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oak
Journal of the American Academy of Dermatology Volume 36, Number 4
Brief communications
647
These outgrowths resembled transversally cut logs (Fig. 2). The largest were from 2 to 3 cm in height and their base ranged from 1 to 2 cm in diameter. The palms and soles 'were thickened but did not show these excrescences. The scalp, face, nails, and genitalia were unaffected. HJstopathologic examination revealed marked hyperkeratosis and acanthosis. The granular layer was prominent and vacuolated with fragmentation of the keratohyalin granules. The stratum malpighii was edematous. There was a mild inflammatory infiltrate in the papillary dermis.
DISCUSSION
The term 114 embraces all ichthyoses that display striking hyperkeratotic verrucous dark b r o w n ridges. Four different types of I H have been described: L a m b e r t type, Curth-Macklin type, Rheydt type, and Bafverstedt type. 4 Our patient belongs to the L a m bert type because o f the resemblance to a porcupine and involvement o f the entire cutaneous surface, except the face, genitals, palms, and soles. L e v e r and Schaumburg-Lever, 5 while emphasizing the symmetric involvement, consider I H to be a f o r m of systematized linear epidermal nevus. According to Pinkus and Mehregan, 6 I H shows histologic changes identical to epidermolytic hyperkeratosis. These changes were present in our patient. Although systemic retinoids have produced limited and temporary response in this and other types o f ichthyoses, 7 they were not tried in this patient.
Fig. 2. Rocky-hard dark brown excrescenses on legs.
REFERENCES
1. Rook A, Wilkinson DS, Ebling FJG. Textbook of dermatology. Oxford: Blackwell Scientific Publications, 1979: 1277. 2. Stedman's Medical Dictionary. Baltimore: Williams & Willdns, 1972:615. 3. Traupe H. The ichthyoses: a guide to clinical diagnosis, genetic counseling and therapy. Berlin: Springer Verlag, 1989. 4. Braun-Falco O, Plewig G, Wolff HH, et al. Dermatology. Berlin: Springer-Verlag, 1991:518-9. 5. Lever WF, Schaumburg-Lever G. Histopathology of the skin. Philadelphia: JB Lippincott, 1975:452-3. 6. Pinkus H, Mehregan AH. A guide to dermatohistopathology. New York: Appleton-Century-Crofts, 1981:326-7. 7. Fitzpatrick TB, Eisen AZ, Wolff K, et al. Dermatology in general medicine. New York: McGraw-Hill, 1993: 859-60.
The effect of oral ibuprofen on patch test reactivity in subjects allergic to poison ivy/oak Elizabeth F. Sherertz, M D Winston-Salem, North Carolina From the Department of Dermatology, Bowman Gray School of Medicine. Presenttedin abstractformat the AmericanContactDermatitisSociety meeting, ! Washington, D,C., December 1993. Reprint~equests:ElizabethF. Sherertz,MD, Departmentof Dermatol-
ogy,BowmanGraySchoolof Medicine,MedicalCenterBoulevard, Winston-Salem, NC 27157. J Am Acad Dermatol 1997;36:647-9. Copyright © 1997 by the AmericanAcademyof Dermatology,Inc. 0190-9622/97155.00 + 0 16/54/79551
648 Brief communications For practical reasons, it would be helpful to know whether nonsteroidal antiinflammatory drugs (NSAIDs) affect patch test reactivity. Over-thecounter NSAIDs, such as aspirin, ibuprofen, and naproxen, are commonly used and could abrogate the inflammatory response in allergic dermatitis and in allergic patch test reactions. A previous study in mice indicated that NSAIDs had tittle effect on models of delayed hypersensitivity. 1 The purpose of this study was to determine the effects of oral ibuprofen on the threshold for patch test reactivity in subjects known to be allergic to poison ivy/ oak.
MATERIAL AND METHODS Forty adults were recruited who had had poison ivy/oak dermatitis at least 1 year earlier, but no more than 3 years before the study.2 Subjects had to have no history of allergy to, or current usage of, oral nonsteroidal antiinflammatory agents, and no history of gastrointestinal disease. Written informed consent was obtained for the Institutional Review Board-approved protocol.
Verification of poison ivy/oak allergy Hollister Stier (West Haven, Conn.) poison ivy/oak extract (1:50 wt/vol) (gift of Dr. Frances Storrs) was diluted to get urushiol equivalents of 0.02 to 5.0 grrd 5 [tl. 3
Finn Chambers were prepared with 5 gl of serial dilutions of the extract as well as a control patch and were placed 7 cm apart on the left side of each subject's back. The patch tests were removed after 48 hours, and readings were done at 72 hours and 168 hours. The lowest dilution giving a grade 2 reaction (erythema, papules, induration) was recorded for each subject. After a 4-week washout period during which no nonsteroidal agents were used and no naturally occurring poison ivy/ oak dermatitis was reported, the subjects returned for the study period.
Ibuprofen study period Twenty-nine subjects were given oral ibuprofen of 400 mg three times daily for 10 days beginning on day 0 of the study period. Five patients served as controls, by following the same protocol but receiving no ibuprofen. The investigator was blinded regarding which subjects received ibuprofen. Repeat poison ivy/oak extract patch testing was done as follows: day 6, repeat patch tests on right side of back to lowest grade 2 dilution of extract; day 8, patch test removal and initial reading; day 9, patch test
Journal of the American Academy of Dermatology April 1997
reading; day 10, finish ibuprofen; day 13, 7 day patch test reading.
RESULTS Thirty-three of the 40 subjects completed the study. Three were dropped after initial poison ivy/ oak allergy verification was negative, despite a positive clinical history. Three were unable to complete the washout period as directed, and in one subject gastrointestinal upset developed during ibuprofen therapy and the drag was discontinued. In the ibuprofen-treated group, 25 of 28 subjects had no difference in patch test reactivity at the same urushiol dilution before and during ibuprofen therapy. Three of the 28 had a less intense positive reaction at the same dilution during ibuprofen therapy. None had total suppression of a positive test. The ibuprofen was stopped 3 days before the final reading to determine whether a rebound inflammatory reaction might occur at the 7-day patch test reading. In no case was the 7-day reaction more intense than that seen at 3 days. In the five control subjects, one of five had a less intense positive reaction at the same dilution.
DISCUSSION Down-regulation (or refractory phase) of doseresponse reactivity to repeat poison ivy/oak patch testing after a 6-week interval was not common in our subjects. 4, 5 Oral ibuprofen did not totally suppress repeat patch test reactions in subjects with hypersensitivity to poison ivy/oak. This indicates a lack of effect of ibuprofen on patch testing. Other medications have been shown to interfere with patch test reactions, including cromolyn, cyclosporine, and cyclophosphamide. 6-8 Because some antiinflammatory effect could occur in patients having patch tests who were taking NSAIDs, more than one reading of patch test results is recommended. Our results suggest that patch testing is likely to be reliable in patients receiving NSAIDs and indicate that some NSAIDs may not be clinically helpful in reducing the inflammation caused by delayed-type cutaneous hypersensitivity reactions such as poison ivy dermatiffs.
REFERENCES 1. TarayreJP, BarbaraM, AliagaM, et al. Comparativeactions of immunosuppressants, glucocorticoids and non-steroidal anti-inflammatory drugs on various models of delayed hy-
Journal of the American Academy of Dermatology Volume 36, Number 4
persensitivity and on a non-immune inflammation in mice. Arzneimittelforschung 1990;40:1125-31. 2. Marks JG Jr, Fowler IF Jr, Sberertz EF, et al. Prevention of poison ivy and poison oak allergic contact dermatitis by quateminm-18 bentonite. J Am Acad Dermatol 1995;33: 212-6. 3. Orchard SM, Fellman JH, Storrs FJ. Poison ivy/oak dermatitis: use of polyamine salts of a linoleic acid dimer for topical prophylaxis. Arch Dermatol 1986;122:783-9. 4. Kalish RS, Mofirnoto C. Quantitation and cloning of human urushiol specific peripheral blood T-cells: isolation of urushiol triggered suppressor T-cells. J Invest Dermatol 1989;92:46-52.
Brief communications
649
5. Hindsen M, Christensen OB. Delayed hypersensitivity reactions following allergic and irritant inflammation. Acta Derm Venereol (Stockh) 1992;72:220-1. 6. Meffert H, Wischnewski GG, Gunther W. Disodium cromoglycate inhibits allergic patch test reactions. Contact Dermatitis 1985;12:18-20. 7. Anderson CD, Groth O. Cytostatic agents and contact allergy: the efferent limb. Contact Dermatitis 1985;12:2432. 8, Higgins EM, McLelland J, Friedmaim PS, et al. Oral cyclosporin inhibits the expression of contact hypersensitivity in man. J Dermatol Sci 1991;2:79-83.
Brief communications
647
These outgrowths resembled transversally cut logs (Fig. 2). The largest were from 2 to 3 cm in height and their base ranged from 1 to 2 cm in diameter. The palms and soles 'were thickened but did not show these excrescences. The scalp, face, nails, and genitalia were unaffected. HJstopathologic examination revealed marked hyperkeratosis and acanthosis. The granular layer was prominent and vacuolated with fragmentation of the keratohyalin granules. The stratum malpighii was edematous. There was a mild inflammatory infiltrate in the papillary dermis.
DISCUSSION
The term 114 embraces all ichthyoses that display striking hyperkeratotic verrucous dark b r o w n ridges. Four different types of I H have been described: L a m b e r t type, Curth-Macklin type, Rheydt type, and Bafverstedt type. 4 Our patient belongs to the L a m bert type because o f the resemblance to a porcupine and involvement o f the entire cutaneous surface, except the face, genitals, palms, and soles. L e v e r and Schaumburg-Lever, 5 while emphasizing the symmetric involvement, consider I H to be a f o r m of systematized linear epidermal nevus. According to Pinkus and Mehregan, 6 I H shows histologic changes identical to epidermolytic hyperkeratosis. These changes were present in our patient. Although systemic retinoids have produced limited and temporary response in this and other types o f ichthyoses, 7 they were not tried in this patient.
Fig. 2. Rocky-hard dark brown excrescenses on legs.
REFERENCES
1. Rook A, Wilkinson DS, Ebling FJG. Textbook of dermatology. Oxford: Blackwell Scientific Publications, 1979: 1277. 2. Stedman's Medical Dictionary. Baltimore: Williams & Willdns, 1972:615. 3. Traupe H. The ichthyoses: a guide to clinical diagnosis, genetic counseling and therapy. Berlin: Springer Verlag, 1989. 4. Braun-Falco O, Plewig G, Wolff HH, et al. Dermatology. Berlin: Springer-Verlag, 1991:518-9. 5. Lever WF, Schaumburg-Lever G. Histopathology of the skin. Philadelphia: JB Lippincott, 1975:452-3. 6. Pinkus H, Mehregan AH. A guide to dermatohistopathology. New York: Appleton-Century-Crofts, 1981:326-7. 7. Fitzpatrick TB, Eisen AZ, Wolff K, et al. Dermatology in general medicine. New York: McGraw-Hill, 1993: 859-60.
The effect of oral ibuprofen on patch test reactivity in subjects allergic to poison ivy/oak Elizabeth F. Sherertz, M D Winston-Salem, North Carolina From the Department of Dermatology, Bowman Gray School of Medicine. Presenttedin abstractformat the AmericanContactDermatitisSociety meeting, ! Washington, D,C., December 1993. Reprint~equests:ElizabethF. Sherertz,MD, Departmentof Dermatol-
ogy,BowmanGraySchoolof Medicine,MedicalCenterBoulevard, Winston-Salem, NC 27157. J Am Acad Dermatol 1997;36:647-9. Copyright © 1997 by the AmericanAcademyof Dermatology,Inc. 0190-9622/97155.00 + 0 16/54/79551
648 Brief communications For practical reasons, it would be helpful to know whether nonsteroidal antiinflammatory drugs (NSAIDs) affect patch test reactivity. Over-thecounter NSAIDs, such as aspirin, ibuprofen, and naproxen, are commonly used and could abrogate the inflammatory response in allergic dermatitis and in allergic patch test reactions. A previous study in mice indicated that NSAIDs had tittle effect on models of delayed hypersensitivity. 1 The purpose of this study was to determine the effects of oral ibuprofen on the threshold for patch test reactivity in subjects known to be allergic to poison ivy/ oak.
MATERIAL AND METHODS Forty adults were recruited who had had poison ivy/oak dermatitis at least 1 year earlier, but no more than 3 years before the study.2 Subjects had to have no history of allergy to, or current usage of, oral nonsteroidal antiinflammatory agents, and no history of gastrointestinal disease. Written informed consent was obtained for the Institutional Review Board-approved protocol.
Verification of poison ivy/oak allergy Hollister Stier (West Haven, Conn.) poison ivy/oak extract (1:50 wt/vol) (gift of Dr. Frances Storrs) was diluted to get urushiol equivalents of 0.02 to 5.0 grrd 5 [tl. 3
Finn Chambers were prepared with 5 gl of serial dilutions of the extract as well as a control patch and were placed 7 cm apart on the left side of each subject's back. The patch tests were removed after 48 hours, and readings were done at 72 hours and 168 hours. The lowest dilution giving a grade 2 reaction (erythema, papules, induration) was recorded for each subject. After a 4-week washout period during which no nonsteroidal agents were used and no naturally occurring poison ivy/ oak dermatitis was reported, the subjects returned for the study period.
Ibuprofen study period Twenty-nine subjects were given oral ibuprofen of 400 mg three times daily for 10 days beginning on day 0 of the study period. Five patients served as controls, by following the same protocol but receiving no ibuprofen. The investigator was blinded regarding which subjects received ibuprofen. Repeat poison ivy/oak extract patch testing was done as follows: day 6, repeat patch tests on right side of back to lowest grade 2 dilution of extract; day 8, patch test removal and initial reading; day 9, patch test
Journal of the American Academy of Dermatology April 1997
reading; day 10, finish ibuprofen; day 13, 7 day patch test reading.
RESULTS Thirty-three of the 40 subjects completed the study. Three were dropped after initial poison ivy/ oak allergy verification was negative, despite a positive clinical history. Three were unable to complete the washout period as directed, and in one subject gastrointestinal upset developed during ibuprofen therapy and the drag was discontinued. In the ibuprofen-treated group, 25 of 28 subjects had no difference in patch test reactivity at the same urushiol dilution before and during ibuprofen therapy. Three of the 28 had a less intense positive reaction at the same dilution during ibuprofen therapy. None had total suppression of a positive test. The ibuprofen was stopped 3 days before the final reading to determine whether a rebound inflammatory reaction might occur at the 7-day patch test reading. In no case was the 7-day reaction more intense than that seen at 3 days. In the five control subjects, one of five had a less intense positive reaction at the same dilution.
DISCUSSION Down-regulation (or refractory phase) of doseresponse reactivity to repeat poison ivy/oak patch testing after a 6-week interval was not common in our subjects. 4, 5 Oral ibuprofen did not totally suppress repeat patch test reactions in subjects with hypersensitivity to poison ivy/oak. This indicates a lack of effect of ibuprofen on patch testing. Other medications have been shown to interfere with patch test reactions, including cromolyn, cyclosporine, and cyclophosphamide. 6-8 Because some antiinflammatory effect could occur in patients having patch tests who were taking NSAIDs, more than one reading of patch test results is recommended. Our results suggest that patch testing is likely to be reliable in patients receiving NSAIDs and indicate that some NSAIDs may not be clinically helpful in reducing the inflammation caused by delayed-type cutaneous hypersensitivity reactions such as poison ivy dermatiffs.
REFERENCES 1. TarayreJP, BarbaraM, AliagaM, et al. Comparativeactions of immunosuppressants, glucocorticoids and non-steroidal anti-inflammatory drugs on various models of delayed hy-
Journal of the American Academy of Dermatology Volume 36, Number 4
persensitivity and on a non-immune inflammation in mice. Arzneimittelforschung 1990;40:1125-31. 2. Marks JG Jr, Fowler IF Jr, Sberertz EF, et al. Prevention of poison ivy and poison oak allergic contact dermatitis by quateminm-18 bentonite. J Am Acad Dermatol 1995;33: 212-6. 3. Orchard SM, Fellman JH, Storrs FJ. Poison ivy/oak dermatitis: use of polyamine salts of a linoleic acid dimer for topical prophylaxis. Arch Dermatol 1986;122:783-9. 4. Kalish RS, Mofirnoto C. Quantitation and cloning of human urushiol specific peripheral blood T-cells: isolation of urushiol triggered suppressor T-cells. J Invest Dermatol 1989;92:46-52.
Brief communications
649
5. Hindsen M, Christensen OB. Delayed hypersensitivity reactions following allergic and irritant inflammation. Acta Derm Venereol (Stockh) 1992;72:220-1. 6. Meffert H, Wischnewski GG, Gunther W. Disodium cromoglycate inhibits allergic patch test reactions. Contact Dermatitis 1985;12:18-20. 7. Anderson CD, Groth O. Cytostatic agents and contact allergy: the efferent limb. Contact Dermatitis 1985;12:2432. 8, Higgins EM, McLelland J, Friedmaim PS, et al. Oral cyclosporin inhibits the expression of contact hypersensitivity in man. J Dermatol Sci 1991;2:79-83.