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Disseminated superficial actinic porokeratosis: Appearance associated with photochemotherapy for psoriasis
Volume 12 Number 6 June, 1985
Reactions to heparin injections
9. Shelley WB, Sayen JJ': Heparin necrosis: An anticoagulant-induced cutaneous infarct. J AM ACADDmRt~ATOL 7:674~677, 1982. 10. Levine LE, Bernstein JE, Soltani K, et al: Hepadninduced cutaneous necrosis unrelated to injection sites.
A sign of potentially lethal complications. Arch Dermatol 119:400-403, 1983. 11. Kelly RA, Gelfand JA, Pincus SH: Cutaneous necrosis caused by systemically administered heparin. JAMA 2,46:1582-1583, 1981.
Disseminated superficial actinic porokeratosis: Appearance associated with photochemotherapy for psoriasis Paul G. Hazen, M,D., James F. Carney, M.D., Allen E. Walker, M . D . , John J. Stewart, M.D., and Conley W. Engstrom, M.D. Cleveland, OH A patient with chronic psoriasis treated with psoralens plus ultraviolet A (PUVA) developed characteristic lesions of disseminated superficial actinic porokeratosis (DSAP). Since other processes associated with ultraviolet irradiation, including epidermal dysplasia, actinic keratoses, squamous cell carcinomas, and keratoacanthomas, have been reported to result from PUVA, it is possible that her DSAP lesions were induced by this therapy. (J AM ACAD DERMATOL 12:1077-1078, 1985.)
CASE REPORT A 30-year-old woman (skin type III) was referred for treatment of psoriasis. Psoriasis had been diagnosed at 11 years of age, and she had been treated with topical steroids, tars, and ultraviolet (UV) light. Because of extensive psoriasis, therapy using psoralens plus ultraviolet A (PUVA) was carried out three times weekly for 18 months from 1976 to 1977. The total amount of UV energy administered was unknown. Her skin responded well to the treatment, and from November, 1977, to October, 1978, no therapy was administered. In October, 1978, her psoriasis recurred. Extensive plaques of psoriasis were noted over the extremities, with fewer lesions on the trunk; an outpatient program of topical steroids, tars, and weekly suberythemogenic doses of UV light (UVB) was instituted. Because of failure to control her psoriasis, weekly PUVA therapy was begun in January, 1983. In February, after six treatments and 19.5 joules/cm ~ of UVA energy, approxiFrom the Departmentof Dermatology,UniversityHospitalsof Cleveland, ClevelandMetropolitan General Hospital. Reprint requests to: Dr. Paul G. Hazen, 14701 Detroit Ave., Lakewood, OH 44107.
mately 20 hyperpigmented macules appeared on the legs (Fig. 1). These were distinct from the lesions of psoriasis. Three weeks later all of the hyperpigmented lesions developed an elevated border consistent with a comoid lamella. A biopsy specimen confirmed the clinical impression of disseminated superficial actinic porokeratosis (DSAP). At that time, persistent plaques of psoriasis were confined only to the elbows and knees. Therapy with PUVA was discontinued. During the next 2 months new lesions continued to appear and older lesions slowly enlarged. At that point new lesions ceased to appear and previous lesions became less prominent. Her psoriasis is currently being managed with topical steroids only. There is no family history of similar lesions or psoriasis. DISCUSSION D S A P is an uncommon process in which lesions appear, usually in sun-exposed areas of skin.l Typical lesions often begin as 0.1 to 0.2 cm keratotic papules that may enlarge slowly to form plaques 1077
Journal of the
1078
American Academyof Dermatology
Hazen et al
Fig. 1. Lower leg of patient shows multiple 6- to 8-mm lesions of DSAP. containing an elevated, keratotic border. 2 The diagnosis of porokeratosis is confirmed by the histologic finding of a parakeratotic column, the cornoid lamella. Epidermal changes, including dyskeratotic cells, vacuolated cells, and liquefaction degeneration of the basal cell layer, may be present. 3 The association of these lesions with artificial or natural UV light exposure has been emphasized previously. Although DSAP has been reported to occur in dark-skinned individuals, 4 it is usually seen in sun-exposed areas of fair-skinned individuals. Summer months are the usual time of onset of new lesions. Artificial UV radiation has also been reported to induce lesions in a previously susceptible subject) A number of cutaneous sequelae have been reported from PUVA therapy. Actinic keratoses and epidermal dystrophy and the appearance of skin neoplasms, including squamous cell carcinomas and multiple keratoacanthomas, have been reported. 6-s The cause of DSAP in our patient is uncertain. Although lesions began to appear while she was receiving PUVA, she had received multiple other therapies including UVB, tars, and topical steroids. Furthermore, the greatest concentration of lesions was in places generally accessible to sun exposure--the arms and legs, However, it is sig-
nificant that both sunlight and standard artificial UVB sources contain substantial quantities of UVA. Other investigators have also noted patients in whom lesions of DSAP have appeared in association with PUVA therapy. 9,t° Reymond et al 9 reported a single patient in whom typical lesions of DSAP appeared after long-term PUVA therapy. Two other patients have also been reported, although in a third patient lesions of DSAP were apparently cleared with PUVA therapy. ,0 Our case may therefore represent the fourth instance of this occurrence. The appearance of lesions of DSAP in a patient receiving PUVA therapy for psoriasis suggests that these lesions may represent another PUVA-induced side effect in skin. The malignant potential of these lesions is currently unknown. Although these lesions are uncommon, the clinician should be alert for their possible development in patients receiving PUVA. REFERENCES
1. ChemoskyME: Porokeratosis:Report of twelvepatients with multiple superficial lesions. South Med J 59:289294, 1966. 2. Chemosky ME: Disseminated superficial actinic porokeratosis. Int J Dermatol 12:152-157, 1973. 3. Sata A, Anton-LamprechtI, SchnyderUW: Ultrastructure of inborn errors of keratinization. VII. Porokeratosis Mibelli and disseminatedsuperficial actinic porokeratosis. Arch DermatolRes 255:271-284, 1976. 4. Mensch F, Hazen PG: Disseminated superficial actinic porokeratosis in a black patient. Cutis 28:51-56, 1981. 5. ChemoskyME, AndersonDE: Disseminatedsuperficial actinic porokeratosis. Clinical studies and experimental productionof lesions. Arch Dermatol99:401-407, 1969. 6. Abel EA, Cox AJ, Farber EM: Epidermaldystrophyand actinic keratosesin psoriasis patients followingoral psoralen phototherapy (PUVA). J AM ACAD DERMATOL 7:333-340, 1982. 7. Stem RS, Thibodeau LA, KleinermanRA, et al: Risk of cutaneous carcinoma treated with oral methoxsalen photochemotherapyfor psoriasis. N Engl J Med 300:809813, 1979. 8. SinaB, AdrianRM: Multiplekeratoacanthomaspossibly induced by psoralens and ultraviolet A photochemotherapy, J AM ACADDERMATOL9:686-688, 1983. 9. Reymond JL, Bean JC, Amblard P: Superficial actinic porokeratosis in a patient undergoing long-term PUVA therapy. Acta Derm Venereol (Stockh) 60:539-540, 1980. 10. Farber EM, Cox AJ, editors: Psoriasis (Third International Psoriasis Symposium).New York, 1982, Grune& Stratton Inc., p. 451.
Reactions to heparin injections
9. Shelley WB, Sayen JJ': Heparin necrosis: An anticoagulant-induced cutaneous infarct. J AM ACADDmRt~ATOL 7:674~677, 1982. 10. Levine LE, Bernstein JE, Soltani K, et al: Hepadninduced cutaneous necrosis unrelated to injection sites.
A sign of potentially lethal complications. Arch Dermatol 119:400-403, 1983. 11. Kelly RA, Gelfand JA, Pincus SH: Cutaneous necrosis caused by systemically administered heparin. JAMA 2,46:1582-1583, 1981.
Disseminated superficial actinic porokeratosis: Appearance associated with photochemotherapy for psoriasis Paul G. Hazen, M,D., James F. Carney, M.D., Allen E. Walker, M . D . , John J. Stewart, M.D., and Conley W. Engstrom, M.D. Cleveland, OH A patient with chronic psoriasis treated with psoralens plus ultraviolet A (PUVA) developed characteristic lesions of disseminated superficial actinic porokeratosis (DSAP). Since other processes associated with ultraviolet irradiation, including epidermal dysplasia, actinic keratoses, squamous cell carcinomas, and keratoacanthomas, have been reported to result from PUVA, it is possible that her DSAP lesions were induced by this therapy. (J AM ACAD DERMATOL 12:1077-1078, 1985.)
CASE REPORT A 30-year-old woman (skin type III) was referred for treatment of psoriasis. Psoriasis had been diagnosed at 11 years of age, and she had been treated with topical steroids, tars, and ultraviolet (UV) light. Because of extensive psoriasis, therapy using psoralens plus ultraviolet A (PUVA) was carried out three times weekly for 18 months from 1976 to 1977. The total amount of UV energy administered was unknown. Her skin responded well to the treatment, and from November, 1977, to October, 1978, no therapy was administered. In October, 1978, her psoriasis recurred. Extensive plaques of psoriasis were noted over the extremities, with fewer lesions on the trunk; an outpatient program of topical steroids, tars, and weekly suberythemogenic doses of UV light (UVB) was instituted. Because of failure to control her psoriasis, weekly PUVA therapy was begun in January, 1983. In February, after six treatments and 19.5 joules/cm ~ of UVA energy, approxiFrom the Departmentof Dermatology,UniversityHospitalsof Cleveland, ClevelandMetropolitan General Hospital. Reprint requests to: Dr. Paul G. Hazen, 14701 Detroit Ave., Lakewood, OH 44107.
mately 20 hyperpigmented macules appeared on the legs (Fig. 1). These were distinct from the lesions of psoriasis. Three weeks later all of the hyperpigmented lesions developed an elevated border consistent with a comoid lamella. A biopsy specimen confirmed the clinical impression of disseminated superficial actinic porokeratosis (DSAP). At that time, persistent plaques of psoriasis were confined only to the elbows and knees. Therapy with PUVA was discontinued. During the next 2 months new lesions continued to appear and older lesions slowly enlarged. At that point new lesions ceased to appear and previous lesions became less prominent. Her psoriasis is currently being managed with topical steroids only. There is no family history of similar lesions or psoriasis. DISCUSSION D S A P is an uncommon process in which lesions appear, usually in sun-exposed areas of skin.l Typical lesions often begin as 0.1 to 0.2 cm keratotic papules that may enlarge slowly to form plaques 1077
Journal of the
1078
American Academyof Dermatology
Hazen et al
Fig. 1. Lower leg of patient shows multiple 6- to 8-mm lesions of DSAP. containing an elevated, keratotic border. 2 The diagnosis of porokeratosis is confirmed by the histologic finding of a parakeratotic column, the cornoid lamella. Epidermal changes, including dyskeratotic cells, vacuolated cells, and liquefaction degeneration of the basal cell layer, may be present. 3 The association of these lesions with artificial or natural UV light exposure has been emphasized previously. Although DSAP has been reported to occur in dark-skinned individuals, 4 it is usually seen in sun-exposed areas of fair-skinned individuals. Summer months are the usual time of onset of new lesions. Artificial UV radiation has also been reported to induce lesions in a previously susceptible subject) A number of cutaneous sequelae have been reported from PUVA therapy. Actinic keratoses and epidermal dystrophy and the appearance of skin neoplasms, including squamous cell carcinomas and multiple keratoacanthomas, have been reported. 6-s The cause of DSAP in our patient is uncertain. Although lesions began to appear while she was receiving PUVA, she had received multiple other therapies including UVB, tars, and topical steroids. Furthermore, the greatest concentration of lesions was in places generally accessible to sun exposure--the arms and legs, However, it is sig-
nificant that both sunlight and standard artificial UVB sources contain substantial quantities of UVA. Other investigators have also noted patients in whom lesions of DSAP have appeared in association with PUVA therapy. 9,t° Reymond et al 9 reported a single patient in whom typical lesions of DSAP appeared after long-term PUVA therapy. Two other patients have also been reported, although in a third patient lesions of DSAP were apparently cleared with PUVA therapy. ,0 Our case may therefore represent the fourth instance of this occurrence. The appearance of lesions of DSAP in a patient receiving PUVA therapy for psoriasis suggests that these lesions may represent another PUVA-induced side effect in skin. The malignant potential of these lesions is currently unknown. Although these lesions are uncommon, the clinician should be alert for their possible development in patients receiving PUVA. REFERENCES
1. ChemoskyME: Porokeratosis:Report of twelvepatients with multiple superficial lesions. South Med J 59:289294, 1966. 2. Chemosky ME: Disseminated superficial actinic porokeratosis. Int J Dermatol 12:152-157, 1973. 3. Sata A, Anton-LamprechtI, SchnyderUW: Ultrastructure of inborn errors of keratinization. VII. Porokeratosis Mibelli and disseminatedsuperficial actinic porokeratosis. Arch DermatolRes 255:271-284, 1976. 4. Mensch F, Hazen PG: Disseminated superficial actinic porokeratosis in a black patient. Cutis 28:51-56, 1981. 5. ChemoskyME, AndersonDE: Disseminatedsuperficial actinic porokeratosis. Clinical studies and experimental productionof lesions. Arch Dermatol99:401-407, 1969. 6. Abel EA, Cox AJ, Farber EM: Epidermaldystrophyand actinic keratosesin psoriasis patients followingoral psoralen phototherapy (PUVA). J AM ACAD DERMATOL 7:333-340, 1982. 7. Stem RS, Thibodeau LA, KleinermanRA, et al: Risk of cutaneous carcinoma treated with oral methoxsalen photochemotherapyfor psoriasis. N Engl J Med 300:809813, 1979. 8. SinaB, AdrianRM: Multiplekeratoacanthomaspossibly induced by psoralens and ultraviolet A photochemotherapy, J AM ACADDERMATOL9:686-688, 1983. 9. Reymond JL, Bean JC, Amblard P: Superficial actinic porokeratosis in a patient undergoing long-term PUVA therapy. Acta Derm Venereol (Stockh) 60:539-540, 1980. 10. Farber EM, Cox AJ, editors: Psoriasis (Third International Psoriasis Symposium).New York, 1982, Grune& Stratton Inc., p. 451.