A bullous pemphigoid-like skin eruption after a chemical burn

A bullous pemphigoid-like skin eruption after a chemical burn

A bullous pemphigoid-like skin eruption after a chemical burn Diana M. Chen, MD, and Janet A. Fairley, MD Milwaukee, Wisconsin Bullous pemphigoid is a...

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A bullous pemphigoid-like skin eruption after a chemical burn Diana M. Chen, MD, and Janet A. Fairley, MD Milwaukee, Wisconsin Bullous pemphigoid is a blistering disorder characterized by antibody deposition in the lamina lucida of the basement membrane zone. In addition to the idiopathic form, there are many agents that have been implicated in inducing bullous pemphigoid or bullous pemphigoid-like lesions. We describe a patient who developed a bullous pemphigoid-like eruption after a chemical burn. (J Am Acad Dermatol 1998;38:337-40.)

Bullous pemphigoid (BP) and bullous pemphigoid-like skin eruptions have occurred after physical trauma,1 thermal burns,2 ultraviolet light exposure,3,4 radiotherapy,5 and systemic medications.6-8 We describe an unusual presentation of a bullous pemphigoid-like skin eruption after exposure to isothiazolinone and glutaraldehyde. CASE REPORT A 49-year-old white man had well-demarcated, red, urticarial plaques containing tense bullae on the anterior trunk, both upper extremities, and left thigh (Fig. 1) that developed after a job-related incident. His job consisted of sampling and chemically treating coolant towers with 15% glutaraldehyde and isothiazoline (a mixture of 1.15% 5-chloro-2-methyl-4-isothiazolin-3-one [MCI] and 0.35% 2-methyl-4-isothiazolin-3-one [MI]) 3 days a week. His method of adding glutaraldehyde and isothiazoline was to alternate between the two chemicals, and he could not recollect which one he was adding at the time he was splattered on the chest and left arm. Ten to 20 minutes after exposure, he developed a burning sensation in his arm. After 6 to 8 hours, the arm and chest became red, and during the next few days, the pain and erythema progressed to involve the abdomen, right arm, and left anterior thigh. He complained of nausea, but denied vomiting, fever, chills, sore throat, dizziness, or diarrhea.

This article is made possible through an educational grant from Ortho Dermatological. From the Department of Dermatology, Medical College of Wisconsin. Reprint requests to: Diana M. Chen, MD, Department of Dermatology, Northwestern University, 222 E. Superior St., Suite 240, Chicago, IL 60611. E-mail: [email protected] Copyright © 1998 by The American Academy of Dermatology, Inc. 0190-9622/98/$5.00 + 0 16/4/85746

Fig. 1. Skin eruption after chemical exposure. On right arm and chest are well-demarcated edematous, red plaques with central clearing. Tense vesicles are present within erythematous plaques. One to 2 weeks after the chemical exposure, blistering and pruritus developed within the erythematous plaques. Nikolsky’s sign was negative. No oral lesions were present. A bacterial culture was negative. The results of complete blood count, basic chemistry

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Fig. 2. Histology suggests bullous pemphigoid. Biopsy specimen from left arm showing subepidermal vesicle with many eosinophils and few neutrophils, and superficial and midperivascular inflammatory infiltrate. (Hematoxylin-eosin stain; original magnification ×400.) panel, and liver function tests were within normal limits. A biopsy specimen showed a subepidermal vesicle containing many eosinophils and a few neutrophils (Fig. 2). A superficial and midperivascular and interstitial inflammatory infiltrate of mostly eosinophils and scattered neutrophils was present. Direct immunofluorescence of perilesional skin revealed linear and fibrillar IgG and C3 deposition in the upper dermis and granular deposits of C3 and linear deposits of fibrin at the dermal-epidermal junction (Fig. 3). Cytoid bodies composed of IgA and IgM were also seen. Indirect immunofluorescence with sodium chloride-split and normal human skin substrates was negative and a complement fixation test was also negative. The patient was treated with triamcinolone 0.1% cream and oral prednisone 80 mg daily with improvement, but after 2 weeks, he was changed to dapsone because of gastrointestinal side effects from prednisone. He continued to develop blisters, despite the daily use of 75 mg of dapsone. Therefore dexamethasone was added, initially 6 mg daily, then 7.5 mg daily. The dexamethasone was discontinued after the patient developed steroid-induced myopathy, and dapsone was increased to 100 mg daily. This dosage was gradually reduced over a 5-month period as his skin condition improved. The patient returned to work 3 weeks after the incident and was given a job that did not require working with chemicals. He has been on no medications and has had no recurrence of his skin lesions for 3 years. DISCUSSION

Glutaraldehyde and isothiazoline are microbicidal and preservative agents used in industrial water coolants to inhibit the growth of microor-

ganisms. Both can cause skin burns and an allergic contact dermatitis. Isothiazoline is a combination isothiazolinone biocide, containing MCI and MI in a ratio of 3:1, with magnesium chloride and magnesium nitrate present as stabilizers. It was first marketed in the United States in 19809 and appears under several brand names, including Kathon CG, Kathon WT, Kathon MW, Kathon LX, Euxyl K 100, and Grotan TK 2. MCI/MI-containing products include paints, shampoos, cosmetics, and household cleaning agents.10 Isothiazolines at higher concentrations are found in industrial products used in water treatment, metal-working fluids, and latex production. Contact allergic reactions have been reported at concentrations as low as 0.0005% MCI/MI11 and skin burns after isothiazoline exposure may be delayed for hours. Tay and Ng12 reported a technician who developed a mid-dermal burn 9 hours after skin contact with MCI/MI. The literature also describes a number of unusual clinical presentations after exposure to isothiazolinone derivatives that mimicked seborrheic dermatitis, lupus erythematosus, or photodermatitis,13 but were histologically consistent with a subacute or chronic dermatitis. We found no reports of glutaraldehyde or isothiazolinone-induced bullous pemphigoidlike eruptions. We suspect that isothiazolinone was the causative agent for the skin eruption in our patient. Although allergic sensitization to glutaraldehyde can occur,14 it is uncommon. There have been several reports of BP within and outside of injured skin15 after a thermal burn, but there are

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Fig. 3. Direct immunofluorescence of peribullous skin using fluorescein-conjugated antihuman C3. Granular deposits of C3 are present at dermal-epidermal junction and linear, fibrillar deposits are seen in upper dermis. (Hematoxylin-eosin stain;original magnification ×400.)

no published reports of chemical burns inducing a bullous pemphigoid-like eruption. There was a report of an industrial chemist who spilled a small amount of isothiazolinone on his left wrist and developed immediate blistering at the site of contact. He continued to work with the biocide, and 1 week later developed blistering in unexposed areas on his left arm and buttocks that lasted for 3 weeks, despite treatment.16 The report does not state what treatments were given, and no skin biopsies were performed. In addition, a bullous pemphigoid-like direct immunofluorescence pattern was found in a patient who was applying Lysol to her skin (Luis A. Diaz, MD, verbal communication, 1978). It has been proposed that in cases of thermal injury, the damaged epithelium may act as a stimulus for antibasement membrane zone antibody production. Many of the patients reported had low circulating antibody titers. Chemical injury to the epidermis might expose a heterogeneous group of antigens, explaining the unusual antibody deposition seen in our patient on direct immunofluorescence. Our patient did not have detectable circulating antibasement membrane zone antibodies, however. Our patient is unique in his clinical presentation and the pattern of antibody deposition at the

basement membrane zone. The clinical appearance and histology was suggestive of bullous pemphigoid, but the immunofluorescence findings do not support this diagnosis. Although immunoelectron microscopy, Western blotting, and immunoprecipitation studies were not performed, the double staining pattern at the dermal-epidermal junction suggests that the antibodies in our patient’s skin are directed at an antigen different from the antigens of typical BP, the 230 kD and the 180 kD antigens. The antigenic targets in drug-induced bullous pemphigoid-like reactions are also heterogeneous.6,7 Many systemic medications that precipitate BP or bullous pemphigoidlike eruptions also contain sulfur, and it has been hypothesized that sulfhydryl groups are important in the induction of drug-induced BP.17 Both MCI and MI in isothiazoline contain sulfur in their ring structure. Whether topical application of these chemicals might expose the sulfhydryl group and trigger an immunologic reaction in the skin is not known. REFERENCES 1. Macfarlane AW, Verbov JL. Trauma-induced bullous pemphigoid. Clin Exp Dermatol 1989;14:245-9. 2. Jevtic A, Grigoris I. Bullous pemphigoid induced by a burn. Aust J Dermatol 1991;32(2):69-70. 3. Pfau A, Hohenleutner U, Hohenleutner S, Eckert F,

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4. 5. 6.

7. 8. 9. 10.

Landthaler M. UV-A-provoked localized bullous pemphigoid. Acta Derm Venereol 1994;74(4):314-6. Preesman AH, Toonstra J, Van der Putte SC. UV-Binduced bullous pemphigoid restricted to mycosis fungoides plaques. Clin Exp Dermatol 1990;15(5):363-6. Sheerin N, Bourke JF, Holder J. Bullous pemphigoid following radiotherapy. Clin Exp Dermatol 1995;20:80-2. Kashihara M, Danno K, Miyachi Y, Horiguchi Y, Imamura S. Bullous pemphigoid-like lesions induced by phenacetin: report of a case and an immunopathologic study. Arch Dermatol 1984;120(9):1196-9. Smith EP, Taylor TB, Meyer LJ, Zone JJ. Antigen identification in drug-induced bullous pemphigoid. J Am Acad Dermatol 1993;29(5):879-82. Hodak E, Ben-Shetrit A, Ingber A, Sandbank M. Bullous pemphigoid—an adverse effect of ampicillin. Clin Exp Dermatol 1990;15:50-2. de Groot AC, Weyland JW. Kathon CG: a review. J Am Acad Dermatol 1988;18:350-8. Nielsen H. Occupational exposure to isothiazolinones. Contact Dermatitis 1994;31:18-21.

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11. Hannuksela M. Rapid increase in contact allergy to Kathon CG in Finland. Contact Dermatitis 1986;15:2114. 12. Tay P, Ng SK. Delayed skin burns from MCI/MI biocide used in water treatment. Contact Dermatitis 1994;30:545. 13. Morren MA, Dooms-Goossens A, Delabie J, DeWolfPeeters C, Marien K, Degreef H. Contact allergy to isothiazolinone derivatives: unusual clinical presentations. Dermatology 1992;184:260-4. 14. Fowler JF. Allergic contact dermatitis from glutaraldehyde exposure. J Occup Med 1989;31(10):852-3. 15. Balato N, Ayala F, Patruno C, Ruocco V. Bullous pemphigoid induced by a thermal burn. Int J Dermatol 1995;34(7):516-7. 16. O’Driscoll JB, Beck MH. Occupational allergic contact dermatitis from Kathon WT. Contact Dermatitis 1988; 19:63. 17. Ruocco V, Sacerdoti G. Pemphigus and bullous pemphigoid due to drugs. Int J Dermatol 1991;30(5):307-12.