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Phenytoin-induced linear IgA bullous disease
Phenytoin-induced linear IgA bullous disease José M. Acostamadiedo, MD,a Charles Perniciaro, MD,b and Roy S. Rogers III, MDc Jacksonville, Florida, and Rochester, Minnesota Drug-induced linear IgA bullous disease most commonly occurs after exposure to vancomycin, but other medications may also trigger the eruption. We describe a 78-year-old man with linear IgA bullous disease related to treatment with phenytoin. (J Am Acad Dermatol 1998;38:352-6.)
Linear IgA bullous disease (LABD) is an acquired autoimmune subepidermal blistering disorder characterized by linear deposition of IgA at the basement membrane zone (BMZ).1-3 In rare cases, this disease is associated with drug exposure.1,4 We describe a case of LABD apparently induced by phenytoin in a 78-year-old man with a cerebral astrocytoma. CASE REPORT A 78-year-old man had progressive ataxia and progressive weakness on the left side. Computed tomographic scanning revealed a large mass in the temporal lobe. A craniotomy was performed, and the tumor was grossly resected. Pathologic examination revealed a grade IV astrocytoma. Postoperatively, the patient received prophylactic treatment with phenytoin (100 mg twice daily) and dexamethasone. External beam radiation therapy was initiated on the seventeenth postoperative day. Four weeks after the operation, tense bullae developed in the inguinal creases bilaterally. The skin eruption progressed rapidly to involve the palms, feet (Fig. 1), perineum, and back, and then it became generalized. The oral mucosa, eyes, and face were spared. Some lesions had a target-like appearance, with a central hemorrhagic area. The initial diagnosis was erythema multiforme caused by phenytoin. Dexamethasone was increased to 4 mg four times daily, and treatment with phenytoin and radiation therapy was discontinued.
This article is made possible through an educational grant from Ortho Dermatological. Nothing in this publication implies that Mayo Foundation endorses Ortho Dermatological. From the Departments of Internal Medicinea and Dermatology,b Mayo Clinic Jacksonville, Jacksonville, Florida, and Department of Dermatology, Mayo Clinic, Rochester, Minnesota.c Reprint requests: Charles Perniciaro, MD, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224. Copyright © 1998 by the American Academy of Dermatology, Inc. 0190-9622/98 $5.00 + 0 16/4/83478
352
Fig. 1. Hemorrhagic bullae of drug-induced linear IgA bullous dermatosis. A biopsy specimen from the edge of a bullous lesion displayed a subepidermal separation (Fig. 2). Spongiosis and a few necrotic keratinocytes were present within the epidermal roof of the blister. Perilesional direct immunofluorescence revealed prominent IgA in a linear pattern at the BMZ (Fig. 3). Linear IgG was also present at the BMZ but with much less intensity than with IgA. IgM, fibrinogen, and C3 staining were unremarkable. Indirect immunofluorescence staining was positive on monkey esophagus with IgA antibasement membrane antibodies (anti-BMZ) at a titer of 1:160. IgG anti-BMZ was detected at a titer of 1:20. Antibodies to the intercellular substance were not present. An indirect immunofluorescence assay using 1 mol/L NaClsplit human skin showed a dermal (blister floor) staining pattern. Four days after phenytoin was discontinued, no new lesions developed. Dapsone (50 mg daily) was given. During the next 10 days, the bullous lesions became denuded and painful erosions ensued (Fig. 4). The skin lesions slowly healed. The patient died of
Journal of the American Academy of Dermatology Volume 38, Number 2, Part 2
Acostamadiedo et al. 353
Fig. 2. Biopsy specimen from edge of bullous lesion demonstrates subepidermal cleft. Isolated necrotic keratinocytes were noted in epidermis. (Hematoxylin-eosin; original
Fig. 3. Direct immunofluorescence of perilesional skin biopsy specimen shows prominent IgA in linear pattern at basement membrane zone. (Original magnification ×400.) complications from his malignancy 9 weeks after admission. DISCUSSION
Clinically, LABD may resemble other bullous dermatoses, such as bullous pemphigoid and dermatitis herpetiformis5-8 but can be differentiated by its characteristic immunofluorescence pattern.6,8-10 As in our patient, linear deposition of IgA is prominent at the BMZ. Chronic bullous disease of childhood, another subepidermal blistering disorder,8 is believed to be a childhood vari-
ant of LABD; the only apparent difference between the two is the younger age at presentation.8,11 LABD is characterized by multiple small vesicles and large bullae in clusters, chiefly on the lower trunk, groin, lower extremities, and perioral skin.6,9 Involvement of the palms and soles was present in at least five of the previously reported cases of drug-induced LABD.1,3,12-14 In our patient, mucosal surfaces were spared, which is common in drug-induced LABD. The direct immunofluorescence staining pattern in LABD is
Journal of the American Academy of Dermatology February 1998
354 Acostamadiedo et al.
Table I. Summary of reported cases of drug-induced linear IgA bullous dermatosis Reference
Sex/age ( yr)
12 13 13 13 1 1 18 22 24 26 27 25 1 17 19 18 28 1 Present case 25 3, 18 20 1
M/68 M/54 F/72 M/54 M/74 M/67 Unknown M/63 M/53 M/79 F/72 M/70 M/69 F/63 M/21 Unknown M/58 M/70 M/78 F/68 M/70 M/58 M/67
30 31 29 14 1 21 16 25
M/26 Unknown F/71 M/6 months F/73 F/58 F/26 M/30
Drug
Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin, rifampin Vancomycin, rifampin Diclofenac Diclofenac Interferon, interleukin-2 Interferon, interleukin-2 Phenytoin Phenytoin Amiodarone Amiodarone Captopril Captopril, trimethoprim-sulfamethoxazole Penicillin Ampicillin Iodine contrast agent Sulfisoxazole Somatostatin Cefamandole Lithium Polychemotherapy
Clinical features
BP, LABD BP EM, BP EM, BP EM, BP BP EM, BP EM, BP BP EM EM EM BP EM, BP DH EM, BP EM, BP BP EM, BP EM, BP EM, LABD EM, BP BP BP ? BP EM BP EM LABD BP
BP, Bullous pemphigoid; DH, dermatitis herpetiformis; EM, erythema multiforme; LABD, linear IgA bullous disease.
linear deposition of IgA along the BMZ,1,9 with occasional C31 and occasional coexistent linear IgG.4 Generally, when both IgA and IgG are present in a linear pattern at the BMZ, the pattern is more consistent with linear IgA dermatosis than with pemphigoid if the fluorescence intensity of IgA is greater than that of IgG, particularly if C3 is absent.8,15 Our patient demonstrated these findings. Also in LABD, the indirect immunofluorescence staining is occasionally positive with antiBMZ IgA,9 which we also found in our patient. Drug-induced LABD has been reported in association with several medications,1,12-14,16-31 most commonly vancomycin (Table I). One other patient with purpura, linear deposition of IgA, and no bullous lesions has been described after treatment with glibenclamide.32 LABD has also been reported to be associated with malignancy,1,7,33-37
connective tissue diseases such as rheumatoid arthritis38 and systemic lupus erythematosus,39 interleukin-2 or interferon-γ therapy (or both) for renal adenocarcinoma,28 and immunosuppressive therapy with cyclosporine after heart transplantation.40 The initial diagnosis of erythema multiforme in our patient was based on the rapidly evolving bullous and target lesions after the administration of phenytoin and cranial irradiation. Several authors have reported erythema multiforme–like or other cutaneous reactions after radiation therapy.41-44 Eight patients were described with erythema multiforme who had intracranial tumors treated with both radiation therapy and phenytoin.45 In all these patients, the eruption began in the area of the radiation port on the scalp and subsequently generalized. Biopsy specimens were not obtained
Journal of the American Academy of Dermatology Volume 38, Number 2, Part 2
Fig. 4. Erosions on back and buttocks at sites of denuded bullae.
from any of these patients for direct immunofluorescence staining. In retrospect, some may have had LABD, although the lesions met the clinical criteria for erythema multiforme. LABD and chronic bullous disease of childhood generally respond to a combined treatment with sulfones and corticosteroids.5,9,46 With druginduced LABD, removal of the offending agent is paramount. Our patient’s skin responded to discontinuation of treatment with phenytoin and radiation, to increasing the dosage of dexamethasone, and to the administration of dapsone. REFERENCES 1. Kuechle MK, Stegemeir E, Maynard B, et al. Druginduced linear IgA bullous dermatosis: report of six cases and review of the literature. J Am Acad Dermatol 1994;30:187-92. 2. Wojnarowska F, Allen J, Collier P. Linear IgA disease: a heterogeneous disease. Dermatology 1994;189(Suppl 1):52-6. 3. Primka EJ III, Liranzo MO, Bergfeld WF, et al. Amiodarone-induced linear IgA disease. J Am Acad Dermatol 1994;31:809-11. 4. Janniger CK, Wiltz H, Schwartz RA, et al. Adult linear IgA bullous dermatosis: a polymorphic disorder. Cutis 1990;45:37-42. 5. Long SA, Argenyi ZB, Piette WW. Arciform blistering in an elderly woman: linear IgA dermatosis (LAD). Arch Dermatol 1988;124:1705, 1708.
Acostamadiedo et al. 355 6. Chorzelski T, Jablonska S. Evolving concept of IgA linear dermatosis. Semin Dermatol 1988;7:225-32. 7. Rasak JC, Sklar JL, Weigand DA. A blistering eruption in an elderly woman: linear IgA dermatosis (LAD). Arch Dermatol 1993;129:231-5. 8. Helm KF, Peters MS. Immunodermatology update: the immunologically mediated vesiculobullous diseases. Mayo Clin Proc 1991;66:187-202. 9. Wilson BD, Beutner EH, Kumar V, et al. Linear IgA bullous dermatosis: an immunologically defined disease. Int J Dermatol 1985;24:569-74. 10. Peters MS, Rogers RS. Clinical correlations of linear IgA deposition at the cutaneous basement membrane zone. J Am Acad Dermatol 1989;20:761-70. 11. Wojnarowska F, Marsden RA, McKee PH, et al. A comparative study of benign chronic bullous dermatosis of childhood and linear IgA dermatosis of adults (abstract). Br J Dermatol 1985;29(suppl):17-8. 12. Baden LA, Apovian C, Imber MJ, et al. Vancomycininduced linear IgA bullous dermatosis (letter to the editor). Arch Dermatol 1988;124:1186-8. 13. Carpenter S, Berg D, Sidhu-Malik N, et al. Vancomycinassociated linear IgA dermatosis: a report of three cases. J Am Acad Dermatol 1992;26:45-8. 14. Safai B, Rappaport I, Matsuoka L, et al. Childhood dermatitis herpetiformis: review of the new aspects and report of a case. J Am Acad Dermatol 1981;4:435-41. 15. Chan LS, Traczyk T, Taylor TB, et al. Linear IgA bullous dermatosis: characterization of a subset of patients with concurrent IgA and IgG anti-basement membrane autoantibodies. Arch Dermatol 1995;131:1432-7. 16. McWhirter JD, Hashimoto K, Fayne S, et al. Linear IgA bullous dermatosis related to lithium carbonate (letter to the editor). Arch Dermatol 1987;123:1120-2. 17. Gabrielsen TO, Staerfelt F, Thune PO. Drug-induced bullous dermatosis with linear IgA deposits along the basement membrane. Acta Derm Venereol 1981;61:439-41. 18. Primka E, Gay D, Bergfeld W. Drug-induced linear IgA disease (histopathologic features of three cases) (abstract). J Cutan Pathol 1996;23:58. 19. Valsecchi R, Serra M, Tornaghi A, et al. Drug-induced bullous dermatosis with linear IgA. G Ital Dermatol Venereol 1982;117:221-3. 20. Klein LE, Shmunes E, Carter JB, et al. Linear IgA bullous dermatosis related to captopril treatment. Cutis 1989;44:393-6. 21. Argenyi ZB, Bergfeld WF, Valenzuela R, et al. Adult linear IgA disease associated with an erythema multiforme–like drug reaction. Cleve Clin J Med 1987;54:445-50. 22. Whitworth JM, Thomas I, Peltz SA, et al. Vancomycininduced linear IgA bullous dermatosis (LABD). J Am Acad Dermatol 1996;34:890-1. 23. Collier PM, Wojnarowska F. Drug-induced linear immunoglobulin A disease. Clin Dermatol 1993;11:52933. 24. Piketty C, Meeus F, Nochy D, et al. Linear IgA dermatosis related to vancomycin (letter to the editor). Br J Dermatol 1994;130:130-1. 25. Espagne E, Prost C, Chosidow O, et al. Linear IgA druginduced dermatosis: report of 3 cases. Ann Dermatol Venereol 1990;117:898-9. 26. Geissmann C, Beylot-Barry M, Doutre MS, et al. Druginduced linear IgA bullous dermatosis (letter to the editor). J Am Acad Dermatol 1995;32:296.
Journal of the American Academy of Dermatology February 1998
356 Acostamadiedo et al. 27. Richards SS, Hall S, Yokel B, et al. A bullous eruption in an elderly woman: vancomycin-associated linear IgA dermatosis (LAD). Arch Dermatol 1995;131:1447-8. 28. Guillaume JC, Escudier B, Espagne E, et al. Bullous dermatosis with linear IgA deposits along the basement membrane during treatment with gamma interferon and interleukin-2. Ann Dermatol Venereol 1990;117:899902. 29. Lemarchand-Venencie F, Vigouroux F, Blanc F, et al. Dermatose bulleuse à IgA linéaire au décours immédiat d’une urographie intra-veineuse. Ann Dermatol Venereol 1987;114:1423-5. 30. Combemale P, Gavaud C, Cozzani E, et al. Linear IgA dermatosis induced by penicillin G. Ann Dermatol Venereol 1993;120:847-8. 31. Boffety B, Sohier J, Venencie PY, et al. Dermatoses bulleuses à IgA linéaire. J Dermatol (Paris) 1981:53-53a. 32. Vaatainen N, Fraki JE, Hyvonen M, et al. Purpura with a linear epidermo-dermal deposition of IgA. Acta Derm Venereol 1983;63:169-70. 33. Sekula SA, Tschen JA, Bean SF, et al. Linear IgA bullous disease in a patient with transitional cell carcinoma of the bladder. Cutis 1986;38:354-6. 34. Vignon D, Guillaume JC, Revuz J, et al. Association of Hodgkin’s disease and linear IgA dermatosis (letter to the editor). Nouv Presse Med 1982;11:603-4. 35. Kienzler JL, Blanc D, Laurent R, et al. Linear IgA bullous dermatosis and Hodgkin’s disease. Ann Dermatol Venereol 1983;110:727-8. 36. Mobacken H, Kastrup W, Ljunghall K, et al. Linear IgA dermatosis: a study of ten adult patients. Acta Derm Venereol 1983;63:123-8. 37. Jablonska S, Chorzelski TP, Beutner EH, et al.
38. 39.
40. 41.
42. 43. 44. 45.
46.
Dermatitis herpetiformis and bullous pemphigoid: intermediate and mixed forms. Arch Dermatol 1976;112:458. Hayakawa K, Shiohara T, Yagita A, et al. Linear IgA bullous dermatosis associated with rheumatoid arthritis. J Am Acad Dermatol 1992;26:110-3. Lau M, Kaufmann-Grunzinger I, Raghunath M. A case report of a patient with features of systemic lupus erythematosus and linear IgA disease. Br J Dermatol 1991;124:498-502. Petit D, Borradori L, Rybojad M, et al. Linear IgA bullous dermatosis after heart transplantation. J Am Acad Dermatol 1990;22:851. Fleischer AB Jr, Rosenthal DI, Bernard SA, et al. Skin reactions to radiotherapy—a spectrum resembling erythema multiforme: case report and review of the literature. Cutis 1992;49:35-9. Maxfield WS, Coleman WP. Cutaneous reactions after radiation therapy: report of 7 cases. Am J Roentgenol Radium Ther Nucl Med 1969;105:636-43. Burnstein HJ. Toxic cutaneous reactions after x-ray therapy. Cutis 1967;3:835-40. Nawalkha PL, Mathur NK, Malhotra YK, et al. Severe erythema multiforme (Stevens-Johnson syndrome) following telecobalt therapy. Br J Radiol 1972;45:768-9. Delattre JY, Safai B, Posner JB. Erythema multiforme and Stevens-Johnson syndrome in patients receiving cranial irradiation and phenytoin. Neurology 1988;38:1948. Chorzelski TP, Jablonska S. IgA linear dermatosis of childhood (chronic bullous disease of childhood). Br J Dermatol 1979;101:535-42.
Linear IgA bullous disease (LABD) is an acquired autoimmune subepidermal blistering disorder characterized by linear deposition of IgA at the basement membrane zone (BMZ).1-3 In rare cases, this disease is associated with drug exposure.1,4 We describe a case of LABD apparently induced by phenytoin in a 78-year-old man with a cerebral astrocytoma. CASE REPORT A 78-year-old man had progressive ataxia and progressive weakness on the left side. Computed tomographic scanning revealed a large mass in the temporal lobe. A craniotomy was performed, and the tumor was grossly resected. Pathologic examination revealed a grade IV astrocytoma. Postoperatively, the patient received prophylactic treatment with phenytoin (100 mg twice daily) and dexamethasone. External beam radiation therapy was initiated on the seventeenth postoperative day. Four weeks after the operation, tense bullae developed in the inguinal creases bilaterally. The skin eruption progressed rapidly to involve the palms, feet (Fig. 1), perineum, and back, and then it became generalized. The oral mucosa, eyes, and face were spared. Some lesions had a target-like appearance, with a central hemorrhagic area. The initial diagnosis was erythema multiforme caused by phenytoin. Dexamethasone was increased to 4 mg four times daily, and treatment with phenytoin and radiation therapy was discontinued.
This article is made possible through an educational grant from Ortho Dermatological. Nothing in this publication implies that Mayo Foundation endorses Ortho Dermatological. From the Departments of Internal Medicinea and Dermatology,b Mayo Clinic Jacksonville, Jacksonville, Florida, and Department of Dermatology, Mayo Clinic, Rochester, Minnesota.c Reprint requests: Charles Perniciaro, MD, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224. Copyright © 1998 by the American Academy of Dermatology, Inc. 0190-9622/98 $5.00 + 0 16/4/83478
352
Fig. 1. Hemorrhagic bullae of drug-induced linear IgA bullous dermatosis. A biopsy specimen from the edge of a bullous lesion displayed a subepidermal separation (Fig. 2). Spongiosis and a few necrotic keratinocytes were present within the epidermal roof of the blister. Perilesional direct immunofluorescence revealed prominent IgA in a linear pattern at the BMZ (Fig. 3). Linear IgG was also present at the BMZ but with much less intensity than with IgA. IgM, fibrinogen, and C3 staining were unremarkable. Indirect immunofluorescence staining was positive on monkey esophagus with IgA antibasement membrane antibodies (anti-BMZ) at a titer of 1:160. IgG anti-BMZ was detected at a titer of 1:20. Antibodies to the intercellular substance were not present. An indirect immunofluorescence assay using 1 mol/L NaClsplit human skin showed a dermal (blister floor) staining pattern. Four days after phenytoin was discontinued, no new lesions developed. Dapsone (50 mg daily) was given. During the next 10 days, the bullous lesions became denuded and painful erosions ensued (Fig. 4). The skin lesions slowly healed. The patient died of
Journal of the American Academy of Dermatology Volume 38, Number 2, Part 2
Acostamadiedo et al. 353
Fig. 2. Biopsy specimen from edge of bullous lesion demonstrates subepidermal cleft. Isolated necrotic keratinocytes were noted in epidermis. (Hematoxylin-eosin; original
Fig. 3. Direct immunofluorescence of perilesional skin biopsy specimen shows prominent IgA in linear pattern at basement membrane zone. (Original magnification ×400.) complications from his malignancy 9 weeks after admission. DISCUSSION
Clinically, LABD may resemble other bullous dermatoses, such as bullous pemphigoid and dermatitis herpetiformis5-8 but can be differentiated by its characteristic immunofluorescence pattern.6,8-10 As in our patient, linear deposition of IgA is prominent at the BMZ. Chronic bullous disease of childhood, another subepidermal blistering disorder,8 is believed to be a childhood vari-
ant of LABD; the only apparent difference between the two is the younger age at presentation.8,11 LABD is characterized by multiple small vesicles and large bullae in clusters, chiefly on the lower trunk, groin, lower extremities, and perioral skin.6,9 Involvement of the palms and soles was present in at least five of the previously reported cases of drug-induced LABD.1,3,12-14 In our patient, mucosal surfaces were spared, which is common in drug-induced LABD. The direct immunofluorescence staining pattern in LABD is
Journal of the American Academy of Dermatology February 1998
354 Acostamadiedo et al.
Table I. Summary of reported cases of drug-induced linear IgA bullous dermatosis Reference
Sex/age ( yr)
12 13 13 13 1 1 18 22 24 26 27 25 1 17 19 18 28 1 Present case 25 3, 18 20 1
M/68 M/54 F/72 M/54 M/74 M/67 Unknown M/63 M/53 M/79 F/72 M/70 M/69 F/63 M/21 Unknown M/58 M/70 M/78 F/68 M/70 M/58 M/67
30 31 29 14 1 21 16 25
M/26 Unknown F/71 M/6 months F/73 F/58 F/26 M/30
Drug
Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin Vancomycin, rifampin Vancomycin, rifampin Diclofenac Diclofenac Interferon, interleukin-2 Interferon, interleukin-2 Phenytoin Phenytoin Amiodarone Amiodarone Captopril Captopril, trimethoprim-sulfamethoxazole Penicillin Ampicillin Iodine contrast agent Sulfisoxazole Somatostatin Cefamandole Lithium Polychemotherapy
Clinical features
BP, LABD BP EM, BP EM, BP EM, BP BP EM, BP EM, BP BP EM EM EM BP EM, BP DH EM, BP EM, BP BP EM, BP EM, BP EM, LABD EM, BP BP BP ? BP EM BP EM LABD BP
BP, Bullous pemphigoid; DH, dermatitis herpetiformis; EM, erythema multiforme; LABD, linear IgA bullous disease.
linear deposition of IgA along the BMZ,1,9 with occasional C31 and occasional coexistent linear IgG.4 Generally, when both IgA and IgG are present in a linear pattern at the BMZ, the pattern is more consistent with linear IgA dermatosis than with pemphigoid if the fluorescence intensity of IgA is greater than that of IgG, particularly if C3 is absent.8,15 Our patient demonstrated these findings. Also in LABD, the indirect immunofluorescence staining is occasionally positive with antiBMZ IgA,9 which we also found in our patient. Drug-induced LABD has been reported in association with several medications,1,12-14,16-31 most commonly vancomycin (Table I). One other patient with purpura, linear deposition of IgA, and no bullous lesions has been described after treatment with glibenclamide.32 LABD has also been reported to be associated with malignancy,1,7,33-37
connective tissue diseases such as rheumatoid arthritis38 and systemic lupus erythematosus,39 interleukin-2 or interferon-γ therapy (or both) for renal adenocarcinoma,28 and immunosuppressive therapy with cyclosporine after heart transplantation.40 The initial diagnosis of erythema multiforme in our patient was based on the rapidly evolving bullous and target lesions after the administration of phenytoin and cranial irradiation. Several authors have reported erythema multiforme–like or other cutaneous reactions after radiation therapy.41-44 Eight patients were described with erythema multiforme who had intracranial tumors treated with both radiation therapy and phenytoin.45 In all these patients, the eruption began in the area of the radiation port on the scalp and subsequently generalized. Biopsy specimens were not obtained
Journal of the American Academy of Dermatology Volume 38, Number 2, Part 2
Fig. 4. Erosions on back and buttocks at sites of denuded bullae.
from any of these patients for direct immunofluorescence staining. In retrospect, some may have had LABD, although the lesions met the clinical criteria for erythema multiforme. LABD and chronic bullous disease of childhood generally respond to a combined treatment with sulfones and corticosteroids.5,9,46 With druginduced LABD, removal of the offending agent is paramount. Our patient’s skin responded to discontinuation of treatment with phenytoin and radiation, to increasing the dosage of dexamethasone, and to the administration of dapsone. REFERENCES 1. Kuechle MK, Stegemeir E, Maynard B, et al. Druginduced linear IgA bullous dermatosis: report of six cases and review of the literature. J Am Acad Dermatol 1994;30:187-92. 2. Wojnarowska F, Allen J, Collier P. Linear IgA disease: a heterogeneous disease. Dermatology 1994;189(Suppl 1):52-6. 3. Primka EJ III, Liranzo MO, Bergfeld WF, et al. Amiodarone-induced linear IgA disease. J Am Acad Dermatol 1994;31:809-11. 4. Janniger CK, Wiltz H, Schwartz RA, et al. Adult linear IgA bullous dermatosis: a polymorphic disorder. Cutis 1990;45:37-42. 5. Long SA, Argenyi ZB, Piette WW. Arciform blistering in an elderly woman: linear IgA dermatosis (LAD). Arch Dermatol 1988;124:1705, 1708.
Acostamadiedo et al. 355 6. Chorzelski T, Jablonska S. Evolving concept of IgA linear dermatosis. Semin Dermatol 1988;7:225-32. 7. Rasak JC, Sklar JL, Weigand DA. A blistering eruption in an elderly woman: linear IgA dermatosis (LAD). Arch Dermatol 1993;129:231-5. 8. Helm KF, Peters MS. Immunodermatology update: the immunologically mediated vesiculobullous diseases. Mayo Clin Proc 1991;66:187-202. 9. Wilson BD, Beutner EH, Kumar V, et al. Linear IgA bullous dermatosis: an immunologically defined disease. Int J Dermatol 1985;24:569-74. 10. Peters MS, Rogers RS. Clinical correlations of linear IgA deposition at the cutaneous basement membrane zone. J Am Acad Dermatol 1989;20:761-70. 11. Wojnarowska F, Marsden RA, McKee PH, et al. A comparative study of benign chronic bullous dermatosis of childhood and linear IgA dermatosis of adults (abstract). Br J Dermatol 1985;29(suppl):17-8. 12. Baden LA, Apovian C, Imber MJ, et al. Vancomycininduced linear IgA bullous dermatosis (letter to the editor). Arch Dermatol 1988;124:1186-8. 13. Carpenter S, Berg D, Sidhu-Malik N, et al. Vancomycinassociated linear IgA dermatosis: a report of three cases. J Am Acad Dermatol 1992;26:45-8. 14. Safai B, Rappaport I, Matsuoka L, et al. Childhood dermatitis herpetiformis: review of the new aspects and report of a case. J Am Acad Dermatol 1981;4:435-41. 15. Chan LS, Traczyk T, Taylor TB, et al. Linear IgA bullous dermatosis: characterization of a subset of patients with concurrent IgA and IgG anti-basement membrane autoantibodies. Arch Dermatol 1995;131:1432-7. 16. McWhirter JD, Hashimoto K, Fayne S, et al. Linear IgA bullous dermatosis related to lithium carbonate (letter to the editor). Arch Dermatol 1987;123:1120-2. 17. Gabrielsen TO, Staerfelt F, Thune PO. Drug-induced bullous dermatosis with linear IgA deposits along the basement membrane. Acta Derm Venereol 1981;61:439-41. 18. Primka E, Gay D, Bergfeld W. Drug-induced linear IgA disease (histopathologic features of three cases) (abstract). J Cutan Pathol 1996;23:58. 19. Valsecchi R, Serra M, Tornaghi A, et al. Drug-induced bullous dermatosis with linear IgA. G Ital Dermatol Venereol 1982;117:221-3. 20. Klein LE, Shmunes E, Carter JB, et al. Linear IgA bullous dermatosis related to captopril treatment. Cutis 1989;44:393-6. 21. Argenyi ZB, Bergfeld WF, Valenzuela R, et al. Adult linear IgA disease associated with an erythema multiforme–like drug reaction. Cleve Clin J Med 1987;54:445-50. 22. Whitworth JM, Thomas I, Peltz SA, et al. Vancomycininduced linear IgA bullous dermatosis (LABD). J Am Acad Dermatol 1996;34:890-1. 23. Collier PM, Wojnarowska F. Drug-induced linear immunoglobulin A disease. Clin Dermatol 1993;11:52933. 24. Piketty C, Meeus F, Nochy D, et al. Linear IgA dermatosis related to vancomycin (letter to the editor). Br J Dermatol 1994;130:130-1. 25. Espagne E, Prost C, Chosidow O, et al. Linear IgA druginduced dermatosis: report of 3 cases. Ann Dermatol Venereol 1990;117:898-9. 26. Geissmann C, Beylot-Barry M, Doutre MS, et al. Druginduced linear IgA bullous dermatosis (letter to the editor). J Am Acad Dermatol 1995;32:296.
Journal of the American Academy of Dermatology February 1998
356 Acostamadiedo et al. 27. Richards SS, Hall S, Yokel B, et al. A bullous eruption in an elderly woman: vancomycin-associated linear IgA dermatosis (LAD). Arch Dermatol 1995;131:1447-8. 28. Guillaume JC, Escudier B, Espagne E, et al. Bullous dermatosis with linear IgA deposits along the basement membrane during treatment with gamma interferon and interleukin-2. Ann Dermatol Venereol 1990;117:899902. 29. Lemarchand-Venencie F, Vigouroux F, Blanc F, et al. Dermatose bulleuse à IgA linéaire au décours immédiat d’une urographie intra-veineuse. Ann Dermatol Venereol 1987;114:1423-5. 30. Combemale P, Gavaud C, Cozzani E, et al. Linear IgA dermatosis induced by penicillin G. Ann Dermatol Venereol 1993;120:847-8. 31. Boffety B, Sohier J, Venencie PY, et al. Dermatoses bulleuses à IgA linéaire. J Dermatol (Paris) 1981:53-53a. 32. Vaatainen N, Fraki JE, Hyvonen M, et al. Purpura with a linear epidermo-dermal deposition of IgA. Acta Derm Venereol 1983;63:169-70. 33. Sekula SA, Tschen JA, Bean SF, et al. Linear IgA bullous disease in a patient with transitional cell carcinoma of the bladder. Cutis 1986;38:354-6. 34. Vignon D, Guillaume JC, Revuz J, et al. Association of Hodgkin’s disease and linear IgA dermatosis (letter to the editor). Nouv Presse Med 1982;11:603-4. 35. Kienzler JL, Blanc D, Laurent R, et al. Linear IgA bullous dermatosis and Hodgkin’s disease. Ann Dermatol Venereol 1983;110:727-8. 36. Mobacken H, Kastrup W, Ljunghall K, et al. Linear IgA dermatosis: a study of ten adult patients. Acta Derm Venereol 1983;63:123-8. 37. Jablonska S, Chorzelski TP, Beutner EH, et al.
38. 39.
40. 41.
42. 43. 44. 45.
46.
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