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Pemphigoid, Cicatricial


BASICS


DESCRIPTION


  • Cicatricial pemphigoid (CP) is an acquired autoimmune subepithelial blistering disorder that mainly affects mucous membranes.
  • In descending order of involvement, CP affects the oral cavity (85%), conjunctivae (65%), skin (25 " ô30%), nasal cavity (20 " ô40%), anogenital region (20%), pharynx (20%), larynx (5 " ô10%), and esophagus (5 " ô15%).
  • The clinical hallmark of CP is scarring; however, it may not be apparent, especially in the oral mucosa.
  • Synonym(s): mucous membrane pemphigoid, oral pemphigoid, desquamative gingivitis, ocular CP, ocular pemphigus (incorrect nomenclature)

EPIDEMIOLOGY


  • Mean onset at age 60 to 80 years
  • Female to male ratio of 2 to 3:1
  • No racial or geographic predilection

Incidence
1/1 million annually é á

ETIOLOGY AND PATHOPHYSIOLOGY


  • Autoantibodies binding to specific epithelial basement membrane components:
    • Type XVII collagen (bullous pemphigoid antigen 2), type VII collagen, laminin-5, laminin-6,α-6 and Ä ▓-4 integrin subunits, 120-kDa undefined epithelial antigen
      • Exclusive ocular mucosal involvement: autoantibodies to Ä ▓-4 subunit of integrin
      • Exclusive oral mucosal involvement: autoantibodies toα-6 subunit of integrin
      • Association with internal malignancy: autoantibodies to antilaminin-5
  • "Epitope spreading " Ł: previous inflammatory events may predispose epithelial basement membrane components to autoreactive T cells
    • Several patients with Stevens-Johnson syndrome developed CP.
    • Association with Sj â Âgren syndrome and ocular CP
  • Mechanism linking the binding of the antibodies to the epithelial basement membrane zone and subsequent scarring process yet to be defined

Genetics
Association with HLA DQB1*0301 é á

GENERAL PREVENTION


None identified é á

COMMONLY ASSOCIATED CONDITIONS


Antilaminin-5 autoantibody " ôpositive patients have a higher risk of internal malignancy. é á

DIAGNOSIS


Diagnosis is based on direct immunofluorescence and clinical presentation. é á

HISTORY


  • Oral: pain, sensitivity, bleeding, mucosal lesions
  • Ocular: burning, dryness/tearing, itching, foreign body sensation, vision changes, photosensitivity
  • Nasal: discharge, pain, congestion, epistaxis
  • Larynx: hoarseness, sore throat, frequent throat clearing, loss of voice
  • Esophagus: dysphagia, odynophagia, unintentional weight loss
  • Anogenital: blisters, erosions, scarring, dyspareunia, hematuria
  • Skin: tense vesicles and bullae, hair loss, pruritus

PHYSICAL EXAM


  • Oral (especially on gingival and palatal mucosa, and less commonly on labial, buccal, and tongue mucosa): erythematous patches, blisters, erosions, reticulate scarring, and/or pseudomembrane-covered erosions, adhesions
    • Patients with restricted oral involvement have mild to moderate disease process with less chance of scarring.
  • Ocular: unilateral/bilateral involvement, conjunctival inflammation and erosions, malalignment of eyelashes or tarsal conjunctivitis may proceed to scar formation, causing symblepharon, trichiasis, neovascularization, and eventually blindness
    • All patients should be seen by an ophthalmologist. Early disease detection requires slit-lamp examination and eversion of eyelids.
  • Nasal: scarring, tissue loss, epistaxis, discharge; may resemble upper respiratory infections
  • Larynx: erosions and edema leading to life-threatening airway obstruction requiring tracheostomy
  • Esophagus: life-threatening stenosis
  • Anogenital: blisters, erosions, scarring, urethral strictures, vaginal/anal stenosis, fusion of labial tissues
  • Skin: tense vesicles/bullae, erosions generally on head, neck, and upper trunk; lesions heal with atrophic scars and milia

DIFFERENTIAL DIAGNOSIS


  • Bullous pemphigoid
  • Pemphigus vulgaris
  • Linear IgA bullous dermatosis
  • Paraneoplastic pemphigus
  • Epidermolysis bullosa acquisita
  • Stevens-Johnson syndrome
  • Erythema multiforme major
  • Drug-induced conjunctival cicatrization
  • Ocular chemical/radiation trauma
  • Lupus erythematosus
  • Lichen planus
  • Lichenoid drug eruptions

DIAGNOSTIC TESTS & INTERPRETATION


  • Direct immunofluorescence (DIF)
    • Linear deposition of IgG, IgA, and/or C3 along the epithelial basement membrane zone
      • Biopsy for DIF are the following:
        • Single mucous membrane involvement: Take biopsy from adjacent inflamed tissue.
        • Multiple mucous membrane involvement: Take biopsy from adjacent nonocular inflamed tissue.
        • Both mucous membrane and skin involvement: Take biopsy from adjacent inflamed skin lesion.
  • Indirect immunofluorescence (low sensitivity)
    • Serum samples tested with chemically separated normal human epithelial substrate split by 1 mol/L NaCl
    • At low titers (1:10 to 1:40), contain anti " ödermal-epidermal junction antibodies
    • Combined IgA and IgG reactivity is associated with more severe disease.
  • Enzyme-linked immunosorbent assay (ELISA)
    • More sensitive test for target antigen but limited access to the test

Test Interpretation
Histopathologic (hematoxylin-eosin [H+E]) é á
  • Early lesions: subepidermal blisters with lymphohistiocytic infiltrates, granulocytes, and plasma cells
  • Late lesions: subepidermal blisters with scant infiltrates, fibroblast proliferations, upper dermis lamellar fibrosis
  • H+E is not a required criterion secondary to difficulty in biopsying a blister, especially in difficult areas such as ocular mucosae.
    • Ocular biopsy may worsen inflammation.

TREATMENT


  • Low-risk patients (oral mucosa é ▒ skin involvement)
    • Topical corticosteroids (moderate to high potency) (1)[A],(2): can use an oral insertable prosthetic device
    • Tetracycline hydrochloride (1 to 2 g/day)
    • Nicotinamide (2 to 2.5 g/day)
    • Nonresponsive disease
      • Prednisone (0.5 mg/kg/day) + dapsone
        • Serious adverse effects of dapsone are rare; check for G6PD deficiency prior to initiation; CBC weekly during first month then monthly for 6 months, then periodically thereafter; LFTs should also be followed.
        • Starting dose: 25 mg/day
      • Increase by 25 to 50 mg/day every 1 to 4 weeks as tolerated up to 150 to 200 mg/day; if no response with prednisone + dapsone, add azathioprine (100 to 150 mg/day) or mycophenolate mofetil (1 g/day)
  • High-risk patients (involvement of any of the following mucosae: ocular, genital, nasopharyngeal, esophageal, laryngeal):
    • Slow moderate progression of disease: dapsone + corticosteroids (1 mg/kg/day) + azathioprine (2 to 2.5 mg/kg/day) or mycophenolate mofetil (1 to 1.5 g/day)
    • Patients with rapid progression of disease (especially ocular, esophageal, or laryngeal involvement): prednisone (1 to 1.5 mg/kg/day) + cyclophosphamide (1 to 2 mg/kg/day)
    • After control of disease, taper prednisone and continue cyclophosphamide
    • Preliminary reports show rituximab é ▒ IV immunoglobulin is effective for treatment-resistant ocular disease.
    • Ocular involvement requires lubricant without preservative:
      • Blepharitis may be treated with tetracycline and lid hygiene.
        • Patients should see the appropriate specialists for systems involved.
  • Extensive side effect profiles, condensed to most important ones " öappropriate monitoring required the following:
    • Azathioprine and mycophenolate mofetil: severe liver toxicity, bone marrow suppression
    • Cyclophosphamide: hemorrhagic cystitis, bone marrow suppression

ADDITIONAL THERAPIES


For patients receiving long-term prednisone and immunosuppressive treatment, add anti-Candida medication to prevent osteoporosis. é á

SURGERY/OTHER PROCEDURES


Surgery for patients with ocular involvement: entropion surgery, tarsorrhaphy, mucous membrane grafting, amniotic membrane transplantation, tectonic keratoplasty, keratoprosthesis. é á

ONGOING CARE


FOLLOW-UP RECOMMENDATIONS


  • Cancer screening for patients with antilaminin-5 autoantibodies
  • All patients should be seen by an ophthalmologist. Early detection of disease is key
  • Long-term follow up with appropriate specialists.

PROGNOSIS


  • IgG and IgA antibasement membrane autoantibodies are associated with more severe disease.
  • Prognosis mostly depends on site involved:
    • Better prognosis and better response to treatment: oral é ▒ skin involvement
    • Poorer prognosis, high likelihood for loss of function and scarring: ocular, genital, nasopharyngeal, esophageal, laryngeal
      • Ocular scarring and blindness
      • Genital and urinary scarring
      • Scarring can only be prevented, not reversed (2).
      • Airway obstruction
      • Esophageal strictures

REFERENCES


11 Kirtschig é áG, Murrell é áD, Wojnarowska é áF, et al. Interventions for mucous membrane pemphigoid and epidermolysis bullosa acquisita. Cochrane Database Syst Rev.  2003;(1):CD004056.22 Culton é áDA, Diaz é áLA. Treatment of subepidermal immunobullous diseases. Clin Dermatol.  2012;30(1):95 " ô102.

ADDITIONAL READING


  • Allen é áCP, Venning é áV. Mucous membrane pemphigoid. In: Lebwohl é áMG, Heymann é áWR, Berth-Jones é áJ, et al, eds. Treatment of Skin Disease: Comprehensive Therapeutic Strategies. 4th ed. Philadelphia, PA: Saunders; 2013:469 " ô472.
  • Chan é áLS. Ocular and oral mucous membrane pemphigoid (cicatricial pemphigoid). Clin Dermatol.  2012;30(1):34 " ô37.
  • Chan é áLS, Ahmed é áAR, Anhalt é áGJ, et al. The first international consensus on mucous membrane pemphigoid: definition, diagnostic criteria, pathogenic factors, medical treatment, and prognostic indicators. Arch Dermatol.  2002;138(3):370 " ô379.
  • Kourosh é áAS, Yancey é áKB. Pathogenesis of mucous membrane pemphigoid. Dermatol Clin.  2011;29(3):479 " ô484.
  • Schiavo é áAL, Puca é áRV, Ruocco é áV, et al. Adjuvant drugs in autoimmune bullous diseases, efficacy versus safety: facts and controversies. Clin Dermatol.  2010;28(3):337 " ô343.
  • Schmidt é áE, Zillikens é áD. Pemphigoid diseases. Lancet.  2013;381(9863):320 " ô332.

CODES


ICD10


L12.1 Cicatricial pemphigoid é á

ICD9


  • 694.60 Benign mucous membrane pemphigoid without mention of ocular involvement
  • 694.61 Benign mucous membrane pemphigoid with ocular involvement

SNOMED


  • Benign mucous membrane pemphigoid (disorder)
  • Benign mucous membrane pemphigoid with ocular involvement
  • Oral involvement by mucous membrane pemphigoid
  • Oral cicatricial pemphigoid (disorder)

CLINICAL PEARLS


  • Patients diagnosed with CP require thorough mucous membrane and skin examinations.
  • Scarring is the clinical hallmark of disease, although it is not always evident.
  • Treatments are disease-modifying rather than curative.
  • Prognosis depends on site involved; oral and/or skin involvement has a better prognosis and better response to treatment. Ocular, genital, nasopharyngeal, esophageal, and laryngeal mucosal involvement are more likely to scar and can lead to life-threatening emergencies such as blindness and airway obstruction.
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