale Antiandrogene (Cyproteronacetat, Chlormadinon) - nur bei gleichzeitiger hormoneller Kontrazeption - Kontraindikation? (gyn., phlebol., internist.) ● extern: - Minoxidil 2%-Lsg. (mind. 6 Monate) - hochdosiert östrogenhaltige Tinkturen ● Haarprothetik N.B. Finasterid ist bei Frauen wegen Teratogenität nicht zugelassen Alopecia areata - kreisrunder Haarausfall ● häufig ● wichtigste entzündliche Alopezie ● Beginn meist als runder Herd mit komplettem Haarverlust ● meist ohne subj. Symptome ● Follikelostien erhalten: keine Atrophie Alopecia areata AA fere totalis AA totalis AA totalis: vollständiger Verlust der Kopfhaare AA universalis: Verlust sämtlicher Haare (auch Körperhaare, Brauen, Wimpern) Alopecia areata Randbereich der Herde Pelade-Haare = Ausrufezeichenhaare = Kommahaare Alopecia areata Zupftest erlaubt Aussagen zur Progredienz Alopecia areata: Nagelveränderungen Rillen, Tüpfel Sandpapiernägel punktförmige Rötungen der Lunulae Isolierte Alopecia areata der Nägel ohne Alopezie Sämtliche Nägel betroffen Î "twenty-nail-dystrophy" Alopecia areata - Poliosis spontanes Nachwachsen unpigmentierter Terminalhaare auch Depigmentierung ohne Haarausfall möglich Î einzelne weiße Strähnen Alopecia areata: Verlauf und Prognose ● über 50% Spontanheilung innerhalb von 1 J. ● Ungünstige Prognose: - Beginn vor der Pubertät - pos. Familienanamnese - Atopie, Autoimmunerkrankungen - Ophiasis-Typ - ausgeprägte Nagelveränderungen - rasche Progredienz - AA totalis / universalis - Dauer > 2 Jahre Ophiasis Alopecia areata ● Ätiologie: T-Zellvermittelte Autoimmunerkrankung multifaktoriell, polygen determiniert ● Pathogenese frühes entzündliches lymphozytäres Infiltrat bienenschwarmartig am Haarbulbus führt zum Abschalten des Haarzyklus ÎMiniaturfollikel Alopecia areata - Therapie ● Wirksam, aber mit ernsten, inakzeptablen Nebenwirkungen: - systemische Glukokortikoide (extrem hohe Dosen erforderlich: z.B. Pulstherapie mit 250mg/die für 1 Woche/Monat) ●Unwirksam, aber leider noch weltweit praktiziert: - topische Glukokortikoide - Anthralin (Dithranol, Cignolin) - Minoxidil ● Unwirksam, aber immer wieder anekdotische Erfolgsmeldungen (hohe Spontanheilungsraten!): - Psychotherapie - Aromatherapie u.a. alternativmedizinische Ansätze -Zink Alopecia areata - topische Immuntherapie ● Prinzip: Erzeugung eines allergischen Kontaktekzems durch obligate Sensibilisatoren - Diphenylcyclopropenon (DCP) - Quadratsäuredibutylester (SADBE) ● Nach Sensibilisierung zunächst halbseitige Anwendung (um Spontanheilung nicht zu übersehen) ● Nach halbseitigem Nachwachsen Behandlung der gesamten Kopfhaut ● bislang effektivste Therapie: - Erfolgsquote über 50% bei lang bestehender schwerer AA ● nur in Spezialzentren mit hoher Erfahrung Alopecia areata - topische Immuntherapie Prof. em. Rudolf Happle & Dr. Karin Echternacht-Happle Alopecia areata - topische Immuntherapie Alopecia areata - topische Immuntherapie Alopecia areata - topische Immuntherapie Nebenwirkungen Wie lautet Ihre Diagnose? Trichotillomanie Bei Rechtshändern: oft linke Kopfregion Histologie: Trichomalazie Traktionsalopezie Alopecia hassica bei hessischer Tracht Vernarbende Alopezien (Beispiele) Vernarbende Alopezien (Beispiele) Tiefe Trichophytie Kerion Celsi phlegmasische Form der Tinea capitis / Tinea barbae Tiefer Befall der Haarfollikel Pusteln, eitrige Sekretion oft narbige Abheilung Vernarbende Alopezien (Beispiele) Lichen planopilaris Vernarbende Alopezien (Beispiele) Lichen planopilaris = Lichen planus follicularis capillitii Lichen ruber der Haarfollikel Endzustand vernarbende Alopezie Vernarbende Alopezien (Beispiele) Morphaea = zirkumskripte Sklerodermie Sonderform: Sklerodermie en coup de sabre Vernarbende Alopezien (Beispiele) Follikulitis decalvans •Erythem, Pusteln •Bündelhaare genetisch bedingte Hypotrichosen ● diffuse Hypotrichosen: Genodermatosen ● umschriebene Hypotrichosen: Mosaikphänotypen diffuse Hypotrichosen, Beispiele Hypohidrotische Ektodermaldysplasie Christ-Siemens-Touraine: X-gekoppelt rezessiv Schwitztest bei einer Konduktorin umschriebene Hypotrichosen Incontinentia pigmenti X-gekoppelt dominant, männlich-letal X-Inaktivierung
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