| 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 |   | 
 
  |   |   | 
 
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  | 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 PPARγ→loss of immune privilege→destruction 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
  steroids→syetemic steroids (for compromise of function & debilitating
  pain) or hydroxychloroquine |