Il pemfigoide bolloso (PB) e una dermatosi bollosa subepidermica, che insorge in eta avanzata ed e caratterizzata da bolle larghe e tese e dal riscontro immunopatologico di depositi di C3 e IgG a livello della membrana basale dell'epidermide. Le mucose sono quasi sempre risparmiate con l'eccezione in alcuni pazienti di bolle o erosioni non cicatrizzanti a livello della mucosa orale (Stanley JR. Bullous pemphigoid. In: Fizpatrick's, Dermatology in General Medicine, Fifth Edition, 1999).
Sono state riportate delle varianti cliniche di pemfigoide bolloso con le stesse caratteristiche istologiche e immunologiche della forma classica. Fra le forme generalizzate di BP, la piu degna di nota e la varieta orticarioide in cui le lesioni sono estese placche eritematose che assomigliano all'orticaria vera e propria, ma durano per piu di 24-48 ore. Talvolta si possono osservare piccole vescicole nel centro o alla periferia della larga placca eritematosa. In alcuni casi le placche hanno un cercine convoluto o margini e bordi circolari. Nel pemfigoide vescicoloso, chiamato anche pemfigoide polimorfo, clinicamente i pazienti sembrano presentare una dermatite erpetiforme con vescicole piccole e pruriginose. In alcuni pazienti tali lesioni evolvono in grandi bolle tese. Nel pemfigoide nodulare si sviluppano dei noduli ipercheratosici, resistenti alla terapia. Questi pazienti sono di solito donne di mezza eta. Tali lesioni persistono per piu di 5 anni, caratterizzate da ricadute e richiedono terapia sistemica con corticosteroidi agenti immunosoppressivi. Il pemfigoide vegetante e stato descritto in pazienti che presentano estese vegetazioni verrucose e purulente che fissurano a livello di inguine e ascelle e lesioni crostose purulente a livello di scalpo, palpebre, volto e zona periombelicale.
La forma localizzata puo essere non cicatrizzante o cicatrizzante. Le lesioni non cicatrizzanti sono spesso presenti a livello delle gambe e sono classificate come pemfigoide pretibiale, ma possono manifestarsi in qualsiasi altra parte del corpo. La forma disidrosica si manifesta con vescicole emorragiche, solitamente limitate alla pianta dei piedi e al palmo delle mani o entrambi. La forma cicatrizzante e chiamata anche pemfigoide di Brunsting Perry in cui le bolle guariscono con cicatrici. Le lesioni sono osservate a livello di capo e collo (Ghohestani RF, Novotney J, Chaudhary M, Agah RS. Bullous pemphigoid: from the bedside to the research laboratory. Clin Dermatol. 2001;19(6):690-6).

La lesione cutanea caratteristica del pemfigoide bolloso e una bolla larga e tesa che insorge su una cute normale o eritematosa. Queste lesioni sono piu comuni a livello dell'addome inferiore, della faccia interna o anteriore della coscia, dell'avambraccio, anche se possono presentarsi ovunque. Le bolle sono solitamente a contenuto limpido, ma puo essere emorragico. La cute erosa in conseguenza alla rottura delle bolle mostra solitamente una facile tendenza alla riepitelizzazione e queste erosioni non tendono ad espandersi. Tuttavia si possono formare nuove piccole vescicole sul margine di vecchie lesioni in via di risoluzione. Le lesioni del pemfigoide solitamente non determinano cicatrici. E' spesso presente prurito, ma non sempre.
Talvolta predomina la componente eritematosa e il paziente puo presentare lesioni orticarioidi, soprattutto nelle prime fasi della malattia. L'eritema puo apparire serpiginoso, con bolle periferiche e puo essere abbastanza esteso.La risoluzione procede solitamente dal centro e puo essere accompagnata da iperpigmentazione.
Lesioni mucose si ritrovano nel 10-35% dei pazienti, solitamente limitate alla mucosa orale, soprattutto quella delle guance. Si osservano bolle intatte o piu spesso erosioni.
Oltre alle caratteristiche cliniche gia descritte, esistono delle manifestazioni non usuali di PB. In tutti questi casi la diagnosi di pemfigoide bolloso e confermata dalla positivita dell'immunofluorescenza. Per esempio talvolta il pemfigoide e caratterizzato da lesioni localizzate, piu spesso agli arti inferiori. In questi pazienti la malattia puo rimanere localizzata per anni o diventare generalizzata. Esiste anche una forma di pemfigoide non bolloso in cui sono presenti solo orticaria e lesioni eczematose in assenza di bolle. Inoltre possono esserci forme nodulari o vegetanti e talvolta il PB puo assomigliare ad una dermatite disidrotica (Stanley JR. Bullous pemphigoid. In: Fizpatrick's, Dermatology in General Medicine, Fifth Edition, 1999).
Nei bambini, soprattutto se piccoli c'e spesso un importante interessamento dei palmi delle mani e delle piante dei piedi. Il coinvolgimento del volto e piu frequente nei bambini rispetto agli adulti e puo essere confuso con impetigine.. L'interessamento delle mucose, soprattutto oculare e orale e piu comune nei bambini rispetto agli adulti.
Il pemfigoide vulvare e una variante morfologica di PB. E caratterizzato da localizzazione vulvare con ricorrenti e spesso emorragiche eruzioni bollose ed erosioni dolorose. Puo presentarsi con prurito e la minzione risulta dolorosa. Le lesioni guariscono senza cicatrizzare e non sono presenti altre localizzazioni (L. Schachner and R. Hansen, Pediatric Dermatology. Third Edition, 2003).

Il pemfigoide bolloso e tipicamente una patologia dell'anziano, e colpisce pazienti per la maggior parte oltre i 60 anni di eta al suo esordio. Anche se puo raramente interessare i bambini, i casi riportati prima del 1970 (quando l'uso dell'immunofluorescenza per la diagnosi e diventato piu diffuso) non erano accurati perche molto spesso consideravano anche i bambini con la malattia bollosa cronica del bambino, che ora viene distinta dal pemfigoide per la presenza di IgA invece che IgG a livello della membrana basale. Non sono note influenze di razza, sesso o etnia nello sviluppo del pemfigoide bolloso (Stanley JR. Bullous pemphigoid. In: Fizpatrick's, Dermatology in General Medicine, Fifth Edition, 1999). L'incidenza del pemfigoide bolloso e stata stimata intorno a 6-10 casi per milione (Yeh SW, Ahmed B, Sami N, Ahmed AR Blistering disorders: diagnosis and treatment Dermatol Clin 2003).
Il pemfigoide bolloso puo rimanere mesi o anni, caratterizzato da riacutizzazioni e remissioni. Sebbene un interessamento esteso possa determinare erosioni molto ampie e compromettere l'integrita della cute, la mortalita e bassa anche in assenza di trattamento. Tuttavia la morte puo incorrere in pazienti anziani e/o debilitati (Harrison's, Principles of Internal Medicine, 15th Edition, 2001).
La prognosi del PB pediatrico e buona e nella maggior parte dei casi riportati ha avuto la durata di un anno o meno, anche se raramente si e protratto oltre (L. Schachner and R. Hansen, Pediatric Dermatology. Third Edition, 2003).
La maggior parte dei casi di BP si presenta sporadicamente in assenza di eventi scatenanti. Tuttavia, ci sono alcune descrizioni di una possibile precipitazione del PB per l'esposizione alla luce UV.
La coesistenza di pemfigoide bolloso e lichen planus, chiamata lichen planus pemfigoide, e ben documentata. Questi casi mostrano aspetti clinici, istologici e immunopatologici di entrambe le patologie (Stanley JR. Bullous pemphigoid. In: Fizpatrick's, Dermatology in General Medicine, Fifth Edition, 1999).
Il PB puo essere associato ad altre malattie autoimmuni come il diabete mellito, l'anemia perniciosa, le malattie infiammatorie croniche della cute, come lichen planus e psoriasi, e a neoplasie maligne (Yeh SW, Ahmed B, Sami N, Razzaque Ahmed A. Blistering disorders: diagnosis and treatment. Dermatol Ther. 2003;16(3):214-23).

L'iniziale formazione della bolla nel PB avviene a livello della lamina lucida, tra le cellule della membrana basale e la lamina densa. Con la formazione della bolla si osserva la perdita dei filamenti di ancoraggio e degli emidesmosomi. Con la degranulazione dei linfociti infiltrati, c'e prima la frammentazione e poi la perdita della lamina densa. Inoltre e stata osservata la degranulazione della mastcellule vicino alla membrana basale.
L'immunofluorescenza diretta della cute perilesionale dei pazienti affetti da pemfigoide ha mostrato depositi lineari di immunoreagenti a livello della membrana basale; nella maggior parte dei pazienti sono state riscontrate IgG, raramente associate con IgD, IgE, IgA. L'immunofluorescenza indiretta ha evidenziato che circa il 70-80% dei pazienti con pemfigoide ha IgG circolanti che si legano alla membrana basale dell'epitelio squamoso stratificato normale. La maggior parte di tali pazienti presentano anche IgE circolanti anti-membrana basale.
A livello della membrana basale sono presenti depositi di C3 e altri componenti sia della via classica che della via alternativa di attivazione del complemento e la proteina regolatrice ?1H. Inoltre componenti attivate del complemento si trovano nel liquido delle bolle e studi in vitro di immunofissazione del complemento dimostrano la capacita del siero dei pazienti con PB di fissare le frazioni del complemento sia della via classica che dell'alternativa a livello della membrana basale. Questi studi suggeriscono che le IgG del pemfigoide attivano il complemento attraverso la via classica con l'attivazione della via alternativa attraverso il meccanismo di amplificazione del C3.
Studi di immunoelettromicroscopia hanno localizzato l'antigene del pemfigoide bolloso nell'emidesmosoma, un organulo ritenuto importante nell'ancorare le cellule basali alla membrana basale. Autoanticorpi si legano sia dentro la cellula alla placca dell'emidesmosoma sia fuori dalla cellula alla faccia extracellulare dell'emidesmosoma.
Gli autoanticorpi di questi pazienti legano due distinte molecole. Tutti i pazienti affetti da PB hanno anticorpi contro una molecola di 230-kDa (adesso chiamata BPAG1). Inoltre nella maggior parte dei pazienti sono presenti autoanticorpi contro una molecola di 180kDa, ora chiamata BPAG2 o collagene di tipo XVII, una molecola transmembrana con un dominio collagenasico extracellulare.
Si pensa che il primo passo nella formazione della bolla sia il legame dell'anticorpo all'antigene del pemfigoide bolloso. Infatti le lesioni del PB si osservano nelle lesioni dove e presente un eccesso di antigene. Il legame delle IgG alla membrana basale attiva la cascata del complemento per la via classica e probabilmente anche l'amplificazione del C3. Le frazioni attivate del complemento causano la chemotassi dei leucociti e la degranulazione delle mastcellule. Alla degranulazione delle mastcellule consegue la chemotassi degli eosinofili dovuta a mediatori come il mediatore chemotattico eosinofilo dell'anafilassi.. Tali mediatori sono presenti nel liquido delle bolle. Infine le proteasi di leucociti e mastcellule determinano la separazione dell'epidermide dal derma.
Come in molte patologie autoimmuni rimane oscura la causa scatenante dalla reazione autoimmune (Stanley JR. Bullous pemphigoid. In: Fizpatrick's, Dermatology in General Medicine, Fifth Edition, 1999).

Oltre agli aspetti immunopatologici, quasi la meta dei pazienti ha elevati livelli di IgE seriche, correlati al titolo di IgG legate alla membrana basale osservato all'immunofluorescenza. Inoltre elevati livelli di IgE sono legati alla presenza di prurito. Infine in circa la meta dei pazienti e presente eosinofilia periferica, talvolta importante ma non correlata ai livelli di IgE.
E fondamentale per la diagnosi la biopsia di una lesione bollosa precoce la cui istologia mostrera che si tratta di una bolla subepidermica, senza necrosi epidermica, con un infiltrato di linfociti, istiociti ed eosinofili a livello del derma superficiale.
Il PB puo essere facilmente distinto dalle altre malattie bollose grazie all'istologia e all'immunofluorescenza (Stanley JR. Bullous pemphigoid. In: Fizpatrick's, Dermatology in General Medicine, Fifth Edition, 1999).

Il trattamento del pemfigoide bolloso e deciso in base all'estensione delle lesioni e al grado di progressione della malattia. Lesioni localizzate possono essere controllate con corticosteroidi topici e intralesionali. Nei pazienti con andamento progressivo della malattia con interessamento di siti multipli e spesso necessario l'uso di corticosteroidi sistemici. Il prednisone determina un buon controllo della malattia e allevia i sintomi, incluso il prurito. In alcuni pazienti si possono usare gli antiistaminici per controllare il prurito. La dose iniziale del prednisone e determinata dalla gravita della malattia e va dai 20 agli 80 mg al giorno. In un sottogruppo di pazienti puo rendersi necessaria una dose '100 mg per ottenere un controllo nella fase acuta della malattia. I pazienti anziani che fanno uso per lungo tempo di alte dosi di corticosteroidi possono presentare effetti collaterali multipli che talvolta richiedono l'ospedalizzazione. E stato osservato che il numero di effetti collaterali e di ospedalizzazioni e direttamente correlato alla quantita totale di prednisone ricevuto.. Per tale motivo il prednisone va progressivamente ridotto. Se durante tale riduzione di dose compaiono nuove lesioni, e necessario passare ad altro trattamento per permettere la continuazione della riduzione della dose di corticosteroidi. Tali farmaci sono gli antiinfiammatori e gli agenti immunosoppressivi. Gli agenti antiinfiammatori utilizzati sono dapsone e antibiotici sistemici in combinazione con nicotinammide. Le dosi di dapsone variano da 100 a 200 mg al giorno. Gli antibiotici che hanno rilevanza clinica sono tetraciclina (2g/die) e eritromicina.
Gli agenti immunosoppressivi utilizzati sono azatioprina (1-2 mg/kg/die), metotrexate (10-20 mg alla settimana), ciclosporina, ciclofosfamide, clorambucile e piu recentemente micofenolato mofetile (2g/die). L'utilizzo di tali farmaci puo determinare effetti collaterali multipli come soppressione midollare, tossicita a livello renale ed epatico,infezioni sistemiche. Per tale motivo e necessario un controllo ematologico periodico per monitorare gli eventuali effetti collaterali. In alcuni pazienti questi trattamenti possono risultare non efficaci alle dosi terapeutiche. Sono stati sperimentati altri trattamenti come la plasmaferesi, la fotochemioterapia extracorporea, e la terapia parenterale con immunoglobuline (IVIG). Recentemente e stato riportato che l'utilizzo a lungo termine delle IVIG ha determinato una sostanziale remissione clinica in pazienti non responsivi alla terapia immunosoppressiva.
Anche l'utilizzo di trattamenti locali e molto importante. Tale terapia consiste nell'applicazione di preparati topici di glucocorticoidi 2-3 volte al giorno. Un altro aspetto della terapia e la prevenzione delle infezioni: il contenuto liquido delle bolle e un buon terreno di coltura per molti patogeni e l'infezione rallenta la guarigione delle lesioni. Per tale motivo e molto importante l'igiene e bagni con permanganato di potassio o di acetato basico di alluminio giornalmente. Lesioni dolorose potrebbero indicare un'infezione locale. In tale caso e necessario eseguire un tampone delle lesioni ed esami colturali multipli in modo da poter effettuare una terapia antibiotica mirata per facilitare la guarigione delle lesioni (Yeh SW, Ahmed B, Sami N, Razzaque Ahmed A. Blistering disorders: diagnosis and treatment. Dermatol Ther. 2003;16(3):214-23).

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