HAIR and Male Pattern Hair Loss모발의 종류와 일생 하나의 동일한 hair follicle( 모낭 ) 에서 네 가지 종류의 털을 만듬 1) 취모 ( Lanugo hair, 배냇머리 , 배냇솜털 ) - 태생 20 주에 처음 나타남 . 가늘고 연한 색깔의 털 . 출생무렵에 탈락 2) 연모 ( Vellus hair, 솜털 ) 3) 중간모 (intermediate hair) 4) 성모 (terminal hair, 종모 ) 연모가 성모로 대치되는 정도는 유전적 소인 및 내분비기관의 영향을 받음모발주기 생장기 ( Anagen ) : hair bulb 가 부드럽고 풍부한 색소함유 . 활발한 세포분열 . 각질화 모발 생산 퇴행기 ( Catagen ): 생장활동 정지 . 급속도로 위축 휴지기 ( Telogen ): 털망울이 건조하고 완전히 각질로 된 곤봉모양 - anagen : telogen = 90-93%: the rest (scalp 에서의 비율 ) - 두피의 hair 개수 : 10 만 -15 만개 정상 hair loss: 50-100 개 /day hair growth on the scalp: 0.37-0.44mm/day : 1cm/month모발에 대한 호르몬의 영향 1) Androgen ① 모든 모발은 androgen 에 의해 영향 받음 ② 두피 모발은 androgen 에 의존하여 성장 하는 것이 아니라 androgen 에 의해 억제 ( 전두부 , 두정부 ) ③ pubic, axillary , beard hair 는 low-dose androgen 에 의해 촉진 ④ 체간부 , 안면부는 high-dose androgen 에 의하여 유지 ＊ Androgen 에 의존하여 성장하는 대표적인 것이 - 남성 : 안면의 턱수염 , 콧수염 ＊ 여성에서 모낭에 작용하는 대표적 androgen - DHEA-S, DHEA * 주로 부신에서 생산2) Androgen, estrogen, glucocorticoid , thyroid H, growth H 역시 모발성장 조절 전신적 중독의 진단에 도움 3) 문제점 : 모발기질은 샴푸 , 염색제 , 탈색제에 영향탈모증의 분류 크게 미만성 / 국소성으로 분류 2. (1) 모발 생성 장애 (2) 내인성 요인에 의한 모발의 절단 (3) 흐트러지는 모발 (Unruly hair) (4) 모발 주기의 이상 (5) 털집의 파괴Diffuse hair loss 1. HAIR SHAFT ABNORMALITIES 1. Hair shaft abnormalities associated with hair breakage 1) Trichorrhexis nodosa ( 결절털찢김증 ) 2) Trichoschisis ( 털부러짐증 ) 3) Pili torti twisting hair dystrophy ( 털꼬임 ) 4) Trichorrhexis invaginata bamboo hair ( 함입털찢김증 ) 5) Monilethrix ( 염주털 ) 2. Hair shaft abnormalities associated with unruly hair 1) Uncombable Hair Syndrome 2) Wooly Hair 3) MARIA-UNNA TYPE OF HEREDITARY HYPOTRICHOSIS 3. Hair shaft abnormalities unassociated with breakage or unruly hair 1) Pili annulati ( 백륜모 ) 2) Pseudo pili annulatiCuticular hair damage gradingDiffuse hair loss 2. ABNORMALITIES OF HAIR CYCLING Atrichia with papular lesion (APL) Acute telogen effluvium ( 휴지기 탈모증 ) chronic telogen effluvium Anagen effluvium ( 생장기 탈모증 ) Loose anagen syndrome Alopecia areata ( 원형 탈모증 )Telogen Effluvium 1) 어느 나이에서 발생 가 loss of body hair ③ nail involvement ④ atopy ⑤ family history ⑥ extensive AA( totalis , universalis ) ⑦ ophiasis * 치료 ① topical corticosteroids ② intralesional corticosteroids- the most effective approach - hydrocortisone acetate(25mg/ml) triamcinolone acetonide (5 to 10mg/ml) subdermal inj./month ③ systemic corticosteroids ④ topical minoxidil solution ⑤ anthralin ⑥ photo(chemo)therapy ⑦ contact immunotherapyFocal hair loss 1. Nonscarring Hair loss Production decline 1) 삼각 ( 측두 ) 탈모증 Triangular (Temporal) Alopecia - Childhood, temporal lesion, 양측성이며 영구적으로 지속 , 유전적 경향 2) 단순 털감소증 ( Hypotrichosis simplex ) 3) Pattern Hair loss a . anagen duration 의 점진적 감소 b . telogen duration 의 증가 c . scalp hair follicle 의 miniaturization( 털집의 파괴보다는 축소 )Male pattern Hair Loss( Androgenetic alopecia)Male pattern Hair Loss( Androgenetic alopecia) - 사춘기 이후 나이에 따라 진행함 70 세 : 80 % 의 남자들이 어느 정도의 balding 가짐 - 최근 baldness 가 coronary artery ds . 및 sudden cardiac death 와 연관성 가진다는 보고 - 남자 : scalp 의 top 중 4 군데 (vertir follicle cycling in normal and balding scalpBasic and specific classification in Korea patients with androgenetic alopecia JAAD 2007Female pattern hair loss 얼굴두피모발의 경계선은 유지 , 크리스마스나무 형태를 보이는 것이 흔함 ① etiology : 20 세 전후 , 40 세 이상 , perimenopause state 때 peak. ② androgen 이 병인 아닐 것 . - 대부분에서 normal androgen level 이 관찰 되고 , androgen 과다의 임상 특징 동반 하지 않음 . - anti-androgenic Tx . 에도 효과 없음 ③ normal androgen level 을 보이면서 menstrual irregularity, hirsuitism , severe acne, 또는 다른 내분비이상 있을 때는 hyperandrogenism 의심Treatment for hair loss ① Topical minoxidil (2 - 5%) 모낭 anagen induction, anagen 주기 증가 , 모발 굵기 증가 - 작용 기전 : ca channel opener activity 가 중요 - nonspecific hair growth promoter, 1 일 2 회 도포 후 약 6 개월 이후 초기반응 , 1 년 후 최대반응 , 사용 중지 이후 2 개월 후 다시 탈모 - 부작용은 facial hypertrichosis 와 irritation 정도안드로겐 과다 생산에 의한 여자의 안드로겐 탈모증 치료 a. 경구 피임약 b. Antiandrogens - Spironolactone : ( 부작용 ) hyperkalemia , irregular mense , breast tenderness - Flutamide : ( 부작용 ) hepatotoxcicity → 두 가지 약은 male fetus 의 feminization 유inea Capitis : 주로 소아에 흔함 5) Acquired localized trichorrhexis nodosa : 만성단순태선이나 발모벽에서 반복적으로 마찰받음 6) Acquired pili torti ( 후천적 꼬임털 , 후천적 염모 ) : 부서지기 쉬운 털의 반 . 외상이나 두피이상의 이차적 변화 7) Bubble hair ( 거품 모발 ) : 고온에 대한 지속적인 노출Unruly Hair 1) Wooly hair nevus ( 양털 모반 , 양모모반 ) : 비유전성 . 2 세경 발생 . 성장하면서 호전되는 경향 2 ) Acquired progressive kinking ( 후천성 진행성 곱슬머리 )Abnormality of cycling 1) Alopecia areata : focal hair loss 로 나타남 2) Syphilis : 2 기 매독의 한 형태로 측두부 탈모 가능 moth-eaten appearance 3) Scalp conditions associated with focal hair loss : Pityriasis Amiantacea , 심한 두피건선 , T cell lymphoma, Langerhans cell histiocytosis 경우 탈모가 동반되기도 함 . 4) Pityriasis Amiantacea : 털의 기저부위에 딱딱한 비늘 .Scarring Alopecia( cicatricial alopecia) Primary cicatricial alopecia 1. Lupus erythematosus 2. Lichen planopilaris ( 털편평태선 , 모공성 편평태선 ) 3. Pseudopelade of Brocq ( 거짓원형탈모증 , 가성독발 ) 4. Central Centrifugal Cicatrical Alopecia (CCCA) 5. Alopecia Mucinosa (=Follicular mucinosis) 6. Keratosis follicularis spinulosa decalvans 7 . Folli
T.R.U.E test ® R1 채웅석Take patient history and perform a physical exam Schedule patient and provide pre-test instructions Apply T.R.U.E TEST panels Remove T.R.U.E TEST at 48 hours; interpret results at 72 and 96 hours Counsel the patient GuildA complete and accurate history is essential. Ask about symptoms (duration and distributing factor) personal and family history of allergies exposure to materials or products at work and at home Take patient Hx . and perform P/EChronic, persistent dermatitis with characteristics indicative of a contact allergy should be evaluated with patch testing T.R.U.E TEST(Allergen Patch test) provides the physician with a ready-to-use test method for identifying the most common contact allergies. Take patient Hx . and perform a P/EIn patients with severe ongoing dermatitis, defer patch testing until acute symptoms subside to avoid eliciting excited skin syndrome and false positives. Two weeks prior to patch testing stop using oral corticosteroids and avoid usot to touch the test substances. Instruct patients to keep the panels dry, in place, and protected from direct sunlight for 48 hours. Apply T.R.U.E TEST panelsInterpret 48-hour reactions after allowing them to subside for a few minutes . Reactions to T.R.U.E TEST should be read 72 to 96 hours after application. This time span is necessary for allergic reactions to develop fully, and for irritant reaction to subside. Interpret ResultsNeomycin sulfate and p- Pheylenediamine (PPD) sometimes cause reactions that appear 4 to 5 days after application. If neomycin or PPD allergies are suspected, reading at 5-7 days may be needed . Neomycin and corticosteroid s are particularly liable to give a late reactions Interpret ResultsAt approximately 2 day (few minutes to 1 hour after remove) the preliminary and should be confirmed at 4 day or 5 day . A second reading is essential to reduce false positive and false negative results. Additional readings may be required depending on patient history and atment as expected 3. Chronic hand and foot eczema 4. Persistent or intermittent eczema of the face, eyelids, ears and perineum 5. Varicose eczemaIn recalcitrant atopic dermatitis, especially at the age of 5 years and over, patch tests are indicated.Reactivity of various test sites Test site Type of reaction Irritant (%) Allergic (%) Upper back 100 100 Lower back 50 95 Upper arm 52 72 Forearm 38 74 Thigh 36 50Causes of false-positive reactions Excessive concentration Impure substance (contaminants) Irritant vehicle Excess allergen applied Uneven dispersion Current or recent dermatitis at patch-test site Current dermatitis at distant sites Pressure effect of hard materials Adhesive tape reactions ‘Angry back’ reaction causing intensification of weak irritants ArtefactCauses of false-negative reactions Insufficient concentration Insufficient amount applied Poor adhesion of patches Patches applied at wrong site Inappropriate vehicle Readings performed too early Substance degraded Pretreatf LCs Second Step : Migration of LC to the Regional LN Third Step : Antigen presentation to Naive T cells at the LN Sensitization PhaseAllergens bind directly to MHC class II molecules inducing a sensitization reaction. MHC class II molecules are coded on the human leukocyte antigen (HLA)-D region genes , and are present on epidermal DCs and LCs. Epicutaneously applied allergen associates with APCs within 6 hours . First StepEpidermal LC take antigens( haptens ) up and become activated with the augmentation of expression of various- costimulatroy molecules , such as CD54, CD80, and CD86 , and the increased production of proinflammatory cytokines such as IL-1ß, TNF- α , and IL-12 . → activation, maturation, and migration of LC → in the absence of co-factors, tolerance would develop First StepThe activated LC express CCR7 and mirgrate to regional LN via afferent lymphatic vessels. Secondary lymphoid-tissue chemokin (SLC)/6Ckine and EBI-1-ligand chemokine (ELC)/MIP-ß , which are ligand fond CD8 T cells, moreover, they may determine the Th1/Th2 differentiation. Although not all the mechanisms are understood, the regulation of IL-12 production is one of the main mechanisms. Third StepFourth phase : Migration of T cells to the skin after sensitization Fifth phase : Cross-Talk Between LC, T cells and keratinocytes at the skin Sixth phase : Induction of inflammation by T cells Elicitation PhaseAfter naive T cells are stimulated by DC, they express chemokine receptors, CCR4 , and respond to its ligand , TARC and MDC . The skin infiltrating lymphocytes in the lesional skin of ACD express CCR10 , whereas basal keratinocytes produce its ligand , CCL27 . → The CCL27-CCR10 interaction play a pivotal role in T-cell-mediated skin inflammation. Fourth phaseKeratinocytes are activated by hapten and release TNF- α and IL-1 α . MCP-1 from keratinocytes seem to drive the influx of T cells. Fifth phaseThe activated hapten -specific T cells that are recruited into the skin lead to the proow}
Contact dermatitis and Ni-associated dermatitis R1 채웅석Contact DermatitisAllergic Contact Dermatitis Immune reaction to an allergen Genetically susceptible Have sufficient contact with a sensitizing chemical Have repeated contact with the substance laterAllergic Contact Dermatitis 적은 양의 chemical 로도 overt allergic reaction 을 일으킴 Specific antigen 에 sensitization 되는 것은 genetic component 와 연관 → specific HLA alleles to allergy to nickel, chromium, and cobaltAllergic Contact Dermatitis In a sensitized individual, ACD appears 1~4 days after contact with the causative allergen. Intial loacation is at the site of contact → propagate immediate vicinity or distant unrelated sitesAllergic Contact Dermatitis Clinical feature Erythema 로 시작하여 edema, papuloveiculation 양상으로 변화 Closely set vesicles, oozing and crusting Intense pruritusIrritant Contact Dermatitis Immunologic reaction 이 없다 Immediate response (3-12 hours) Reaction 의 강도는 applied 된 chemical dose 와 비례 chemical concentration, duration of exposure, and general skin integrity 와 관련Irritant Contact Dermatitis Casuses of ICD Animal products Cosmetics Degreasing agents Detergents Foods Dusts/friction Low humidity Metal working Tear gases Topical medicaments Solvents Water/wet workContact Dermatitis Two main types of contact dermatitis * Irritant contact dermatitis (ICD) is due to the pro-inflammatory and toxic effects of xenobiotics able to activate the skin innate immunity * Allergic contact dermatitis (ACD) requires the activation of antigen specific acquired immunity leading to the development of effector T cells which mediate the skin inflammation.Contact DermatitisContact DermatitisAllergic Contact Dermatitis ACD is the classic presentation of delayed-type(type IV) hypersensitivity responses to exogenous agents ## S ystemic disease ## hapten specific T cell mediated skin inflammationAllergic Contact Dermatitis ## Three phase Sensitization Elicitation Resolution ## Contact Sensitivity(CS) or Contact Hypersensitiviy (CHS) : skin inflammation induced by hapten painting of the skinAllergic Contact Dermatitis Sensitization phase (induction phase of CS) Low-molecular-weight electrophilic or hydrophilic hapten chemicals → → epidermal carrier proteins 과 covalent linkage → hapten -protein complex (complete allergen) Hepten chemical 은 metabolic biotransformation 을 거치면서 allergic response 를 보일 수 있다 . Non-immunogenic carrier 와 complex 를 이룰 때 tolerance 를 나타냄Allergic Contact DermatitisAllergic Contact DermatitisAllergic Contact Dermatitis ## Treatment Avoidance of allergic contactants Topical steroids If ACD is widespread and severe → systemic corticosteroids for a short period Pimecrolimus / Tacrolimus Phototherapy (short wave UVB light)Allergic Contact DermatitisContact DermatitisAllergic Contact Dermatitis Ni : most common allergenNi-associated ACD Randomly patch tested 657 patients aged 15 to 69 years in 1990 : 1998 년에 365 명의 같은 환자에게 re-test : 1990 년에 시행한 patch test 에서 음성을 보인 사람들 중에서 12% 는 한가지 또는 그 이상에서 양성을 보임 6% 는 nickel 에 incident allergy 를 보임 Risk factor → female gender, young age, prior ear piercingNi-associated ACD In another study, - Female child male child - Neck and antecubital / popliteal fossae Atopic dermatitis non-atopic dermatitisIndustrial Exposures to Nickel Alkaline batteries Blackening zinc and brass Ceramics Coating(electroplating) Dyes Electrical wiring Enamel Fuel additives Insecticides Magnet cores Nickel alloys Paint for glassMetal Allergy Demographics Nickel Female Male Incidence incresing overall Younger older Cobalt Female Male Incidence increasing Younger older Association with nickelAllergic Contact Dermatitis ## Treatment Avoidance of allergic contactants Topical steroids If ACD is widespread and severe → systemic corticosteroids for a short period Reducing the total body load of nickel Metal- chelator ( disulfiram ) was limited by serious side effectsNi-associated food Reducing the total body load of nickel 가급적 피하는 것이 좋은 음식 : 녹차 , 홍차 , 밀가루 음식 , 감자칩 , 커피 , 땅콩 , 피자 되도록 피하는 것이 좋은 음식 : 새우 , 홍합 , 대두콩 , 양배추 , 부추 , 상추 , 시금치 , 완두콩 , 메밀 , 수수 , 파인애플 , 코코아 , 아몬드 , 두유 , 튀긴고기류 증상을 악화시킬 수 있는 음식 : 맥주 , 포도주 , 신맛이 나는 과일 주스 등니켈에 대한 직접적인 피부 접촉을 피하여도 증상이 사라지지 않는 경우 니켈에 의한 전신성 접촉 피부염을 생각해 보아야 한다 . 3 주 후 병변 호전 양상 8 주 후 재발 없이 피부 병변 소실Ni 에 의한 알레르기성 접촉 피부염은 인구의 7-10% 티백형 녹차 / 홍차 , 쵸콜렛 , 감자칩 , 밀가루 김치 / 깍두기Reference Fitzpatric’s dermatology in general 7 th edition Allergic contact dermatitis. Eur J Dermatol 2004;14:284-5 Effector and regulatory mechanisms in allergic contact dermatitis. Allergy 2009;64:1699-1714 Allergic and irritant contact dermatitis. Eur J Dermatol 2009;19(4):325-32{nameOfApplication=Show}
Hereditary Angioedema (HAE) R1 채웅석Urticaria vs Angioedema Urticaria : wheal and flare ( present in the superficial dermis and involve the venular plexus in that location ) Angioedema : rapid swelling of the dermis, subcutaneous tissue, mucosa and submucosal tissues Less pruritus , but pain or burning sensation may be presentAngioedema classification Hereditary angioedema (HAE) caused by genetic mutation ( tyep I, II : AD type III : XD) distinguished by the underlying genetic abnormality and lab. (C1NH,C4,C1q) Acquired angioedema usually caused by allergy and occurs together with other allergic symptoms and urticaria Happen as a side-effect to certain medication (particularly ACE inhibitors)Hereditary Angioedema (HAE)HAE Recurrent episodes of non- pruritic , non-pitting, subcutaneous or submucosal edema Typically involving the arms, legs, hands, feet, bowels, genitalia, trunk, face, tongue, or larynx. Begin in childhood, worsen around puberty, and persist throughout life, with unpredictable severity Increased frequency of autoimmune disease ( especially golmerulonephritis ) Prevalence : estimated 1/10,000~150,000Signs and symptoms Prodrome (usually a tingling sensation) A third are accompanied by erythema marginatum , a non- pruritic , serpiginous rash Swelling classically worsens slowly over the first 24 hours, then gradually subsides over the subsequent 48 to 72 hours. Oropharyngeal swelling is less frequent, but half of patients have had at least on episode of laryngeal angioedema during their life timeSigns and symptoms Abdomen or oropharynx can be associated with significant risk of illness and death Abdomen pain last from 1-5 days on average with high WBC (often indistinguishable from acute appendicitis) Have no direct identifiable cause mild trauma such as dental work can cause attacksPathogenesisAD AD XD Mutation in the C1-inhibitor gene Truncated and mis -folded proteins that are not efficiently secreted Involve exon 8, resulting in a mutant protein that is secreted but is dysfuctional J Allergy Clin Immunol 2010 NovSLE and cryoglobulinemia J Allergy Clin Immunol 2010 NovManagement Allergic Angioedema avoidance of the allergen and use of antihistamines( cetirizine ) may prevent future attacks Drug induced Angioedema ACEi block the enzyme ACE so that it can no longer degrade bradykinin common in African-American change to ARB (but some risk remains)Management Hereditary Angioedema Dose not respond to antihistamines, corticosteroids, or epinephrine Treatment of acute attack Shot-term prophylaxis to prevent an attack Long-term prophylaxis to minimize the frequency and severity of reccurent attacksTreatment of acute attack Purified C1-inhibitor replacement therapy (main treatment, 500 to 2000U IV) Fresh-frozen plasma (exacerbate in some patients) Epinephrine : transient benefit 17 α - alkylated androgens and antifibrinolytic drugs are not effectiveTreatment of acute attack Change in voice, loss of the ability to swallow, difficulty breathing → intubation should be considered → immediate backup tracheotomyShot-term prophylaxis Trigger an attack situation : dental work, invasive medical procedures, and surgical procedures C1 inhibitor (500 to 1500 U given 1 hour before the provoking event) Fresh-frozen plasma 2U (1 to 12 hours before) High-dose 17 α - alkylated androgens ( danazol 200mg orally tid , 5 to 10 days before)Long-term prophylaxis 17 α - alkylated androgens Anti- fibrinolytic drugGleich’s syndrome Unexplained angioedema with high eosinophil counts{nameOfApplication=Show}
True patch test
