1192 Correspondence
jet injection stem from the lack of standardization of the type of jet injector and the parameters used among various studies. The amount of pain can be reduced with the use of appropriate parameters. Pain severity correlates with the jet’s depth of penetration.7 We have observed that low driving pressure, low volume per spurt, smaller nozzle diameter and a longer distance (2–3 mm) between the tip of the nozzle and skin surface allow more superficial penetration of the jet into the skin.7 A low-pressure jet injector provides rapid, adequate and painless anaesthesia for a variety of dermatological procedures. The lack of needle use and the rapidity of the procedure reduce apprehension in the needle-phobic patient.8 For needle-phobic patients, the direct injection of BTX-A into the palms with the needle-free injector is also a justifiable option despite a 5–10% waste of BTX-A occurring through splash and splatter. Traditional jet injectors, such as Dermojetâ, have fixed driving pressures due to their spring-loaded mechanism. They are high-pressure devices with driving pressure varying between 1400 and 2000 psi. These devices do not work universally on different areas of the body and some manufacturers even warn against their use on the hands and fingers. Driving pressures used in our practice do not usually exceed 140 psi, which is at least 10 times lower than the driving pressure used in traditional jet injectors. Complications with higher-pressure traditional injectors include pain8 and considerable harm to vital nerves and vessels.9 The disadvantages of jet injection with the lowest possible pressure (140 psi) capable of inducing a subepidermal weal are minimal. The risk of infection is low with disposable anticontaminant devices and spacers combined with the use of advanced sterilization techniques.10 Soaking the hands in lukewarm water for 5–10 min helps induce a subepidermal weal with lower pressures. The driving pressure should be increased only when the weal fails to appear. At that time, it can be increased by increments of 10 psi until the anaesthetic weal becomes visible or a tiny blood spot appears into which BTX-A can be injected in a painless manner. The versatility of the pressure settings is because the new jet injectors are powered by carbon dioxide, which allows delivery of the injectate at the desired depth. Using a sterile jet injector on each patient avoids transmission of infection between patients. Because needle phobia is prevalent and has remained a therapeutic challenge, the importance of embracing needle-free injection systems in dermatology cannot be overemphasized. 1
McGill University, 845 Sherbrooke St W, Montreal, QC H3A 0G4, Canada 2 Division of Dermatology, Department of Medicine, St-Luc Hospital, Montreal University Hospital Center, 264, Boul. Rene-Levesque East, Montreal, QC, H2X 1P1, Canada Correspondence: Antranik Benohanian. E-mail: [email protected]
L. PATAKFALVI1 A. BENOHANIAN2
British Journal of Dermatology (2014) 170, pp1187–1207
References 1 Benohanian A. Needle-free anesthesia: a promising technique for the treatment of palmoplantar hyperhidrosis with botulinum toxin A. Therapy 2006; 3:591–6. 2 Hayton M, Stanley J, Lowe N. A review of peripheral nerve blockade as local anaesthesia in the treatment of palmar hyperhidrosis. Br J Dermatol 2003; 149:447–51. 3 Solomon P. Modified Bier block anesthetic technique is safe for office use for botulinum a toxin treatment of palmar and plantar hyperhidrosis. Dermatol Online J 2007; 13:6. 4 Saijo M, Ito E, Ichinohe T, Kaneko Y. Lack of pain reduction by a vibrating local anesthetic attachment: a pilot study. Anesth Prog 2005; 52:62–4. 5 Kontochristopoulos G, Gregoriou S, Zakopoulou N, Rigopoulos D. Letter: cryoanalgesia with dichlorotetrafluoroethane spray versus ice packs in patients treated with botulinum toxin-A for palmar hyperhidrosis: self-controlled study. Dermatol Surg 2006; 32:873–4. 6 Nantel-Battista M, Richer V, Marcil I, Benohanian A. Treatment of nail psoriasis with intralesional triamcinolone acetonide using a needlefree jet injector: a prospective trial. J Cutan Med Surg 2014; 18:38–42. 7 Mitragotri S. Current status and future prospects of needle-free liquid jet injectors. Nat Rev Drug Discov 2006; 5:543–8. 8 Benohanian A. Needle-free anaesthesia prior to botulinum toxin type A injection treatment of palmar and plantar hyperhidrosis. Br J Dermatol 2007; 156:593–6. 9 Naumann M, Bergmann I, Hofmann U et al. Botulinum toxin for focal hyperhidrosis: technical considerations and improvements in application. Br J Dermatol 1998; 139:1123. 10 Lamontagne L, Brassard D. Control of risk transmission of hepatitis virus in a murine model using the Med-Jetâ (MIT, Inc.) Injector. Research report of the Viro-Immunology Laboratory Animal Diseases Department of Biological Sciences, University of Quebec at Montreal, Canada, April 2002.
Supporting Information Additional Supporting Information may be found in the online version of this article at the publisher’s website: Video S1. Needle-free anaesthesia for the treatment of palmar hyperhidrosis. Intradermal anaesthetic weals with 2% lidocaine are induced with the Jetâ injector. Each anaesthetic weal is then painlessly injected with 2–3 units of onabotulinumtoxinA. Funding sources: None. Conflicts of interest: None declared.
A case of concurrent pemphigoid vegetans and pemphigus vegetans resolving without oral corticosteroid DOI: 10.1111/bjd.12802 DEAR EDITOR, Pemphigoid vegetans and pemphigus vegetans are variants of bullous pemphigoid and pemphigus vulgaris, respec-
© 2013 British Association of Dermatologists
Correspondence 1193
(a)
(c)
Fig 1. (a) Vegetating nodules in both inguinal areas at first presentation. (b) Lesions had completely resolved 4 months later. (c,d) A biopsy specimen revealed marked acanthosis and intraepidermal abscesses. (e) Subepidermal cleft (arrows). (f) Intraepidermal blisters with acantholytic cells (arrows). (g) Direct immunofluorescence(IF) showing IgG deposits at the basement membrane zone (arrows) but not at the keratinocyte cell surfaces. (h) Indirect IF of 1 mol L 1 NaCl-split skin demonstrating circulating IgG antibodies reacting with epidermal side of the split.
(f)
tively, and both typically show elevated skin lesions on the intertriginous areas.1–6 We report a patient with inguinal nodular lesions, diagnosed as concurrent pemphigoid vegetans and pemphigus vegetans. The skin lesions resolved completely with only topical corticosteroid and ketoconazole. An 85-year-old Japanese male presented with itchy nodular lesions on the inguinal areas, which had gradually enlarged over 5 months. Antifungal ointments had been prescribed by a local dermatologist because fungal components were identified microscopically. Physical examination revealed lobulated nodules on both inguinal areas (Fig. 1a). The lesions in the right inguinal region were 43 9 24 mm in size and 14 mm high, while those in the left inguinal region were 35 9 77 mm in size and 20 mm high. Erosions and crusts on the surface of the nodules, as well as peripheral erythematous macules, were noted. No vesicles or pustules were observed around the nodular lesions. No mucous membrane lesions were observed. All laboratory data were within normal limits, except for slightly reduced haemoglobin (125 gdL 1; normal 136–173). Tumour stage of extramammary Paget disease was suspected and skin biopsy was taken from the nodular lesion. Histo© 2013 British Association of Dermatologists
(b)
(d)
(e)
(g)
(h)
pathology revealed remarkable acanthosis with intraepidermal abscesses of neutrophils and eosinophils and marked oedema in the upper dermis (Fig. 1c,d). In some areas, there were minimal but apparent subepidermal clefts (Fig. 1e) and intraepidermal acantholytic blisters (Fig. 1f). Infiltration of eosinophils and lymphocytes were also seen in the dermis. Direct immunofluorescence (IF) revealed deposits of IgG and C3, but not IgA or IgM, at the epidermal basement membrane zone (BMZ), but not at keratinocyte cell surfaces (Fig. 1g). Indirect IF demonstrated that IgG antibodies in the patient’s serum reacted with the BMZ in both normal human skin and monkey oesophagus, and bound to the epidermal side of 1 mol L 1 NaCl-split human skin (Fig. 1h). However, no IgG reactivity with cell surfaces was found in any substrates. No positive staining was seen for IgA antibodies. Enzyme-linked immunosorbent assays (ELISAs) (MBL, Nagoya, Japan) for IgG antibodies gave positive results for BP230 (index 38, normal < 9) and desmoglein (Dsg) 1 (index 47, normal < 14), while no antibodies to either BP180 or Dsg3 were detected. To verify these results, the same serum was also investigated by indirect IF using biochips, the Dermatology British Journal of Dermatology (2014) 170, pp1187–1207
1194 Correspondence
Mosaic No. 7 (EUROIMMUN AG, Luebeck, Germany). This study showed that the IgG antibodies in the patient’s serum reacted with both Dsg1 (9100) and Dsg3 (910), and showed positive cell surface staining on primate oesophagus. In contrast, this study showed negative results for both BP230 and BP180. This is well explained by the fact that the ELISAs used a longer recombinant protein of BP230 than the biochips did. Novel ELISAs using eukaryotic recombinant human desmocollins 1–3 gave negative results for both IgG and IgA antibodies (data not shown). There were no positive reactions for either IgG or IgA antibodies in immunoblot analyses of various preparations, including normal human epidermal and dermal extracts, recombinant proteins of BP180 NC16a and C-terminal domains, and purified human laminin-332. The diagnosis of concurrent pemphigoid vegetans and pemphigus vegetans was made, based on the histopathological findings and reactivity with BP230, Dsg1 and Dsg3. The patient was treated effectively with topical corticosteroid and ketoconazole, and the lesions resolved completely in approximately 4 months (Fig. 1b). ELISA values for BP 230 and Dsg1 decreased to normal ranges. To our knowledge, this is the first case of concurrent pemphigoid vegetans and pemphigus vegetans. We found nine cases of pemphigoid vegetans in the literature,1–4 and target antigens were reported in only two cases. One patient reacted with BP230 and the 160 kDa, 130 kDa and 95 kDa proteins;3 while the other patient reacted with BP230 and BP180.4 In our case, only BP230 was detected as BMZ autoantigens. Although BP230 is not considered as a primary pathogenic autoantigen, it may play a role in local inflammatory response.7 It is also reported that anti-BP230 autoreactivity is associated to localized bullous pemphigoid, rather than the generalized type.8 These results suggest that anti-BP230 autoantibodies might be relevant to the pathogenesis in our patient. The target antigen in pemphigus vegetans is mainly Dsg3. However, anti-Dsg1 antibodies, in addition to anti-Dsg3 antibodies, were occasionally detected.5,9,10Anti-Dsg1 antibodies in our patient might have induced acantholytic change although low titres of anti-Dsg3 antibodies were also detected in one test. Dual IgG reactivity with BP230 and Dsg1, as well as weak reactivity with Dsg3, might contribute to the localized extensively vegetating skin lesions in our case. However, the large nodular lesions were self-limited. A case of pemphigus vegetans localized to the scalp was successfully treated with topical steroid exclusively.6 Although no periodic acid-Schiff-positive spores were found in the skin biopsy, a local dermatologist had prescribed antifungal ointment in addition to topical steroid. Thus, it may be plausible that fungal infection triggered the inflammation on the intertriginous regions in our patient.
examining our patient’s serum with the Dermatology Mosaic No. 7 containing primate oesophagus, human salt-split-skin, recombinant BP180-NC16A-4X, recombinant BP230gC, recombinant desmoglein (Dsg) 1 and recombinant Dsg3. 1
Department of Dermatology, Faculty of Medicine, Oita University, Hasama, Yufu 879-5593, Japan 2 Department of Dermatology, Kurume University School of Medicine, Kurume University Institute of Cutaneous Cell Biology, 67 Asahimachi, Kurume, Fukuoka 830-0011, Japan Correspondence: Sakuhei Fujiwara. E-mail: [email protected]
Y. HATANO1 K. ISHIKAWA1 H. KOGA2 N. ISHII2 T. HASHIMOTO2 N. TAKEO1 H. SHIMADA1 T. SAKAI1 O. OKAMOTO1 S. FUJIWARA1
References 1 Winkelmann RK, Su WP. Pemphigoid vegetans. Arch Dermatol 1979; 115:446–8. 2 Kim J, Chavel S, Girardi M, McNiff JM. Pemphigoid vegetans: a case report and review of the literature. J CutanPathol 2008; 35:1144–7. 3 Chan LS, Dorman MA, Agha A et al. Pemphigoid vegetans represents a bullous pemphigoid variant Patient’s IgG autoantibodies identify the major bullous pemphigoid antigen. J Am Acad Dermatol 1993; 28:331–5. 4 Suda-Takayanagi T, Hara H, Ohyama B et al. A case of pemphigoid vegetans with autoantibodies against both BP180 and BP230 antigens. J Am Acad Dermatol 2011; 64:206–8. 5 Cozzani E, Christana K, Mastrogiacomo A et al. Pemphigus vegetans Neumann type with anti-desmoglein and anti-periplakin autoantibodies. Eur J Dermatol 2007; 17:530–3. 6 Zaraa I, Sellami A, Bouguerra C et al. Pemphigus vegetans: a clinical, histological, immunopathological and prognostic study. J EurAcad Dermatol Venereol 2011; 25:1160–7. 7 Guo L, Degenstein L, Dowling J et al. Gene targeting of BPAG1: abnormalities in mechanical strength and cell migration in stratified epithelia and neurologic degeneration. Cell 1995; 81: 233–43. 8 Thoma-Uszynski S, Uter W, Schwietzke S et al. BP230- and BP180-specific auto-antibodies in bullous pemphigoid. J Invest Dermatol 2004; 122:1413–22. 9 Hashimoto K, Hashimoto T, Higashiyama M et al. Detection of anti-desmocollins I and II autoantibodies in two cases of Hallopeau type pemphigus vegetans by immunoblot analysis. J DermatolSci 1994; 7:100–6. 10 Powell AM, Albert S, Oyama N et al. Paraneoplastic pemphigus secondary to fludarabine evolving into unusual oral pemphigus vegetans. J Eur Acad Dermatol Venereol 2004; 18:360–4. Funding sources: No external funding. Conflicts of interest: None declared.
Acknowledgments We gratefully appreciate Drs Christian Probst and Lars Komorowski, EUROIMMUN AG, Luebeck, Germany, for kindly British Journal of Dermatology (2014) 170, pp1187–1207
© 2013 British Association of Dermatologists
jet injection stem from the lack of standardization of the type of jet injector and the parameters used among various studies. The amount of pain can be reduced with the use of appropriate parameters. Pain severity correlates with the jet’s depth of penetration.7 We have observed that low driving pressure, low volume per spurt, smaller nozzle diameter and a longer distance (2–3 mm) between the tip of the nozzle and skin surface allow more superficial penetration of the jet into the skin.7 A low-pressure jet injector provides rapid, adequate and painless anaesthesia for a variety of dermatological procedures. The lack of needle use and the rapidity of the procedure reduce apprehension in the needle-phobic patient.8 For needle-phobic patients, the direct injection of BTX-A into the palms with the needle-free injector is also a justifiable option despite a 5–10% waste of BTX-A occurring through splash and splatter. Traditional jet injectors, such as Dermojetâ, have fixed driving pressures due to their spring-loaded mechanism. They are high-pressure devices with driving pressure varying between 1400 and 2000 psi. These devices do not work universally on different areas of the body and some manufacturers even warn against their use on the hands and fingers. Driving pressures used in our practice do not usually exceed 140 psi, which is at least 10 times lower than the driving pressure used in traditional jet injectors. Complications with higher-pressure traditional injectors include pain8 and considerable harm to vital nerves and vessels.9 The disadvantages of jet injection with the lowest possible pressure (140 psi) capable of inducing a subepidermal weal are minimal. The risk of infection is low with disposable anticontaminant devices and spacers combined with the use of advanced sterilization techniques.10 Soaking the hands in lukewarm water for 5–10 min helps induce a subepidermal weal with lower pressures. The driving pressure should be increased only when the weal fails to appear. At that time, it can be increased by increments of 10 psi until the anaesthetic weal becomes visible or a tiny blood spot appears into which BTX-A can be injected in a painless manner. The versatility of the pressure settings is because the new jet injectors are powered by carbon dioxide, which allows delivery of the injectate at the desired depth. Using a sterile jet injector on each patient avoids transmission of infection between patients. Because needle phobia is prevalent and has remained a therapeutic challenge, the importance of embracing needle-free injection systems in dermatology cannot be overemphasized. 1
McGill University, 845 Sherbrooke St W, Montreal, QC H3A 0G4, Canada 2 Division of Dermatology, Department of Medicine, St-Luc Hospital, Montreal University Hospital Center, 264, Boul. Rene-Levesque East, Montreal, QC, H2X 1P1, Canada Correspondence: Antranik Benohanian. E-mail: [email protected]
L. PATAKFALVI1 A. BENOHANIAN2
British Journal of Dermatology (2014) 170, pp1187–1207
References 1 Benohanian A. Needle-free anesthesia: a promising technique for the treatment of palmoplantar hyperhidrosis with botulinum toxin A. Therapy 2006; 3:591–6. 2 Hayton M, Stanley J, Lowe N. A review of peripheral nerve blockade as local anaesthesia in the treatment of palmar hyperhidrosis. Br J Dermatol 2003; 149:447–51. 3 Solomon P. Modified Bier block anesthetic technique is safe for office use for botulinum a toxin treatment of palmar and plantar hyperhidrosis. Dermatol Online J 2007; 13:6. 4 Saijo M, Ito E, Ichinohe T, Kaneko Y. Lack of pain reduction by a vibrating local anesthetic attachment: a pilot study. Anesth Prog 2005; 52:62–4. 5 Kontochristopoulos G, Gregoriou S, Zakopoulou N, Rigopoulos D. Letter: cryoanalgesia with dichlorotetrafluoroethane spray versus ice packs in patients treated with botulinum toxin-A for palmar hyperhidrosis: self-controlled study. Dermatol Surg 2006; 32:873–4. 6 Nantel-Battista M, Richer V, Marcil I, Benohanian A. Treatment of nail psoriasis with intralesional triamcinolone acetonide using a needlefree jet injector: a prospective trial. J Cutan Med Surg 2014; 18:38–42. 7 Mitragotri S. Current status and future prospects of needle-free liquid jet injectors. Nat Rev Drug Discov 2006; 5:543–8. 8 Benohanian A. Needle-free anaesthesia prior to botulinum toxin type A injection treatment of palmar and plantar hyperhidrosis. Br J Dermatol 2007; 156:593–6. 9 Naumann M, Bergmann I, Hofmann U et al. Botulinum toxin for focal hyperhidrosis: technical considerations and improvements in application. Br J Dermatol 1998; 139:1123. 10 Lamontagne L, Brassard D. Control of risk transmission of hepatitis virus in a murine model using the Med-Jetâ (MIT, Inc.) Injector. Research report of the Viro-Immunology Laboratory Animal Diseases Department of Biological Sciences, University of Quebec at Montreal, Canada, April 2002.
Supporting Information Additional Supporting Information may be found in the online version of this article at the publisher’s website: Video S1. Needle-free anaesthesia for the treatment of palmar hyperhidrosis. Intradermal anaesthetic weals with 2% lidocaine are induced with the Jetâ injector. Each anaesthetic weal is then painlessly injected with 2–3 units of onabotulinumtoxinA. Funding sources: None. Conflicts of interest: None declared.
A case of concurrent pemphigoid vegetans and pemphigus vegetans resolving without oral corticosteroid DOI: 10.1111/bjd.12802 DEAR EDITOR, Pemphigoid vegetans and pemphigus vegetans are variants of bullous pemphigoid and pemphigus vulgaris, respec-
© 2013 British Association of Dermatologists
Correspondence 1193
(a)
(c)
Fig 1. (a) Vegetating nodules in both inguinal areas at first presentation. (b) Lesions had completely resolved 4 months later. (c,d) A biopsy specimen revealed marked acanthosis and intraepidermal abscesses. (e) Subepidermal cleft (arrows). (f) Intraepidermal blisters with acantholytic cells (arrows). (g) Direct immunofluorescence(IF) showing IgG deposits at the basement membrane zone (arrows) but not at the keratinocyte cell surfaces. (h) Indirect IF of 1 mol L 1 NaCl-split skin demonstrating circulating IgG antibodies reacting with epidermal side of the split.
(f)
tively, and both typically show elevated skin lesions on the intertriginous areas.1–6 We report a patient with inguinal nodular lesions, diagnosed as concurrent pemphigoid vegetans and pemphigus vegetans. The skin lesions resolved completely with only topical corticosteroid and ketoconazole. An 85-year-old Japanese male presented with itchy nodular lesions on the inguinal areas, which had gradually enlarged over 5 months. Antifungal ointments had been prescribed by a local dermatologist because fungal components were identified microscopically. Physical examination revealed lobulated nodules on both inguinal areas (Fig. 1a). The lesions in the right inguinal region were 43 9 24 mm in size and 14 mm high, while those in the left inguinal region were 35 9 77 mm in size and 20 mm high. Erosions and crusts on the surface of the nodules, as well as peripheral erythematous macules, were noted. No vesicles or pustules were observed around the nodular lesions. No mucous membrane lesions were observed. All laboratory data were within normal limits, except for slightly reduced haemoglobin (125 gdL 1; normal 136–173). Tumour stage of extramammary Paget disease was suspected and skin biopsy was taken from the nodular lesion. Histo© 2013 British Association of Dermatologists
(b)
(d)
(e)
(g)
(h)
pathology revealed remarkable acanthosis with intraepidermal abscesses of neutrophils and eosinophils and marked oedema in the upper dermis (Fig. 1c,d). In some areas, there were minimal but apparent subepidermal clefts (Fig. 1e) and intraepidermal acantholytic blisters (Fig. 1f). Infiltration of eosinophils and lymphocytes were also seen in the dermis. Direct immunofluorescence (IF) revealed deposits of IgG and C3, but not IgA or IgM, at the epidermal basement membrane zone (BMZ), but not at keratinocyte cell surfaces (Fig. 1g). Indirect IF demonstrated that IgG antibodies in the patient’s serum reacted with the BMZ in both normal human skin and monkey oesophagus, and bound to the epidermal side of 1 mol L 1 NaCl-split human skin (Fig. 1h). However, no IgG reactivity with cell surfaces was found in any substrates. No positive staining was seen for IgA antibodies. Enzyme-linked immunosorbent assays (ELISAs) (MBL, Nagoya, Japan) for IgG antibodies gave positive results for BP230 (index 38, normal < 9) and desmoglein (Dsg) 1 (index 47, normal < 14), while no antibodies to either BP180 or Dsg3 were detected. To verify these results, the same serum was also investigated by indirect IF using biochips, the Dermatology British Journal of Dermatology (2014) 170, pp1187–1207
1194 Correspondence
Mosaic No. 7 (EUROIMMUN AG, Luebeck, Germany). This study showed that the IgG antibodies in the patient’s serum reacted with both Dsg1 (9100) and Dsg3 (910), and showed positive cell surface staining on primate oesophagus. In contrast, this study showed negative results for both BP230 and BP180. This is well explained by the fact that the ELISAs used a longer recombinant protein of BP230 than the biochips did. Novel ELISAs using eukaryotic recombinant human desmocollins 1–3 gave negative results for both IgG and IgA antibodies (data not shown). There were no positive reactions for either IgG or IgA antibodies in immunoblot analyses of various preparations, including normal human epidermal and dermal extracts, recombinant proteins of BP180 NC16a and C-terminal domains, and purified human laminin-332. The diagnosis of concurrent pemphigoid vegetans and pemphigus vegetans was made, based on the histopathological findings and reactivity with BP230, Dsg1 and Dsg3. The patient was treated effectively with topical corticosteroid and ketoconazole, and the lesions resolved completely in approximately 4 months (Fig. 1b). ELISA values for BP 230 and Dsg1 decreased to normal ranges. To our knowledge, this is the first case of concurrent pemphigoid vegetans and pemphigus vegetans. We found nine cases of pemphigoid vegetans in the literature,1–4 and target antigens were reported in only two cases. One patient reacted with BP230 and the 160 kDa, 130 kDa and 95 kDa proteins;3 while the other patient reacted with BP230 and BP180.4 In our case, only BP230 was detected as BMZ autoantigens. Although BP230 is not considered as a primary pathogenic autoantigen, it may play a role in local inflammatory response.7 It is also reported that anti-BP230 autoreactivity is associated to localized bullous pemphigoid, rather than the generalized type.8 These results suggest that anti-BP230 autoantibodies might be relevant to the pathogenesis in our patient. The target antigen in pemphigus vegetans is mainly Dsg3. However, anti-Dsg1 antibodies, in addition to anti-Dsg3 antibodies, were occasionally detected.5,9,10Anti-Dsg1 antibodies in our patient might have induced acantholytic change although low titres of anti-Dsg3 antibodies were also detected in one test. Dual IgG reactivity with BP230 and Dsg1, as well as weak reactivity with Dsg3, might contribute to the localized extensively vegetating skin lesions in our case. However, the large nodular lesions were self-limited. A case of pemphigus vegetans localized to the scalp was successfully treated with topical steroid exclusively.6 Although no periodic acid-Schiff-positive spores were found in the skin biopsy, a local dermatologist had prescribed antifungal ointment in addition to topical steroid. Thus, it may be plausible that fungal infection triggered the inflammation on the intertriginous regions in our patient.
examining our patient’s serum with the Dermatology Mosaic No. 7 containing primate oesophagus, human salt-split-skin, recombinant BP180-NC16A-4X, recombinant BP230gC, recombinant desmoglein (Dsg) 1 and recombinant Dsg3. 1
Department of Dermatology, Faculty of Medicine, Oita University, Hasama, Yufu 879-5593, Japan 2 Department of Dermatology, Kurume University School of Medicine, Kurume University Institute of Cutaneous Cell Biology, 67 Asahimachi, Kurume, Fukuoka 830-0011, Japan Correspondence: Sakuhei Fujiwara. E-mail: [email protected]
Y. HATANO1 K. ISHIKAWA1 H. KOGA2 N. ISHII2 T. HASHIMOTO2 N. TAKEO1 H. SHIMADA1 T. SAKAI1 O. OKAMOTO1 S. FUJIWARA1
References 1 Winkelmann RK, Su WP. Pemphigoid vegetans. Arch Dermatol 1979; 115:446–8. 2 Kim J, Chavel S, Girardi M, McNiff JM. Pemphigoid vegetans: a case report and review of the literature. J CutanPathol 2008; 35:1144–7. 3 Chan LS, Dorman MA, Agha A et al. Pemphigoid vegetans represents a bullous pemphigoid variant Patient’s IgG autoantibodies identify the major bullous pemphigoid antigen. J Am Acad Dermatol 1993; 28:331–5. 4 Suda-Takayanagi T, Hara H, Ohyama B et al. A case of pemphigoid vegetans with autoantibodies against both BP180 and BP230 antigens. J Am Acad Dermatol 2011; 64:206–8. 5 Cozzani E, Christana K, Mastrogiacomo A et al. Pemphigus vegetans Neumann type with anti-desmoglein and anti-periplakin autoantibodies. Eur J Dermatol 2007; 17:530–3. 6 Zaraa I, Sellami A, Bouguerra C et al. Pemphigus vegetans: a clinical, histological, immunopathological and prognostic study. J EurAcad Dermatol Venereol 2011; 25:1160–7. 7 Guo L, Degenstein L, Dowling J et al. Gene targeting of BPAG1: abnormalities in mechanical strength and cell migration in stratified epithelia and neurologic degeneration. Cell 1995; 81: 233–43. 8 Thoma-Uszynski S, Uter W, Schwietzke S et al. BP230- and BP180-specific auto-antibodies in bullous pemphigoid. J Invest Dermatol 2004; 122:1413–22. 9 Hashimoto K, Hashimoto T, Higashiyama M et al. Detection of anti-desmocollins I and II autoantibodies in two cases of Hallopeau type pemphigus vegetans by immunoblot analysis. J DermatolSci 1994; 7:100–6. 10 Powell AM, Albert S, Oyama N et al. Paraneoplastic pemphigus secondary to fludarabine evolving into unusual oral pemphigus vegetans. J Eur Acad Dermatol Venereol 2004; 18:360–4. Funding sources: No external funding. Conflicts of interest: None declared.
Acknowledgments We gratefully appreciate Drs Christian Probst and Lars Komorowski, EUROIMMUN AG, Luebeck, Germany, for kindly British Journal of Dermatology (2014) 170, pp1187–1207
© 2013 British Association of Dermatologists
