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Abnormal epidermal changes after argon laser treatment
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Abnormal epidermal changes after argon laser treatment Reinhard A. Neumann, MD, a Robert M. Knobler, MD, a Elisabeth Aberer, M D , a Wolfgang Klein, Dr.rer.nat., b Franz Kocsis,u and Elisabeth Ott b Seibersdorf and
Vienna, Austria A 26-year-old woman with a congenital port-wine stain on the forehead was treated three times at 2-month intervals with an argon laser. Six months after the last treatment, moderate blanching and mild scaling confined to the treated area was observed. A biopsy specimen of the treated area revealed a significant decrease in ectatie vessels. However, epidermal changes similar to those of actinic keratosis with disorganized cell layers and marked cytologic abnormalities were seen. Analysis of peripheral blood lymphocytes for a defect in DNA repair was negative. Multiple, argon laser-induced photothermal effects may be responsible for the changes observed in our case and may lead to premalignant epidermal transformation. (J AM ACAD DERMA'rOL 1991;24:369-75.) The principle of argon laser treatment is the selective absorption of light in the hemoglobin of intravasal erythrocytes and conversion into thermal energy. This process results in thrombosis and subsequent obliteration of vessels. A concomitant effect is heat transfer to surrounding tissues and a limited epidermal second-degree burn. Because the action spectrum of most lasers lies outside the range of known photocarcinogenesis, lasers have been considered to be relatively safe instruments with regard to possible oncogenic side effects. 1"3 Repeated exposure to heat may cause erythema ab igne (EAI) with histologic features similar to perilesional 4, 5 and lesional skin 4, 6 in actinic keratoses. The evolution of squamous cell carcinoma has been described in EAI. 7"9 Furthermore, ample evidence exists that burn scars have the potential to develop similar malignant lesions.l~ 1~ Heat has been suggested to play a significant role in cutaneous carcinogenesis in many studies./2-15 W e describe a patient in whom abnormal epidermal changes developed after argon laser treatment of a port-wine stain.
CASE REPORT A 26-year-old woman had an untreated nevus flammeus on the left eyebrow, eyelid, and left side of the fore-
head (Fig. 1, A). The surface was smooth. The lesion had been concealed by skin-colored makeup and protected with sunscreens for the last 8 years. Before laser treatment a 4 mm punch biopsy specimen was taken. The first treatment with the argon laser was followed by two further sessions at 2-month intervals. Six months after the last treatment, the port-wine stain showed only moderate blanching with sigm of mild scaling confined to the treated area. The adjacent untreated area showed no changes. At this time two additional 4 mm punch biopsy specimens were obtained, one from a representative blanched area and one from adjacent lesional but untreated skin. Treatment was continued. The patient was seen 2 months later and had moderate blanching of the entire lesion (Fig. 1, B).
Treatment For therapy a Coherent 920 S argon laser (Coherent Inc., Palo Alto, Calif.) was used. The pulse duration was 0.2 seconds, the diameter of the laser beam varied from 1.5 to 2.0 mm, and the energy output ranged from 2.5 to 3.0 W, corresponding to an h-radiance of 79 to 142 W / cm2 and an energy fluence of 15 to 28 joules/cm 2. The laser spots were placed carefully at 0.5 to 1 mm distances to avoid overlapping. Posttreatment healing was normal, with complete re, pithelialization. No scar formation was observed. During the treatment period the patient used sunscreens and continued to avoid sun exposure.
Histologic findings From the Department of Dermatology II, University of Vienna,j and the Institute of Biology, Austrian Research Centre, Seibersdorf.b Reprint requests: Reinhard A. Neumann, MD, Department of Dermatology II, University of Vienna, Alserstrasse 4, 1090 Vienna, Austria.
16/4/19010
The two biopsy specimens from the untreated portwine stain taken before treafment and 10 months later revealed multiple ectatic vessels in the papillary dermis and to a lesser degree in deeper layers (Fig. 2). The epidermis in both specimens appeared normal (Fig. 3). 369
3"70 Neumann et aL
Journal of the American Academy of Dcrmatology
Fig. 1. Nevus flarnrneus on left side of forehead before argon laser treatment (A) and moderate blanching of treated area (B).
Fig. 2. Multiple ectatie vessels in dermis of port-wine stain before laser therapy. (Hematoxylin-eosin stain; •
A specimen of treated skin showed a significant decrease in the number of ectatic vessels. Capillary proliferations with small lumina were observed (Fig. 4). The epidermis was acanthotic with disarrangement of keratinoeytes (Fig. 4). At higher magnification this perturbation of keratinocyte maturation was striking (Fig. 5). In most sections, in addition to disarray of keratinocytes, an
irregularity of cell size and shape was present (Figs. 5 and 6). Heterochromaticity of nuclei could be found throughout the epidermis (Figs. 5 and 6). In some sections focal parakeratosis was present (Fig. 7). Frequently, multinucleate cells with up to five nuclei were detected (Figs. 7 and 8). Occasionally, large, bizarre, bowenoid-like nuclei were present (Fig. 8).
Volume 24 Number 2, Part 2 February 1991
Epidermal changes after argon laser treatment 371
Fig. 3. Normal epidermis covering port-wine stain before laser treatment. (Hematoxylineosin stain; •
Fig. 4. Significant decrease of ectatic vessels after argon laser treatment. Proliferating capillary vessels with small lumina are distributed throughout dermis. Epidermis is acanthotic with disarrangement of cells. (Hematoxylin-eosin stain; •
DNA repair analysis To exclude other cofactors that may predispose to premalignant changes, we also evaluate the DNA repair mechanisms of the patient's peripheral blood lymphocytes. Lymphocytes were separated from blood by a Ficoll/Urograffin gradient technique (Schering Inc., Berlin, West Germany).
Unscheduled DNA synthesis was measured after incorporation of 3H-thymidine (New England Nuclear Research Products, Dreieich, West Germany; specific activity 2.96 TBq/mmol) into the DNA of the cells by autoradiography. 100 cells per slide were examined in the light microscope (• and silver grains per nucleus were counted. Replicative DNA synthesis was also esti-
3'72
Journal of the American Academy of Dermatology
Neumann et aL
Fig. 5. Perturbation of keratinocytic maturation. Noteheterochromaticityofkeratinocytic nuclei. (Hematoxylin-eosin stain; x400.) Table I. Results of D N A repair analysis Control l
Unscheduled DNA synthesis (mean No. of silver grains/nucleus) Replicative DNA synthesis (cpm/t~g DNA) DNA repair synthesis (cpm/#g DNA) Supercoiled DNA (values as ratio to front) cpm,
0.32
Patient
0.44
140
145
190
182
0.76
0.74
Counts per minute,
mated by incorporation of the labeled precursor thymidine into DNA and by liquid scintillation counting. To measure repair synthesis, the lymphocytes were irradiated by ultraviolet light at 254 nm and at an incident dose rate of 20 joules/m 2, Investigations on sedimentation of supercoiled DNA were done according to the modified procedure of Cook and Brazell? 6 Lymphocyte suspension was lysed on the top of a continuous sucrose gradient. Gradients were spun in an ultracentrifuge for 60 minutes at 20 ~ C at 30,000 rpm. Sedimentation distance of DNA as measured from the top of the gradients was related to the whole length of the gradient. RESULTS (Table I) The data are mean values of estimations performed in triplicate for the control and the patient.
Results of the control are in the range of historical data. No distinct deviations in the results of the patient from the control were found. A few of the patient's blood lymphocytes showed enhanced silver grain counts per nucleus (5 cells from 100 cells counted; control, 1 from 100); on the basis of historical data, these cells should not be classified as "induced" cells. DISCUSSION The high photon density of laser light effectively destroys tissues by heat. Within the epidermis the basal cell layer displays the greatest thermal changes. 17 Abnormal epidermal changes after argon laser treatment as seen in our case have not been previously described. Few reports cover sufficiently long periods of observation after laser therapy; Finley et al. 17 and Landthaler et al. TMnoted a normal epidermis 489 and 4 months after laser application, respectively. Solomon et al. 19 and Buecker et al. 2~ studied biopsy specimens 18 months to 3 years after laser impact and also found no pathologic epidermal changes. Apfelberg et al. 3 used a heteroploid mouse fibroblast cell line of the BALB/3T3 strain for in vitro assay to quantify a possible carcinogenic effect of argon and carbon dioxide laser exposure. Their study provided no evidence for laser-induced oncogenesis.
Volume 24 Number 2, Part 2 February 1991
Epidermal changes after argon laser treatment 373
~j .tP.
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Fig. 6, A, Striking disarrangement of keratinocytes and nuclear atypia. B, Photomicrograph of same section at higher magnification showing hyperchromaticity of several keratinocytes (arrows). (Hematoxylin-eosin stain; A, X400; B, xl000.) EAI, a reticular erythema induced by repeated heat exposure, sometimes histologically reveals epidermal changes similar to those seen in actinic keratosis, 4,6,21 referred to as "thermal keratosis. ''7 Development of squamous cell carcinoma from EAI 79 and direct heat-induced malignant transfor-
mation (e.g., kang cancer in northern China or kangfi cancer in India 22) have been described. However, in many cases of EAI, only changes similar to those observed in perilesional skin of actinic keratosis can be found, 5' 6 with loss of the rete pattern, marked cytologic abnormalities with irreg-
374
Neumann et al.
Journal of the American Academy of Dermatology
Fig. 7. Focal parakeratosis and multinucleate cells ~arrowheads) after laser treatment. (Hematoxylin-eosin stain; X400.)
Fig. 8. Irregularity of nuclei and bowenoid degeneration of cells (short arrow). Note several multinucleate cells (arrows). (Hematoxylin-eosin stain; x600.) ularity of cell size and shape, and formation of multinucleate cells. These different histologic findhags in the same condition may be interpreted as a gradual stepwise progression to premalignant degeneration. Although clear-cut anaplastic keratinocytic nuclear atypia is not present, the observed clinical and histologic changes found ha our patient are common features observed in perilesional and lesional skin of actinic keratosis. 4"6 Our findings may also provide evidence for a perturbation of the synchronous pattern of keratinocyte differentiation. These findings have also been re-
ported in skin biopsy specimens of acute graftversus-host disease, immunodeficiency states, and allograft transplant recipients. After laser treatment the microenvironment may be altered by the significant decrease in blood supply. This may in turn induce transient metabolic changes in the epidermal cell cycle that lead to the pathologic changes. However, the observation period of 6 months seems too long to interpret these changes as truly physiologic. Although the port-wine stain in our patient was located on a sun-exposed site, the patient had used makeup and sunscreens, thus rendering unlikely sunlight as a contributing factor for the observed
Volume 24 Number 2, Part 2 February 1991
Epidermal changes after argon laser treatment 375
changes. T h e evaluation of D N A repair mechanisms in the patient's peripheral blood lymphocytes presented no evidence for any predisposing oncogenic factors. N o r m a l l y histopathologic changes after argon laser impact in port-wine stains show beginning reepithelialization within 48 to 72 hours. 18 However, laser treatment also produces repetitive minimal burn scars that have, although rarely, a potential for malignant degeneration 1~ 11 with a known lag time of 20 to 30 years. To our knowledge this is the first report of abnormal epidermal changes after argon laser treatment. One explanation for these unexpected short-term changes might be the time-dose relationship, which suggests that repeated impacts of high energies in short intervals m a y dramatically accelerate premalignant transformation or prevent effective D N A repair.
7. Arrington JH, Loekman DS. Thermal keratosis and squamous cell carcinoma in situ associated with erythema ab igne. Arch Dermatol 1979;115:1226-8. 8. Peterkin GAG. Malignant change in erythema ab igne. Br Med J 1955;2:1599-602. 9. Cross F. On a turf (peat) fire cancer: malignant change superimposed on erythema ab igne. Proc R Soc Med 1967; 60:1307-8. 10. Lawrernce EA. Carcinoma arising in the scars of thermal burns. Surg Gynecol Obstet 1952;95:579-88. 11. Florey HW, ed. General pathology. 4th ed. Philadelphia: WB Saunders, 1970. 12. Freeman RG, Knox JM. Influence of temperature on ultraviolet injury. Arch Dermatol 1964;89:858-64. 13. Corry PM, Robinson S, Getz S. Hyperthermic effects on DNA repair mechanisms. Radiology 1977;123:475-9. 14. Roth D, London M. Acridine probe study into synergistic DNA-denaturing action of heat and ultraviolet light in squamous cells. J Invest Dermatol 1977;69:368-72. 15. Schwartz RA. Infrared radiation as a carcinogenic agent. Br J Dermatol 1978;99:460-1. 16. Cook PR, Brazell IA. Supercoils in human DNA. J Cell Sci 1975; 19:261-79. 17. Finley JL, Barsky SH, Geer DE, et al. Healing of port-wine stains after argon laser therapy. Arch Dermatol 1981;
REFERENCES
18. Landthaler M, Dorn M, Haina D, et al. Morphologisehe Untersuchungen zur Behandlung yon Naevi flammei mit dem Argonlaser. Hautarzt 1983;34:548-54. 19. Solomon H, Goldman L, Henderson B, et al. Histopathology of the laser treatment of port-wine lesions. J Invest Dermatol 1968;50:141-6. 20. Bueeker JW, Ratz JL, Richfield DF. Histology of portwine stain treated with carbon dioxide laser. J AM AC^D DERMATOL 1984;10:1014-9. 21. Kligman A M. Early destructive effect ofsunlight on human skin. JAMA 1969;210:2377-80. 22. Kligman LH, Kligman AM. Reflections on heat. Br J Dermatol 1984;110:369-75.
1. Arndt KA, Noe JM. Lasers in dermatology. Arch Dermatol 1982;118:293-5. 2. Landthaler M, Haina D, Waidelich W, et al. A three-year experience with the argon laser in dermatotherapy. J Dermatol Surg Oncol 1984;10:455-61. 3. Apfelberg DB, Mittelman H, Chadi B, et al. Investigation of carcinogenic effects of in vitro argon and CO2 laser exposure of fibroblasts. Laser Surg Meal 1984;4:173-9. 4. Finlayson GR, Sams WM, Smith JG. Erythema ab igne: a histopathological study. J Invest Dermatol 1966;46: 104-7. 5. Pearse AD, Marks R. Actinic keratoses and the epidermis on which they arise. Br J Dermatol 1977;96:45-50. 6. Sharad P, Marks R. The wages of warmth: changes in erythema ab igne. Br J Dermatol 1977;97:179-86.
117:486-9.
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Abnormal epidermal changes after argon laser treatment Reinhard A. Neumann, MD, a Robert M. Knobler, MD, a Elisabeth Aberer, M D , a Wolfgang Klein, Dr.rer.nat., b Franz Kocsis,u and Elisabeth Ott b Seibersdorf and
Vienna, Austria A 26-year-old woman with a congenital port-wine stain on the forehead was treated three times at 2-month intervals with an argon laser. Six months after the last treatment, moderate blanching and mild scaling confined to the treated area was observed. A biopsy specimen of the treated area revealed a significant decrease in ectatie vessels. However, epidermal changes similar to those of actinic keratosis with disorganized cell layers and marked cytologic abnormalities were seen. Analysis of peripheral blood lymphocytes for a defect in DNA repair was negative. Multiple, argon laser-induced photothermal effects may be responsible for the changes observed in our case and may lead to premalignant epidermal transformation. (J AM ACAD DERMA'rOL 1991;24:369-75.) The principle of argon laser treatment is the selective absorption of light in the hemoglobin of intravasal erythrocytes and conversion into thermal energy. This process results in thrombosis and subsequent obliteration of vessels. A concomitant effect is heat transfer to surrounding tissues and a limited epidermal second-degree burn. Because the action spectrum of most lasers lies outside the range of known photocarcinogenesis, lasers have been considered to be relatively safe instruments with regard to possible oncogenic side effects. 1"3 Repeated exposure to heat may cause erythema ab igne (EAI) with histologic features similar to perilesional 4, 5 and lesional skin 4, 6 in actinic keratoses. The evolution of squamous cell carcinoma has been described in EAI. 7"9 Furthermore, ample evidence exists that burn scars have the potential to develop similar malignant lesions.l~ 1~ Heat has been suggested to play a significant role in cutaneous carcinogenesis in many studies./2-15 W e describe a patient in whom abnormal epidermal changes developed after argon laser treatment of a port-wine stain.
CASE REPORT A 26-year-old woman had an untreated nevus flammeus on the left eyebrow, eyelid, and left side of the fore-
head (Fig. 1, A). The surface was smooth. The lesion had been concealed by skin-colored makeup and protected with sunscreens for the last 8 years. Before laser treatment a 4 mm punch biopsy specimen was taken. The first treatment with the argon laser was followed by two further sessions at 2-month intervals. Six months after the last treatment, the port-wine stain showed only moderate blanching with sigm of mild scaling confined to the treated area. The adjacent untreated area showed no changes. At this time two additional 4 mm punch biopsy specimens were obtained, one from a representative blanched area and one from adjacent lesional but untreated skin. Treatment was continued. The patient was seen 2 months later and had moderate blanching of the entire lesion (Fig. 1, B).
Treatment For therapy a Coherent 920 S argon laser (Coherent Inc., Palo Alto, Calif.) was used. The pulse duration was 0.2 seconds, the diameter of the laser beam varied from 1.5 to 2.0 mm, and the energy output ranged from 2.5 to 3.0 W, corresponding to an h-radiance of 79 to 142 W / cm2 and an energy fluence of 15 to 28 joules/cm 2. The laser spots were placed carefully at 0.5 to 1 mm distances to avoid overlapping. Posttreatment healing was normal, with complete re, pithelialization. No scar formation was observed. During the treatment period the patient used sunscreens and continued to avoid sun exposure.
Histologic findings From the Department of Dermatology II, University of Vienna,j and the Institute of Biology, Austrian Research Centre, Seibersdorf.b Reprint requests: Reinhard A. Neumann, MD, Department of Dermatology II, University of Vienna, Alserstrasse 4, 1090 Vienna, Austria.
16/4/19010
The two biopsy specimens from the untreated portwine stain taken before treafment and 10 months later revealed multiple ectatic vessels in the papillary dermis and to a lesser degree in deeper layers (Fig. 2). The epidermis in both specimens appeared normal (Fig. 3). 369
3"70 Neumann et aL
Journal of the American Academy of Dcrmatology
Fig. 1. Nevus flarnrneus on left side of forehead before argon laser treatment (A) and moderate blanching of treated area (B).
Fig. 2. Multiple ectatie vessels in dermis of port-wine stain before laser therapy. (Hematoxylin-eosin stain; •
A specimen of treated skin showed a significant decrease in the number of ectatic vessels. Capillary proliferations with small lumina were observed (Fig. 4). The epidermis was acanthotic with disarrangement of keratinoeytes (Fig. 4). At higher magnification this perturbation of keratinocyte maturation was striking (Fig. 5). In most sections, in addition to disarray of keratinocytes, an
irregularity of cell size and shape was present (Figs. 5 and 6). Heterochromaticity of nuclei could be found throughout the epidermis (Figs. 5 and 6). In some sections focal parakeratosis was present (Fig. 7). Frequently, multinucleate cells with up to five nuclei were detected (Figs. 7 and 8). Occasionally, large, bizarre, bowenoid-like nuclei were present (Fig. 8).
Volume 24 Number 2, Part 2 February 1991
Epidermal changes after argon laser treatment 371
Fig. 3. Normal epidermis covering port-wine stain before laser treatment. (Hematoxylineosin stain; •
Fig. 4. Significant decrease of ectatic vessels after argon laser treatment. Proliferating capillary vessels with small lumina are distributed throughout dermis. Epidermis is acanthotic with disarrangement of cells. (Hematoxylin-eosin stain; •
DNA repair analysis To exclude other cofactors that may predispose to premalignant changes, we also evaluate the DNA repair mechanisms of the patient's peripheral blood lymphocytes. Lymphocytes were separated from blood by a Ficoll/Urograffin gradient technique (Schering Inc., Berlin, West Germany).
Unscheduled DNA synthesis was measured after incorporation of 3H-thymidine (New England Nuclear Research Products, Dreieich, West Germany; specific activity 2.96 TBq/mmol) into the DNA of the cells by autoradiography. 100 cells per slide were examined in the light microscope (• and silver grains per nucleus were counted. Replicative DNA synthesis was also esti-
3'72
Journal of the American Academy of Dermatology
Neumann et aL
Fig. 5. Perturbation of keratinocytic maturation. Noteheterochromaticityofkeratinocytic nuclei. (Hematoxylin-eosin stain; x400.) Table I. Results of D N A repair analysis Control l
Unscheduled DNA synthesis (mean No. of silver grains/nucleus) Replicative DNA synthesis (cpm/t~g DNA) DNA repair synthesis (cpm/#g DNA) Supercoiled DNA (values as ratio to front) cpm,
0.32
Patient
0.44
140
145
190
182
0.76
0.74
Counts per minute,
mated by incorporation of the labeled precursor thymidine into DNA and by liquid scintillation counting. To measure repair synthesis, the lymphocytes were irradiated by ultraviolet light at 254 nm and at an incident dose rate of 20 joules/m 2, Investigations on sedimentation of supercoiled DNA were done according to the modified procedure of Cook and Brazell? 6 Lymphocyte suspension was lysed on the top of a continuous sucrose gradient. Gradients were spun in an ultracentrifuge for 60 minutes at 20 ~ C at 30,000 rpm. Sedimentation distance of DNA as measured from the top of the gradients was related to the whole length of the gradient. RESULTS (Table I) The data are mean values of estimations performed in triplicate for the control and the patient.
Results of the control are in the range of historical data. No distinct deviations in the results of the patient from the control were found. A few of the patient's blood lymphocytes showed enhanced silver grain counts per nucleus (5 cells from 100 cells counted; control, 1 from 100); on the basis of historical data, these cells should not be classified as "induced" cells. DISCUSSION The high photon density of laser light effectively destroys tissues by heat. Within the epidermis the basal cell layer displays the greatest thermal changes. 17 Abnormal epidermal changes after argon laser treatment as seen in our case have not been previously described. Few reports cover sufficiently long periods of observation after laser therapy; Finley et al. 17 and Landthaler et al. TMnoted a normal epidermis 489 and 4 months after laser application, respectively. Solomon et al. 19 and Buecker et al. 2~ studied biopsy specimens 18 months to 3 years after laser impact and also found no pathologic epidermal changes. Apfelberg et al. 3 used a heteroploid mouse fibroblast cell line of the BALB/3T3 strain for in vitro assay to quantify a possible carcinogenic effect of argon and carbon dioxide laser exposure. Their study provided no evidence for laser-induced oncogenesis.
Volume 24 Number 2, Part 2 February 1991
Epidermal changes after argon laser treatment 373
~j .tP.
a
j
,J
Fig. 6, A, Striking disarrangement of keratinocytes and nuclear atypia. B, Photomicrograph of same section at higher magnification showing hyperchromaticity of several keratinocytes (arrows). (Hematoxylin-eosin stain; A, X400; B, xl000.) EAI, a reticular erythema induced by repeated heat exposure, sometimes histologically reveals epidermal changes similar to those seen in actinic keratosis, 4,6,21 referred to as "thermal keratosis. ''7 Development of squamous cell carcinoma from EAI 79 and direct heat-induced malignant transfor-
mation (e.g., kang cancer in northern China or kangfi cancer in India 22) have been described. However, in many cases of EAI, only changes similar to those observed in perilesional skin of actinic keratosis can be found, 5' 6 with loss of the rete pattern, marked cytologic abnormalities with irreg-
374
Neumann et al.
Journal of the American Academy of Dermatology
Fig. 7. Focal parakeratosis and multinucleate cells ~arrowheads) after laser treatment. (Hematoxylin-eosin stain; X400.)
Fig. 8. Irregularity of nuclei and bowenoid degeneration of cells (short arrow). Note several multinucleate cells (arrows). (Hematoxylin-eosin stain; x600.) ularity of cell size and shape, and formation of multinucleate cells. These different histologic findhags in the same condition may be interpreted as a gradual stepwise progression to premalignant degeneration. Although clear-cut anaplastic keratinocytic nuclear atypia is not present, the observed clinical and histologic changes found ha our patient are common features observed in perilesional and lesional skin of actinic keratosis. 4"6 Our findings may also provide evidence for a perturbation of the synchronous pattern of keratinocyte differentiation. These findings have also been re-
ported in skin biopsy specimens of acute graftversus-host disease, immunodeficiency states, and allograft transplant recipients. After laser treatment the microenvironment may be altered by the significant decrease in blood supply. This may in turn induce transient metabolic changes in the epidermal cell cycle that lead to the pathologic changes. However, the observation period of 6 months seems too long to interpret these changes as truly physiologic. Although the port-wine stain in our patient was located on a sun-exposed site, the patient had used makeup and sunscreens, thus rendering unlikely sunlight as a contributing factor for the observed
Volume 24 Number 2, Part 2 February 1991
Epidermal changes after argon laser treatment 375
changes. T h e evaluation of D N A repair mechanisms in the patient's peripheral blood lymphocytes presented no evidence for any predisposing oncogenic factors. N o r m a l l y histopathologic changes after argon laser impact in port-wine stains show beginning reepithelialization within 48 to 72 hours. 18 However, laser treatment also produces repetitive minimal burn scars that have, although rarely, a potential for malignant degeneration 1~ 11 with a known lag time of 20 to 30 years. To our knowledge this is the first report of abnormal epidermal changes after argon laser treatment. One explanation for these unexpected short-term changes might be the time-dose relationship, which suggests that repeated impacts of high energies in short intervals m a y dramatically accelerate premalignant transformation or prevent effective D N A repair.
7. Arrington JH, Loekman DS. Thermal keratosis and squamous cell carcinoma in situ associated with erythema ab igne. Arch Dermatol 1979;115:1226-8. 8. Peterkin GAG. Malignant change in erythema ab igne. Br Med J 1955;2:1599-602. 9. Cross F. On a turf (peat) fire cancer: malignant change superimposed on erythema ab igne. Proc R Soc Med 1967; 60:1307-8. 10. Lawrernce EA. Carcinoma arising in the scars of thermal burns. Surg Gynecol Obstet 1952;95:579-88. 11. Florey HW, ed. General pathology. 4th ed. Philadelphia: WB Saunders, 1970. 12. Freeman RG, Knox JM. Influence of temperature on ultraviolet injury. Arch Dermatol 1964;89:858-64. 13. Corry PM, Robinson S, Getz S. Hyperthermic effects on DNA repair mechanisms. Radiology 1977;123:475-9. 14. Roth D, London M. Acridine probe study into synergistic DNA-denaturing action of heat and ultraviolet light in squamous cells. J Invest Dermatol 1977;69:368-72. 15. Schwartz RA. Infrared radiation as a carcinogenic agent. Br J Dermatol 1978;99:460-1. 16. Cook PR, Brazell IA. Supercoils in human DNA. J Cell Sci 1975; 19:261-79. 17. Finley JL, Barsky SH, Geer DE, et al. Healing of port-wine stains after argon laser therapy. Arch Dermatol 1981;
REFERENCES
18. Landthaler M, Dorn M, Haina D, et al. Morphologisehe Untersuchungen zur Behandlung yon Naevi flammei mit dem Argonlaser. Hautarzt 1983;34:548-54. 19. Solomon H, Goldman L, Henderson B, et al. Histopathology of the laser treatment of port-wine lesions. J Invest Dermatol 1968;50:141-6. 20. Bueeker JW, Ratz JL, Richfield DF. Histology of portwine stain treated with carbon dioxide laser. J AM AC^D DERMATOL 1984;10:1014-9. 21. Kligman A M. Early destructive effect ofsunlight on human skin. JAMA 1969;210:2377-80. 22. Kligman LH, Kligman AM. Reflections on heat. Br J Dermatol 1984;110:369-75.
1. Arndt KA, Noe JM. Lasers in dermatology. Arch Dermatol 1982;118:293-5. 2. Landthaler M, Haina D, Waidelich W, et al. A three-year experience with the argon laser in dermatotherapy. J Dermatol Surg Oncol 1984;10:455-61. 3. Apfelberg DB, Mittelman H, Chadi B, et al. Investigation of carcinogenic effects of in vitro argon and CO2 laser exposure of fibroblasts. Laser Surg Meal 1984;4:173-9. 4. Finlayson GR, Sams WM, Smith JG. Erythema ab igne: a histopathological study. J Invest Dermatol 1966;46: 104-7. 5. Pearse AD, Marks R. Actinic keratoses and the epidermis on which they arise. Br J Dermatol 1977;96:45-50. 6. Sharad P, Marks R. The wages of warmth: changes in erythema ab igne. Br J Dermatol 1977;97:179-86.
117:486-9.