Sunday, April 26, 2020

人類最常見的癌症:皮膚的基底細胞癌

基底細胞癌是最常見的皮膚癌,會在皮膚表面造成型態特殊的丘疹或是潰瘍,多半只會造成局部的侵犯。只要能徹底將病灶移除,極少發展成遠處的轉移。


人類身上最常見的癌症是什麼?這答案不是很響亮,但很明確就是皮膚上面的「基底細胞癌(basal cell carcinoma)」。根據國外統計這種癌症的案例數佔了所有皮膚癌的75%,所有人類惡性腫瘤案例的25%(1),在臺灣雖然比例不至於那麼誇張,但在皮膚癌中基底細胞癌還是占了所有案例的五成(2)。這種癌症雖然不太會四處轉移,卻會破壞附近皮膚的結構,在皮膚上面形成經久不癒的潰瘍。偏偏基底細胞癌又好發於頭頸部,容易造成顏面五官的一些傷害。


基底細胞癌的臨床特徵


一般臨床上看到的基底細胞癌多半是結節型(nodular),是一個看起來略為透亮(半透明)、邊緣隆起的丘疹(圖1),上面往往會出現黑色素斑點,乍看之下像一個黑痣,但卻黑得不是很完全。它們發展到最後中央會出現長久不癒的潰瘍(圖2)

圖1:典型的結節型基底細胞癌,位於上嘴唇,上面會有一些黑色斑點,但往往不會擴及整個病灶,彷彿一個黑得不太完全的黑痣。

圖2:結節型基底細胞癌發展到最後變成一個長久不癒的潰瘍,位於鼻翼外側臉頰。

某些亞型(色素型 pigmented type,如圖3)會整個呈黑色。常伴隨血管擴張,中央有時也會出現潰瘍,常被以為是惡名昭彰的黑色素瘤。實際上黑色素瘤的黑色會有很多不同的層次,不會只有一兩種色階。

有種基底細胞癌是一塊邊緣清楚的紅色斑塊,表層稍微粗糙類似濕疹,但周圍沒有出現類似的病灶,擦濕疹的藥膏也不太會好,這就可能是表淺型(superficial type,圖4)的基底細胞癌。
圖3:色素型基底細胞癌,位於髮際線,看起來很黑又有潰瘍,常被誤以為為是黑色素瘤。但本例整個全黑且邊緣相對隆起,並非黑色素瘤特徵。
圖4:表淺型基底細胞癌,是一塊位於胸口,邊緣清楚的紅色斑塊,表面稍微粗糙類似濕疹但以濕疹方式治療無效。

另外有兩種比較侵略性的基底細胞癌,比起其他各型的基底細胞癌更容易復發。有些看起來是一塊偏白稍硬的斑塊,乍看之下很像一個疤痕或是自體免疫的硬斑症(morphea),這種稱為硬斑型/硬化型(morpheaform/sclerosing,圖4)基底細胞癌。還有一些看起來像是表層被抓破的小丘疹,切片之後發現雖然是基底細胞癌,但部分已經出現像鱗狀細胞癌的分化,稱為基底鱗狀癌(basosquamous carcinoma),這兩種基底細胞癌的亞型有相對較高的轉移率,跟其他幾乎不轉移的亞型大不相同。
圖4:硬斑型基底細胞癌,看起來是一塊偏白稍硬的斑塊,常被誤認為是一個疤痕。

由於基底細胞癌跟紫外光曝曬有關,好發的區域常在頭頸部,但身體各處都可能出現。基底細胞癌的各種亞型好發於不同的位置,例如結節型色素型硬斑型在頭頸部較多,表淺型則常出現於軀幹

基底細胞癌的型態變化很大,因此皮膚上如果出現任何不明的病灶,最好找皮膚科醫師確定。

基底細胞癌的好發族群與誘發因素


目前所知所有的基底細胞癌幾乎都是因為紫外光曝曬導致PTCH1基因突變,活化細胞中的一條訊息傳導路徑(Hedgehog signaling pathway)所致(1)

基底細胞癌好發於老年人,大多發生於60歲以上的人,但近年來有年輕化的趨勢。男性的比例稍高於女性;膚色較白的人則比膚色較黑的人容易得基底細胞癌,都與紫外光的作用有關。

基底細胞癌的治療與預後


基底細胞癌如能及早治療,病人的壽命與都與正常人無異。目前最好的方式還是讓皮膚外科醫師把整個病灶都切下來進行病理化驗,才能確認是否有切乾淨(圖5),這也是復發率最低的方式。(1, 3)
圖5:鼻子上的基底細胞癌,在其他醫院確診後轉給筆者治療。經手術廣泛切除達到安全距離(safe margin)後,考量直接縫合張力過大,以皮瓣手術關閉傷口。半年之後除了膚色稍白尚未完全恢復外,疤痕相當輕微,幾乎看不出來。


至於某些不適合手術的地方(例如眼皮),則可以使用刮除加上電燒(curettage & desiccation)的方式來清除腫瘤,對於小於1公分的基底細胞癌有很高的治癒率(1, 3)

此外液態氮冷凍治療、外用的5-fluorouracil藥膏、外用imiquimod(樂得美)藥膏、光動力療法、與放射治療(radiotherapy)都可以治療無法手術切除的基底細胞癌。其中最不影響外觀的是光動力療法(photodynamic therapy),但復發率相對略高,治療之後最好規律追蹤二到三年(1)。但上述的5-fluorouracil藥膏與光動力療法的5-Aminolevulinic acid藥膏需要專案申請,使用上並不普及。筆者也是經過很多年的努力,才幫自己所屬的醫院收集到上述所有的治療。

當然,這些非外科的治療不能確認癌細胞有無徹底清除乾淨,因此未來還是需要長期追蹤,確保沒有殘存的癌細胞復發。不過基底細胞癌是相對溫和的皮膚癌,就算復發,只要進一步切除乾淨還是可以治癒,也不容易產生轉移。

一般除非是硬斑型基底鱗狀癌等亞型、或是病理下出現侵犯神經的特徵、大於7.5公分拖了很久都沒處理的病灶,才可能出現淋巴結、肺部、與骨頭的轉移。轉移的案例很稀少,轉移率遠小於1%。然而轉移的案例預後就很差,剩餘壽命的中位數僅10個月(1, 4),與很早就進行手術切除根治的病例(壽命同正常人)相比可說是天壤之別。因此,早期診斷早期治療,依然是對於癌症最有效的處理方式。

降低基底細胞癌風險的方法



一般得過基底細胞癌的病人大約有40-50%在五年內會在其他地方出現基底細胞癌。目前發現每日早晚各服用一次500mg的菸鹼醯胺(nicotinamide,維生素B3的醯胺化合物),或是服用關節痛使用的非類固醇抗發炎藥celecoxib(需醫師開立)能降低得基底細胞癌的風險(1)。考量菸鹼醯胺很安全且對皮膚有不少其他好處(5),曾確診過基底細胞癌的病人可以適度補充。

參考資料

(1) Fitzpatrick's Dermatology, 9th edition, p. 1884-1897.
(2) 臺灣癌症登記中心年報 http://tcr.cph.ntu.edu.tw/uploadimages/Y98-ALL.pdf
McKee's Pathology of the Skin, 5th edition, p. 1192-1196.
(3) Surgery of the skin, 3rd edition, p. 718-719.
(4) Update on metastatic basal cell carcinoma: a summary of published cases from 1981 through 2011. JAMA Dermatol. 2013;149(5):615-616.
(5) http://www.skin168.net/2012/02/b3.html (皮膚科王修含醫師的網頁)

國泰皮膚科線上教室:Clinical Patterns in Dermatology(12) Granulomatous & Necrobiotic Lesions(1) 3.0

本次因為疫情關係取消實體課程,結果沒有比較簡單,做了超過一個月才完成,弄到皮專考完一周才完成,實在是來討罵的。

但這次錄音實在歷經很多困難。比如假日被迫在家帶小孩,從早上七點開始就很難找到超過10分鐘的安靜時間,還要整天都與大便為伍。希望大家有小孩之後不要像煜彬這麼悲慘。

課程連結已經寄送到各位信箱。如有皮膚科醫師沒收到請私訊。


Wednesday, April 8, 2020

別被它的溫和外表騙了!紅紅的厚皮居然是鱗狀細胞癌原位癌。

鱗狀細胞癌原位癌又稱為波文氏症(Bowen disease),臨床上往往是一片紅色、邊界清楚、略為增厚、表面粗糙的皮膚。手術切除是最好的治療方式,對於某些不適合開刀的病灶可使用光動力療法等非手術療法。


有時老人的皮膚上會出現一塊紅色、邊界清楚、略為增厚、表面粗糙的皮膚。由於不癢不痛,很多人往往不以為意,但別被它溫和的外表騙了,這塊病灶可能就是鱗狀細胞癌的原位癌/波文氏症(squamous cell carcinoma in situ/Bowen disease)。

鱗狀細胞癌原位癌是指癌變的細胞還位於表皮基底膜(basement membrane)以上的淺層病灶,只要手術移除就等同治癒。但如果癌細胞吃穿了表皮的基底膜(basement membrane),接下來轉移到淋巴結或遠處其他器官的機率就會大增,所幸一般只有大約5%的病灶會演變成侵入性的鱗狀細胞癌。(1)

鱗狀細胞癌原位癌(波文氏症)的臨床特徵


鱗狀細胞癌原位癌好發於頭頸部與四肢這些容易受到日光曝曬的位置,但全身到處都可能出現,也可能出現於皮膚皺褶處、甲床或指甲附近。臨床上看起來是一塊邊緣不規則但界限清楚的粉紅色或紅色斑塊(圖1, 2, 3),會隨著時間逐漸變大,也可能會出現隆起的結節或是疣狀的增生(圖4)。因為表面往往有鱗屑脫落、結痂或是角質增生,有時會呈現灰色或棕色(圖5)。(1, 2)
圖1  典型的鱗狀細胞癌原位癌:一塊紅色、邊界清楚、略為增厚、表面粗糙的皮膚
圖2  頭頸部的鱗狀細胞癌原位癌:呈現紅色、粗糙的厚皮


圖3  與圖2相同病人頭頸部另一處的鱗狀細胞癌原位癌:鱗狀細胞癌原位癌有時會有多處病灶,因為附近的皮膚往往也累積了相當程度的DNA突變。

圖4  出現疣狀增生的鱗狀細胞癌原位癌
圖5  結痂的臨床細胞癌原位癌,呈現棕色與黃灰色的痂

由於長得很慢沒症狀,頂多略為搔癢,因此很容易被忽略。最後病人來門診的時候往往已經長達數公分,雖然多半還沒穿過基底膜,切除後大多仍可根治,卻還是會造成很大的傷疤。
圖6  色素型的鱗狀細胞癌原位癌(pigmented squamous cell carcinoma in situ),可能會被誤以為是老人斑。

鱗狀細胞癌原位癌有時會被誤以為是乾癬(psoriasis)、慢性濕疹、扁平苔蘚(lichen planus)或是黴菌感染(癬),但上述這些疾病多半伴隨明顯搔癢。少數的鱗狀細胞癌原位癌會有色素增生(圖6),常會被誤以為是老人斑(seborrheic keratosis)等良性病灶,此時最好還是由皮膚科醫師實際看診後決定是否進一步接受切片檢查,以免誤放皮膚癌或是過度治療。

鱗狀細胞癌原位癌(波文氏症)的誘發因子與好發族群


引起波文氏症的主要原因是紫外光的曝曬,另外使用免疫抑制的藥物、接受放射治療、以及受到人類乳突病毒(human papillomavirus)感染也都可能誘發波文氏症。在台灣西南沿海過去飲用深井水造成的慢性砷中毒(arsenism)除了會造成烏腳病,也會誘發鱗狀細胞癌。
由此可知,鱗狀細胞癌原位癌多半發生於六十歲以上的老人男性的盛行率較高,可能跟接受較多日光曝曬有關。免疫力受到抑制的人出現鱗狀細胞癌原位癌的年齡則會提早。

鱗狀細胞癌原位癌的治療方式


鱗狀細胞癌原位癌如能及早治療,病人的壽命與都與正常人無異。主要治療方法是手術切除,因為這類腫瘤一旦吃穿基底膜就可能變成淋巴或遠處轉移。要評估有沒有吃穿基底膜,最好的方式還是讓皮膚外科醫師把整個病灶都切下來進行病理化驗,才能確認是否有轉移(圖7, 8)。(1, 3)

圖7  手術切除並轉皮瓣縫合是最能確保根治的作法

圖8  手術切除得當,也可以兼顧美觀。本例是筆者幫106歲的人瑞切除額頭多年的鱗狀細胞癌,經過半年後回診追蹤,除了色素稍有不均之外,彷彿什麼事都沒發生過。

至於某些不適合手術的地方(例如眼皮),則可以使用光動力療法電燒氣化型雷射(二氧化碳雷射)三氯冰醋酸藥物燒灼液態氮冷凍治療外用的5-fluorouracil藥膏、或是外用imiquimod(樂得美)藥膏來治療。其中實證效果最佳,且最不影響外觀的是光動力療法(photodynamic therapy)。(1)但上述許多藥物需要專案申請,使用上並不普及。筆者也是經過很多年的努力,才幫自己所屬的醫院收集到上述所有的治療。

當然,這些非外科的治療不能確認癌細胞有無吃穿基底膜,因此未來還是需要長期追蹤,確保沒有殘存的癌細胞復發。

鱗狀細胞癌原位癌的後續追蹤


儘管進行了徹底的治療,鱗狀細胞癌原位癌患者其他處皮膚仍有可能在往後數年中陸續長出非黑色素的皮膚癌。這是因為附近的皮膚往往也累積了相當程度的DNA突變,只要再接受到臨門一腳的刺激就可能變成癌細胞。因此得過鱗狀細胞癌原位癌的病人都要比一般人更警覺,更要時常檢查自己的皮膚有無異常病灶出現。



參考資料

(1) Fitzpatrick's Dermatology, 9th edition, p. 1867-1871.
(2) McKee's Pathology of the Skin, 5th edition, p. 1192-1196.
(3) Surgery of the skin, 3rd edition, p. 718-719.

Wednesday, April 1, 2020

[考生加油] Dermatological Recall: Chapter 32 Lichen Planus Part 2


口腔的扁平苔蘚除了造成疼痛,長期下來也有癌變的危險。扁平苔蘚不容易治療,常常需要另加上口服藥才能控制。很多位於頭皮、指甲的扁平苔蘚如果沒有及時治療,甚至可能造成不可逆的毛髮與指甲脫失。

Chapter 32 :: Lichen Planus Part 2

:: Aaron R. Mangold & Mark R. Pittelkow

鄭煜彬(20200329)

MALIGNANT TRANSFORMATION

 

How about the risk of malignant transformation in oral LP?

Low risk (0.6-1.9%)

What are the risk factors of malignant transformation in oral LP?

Long-standing dz, erosive or atrophic types, tobacco use, esophageal involvement, oncogenic subtypes of HPV (type 16)

What is the stage of malignant transformation in oral LP?

In situ carcinoma or with a microinvasive pattern.

Where is the common sites of malignant transformation in oral LP?

Tongue> buccal mucosa>gingiva>>>lip

What are the features of malignant transformation in oral LP?

Invasive SCC:

1.          Indurated, nonhealing ulcers

2.          Exophytic lesions with a keratotic surface.

3.          Red atrophic plaques(correlate with SCC in situ)

What are the risk factors of SCC in LP ?

1.          Hypertrophic or verrucous LP

2.          LP on the lower extremity

3.          A history of arsenic exposure

4.          A history of x-ray exposure

5.          Long-standing disease (average, 12 ys)

DIAGNOSIS

 

What should you do for the vesiculobullous disease or erosive disease of LP?

Histopathology, DIF, IIF, & ELISA (to differentiate from immunobullous dzs)

Laboratory testing is not required

What laboratory testing should be performed in LP?

Tests for dyslipidemia

What laboratory testing should be performed in oral LP?

Patch tests of mercury, gold, chromate, flavoring agents, acrylate, & thimerosal

What laboratory testing should be performed in LLP?

Testing for thyroid abnormalities: TSH, antithyroid peroxidase antibodies, & anti-thyroglobulin antibodies.

When should you check HCV in the case of LP?

Oral LP, risk factors for HCV (liver function, IV drug use, blood transfusion

prior to 1992, & high risk sex), in endemic areas (East and Southeast Asia, South America, the Middle East, & Southern Europe)臺灣是流行區

PATHOLOGY

 

What are the major pathologic findings of LP?

Epidermis: hyperkeratosis, wedge-shaped areas of hypergranulosis, & elongation of rete ridges (sawtooth)

l  Basal epidermal keratinocyte damage (effacement of DEJ)

 

l  A lichenoid-interface lymphocytic reaction: a dense, continuous, & band-like lymphohistiocytic infiltrate at the DEJ

What are the 2 absent features in LP?

Parakeratosis & eosinophils

What is the apoptotic cells at the papillary dermis of LP ?

Colloid-hyaline bodies=Civatte bodies= eosinophilic bodies.

What is the difference between lichenoid drug eruptions & classic LP?

Eosinophils (in 2/3 lichenoid drug eruption)

What is the difference between hypertrophic LP & classic LP?

Eosinophils (in 1/5 hypertrophic LP, thus they are very itchy.)

What is Max Joseph cleft formation in LP?

Separation of the epidermis in small clefts under severe inflammation of LP.

What are the features of late disease of LP?

Scarring (an atrophic epidermis, effacement of the rete ridges, dermal fibrosis), colloid bodies & melanophages.

What is difference between late disease of LP & poikiloderma?

LP: colloid bodies (+)

What are the features of hypertrophic LP?

Hyperkeratosis, acanthosis, papillomatosis, thick-ened collagen bundles in the dermis, & Eφ.

What are the differences between mucosal/genital LP & cutaneous LP?

Parakeratosis & an absent granular layer, plasma cells.

What are the features of LPP?

A perifollicular, lymphohistiocytic inflammation at only isthmus & infundibulum + scarring alopecia (perifollicular fibrosis, scarring, & follicular atrophy)

What is the features of DIF in LP?

1.      IgM(±IgG, IgA) on the apoptotic cells(colloid bodies) at the DEJ

2.      Shaggy deposition of fibrinogen at the DEJ

3.      Multiple Ig conjugates(IgM, IgG, IgA): consider LE

What is the role of DIF in LP?

1.      More important in oral LP

2.      Atypical disease

3.      Ulcerative and vesiculobullous LP

Where is the optimal location for biopsy of cutaneous LP?

1.      Proximal trunk

2.      Avoidance of the distal extremities.

How do you select optimal location for biopsy of LPP & nail LP?

With dermoscopy.

Where is the proper location of biopsy of nail LP? 

Surficial change (trachyonychia & pitting): matrix

Change of plate(chromonychia, nail plate fragmentation), subungual change(splinter hemorrhage, onycholysis, & subungual debris): nail bed.

Where are the proper locations of DIF of LP ?

1.      Mouth floor & ventral tongue

2.      Can be 1 cm from the lesion

DIFFERENTIAL DIAGNOSIS

 

 

 

 

 

CLINICAL COURSE AND PROGNOSIS

 

How long is the duration of most cutaneous LP?

Resolves within 1-2 years

How much is the recurrence rate of LP?

20%, common in generalized cutaneous disease.

What is the relationship between duration & the extent/sites of LP?

Short to Long: generalized cutaneous < nongeneralized cutaneous < cutaneous & mucosal < mucosal < hypertrophic <LPP

What is the most common manifestation of LP sequelae?

Postinflammatory hypo-/hyperpigmentation (in higher Fitzpatrick skin types)

 

TREATMENT(challenging & discouraging)

 

How can you decrease the severity of LP?

Discontinue exacerbating drugs, minimize trauma, & reduce microbial overgrowth

What is most specific tx of lichenoid dzs?

Janus kinase (JAK) inhibitors (target CD8-Tc cells, also works in DM, AA, & vitiligo)

CUTANEOUS LICHEN PLANUS 

 

What are the choices of skin-directed Tx of cutaneous LP?

Topical: steroids(±occlusion), calcipotriene, calcineurin inhibitors (esp. combination of steroids)

IL: steroids (5-10 mg/mL monthly ± topical steroids)

Phototherapy: NBUVB, BBUVB, UVA, PUVA

What are the special applications of hypertrophic LP?

Occlusion of topical steroids, IL steroids.

What are the systemic Tx of LP?

1st: oral steroids

2nd: sulfasalazine, metronidazole, acitretin, hydroxychloroquine/ chloroquine, methotrexate, mycophenolate mofetil (MMF), & azathioprine

3rd: cyclosporine

How do you choose the systemic Tx of LP ?

Refractory/ulcerative: target lymphocutes (methotrexate, MMF,

and azathioprine)

Generalized/hypertrophic: indirectly on lymphocytes (sulfasalazine & metronidazole) or cellular

differentiation (acitretin)

How much is the dose of systemic prednisolone for cutaneous LP?

0.3-1 mg/kg/ day for 4-6 wks.

Why is corticosteroid-sparing agents very important for cutaneous LP therapies?

Relapse is common after DC steroid

What drug in 2nd line therapies has highest efficacy for cutaneous LP?

Sulfasalazine (1-2.5 g/day)

What is adverse effects of sulfasalazine?

Agranulocytosis & liver function

What is the role of metronidazole in the Tx of cutaneous LP?

1.      The first-line nonimmunosuppressive systemic agent (250mg tid or 500mg bid)

2.      Effective in generalized cutaneous LP.

What is adverse effects of metronidazole?

Sensory peripheral neuropathy

What is the role of acitretin in the therapies of cutaneous LP ?

Highly effective for hypertrophic LP (30 mg/day)

What is adverse effects of acitretin?

Mucocutaneous side effects(xerosis, scaling) and hyperlipidemia

What is the role of antimalarials in the Tx of cutaneous LP ?

Chloroquine: cutaneous LP.

Hydroxychloroquine: LPP, & actinic LP, favorable side effects

What is the role of methotrexate in the Tx of cutaneous LP ?

Works for recalcitrant disease, hypertrophic LP, & LPP

What is drawbacks of MMF, azathioprine, & cyclosporine?

MMF: expensive, delayed response (needs steroids)

Azathioprine: suppressive effects on T + B lymphocytes & poor tolerability

Cyclosporine: expensive, frequent relapses, long-term side effects (kidney insufficiency & lymphoma)

ORAL LICHEN PLANUS

 

What is the cornerstone of Tx in oral LP?

Good oral hygiene with regular professional dental cleanings

How can patients minimize exacerbating factors of oral LP?

Avoiding contact allergens(removal of amalgams, gold), DC drug, reducing oral microbes & trauma

What are the skin-directed Tx of oral LP?  

1st: topical sterods in orabase.(Stronger agents: clobetasol & fluocinonide + more occlusive preparations + 2-6 times daily)

2nd: topical tacrolimus/ pimecrolimus

3rd: topical cyclosporine/tretinoin

What is the major complication of topical steroids?

Fungal infection

How can you manage the major complication topical steroids?

Oral chlorohexidine gluconate mouthwash, topical anticandidal medications, oral fluconazole

What is the side effect of topical calcineurin inhibitors for oral LP?

Transient burning (improved by combination of topical steroids)

What is the role of IL steroid in the Tx of oral LP?

Last line (after exhausting topical therapies, 10-40mg/ml, Q 1-4 wks)

What are the systemic Tx of oral LP?  

1st: oral steroids

2nd: acitretin, hydroxychloroquine/ chloroquine, methotrexate, MMF

3rd: cyclosporine, azathioprine…

How much is the dose of systemic prednisolone for oral LP?

1.5-2 mg/kg/ day for 4-6 wks.

What are the concerns of systemic Tx in oral LP? (2)

1.      iatrogenic candida infections

2.      risk of oral SCC under erosive & refractory LP & immunosuppression

What drugs are preferred in oral LP?  (4)

Erosive LP

1.      MMF

2.      Hydroxychloroquine (less immunosuppressive)

3.      Methotrexate (less immunosuppressive)

Hyperkeratotic/noneroded LP

4.      Acitretin (antiploliferative, less immunosuppressive)

How much is the dose of systemic steroids for oral LP?

Prednisolone: 1.5-2 mg/kg (higher than skin, more side effects)

Betamethasone: 5 mg on 2 consecutive days weekly (pulse tx: less side effects)

What oral drugs can be considered in oral LP?

1.      Acitretin 30mg/day

2.      Alitretinoin 30mg/day (臺灣沒有)

What are first choices of steroid-sparing agents for oral LP? (2)

1.      Methotrexate (10-15mg/wk)

2.      MMF (2-3g/day)

Tx of LPP

 

Why does LPP & FFA cause scarring alopecia?

Deficiency of PPARγloss of immune privilegedestruction of the bulge

What are the skin-directed Tx of LPP?  

1st: mid to high potency steroids(topical or IL)

2nd: calcineurin inhibitors

What are the systemic Tx of LPP?  

1st: prednisolone 1 mg/kg/day

2nd: Hydroxychloroquine (+ doxycycline, not monotherapy), MMF, methotrexate

3rd: cyclosporine (monotherapy)

Tx of FFA

 

What are the skin-directed Tx of FFA?  

IL steroid, topical minoxidil (combine hydroxychloroquine or others)

 

What are the systemic Tx of FFA?  

1.      5 α-reductase inhibitors (finasteride 2-5mg/day or dutasteride 0.5mg every 1-7 days)

2.      Systemic steroids + MTX & MMF

3.      Cyclosporine (monotherapy)

NAIL LICHEN PLANUS

 

What is the goal of the therapy of nail LP?

Stop the disease (prevent irreversible pterygium), not reverse it.

What is the therapies of nail LP?

Ultrapotent topical & intralesional steroidssyetemic steroids (for compromise of function & debilitating pain) or hydroxychloroquine