Fil. 10-review art5/clinical

REVIEW ARTICLE
Walaiorn
Pratchyapruit, M.D.
Patchnee
Tohtubtiang, M.D.
Institute of Dermatology
■The purpose of the authors is to familiarize the logic inflammatory cells namely: eosinophils, polymor- readers with the principles that master the diagnosis phonuclear cells, mast cells, macrophages involve in and management of bullous pemphigoid (BP), its pathophysiologic process of BP (see detail in part I).
variants and pemphigoid gestationis (PG). Our aim This topic will describe only some interesting practical was not to be all-inclusive but illustrative. There are some other points of view on BP that have not been discussed here because of the limited scope of this article. As mentioned earlier in part I, BP the most Most common presentation of BP is generalized common chronic acquired autoimmune bullous dis- bullous form. There are multiple tense blisters on ease, most affects elderly patients. BP autoantibodies, erythematous base or normal skin with a predilection most common IgG, react against hemidesmosomal on the trunk and flexural areas. The lesions usually protein of skin basement membrane zone (BMZ) then heal without scarring or milia formation. This clinical activates complement and inflammatory mediators; finding makes it different from EB or EBA. Some cytokines and proteinase to degrade hemidesmosomal patients initially present with pruritic urticarial, irreg- proteins. NC16a domain is now considered to be the ular bordered plaques. Nearly two-thirds of the pa- most pathogenic site of BP.1 Many types of immuno- tients had prodromal symptoms. These eruptions, par- ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
ticularly as an early symptom, may cause misin- reveals IgG on the blister roof (epidermal side of split terpretation in patients with BP.2 The duration of the prodromal eruptions was up to 6 weeks if papular It is not known when in the course of the disease and/or urticarial and up to 2 years if eczematous, the DIF will be positive. Some patients have IIF- before the blisters appeared. About 10-25% of BP positive 1 and 2 weeks respectively before the blisters patients have mucous membrane involvement. Fifty appeared. The diagnosis of BP can be archieved in percent of oral pemphigoid patients have been re- most patients by the above tests. However, some ported to experience disease progression to involve cases need laborious investigative techniques such as other mucosal tissues, including the eye and larynx.3 immunoblotting and immuno precipitation, which may BP has better prognosis than other blistering dis- eases. Courses of disease are vary. If untreated, the disease can persist for months or years, with periods of spontaneous remission and exacerbation. In most 1. Chronic bullous disease of childhood (CBDC) treated patients, BP remits within 5 years and has long-term remission after that. The present report of mortality rate is about 6-41% most due to side effect of treatment and secondary infection. Disease activity relates to circulating immune complex levels and serum levels of Ab to BP180 NC16a, but not relates BP may present with several distinct clinical The following tests should be performed to 1. Histopathologic analysis from normal-appear- ing perilesional skin shows subepidermal blister with CP as a clinical subset of BP, characterized by chronic inflammation and scarring at the mucous 2. DIF study presents deposits of IgGs (70-90% membrane, especially the oral and ocular mucosae.
of patients) and complement C3 (90-100% of patients) Sometimes, minimal skin involvement is obscured.
However, it differs from BP in some significant ways: 3. IIF study shows the presence of circulating (a) in CP mucosal involvement with clinical scarring IgG in the patientsû serum at BMZ. The SSS substrate is prominent; (b) there is a prominent IgA antibody ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
response alone or in addition to the IgG antibody There is much overlap among the three types response; and (c) there is a heterogeneous antibody of localized cutaneous BP; BPP, OCP, MMP-CP.
response in CP. Esophageal involvement in CP is a They all tend to affect the same age group, in general, rare, but often devastating manifestation. CP has been and may remain regional or be associated with a referred to by a variety of designations based largely generalized eruption consistent with BP. DIF findings on its site of involvement. Occular CP with clinical are identical, as well, with linear IgG and C3 at the disease restricted to ocular mucosa is characterized BMZ. IIF tends to be negative for all three variants, by the absence of circulating Abs and the presence with a tendency to positivity with increased extent of in vivo-bound fibrin deposition at the patientsû and severity of skin involvement. There are diffe- BMZ. Anti-laminin-CP are reported to have IgG Abs rences, though, between them. BPP tends to affect men targeting a lower LL component epiligrin. Brunsting- more than women and lacks mucous membrane Perry pemphigoid (BPP) described in patients with involvement. BPP is unlike benign MMP-CP (BMMP- locally recurrent and scarring subepidermal blistering CP) and localized cutaneous nonscarring BP. Localized cutaneous non-scarring BP usually involves the legs, whereas the other two conditions affect the head and prises a heterogeneous group of disorders characterized neck, with resultant scarring. Histology is similar to by subepidermal separation and the deposition of Igs that seen in BP, but dermal fibrosis and sclerosis result and complement along the BMZ. MMP affects 2-5 in skin affected by BMMP-CP and BPP. Localized cases per 100,000 and more than 85% of patients have cutaneous nonscarring BP is more amenable to topical oral involvement. MMP is now the preferred term steroid therapy, whereas BMMP-CP and BPP are when the condition is primarily mucosal, and BP when more persistent and resistant to systemic immuno- the condition primarily involves the skin. Oral variant suppressive therapy. Clinical, histologic, and immu- or MMP always presents with erosive patches and nologic similarities among the pemphigoid variants desquamative gingivitis.8 Ocular CP, the patients have may reflect common antigenic features. On the other disease that is limited to conjunctival mucous mem- hand, clinical, histologic, and immunologic differences brane. It begins as a non-specific chronic conjunctivitis may imply that there are more than one BP antibody leading progressively to subconjunctival fibrosis with directed at a variety of antigenic structures (as Table symplepharon formation and forniceal shortening, fi- nally resulting in blindness. In contrary to pemphigus vulgaris, two-thirds of the BP cases begin with oral leison-mainly the buccal mucosa and palate, rarely the present with a persistent vesiculobullous eruption ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
similar to dyshidrosiform dermatitis.
A patient gives history of intensive pruritus and excoriated papules resembling subacute prurigo.
It presents as dermatitis herpetiformis-liked Histopathologic study shows signs of chronic derma- lesion, but granular IgA autoantibody at dermal pa- titis, whereas findings by DIF and IIF are compatible pillae should not be found. An unusual generalized with BP. The autoantibodies show the same specificity vesicular eruption in the pediatric warrant this diag- LPP is a very rare clinical variants of BP.
The overlapping clinical features of both LPP may be due to intake of drugs such as cinnarizine, prurigo nodularis and BP lesions are present. It is captopril, ramipril, furosemide and simvastatin.19 One more common in elderly women and is relatively case has skin lesion associating with hepatitis B viral resistant to therapy.16 The blisters arising from nor- infection.20 The patient with LPP has bullae arising mal-appearing or nodular skin but it may or may not on lichen planus papules and on uninvolved skin. The develop in some patients.17 They has fulfilled criteria lesion confines on the face, neck, trunk, elbows, and of BP by histopathologic examination, DIF and IIF feet. Histologic study reveals subepidermal blister.
studies. The nodular plaque skin shows an expression The localization of the immune deposits is consistent of alpha-6 and beta-1 integrin subunits, mediators of with a diagnosis of BP, CP, EBA. A linear deposits matrix-cell signaling and proliferation, at the basal and of IgG,C3 and cytoid bodies along the BMZ on IIF the suprabasal epidermis which is a pattern of hyper- of peribullous skin demonstrates IgG deposited on the proliferative dermatoses.18 The role of anti-BMZ Abs epidermal side of SSS support the diagnosis.21 Sera in the development of the eruption, or the role of the from some patients with LPP bind to C-terminal eruption in the development and persistence of Abs, portions of NC16a. One caseûs serum reacts to BP180 is not clear. In these variants of BP, the presence of Ag and 200 kDa Ag.22 Only a few cases have been Abs may not sufficient for the development of blisters.17 One case has IgA anti-intercellular Abs (intracellular domain of desmoglein 1) in addition to IgG anti-BMZ Abs. Interestingly, sera from both localized BP and pemphigoid nodularis showed Bullae may arise at the site of pre-existing a lower end point of titer of Ab to NC16a do- LP-like or prurigo nodularis-like eruptions, and clini- cally uninvolved skin. DIF finding of linear deposits ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
of IgG and/or C3 at the BMZ in perilesional skin characterized by an erythroderma with or without is found. The disease spectrum of LPP and pem- blister formation.24,25 The patients with erythrodermic phigoid nodularis differs from that of classical BP BP have circulating IgGs bind to the epidermal side phenotype, and their presentations are often indolent.
of SSS in a pattern identical to generalized BP.
LPP may predominantly affect a younger age group Immunoprecipitation study reveals that patients with and is responsive to standard treatments used in erythrodermic BP has circulating IgG which recognizes, acquired ABD, while pemphigoid nodularis is more to varying degrees, the 230 and 180 kDa BPAgs.
common in elderly women and is relatively resistant However, sera from erythrodermic patients without to therapy. LPP lesion may persist for long period blisters fails to recognize any specific polypeptides.24 of time before subsequently developed a nodular eruption with a concurrently detected anti BP180 The elderly patients present with a prodromal generalized pruritus as the dominant or single pre- senting feature. Some patients have rare vesicles at It is defined by the concurrence of BP and presentation. All have excoriations and some cases LP lesions. The patients have a severe lichenoid presents with minimal urticarial or eczematous pa- erythroderma associated with BP lesion involving the pules. Routine skin biopsies are largely nonspecific.
skin and mucosa. Histologic and DIF of skin and All patients have confirmation of the diagnosis by mucosal lesion are consistent with the diagnosis of either IIF or DIF or both. It joins the remarkable BP associated with a lichenoid dermatitis. Immunoblot clinical finding of generalized pruritus with the un- analysis of sera detected anti-BP230 and anti-BP180.
derlying diagnosis of BP. Elderly patients with severe IEM shows IgG deposit localizes in the LL and the or persistent unexplained generalized pruritus should HD. The patients have the common HLA-DR 10 have IF testing to exclude BP as the cause of the haplotype. This a particular type of lichenoid erythro- generalized pruritus. Establishing an early diagnosis dermic BP is probably determined by genetic fac- permits the prompt institution of effective therapy.
tors.23 Interestingly, other autoimmune bullous skin diseases such as paraneoplastic pemphigus or bullous lupus erythematosus may also be associated with It has clinical manifestation similar to pem- phigus vegetans. Most patients present with multiple well-circumscribed, erythematous, erosive, and vegeta- ting plaques at intertriginous region such as axilla, Erythrodermic BP is a very unusual variant, inframammary†and†neck. However,†histopathologic ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
and immunological studies show a typical BP. Immu- LVPC). Clinical†features†and†immunopathological noblot analysis and IIF on SSS are negative.27 data have suggested that LVPC to be a morphological variant of BP. However, vulval pemphigoid can be BP confined to vulva and CP. The age onset of these An autoimmune blistering disorder that may variants ranges between 6 and 13 years. All present very rarely occur in childhood. Only a few cases have with vulva discomfort and erosions with or without been described in infant less than 4 months of age.
oral, perianal and eye involvement.34 Epitope targets There is considerable clinical and histologic overlap of the Abs from these patients have not been defined with other acquired or congenital blistering disorders.
in detail. Circulating IgG Abs directs against BP180, A definite diagnosis of childhood BP requires DIF its 120-kDa soluble ectodomain and against the C- and, in some cases, characterization of the target terminus of BP180. No reactivity is detected towards antigen. Although the cause of childhood BP is the NC16a BP180. Linear IgG and C3 deposits are unknown, drug intake and vaccination; hepatitis B found along the cutaneous BMZ. On SSS, IgG Abs vaccine, tetanus toxoid, antiinfluenza vaccine as well are shown to bind to the epidermis. LVPC is a variant as hepatitis B surface antigen have been incriminated of BP in which DIF combined with IB can deliver in some cases.28-30 Besides, there is evidence that valuable diagnostic information for differential diag- childhood BP associated with chronic renal allograft nosis. However, differentiation between the scarring rejection31 and a solid organ transplantation.32 There and non-scarring course of the disease cannot be made are criteria for diagnosis childhood BP as follows33 with the present diagnostic markers and therefore (1) patients 18 years or younger with the clinical careful follow-up of patients with LVPC is required.35 appearance of tense bullae on erythematous or non- In general, clinical, histological and immunopathological erythematous skin with or without mucous membrane findings in childhood BP appear to be not different involvement, and histopathologic study showing sub- form the adult. Nevertheless, mucosal and palm & epidermal bulla formation with eosinophils. (2) DIF sole lesions seem to occur more frequently in child- showing the linear deposition of IgG and/or C3 at hood BP.36 Childhood BP has to be differential the BMZ and/or positive IIF showing IgG antibodies diagnosed with chronic bullous dermatosis of child- reactive with antigens at the BMZ. Two subtypes hood (CBDC). The differrence of both diseases are of childhood BP have been described. First, infantile BP mostly presents at the first year of life. Blisters usually are on palms and soles. Second, self-limited localized form presents with non-scarring BP-liked on vulva (localized vulval pemphigoid of childhood- terized by the presence of IgG Abs to the dermal side ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
Table 1 Difference of childhood bullous pemphigoid (BP) and Chronic bullous disease of Childhood (CBDC)37,38 Centripedal, perioral, pelvic region spare palms & more peripheral esp. on palms & soles of SSS together with the reactivity of these Abs to serum contains Abs direct against a 105-kDa dermal a novel 200-kDa antigen on IB of a dermal extract.
Ag and BP230 Ag. This unique bullous dermatosis Up to now, there are a few cases of p-200 BP reported.
resembled severe toxic epidermal necrolysis clinically.
Patients present with a bullous eruption on the whole The histologic findings resemble dermatitis herpeti- body, which clinically resembles BP, DH, LAD, or formis. DIF detected linear IgG and C3 deposition at EBA. Some cases have severe mucous membrane the cutaneous BMZ of lesional and perilesional skin.
involvement.39 A number of patients often associates Direct and indirect IEM localized the IgG deposits with psoriasis.40-42 A histopathological examination of to the lowest portion of the LL. The patientûs auto- a lesional skin biopsy specimen shows an area of DEJ antibodies, belonging to the IgG1 subclass, labeled separation and mixed dermal inflammatory infiltrates BMZ of normal intact human skin, oral mucosa, and consisting of lymphocytes, PMNs, and Eo. DIF shows conjunctiva, and localized to the dermal side of SSS a linear deposition of IgG and C3 at the BMZ. The normal adult and neonatal human skin, but failed to antibodies are mainly of the IgG4 subclass.39 On IEM, react with human fetal skin up to 142 gestational days.
these Abs deposit at the LL-LD40,43 interface. The The patientûs Abs fail to react with BP Ags or EBA patient shows good response to the treatment with Ag (type VII collagen) by immunoblotting. Instead, systemic corticosteroids and dapsone.
the patientûs Abs unequivocally labels a 105 protein in cellular extracts and conditioned media of human cultured keratinocytes and dermal fibroblasts. The Several cases have been reported of patients titer of the patientûs antibody against the cutaneous with immune mediated subepidermal blistering dis- BMZ and the intensity of the antibody reactivity orders whose Abs react to antigens present on both against the 105-kD protein paralleled the patientûs the dermal and epidermal side of SSS. The patientûs disease activity. This patientûs disease represents a ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
novel Ag and this patientûs disease represents a deep LL pemphigoid, distinguishable from all other known Nowadays, there are neither estimate optimum treatment nor gold standard treatment of BP. There are two different ideas of treatment. The first, the smallest dose of systemic therapy to control the disease is given. The second, high dose systemic CBDC, dermatitis herpetiformis, BP and IgA BP. IgA therapy is initially introduced and then tapered off BP is distinguished from cases of dermatitis herpeti- once control the disease. The aim of treatment is formis by the clinical features and the site of IgA to suppress the clinical signs and symptoms of BP deposition on IEM. It is distinguished from cases of without over-treating the patient, because BP tends BP with linear IgA by the absence of circulating IgG to spontaneously remit in most patients within ap- anti-BMZ antibody, the therapeutic response to dap- proximately 5 years. Principle of treatment in BP sone and the frequent occurrence of circulating IgA anti-BMZ antibody. The dual antibody response- 1. The most effective drugs or intervention with there are both IgG and IgA autoantibodies to BMZ target antigens found in some cases of childhood 2. Combination therapy offers any advantages blistering. Although the reason why these children have mixed immunologic response is not known. The 3. Both antimicrobials, such as tetracyclines, presence of IgA is associated with a good response minocycline, erythromycin, dapsone, or sulfonamides to treatment with antimicrobials (dapsone, sulphonamide, and its combination such as tetracycline and niacina- erythromycin) and the clinical course is no more protracted than found in children with a single anti- The aims of treatment can be concluded as 1. To suppress the inflammatory process (corti- costeroids-both topical and systemic, systemic antibiotics, Occasionally, BP can present as localized anti-inflammatory drugs). Topical steroid is good for typical BP lesion. A few unusual features of BP have LPP in a child treated.53 An anti-p200 pemphigoid been described i.e. the blister limited to psoriatic shows good response to the treatment with systemic plaque, presented with psoriasis on vitiligo lesion or as an extensive erosive BP, or a combination of BP 2. To suppress pathogenic antibody (high dose and erythema multiforme. The lesion localizes at corticosteroid, azathioprine, MTX, cyclophosphamide, mycophenolate mofetil, combined antiCD-20/antiCD ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
Table 2 Difference between bullous pemphigoid (BP) and pemphigoid gestationis (PG) Pregnancy, hornonal therapy, trophoblastic CA, Associated with HLA B8, DR3, DR4, C4 null alleles 25, leflunomide, mitomycin C for ocular CP). Topical make the disease be tolerable to patients is an aim tacrolimus was tried successfully in a resistant case of treatment. Drugs can be reduced if disease activity is suppressed, although it is not complete suppression.
3. Remove pathogenic antibody and inflamma- It is not necessory to adjust dose if occasional and tory mediators (plasmapheresis and double-filtration 4. Immune-modulating†treatment†(intravenous The similarities and difference of PG and BP have been summarized here. (Table 2.)64-66 The patients are classified mainly on severity into 3 groups. Localized or mild cases can be treated 1. All PG and more than 50% BP sera contain with potent topical corticosteroid e.g. clobetasol pro- IgG autoantibodies that avidly bind complement in pionate or low doses of systemic corticosteroid (20 mg or 0.3 mg/kg/d). Mild to moderate cases can be 2. Both show histopathologically subepidermal treated with higher doses of systemic corticosteroid bullae with eosinophil infiltration.
(40 mg or 0.6 mg/kg/d). Some patients have a good 3. Immunofluorescence (IIF) and immunoelec- response to tetracycline plus nicotinamide. For severe tron microscopy (IEM) reveal C3 and IgG in LL of cases, high doses systemic corticosteroid (50-70 mg or 0.75 mg/kg/d) or immunosuppressive drugs should 4. Both have a common epitope on extracellular be used. To suppress clinical signs sufficiently to ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
rtodime has also reported with contradictory results.67 Treatment is essentially based on cortico- New treatment modalities in PG68-71 such as cyclo- steroid; local for pauci-bullous and/or limited forms sporine, intravenous immunoglobulin and tetracycline, and systemic corticosteroid therapy for the severe doxycycline combined with nicotinamide, pulse-dose forms. So far, systemic corticosteroids have been the intravenous cyclophosphamide, chemical oophorec- main PG therapy and the use of cyclophosphamide, tormy with goserelin in post partum have shown dapsone, pyridoxine, methotrexate, plasmapheresis or promise and warrant further evaluation.
BMZ = basement membrane zone, BP = bullous pemphigoid, BPP = Brunsting-Perry pemphigoid, CBDC = chronic bullous disease of childhood, CP = cicatricial pemphigoid, DEJ = dermoepidermal junciton, DH = dermatitis herpetiformis, DIF = direct immunofluorescence, EBA = epidermolysis bullosa acquisita, Eo = eosinophils, IB = immunoblotting assay, IEM = indirect immunoelectron microscopy, LAD = linear IgA bullous dermatosis, LVPC = localized vulval pemphigoid of childhood, MMP = mucous membrane pemphigoid, PMNs = polymorphonuclear cells, SSS = salt split skin.
Kawahara Y, Matsumura K, Hashimoto T, Nishikawa T. Immunoblot analysis of autoantigens in localized pemphigoid and pemphigoid nodularis. Acta Derm Venereol 1997;77:187-90.
Asbrink E, Hovmark A. Clinical variations in bullous pemphigoid with respect to early symptoms. Acta Derm Venereol Sami N, Bhol KC, Ahmed AR. Treatment of oral pemphigoid with intravenous immunoglobulin as monotherapy: long-term follow-up: influence of treatment on antibody titres to human alpha-6 integrin. Clin Exp Immunol Schmidt E, Sitaru C, Schubert B, Wesselmann U, Kromminga A, Brocker EB. Subacute prurigo variant of bullous pemphigoid: autoantibodies show the same specificity compared with classic bullous pemphigoid. J Am Acad Dermatol Harman KE, Bhogal BS, Eady RA, McGrath JA, Black MM. Defining target antigens in linear IgA disease using skin from subjects with inherited epidermolysis bullosa as a substrate for indirect immunofluorescence microscopy.
Shahab RK, Loo DS. Bullous scabies. J Am Acad Dermatol 2003;49:346-50.
Martalo O, Fraiture AL, Pierard-Franchimont C, Pierard GE. A conjugally exacerbated allergy: procuration dermatosis.
Rev Med Liege 2002;57:320-3. (Article in French) Antonelli JR, Bachiman R, Scherer W. Mucous membrane pemphigoid: a disease of the elderly. Spec Care Dentist Kim YJ, Kim MY, Kim Ho, Park YM. Dyshidrosiform bullous pemphigoid. Acta Derm Venereol 2004;84:253-5.
10. Requena L, Vazquez F, Yus ES. Vesicular pemphigoid. Cutis 1991;47:333-6.
11. Komine M, Nishiro K, Asahina A, Matsuyama T, Furue M, Tsuchida T, et al. Vesicular pemphigoid. Int J Dermatol 12. Geyer AS, Zillikens D, Skrobek C, Cohen B, Anhalt GJ, Nousari HC. Vesicular pemphigoid in a 16-year-old. J ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
13. Stoh S, Seishima M, Izumi T, Ito A, Kamiya H, Kitajima Y. A vesicular variant of bullous pemphigoid with autoantibodies against unidentified 205- and 105-kDa proteins at the basement membrane zone. Br J Dermatol 14. Ohnishi Y, Tajima S, Ishibashi A, Fujawara S. A vesicular bullous pemphigoid with an autoantibody against plectin.
15. Fujisawa H, Ishii Y, Teteishi T, Kawachi Y, Ostuka F, Amagai M. Pemphigoid nodularis with IgA autoantibodies against the intracellular domain of desmoglein 1. Br J Dermatol 2000;142:143-7.
16. Sakuma-Oyama Y, Powell AM, Albert S, Oyama N, Bhogal BS, Black MM. Lichen planus pemphigoides evolving into pemphigoid nodularis. Clin Exp Dermatol 2003;28:613-6.
17. Powell AM, Albert S, Gratian MJ, Bittencourt R, Bhogal BS, Black MM. Pemphigoid nodularis (non-bullous): a clinicopathological study of five cases. Br J Dermatol 2002;147:343-9.
18. Schachter M, Brieva JC, Jones JC, Zillikens D, Skrobek C, Chan LS. Pemphigoid nodularis associated with autoantibodies to the NC16A domain of BP180 and a hyperproliferative integrin profile. J Am Acad Dermatol 19. Stoebner PE, Michot C, Ligeron C, Durand L, Meynadier J, Meunier L. Simvastatin-induced lichen planus pemphi- goides. Ann Dermatol Venereol 2003;130:187-90. (Article in French) 20. Chimanovitch I, Hamm H, Georgi M, Kroiss M, Stolz W, Apitz C, et al. Bullous pemphigoid of childhood: autoantibodies target the same epitopes within the NC16A domain of BP180 as autoantibodies in bullous pemphigoid of adulthood. Arch Dermatol 2000;136:527-32.
21. Bouloc A, Vignon-Pennamen MD, Caux F, Teillac D, Wechsler J, Heller M, et al. Lichen planus pemphigoides is a heterogeneous disease: a report of five cases studied by immunoelectron microscopy. Br J Dermatol 1998;138:972- 22. Yoon KH, Kim SC, Kang DS, Lee IJ. Lichen planus pemphigoides with circulating autoantibodies against 200 and 180 kDa epidermal antigens. Eur J Dermatol 2000;10:212-4.
23. Joly P, Tanasescu S, Wolkenstein P, Bocquet H, Gilbert D, Thomine E, et al. Lichenoid erythrodermic bullous pemphigoid of the African patient. J Am Acad Dermatol 1998;39:691-7.
24. Korman NJ, Woods SG. Erythrodermic bullous pemphigoid is a clinical variant of bullous pemphigoid. Br J Dermatol 25. Scrivener Y, Cribier B, Le Coz C, Boehm N, Jelen G, Heid E, et al. Erythroderma with immunoglobulin deposits along the basal membrane: pemphigoid erythroderma? Ann Dermatol Venereol 1998;125:13-7. (Article in French) 26. Alonso-Llamazares J, Rogers RS, Oursler JR, Calobrisi SD. Bullous pemphigoid presenting as generalized pruritus: observations in six patients. Int J Dermatol 1998;37:508-14.
27. Delpuget-Bertin N, Bernard P, Bedane C, Boulinguez S, Garnier A, Bonnetblanc JM. Pemphigoid vegetans: an immunoelectron microscopic study. Ann Dermatol Venereol 1997;124:467-9. (Article in French) 28. Erbagci Z. Childhood bullous pemphigoid following hepatitis B immunization. J Dermatol 2002;29:781-5.
29. Baykal C, Okan G, Sarica R. Childhood bullous pemphigoid developed after the first vaccination. J Am Acad 30. Amos B, Deng JS, Flynn K, Suarez S. Bullous pemphigoid in infancy: case report and literature review. Pediatr 31. Yamazaki S, Yokozeki H, Katayama I, Komai R, Hashimoto T, Nishioka K. Childhood bullous pemphigoid associated with chronic renal allograft rejection. Br J Dermatol 1998;138:547-8.
32. Morelli JG, Weston WL. Childhood immunobullous disease following a second organ transplant. Pediatr Dermatol 33. Nemeth AJ, Klein AD, Gould EW, Schachmer LA. Childhood bullous pemphigoid: clinical and immunological features, ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
treatment and prognosis. Arch Dermatol 1991;127:378-86.
34. Farrell AM, Kirtschig G, Dalziel KL, Allen J, Dootson G, Edwards S, et al. Childhood vulval pemphigoid: a clinical and immunopathological study of five patients. Br J Dermatol 1999;140:308-12.
35. Rico MJ. Autoimmune blistering diseases in children. Semin Dermatol 1995;14:54-9.
36. Nagano T, Tani M, Adachi A, Takanaga T, Sakanoto S, Kodama S, et al. Childhood bullous pemphigoid: Immunohistochemical, immunoelectron microscopic, and Western blot analysis. J Am Acad Dermatol 1994;30:884- 37. Fisler RE, Saeb M, Liang MG, Howard RM, McKee PH. Childhood bullous pemphigoid: a clinicalpathologic study and review of the literature. Am J Dermatopathol 2003;25:183-9.
38. Marsden RA, McKee PH, Bhogal B. A study of benign chronic dermatosis of childhood and comparison with dermatitis herpetiformis and bullous pemphigoid occurring in childhood. Clin Exp Dermatol 1980;5:159-72.
39. Zillikens D, Kawahara Y, Ishiko A, Shimizu H, Mayer J, Rank CV, et al. A novel subepidermal blistering disease with autoantibodies to a 200-kDa antigen of the basement membrane zone. J Invest Dermatol 1996;106:1333-8.
40. Kawahara Y, Zillikens D, Yancey KB, Marinkovich MP, Nie Z, Hashimoto T, et al. Subepidermal blistering disease with autoantibodies against a novel dermal 200-kDa antigen. J Dermatol Sci 2000;23:93-102.
41. Umemoto N, Demitsu T, Toda S, Noguchi T, Suzuki SI, Kakurai M, et al. A case of anti-p200 pemphigoid clinically mimicking inflammatory epidermolysis bullosa acquisita Br J Dermatol 2003;148:1058-60.
42. Chen KR, Shimizu S, Miyakawa S, Ishiko A, Shimizu H, Hashimoto T. Coexistence of psoriasis and an unusual IgG-mediated subepidermal bullous dermatosis: identification of a novel 200-kDa lower lamina lucida target antigen.
43. Georgi M, Jainta S, Brocker EB, Zillikens D. Autoantigens of subepidermal bullous autoimmune dermatoses. Hautarzt 44. Cotell SL, Lapiere JC, Chen JD, Iwasaki T, Krusinski PA, Chan LS, et al. A novel 105-kDa lamina lucida autoantigen: association with bullous pemphigoid. J Invest Dermatol 1994;103:78-83.
45. Chan LS, Fine JD, Briggaman RA, Woodley DT, Hammerberg C, Drugge RJ, et al. Identification and partial charac- terization of a novel 105-kDalton lower lamina lucida autoantigen associated with a novel immune-mediated subepidermal blistering disease. J Invest Dermatol 1993;101:262-7.
46. Jazia B, Jones RR, Goolamali SK. IgA bullous pemphigoid: a distinct blistering disorder: case report and review of the literature. Br J Dermatol 1980;102:719-25.
47. Domloge-Hultsch N, Utecht L, James W, Yancey KB. Autoantibodies from patients with localized and generalized bullous pemphigoid immunoprecipitate the same 230-kd keratinocyte antigen. Arch Dermatol 1990;126:1337-41.
48. Kobayashi TT, Elston DM, Libow LF, David-Bajar K. A case of bullous pemphigoid limited to psoriatic plaques.
49. Pasic A, Ljubojevic S, Lipozencic J, Marinovic B, Loncaric D. Coexistence of psoriasis vulgaris, bullous pemphigoid and vitiligo: a case report. J Eur Acad Dermatol Venereol 2002;16:426-7.
50. Cordel N, Courville P, Martel P, Musette P, Joly P. Extensive erosive bullous pemphigoid: an atypical and serious clinical variant. Br J Dermatol 2002;146:537-9.
51. Hayakawa K, Shiohara T. Atypical bullous disease showing features of both erythema multiforme and bullous pemphigoid. Acta Derm Venereol 2002;82:196-9.
52. Tomita M, Tanei R, Hamada Y, Fujimura T, Katsuoka K. A case of localized pemphigoid with loss of toenails.
53. Hofmann-Wellenhof R, Salmhofer W, Kerl H. Lichen planus pemphigoides in a 9-year-old child: successful treatment with topical corticosteroids. Pediatr Dermatol 1999;16:70-1.
54. Egan CA, Yee C, Zillikens D, Yancey KB. Anti-p200 pemphigoid: diagnosis and treatment of a case presenting ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548
REVIEW ARTICLE
as an inflammatory subepidermal blistering disease. J Am Acad Dermatol. 2002;46:786-9.
55. Szabolcs P, Reese M, Yancey KB, Hall RP, Kurtzberg J. Combination treatment of bullous pemphigoid with anti- CD20 and anti-CD25 antibodies in a patient with chronic graft-versus-host disease. Bone Marrow Transplant 56. Rivas Jara L, Celis Sanchez J. Mitomycin C treatment for ocular cicatricial pemphigoid. Arch Soc Esp Oftalmol 57. Boedeker CC, Termeer CC, Staats R, Ridder GJ. Cicatricial pemphigoid in the upper aerodigestive tract: diagnosis and management in severe laryngeal stenosis. Ann Otol Rhinol Laryngol 2003;112:271-5.
58. Chuh AAT. The application of topical tacrolimus in vesicular pemphigoid. Br J Dermatol 2004;150:622-3.
59. Ko MJ, Chu CY. Topical tacrolimus therapy for localized bullous pemphigoid. Br J Dermatol 2003;149:1079-81.
60. Hatano Y, Katagiri K, Arakawa S, Umeki T, Takayasu S, Fujiwara S. Successful treatment by double-filtration plasmapheresis of a patient with bullous pemphigoid: effects in vivo on transcripts of several genes for chemokines and cytokines in peripheral blood mononuclear cells. Br J Dermatol 2003;148:573-9.
61. Khumalo NP, Murrell DF, Wojnarowska F, Kirtschig G. A systemic review of treatments for bullous pemphigoid.
62. Fontaine J, Joly P, Roujeau JC. Treatment of bullous pemphigoid. J Dermatol 2003;30:83-9.
63. Wojnarowska F, Kirtschig G, Highet AS, Venning VA, Khumalo HP. Guidelines for the management of bullous pemphigoid. Br J Dermatol 2002;147:214-21.
64. Amato L, Mei S, Gallerani I, Moretti S, Fabbri P. A case of chronic herpes gestationis: persistent disease or conversion to bullous pemphigoid? J Am Acad 2003;49:302-7.
65. Triffet MK, Gibson LE, Leiferman KM. Severe subepidermal blistering disorder with features of bullous pemphigoid and herpes gestationis. J Am Acad Dermatol 1999;40:797-801.
66. Soh H, Hosokawa H, Miyauchi H, Izumi H, Asada Y. The distribution of IgG subclasses autoantibodies in bullous pemphigoid analysed by immunofluorescence and immunoblotting. Arch Dermatol Res 1991;283:400-4.
67. Schmutz JL. Specific dermatoses of pregnancy. Presse Med 2003;32:1813-7. (Article in French) 68. Kroumpouzos G, Cohen LM. Specific dermatoses of pregnancy: an evidence-based systematic review. Am J Obstet 69. Amato L, Coronella G, Berti S, Gallerani I, Moretti S, Fabbri P. Successful treatment with doxycycline and nicotinamide of two cases of persistent pemphigoid gestationis. J Dermatolog Treat 2002;13:143-6.
70. Castle SP, Mather-Mondrey M, Bennion S, David-Bajar K, Huff C. Chronic herpes gestationis and antiphospholipid antibody syndrome successfully treated with cyclophosphamide. J Am Acad Dermatol 1996;34:333-6.
71. Garvey MP, Handfield-Jones SE, Black MM. Pemphigoid gestationis--response to chemical oophorectomy with goserelin. Clin Exp Dermatol 1992;17:443-5.
ªï∑’Ë 10 ∫—∫∑’Ë 1
‡¡…“¬π 2548

Source: http://www.inderm.go.th/alumni/journal_alumni/j_18/fil.%2010-Rev%20art5.pdf