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Exacerbation and induction of psoriasis by angiotensin-converting enzyme inhibitors
Journal of the American Academy of Dermatology Volume 30, Number 6
almost 30 years ago, should have been cited in our references. Dr. Behl and his colleagues successfully used thin split-thickness skin grafts taken "free hand" with a razor blade and transplanted them to the area of vitiligo that had been tangentially excised with a razor blade. Their results seem to have been satisfactory in the small areas treated. Our article described a "new" technique that allows precision in the removal of the epidermis of the nonpigmented skin (by dermabrasion) and precision in the thickness of epithelial sheet grafts (unlimitedin size) because ofthe availabilityof newinstrumentation (Zimmer Air Dermatome). Since the publication of our article, we have used our procedure on several additional patients with excellent results and without any complications (failure of repigmentation, scarring, or loss of pigmentation after the procedure). We have repigmented areas as large as 200
cnr', Arthur M. Kahn, M D 9201 Sunset Blvd., Suite 516 Los Angeles, CA 90069
Exacerbation and induction of psoriasis by angiotensin-converting enzyme inhibitors To the Editor: We read with interest the report of Gilleaudeau et a1. (J AMACAD DERMATOL 1993;28:4902), describing flares of psoriatic lesions induced by angiotensin-converting enzyme (ACE) inhibitors. The authors state that ACE inhibitors have not been mentioned in the literature to exacerbate psoriasis. We refer the authors to our publication in Dermatalogica (1990;181:51-3) entitled "Psoriasis Related to Angiotensin-converting Enzyme Inhibitors,"] in which we presented two cases of psoriasis attributed to the induction and exacerbation of ACE inhibitors. We proposed twopossible mechanismsfor the psoriaticeruption: (1) an allergic immune-mediated reaction and (2) a pharmacologic dose-dependent response, as a result of ACE inhibitors induced augmentation of kinin levels in the skin.! now suggested by Gilleaudeau et a1. Thus the report of Gilleaudeau et a1. supports our finding that the list of drugs known to induce or exacerbate psoriasis should include ACE inhibitors.
A. Tamir, MD R. Wolf, MD S. Brenner, M D Department of Dermatology Tel-Aviv Sourasky Medical Center Sackler Faculty of Medicine Tel-Aviv University Tel-Aviv, Israel
Correspondence
1045
REFERENCES 1. Wolf R, Tamir A, Brenner S. Psoriasis related to angiotensin-converting enzyme inhibitors. Dermatologica 1990;181: 51-3. 2. Wilkin JK, Hammond JJ, Walter MK. The captoprilinduced eruption. Arch Dermatol 1980;116:902-5.
Unilaterallaterothoracic exanthem To the Editor: Drs. Bodemer and de Prost (J AM ACAD DERMATOL 1992;27:693-6) presented an interesting series of 18 children in France with a newly described Iaterothoracic exanthem. Laur (J AM ACAD DERMATOL 1993;29:799-800) expanded this to include an initial series of 175 patients and 200 subsequent cases seenduring the past 30 years. We have seen a similar case, which to our knowledge is the first case reported in the United States. A 14-month-old white girl had an 8-day history of centrifugally spreading, mildly pruritic, annular papules and plaques. These originated on the left abdominal wall and extended to the left upper and lower extremities.The patient had been in good health other than receiving amoxicillin 2 months before for an upper respiratory tract infection. A skin biopsy specimen showed a spongiotic dermatitis with a perivascular Iymphohistiocytic infiltrate. She was treated with topical steroids with eventual resolution at 8 weekswith mild residual hyperpigmentation. Our patient is similar to those reported by Bodemer and de Prost. Their cases occurred between ages 14 months and 4 years, were seen more frequently in girls than in boys, and were initially unilateral and localized with occurrence on the left side ofthe trunk twice as often as the right side. The exanthem was centrifugally extending, morbilliform, and showedvariable dissemination between the first and second week.Lesions in all patients cleared by 4 weeks.A viral cause was postulated, but not confirmed. Michele Maroon, MD Elizabeth Magill Billingsley, MD Department of Dermatology Geisinger Medical Center Danville, PA 17822
Activated macrophages and radicals in scleroderma To the Editor: With great interest we read the article by Dr. Murrell inwhich radical-mediated tissue damage was proposedas the central mechanism in the pathogenesisof scleroderma (J AM ACAD DERMATOL 1993;28:78·85). The author proposed that the actual cause of chronic endothelial injury is increased generation of oxygen free
almost 30 years ago, should have been cited in our references. Dr. Behl and his colleagues successfully used thin split-thickness skin grafts taken "free hand" with a razor blade and transplanted them to the area of vitiligo that had been tangentially excised with a razor blade. Their results seem to have been satisfactory in the small areas treated. Our article described a "new" technique that allows precision in the removal of the epidermis of the nonpigmented skin (by dermabrasion) and precision in the thickness of epithelial sheet grafts (unlimitedin size) because ofthe availabilityof newinstrumentation (Zimmer Air Dermatome). Since the publication of our article, we have used our procedure on several additional patients with excellent results and without any complications (failure of repigmentation, scarring, or loss of pigmentation after the procedure). We have repigmented areas as large as 200
cnr', Arthur M. Kahn, M D 9201 Sunset Blvd., Suite 516 Los Angeles, CA 90069
Exacerbation and induction of psoriasis by angiotensin-converting enzyme inhibitors To the Editor: We read with interest the report of Gilleaudeau et a1. (J AMACAD DERMATOL 1993;28:4902), describing flares of psoriatic lesions induced by angiotensin-converting enzyme (ACE) inhibitors. The authors state that ACE inhibitors have not been mentioned in the literature to exacerbate psoriasis. We refer the authors to our publication in Dermatalogica (1990;181:51-3) entitled "Psoriasis Related to Angiotensin-converting Enzyme Inhibitors,"] in which we presented two cases of psoriasis attributed to the induction and exacerbation of ACE inhibitors. We proposed twopossible mechanismsfor the psoriaticeruption: (1) an allergic immune-mediated reaction and (2) a pharmacologic dose-dependent response, as a result of ACE inhibitors induced augmentation of kinin levels in the skin.! now suggested by Gilleaudeau et a1. Thus the report of Gilleaudeau et a1. supports our finding that the list of drugs known to induce or exacerbate psoriasis should include ACE inhibitors.
A. Tamir, MD R. Wolf, MD S. Brenner, M D Department of Dermatology Tel-Aviv Sourasky Medical Center Sackler Faculty of Medicine Tel-Aviv University Tel-Aviv, Israel
Correspondence
1045
REFERENCES 1. Wolf R, Tamir A, Brenner S. Psoriasis related to angiotensin-converting enzyme inhibitors. Dermatologica 1990;181: 51-3. 2. Wilkin JK, Hammond JJ, Walter MK. The captoprilinduced eruption. Arch Dermatol 1980;116:902-5.
Unilaterallaterothoracic exanthem To the Editor: Drs. Bodemer and de Prost (J AM ACAD DERMATOL 1992;27:693-6) presented an interesting series of 18 children in France with a newly described Iaterothoracic exanthem. Laur (J AM ACAD DERMATOL 1993;29:799-800) expanded this to include an initial series of 175 patients and 200 subsequent cases seenduring the past 30 years. We have seen a similar case, which to our knowledge is the first case reported in the United States. A 14-month-old white girl had an 8-day history of centrifugally spreading, mildly pruritic, annular papules and plaques. These originated on the left abdominal wall and extended to the left upper and lower extremities.The patient had been in good health other than receiving amoxicillin 2 months before for an upper respiratory tract infection. A skin biopsy specimen showed a spongiotic dermatitis with a perivascular Iymphohistiocytic infiltrate. She was treated with topical steroids with eventual resolution at 8 weekswith mild residual hyperpigmentation. Our patient is similar to those reported by Bodemer and de Prost. Their cases occurred between ages 14 months and 4 years, were seen more frequently in girls than in boys, and were initially unilateral and localized with occurrence on the left side ofthe trunk twice as often as the right side. The exanthem was centrifugally extending, morbilliform, and showedvariable dissemination between the first and second week.Lesions in all patients cleared by 4 weeks.A viral cause was postulated, but not confirmed. Michele Maroon, MD Elizabeth Magill Billingsley, MD Department of Dermatology Geisinger Medical Center Danville, PA 17822
Activated macrophages and radicals in scleroderma To the Editor: With great interest we read the article by Dr. Murrell inwhich radical-mediated tissue damage was proposedas the central mechanism in the pathogenesisof scleroderma (J AM ACAD DERMATOL 1993;28:78·85). The author proposed that the actual cause of chronic endothelial injury is increased generation of oxygen free