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Elastolysis of the earlobes
Volume 14 Number 1 January, 1986
Treatment of pilar cyst with solcoderrn solution To the Editor: The treatment of a pilar cyst with a solution of Solcodenn is described. Solcodenn solution has been used in Israel for some years for the treatment of skin lesions. The method and follow-up of this treatment are well established. A trial treatment of a pilar cyst with Solcoderm was undertaken successfully. Case report. A healthy 40-year-old woman came to our dennatologic clinic because of a scalp lesion of several years' duration that had recently started to grow. On examination the lesion was about 5 Cm in diameter, 3 cm in depth, and yellow in color. Histologic examination from a punch biopsy showed the lesion to have a wall composed of epithelial cells. The peripheral layer of cells had a palisade arrangement, and the cyst contained a homogeneous eosinophilic material. The patient refused an operation because she was afraid of the surgical procedure but was willing to try conservative treatment. Treatment twice monthly with an application of the Solcodenn*" material (0.05 mlJtimc) was started. There was a delayed reaction ending with a scab formation, which detached by itself. Fourteen days later the patient underwent a second application of Solcodenn, and these applications were continued in the same way for about 4 months. The lesion disappeared without any scar formation. Discussion. Solcoderm as compared to plain nitric acid has shown its superior effect in mummification of tumors and skin lesions. 2 The treatment has proved to be successful in eradicating the tumor without causing any injury to the surrounding normal tissue and without damaging the hair around the lesion when it is located on the scalp. To our knowledge, Solcoderm has been tried on various skin tumors, among them, seborrheic keratosis, compound nevus, common warts, condyloma acuminatum, basal cell epithelioma, trichoepithelioma, solar keratosis, Dubreuilh melanosis, fibroma, and papilloma. 3-s While only one application is usually needed to treat a lesion such as solar keratosis, in this case several applications were needed because of the depth of the tumor (3 cm). As far as we know this is the first attempt to treat a pilar cyst with Solcoderm. The uneventful follow-up *Solcoderm as currently marketed is a specially prepared and packaged solution of organic acids (lactic, oxalic, acetic) and copper ions in moderately strong (6 to 7 normal) nitric acid. The exact composition is: copper ions, 15 ppm; oxalic acid, 40 mg/ml; lactic acid, 3 mg/ml; nitrate, 410 mg/ml; acetic acid, 40 mg/ml.
Correspondence
145
and avoidance of surgery make trying again worthwhile.
S. Brenner, M.D., Department of Dermatology Ichilov Municipal-Governmental Center Weizmann St., Tel Aviv 61 239, Israel REFERENCES 1. Weiner M: In vitro models reflecting the action of strong acids on integumental tissue. Dermatologica 168(suppl 1): 7-11, 1984. 2. Weiner M, Semah D, Schewach-Millet M, Cesarini J: Preclinical and clinical evaluation of topical acid products for skin tumors. Clin Pharmacol Ther 33:77-83, 1983. 3. Haim S, Cohen A: Solcoderm treatment of epidennal growth including intradermal nevi. Dermatologica 168 (suppl 1):46-48, 1984. 4. Feuerman EJ, Katzenelson W, Halevy S: Solcoderm in the treatment of solar and seborrheic keratoses. Dennatologica 168(suppl 1):33-35, 1984. 5. Weiner M, Semah D, Schewach-Millet M: Double-blind study of variables influencing the clinical effect of 801coderm. Dennatologlca 168(suppl 1):26-30, 1984.
Elastolysis of the earlobes To the Editor: A mother brought her 15-year-old daughter in to be seen for droopy earlobes. She had noted that her daughter's earlobes were "flapping in the breeze" during a drive in their car with the windows down. The mother is a hairdresser and began to observe earlobes. She thought that her daughter's earlobes were similar to those of clients 80 to 90 years old. We report this unusual presentation of acquired elastic tissue loss (Case 1) and a similar case brought to our attention by review of our photographic files (Case 2). Case 1. A healthy 15-year-old girl presented with wrinkling and drooping of her earlobes. These changes had occurred gradually over 18 months and were not preceded or accompanied by swelling, erythema, infection, or pruritus. Her ears had been pierced many years earlier, but she denied any adverse reactions or wearing large, heavy earrings. She described recurrent urticarial lesions over the preceding 3 to 4 years but denied involvement of the head and neck. Her history was negative for easy bruising, abnormal scarring, or musculoskeletal symptoms, and her family history was negative for similar skin changes_ The skin of the ears was lax and wrinkled (Fig. 1), and the earlobes were elongated. The upper and lower eyelids were mildly atrophic and wrinkled. Striae were present over both breasts. The remainder of her skin was nonnal in appearance except for mild acne vulgaris. There was diffuse
146
Correspondence
Fig. 1. Case 1. Fine wrinkling and drooping of earlobes of 1 V2 years' duration in a IS-year-old girl. Laxity of the upper and lower eyelids also was present but it was less obvious. hypermobility of the joints that was thought to represent the benign hypennobility syndrome. Otherwise, the results of physical examination were unremarkable. The following laboratory studies gave negative or normal results: complete blood cell count, urinalysis, thyroid studies, erythrocyte sedimentation rate, serum protein electrophoresis, sodium, potassium, calcium, phosphorus, chloride, glucose, alkaline phosphatase, aspartate aminotransferase (AST; SOOT), lactate dehydrogenase (LDH), bilirubin (total and direct), creatinine, uric acid, CH~o, antinuclear antibodies, anti-deoxyribonucleic acid (DNA), antitrypsin, and direct immunofluorescence study of a skin biopsy specimen from the earlobe. Histologic study (elastin Giemsa stain) of skin from the earlobe showed a marked decrease in elastic tissue throughout the dermis and a mild perivascular and periappendageal mononuclear cell infiltrate. Case 2. A 29-year-old woman presented in 1955 with relaxed, wrinkled skin of the face and earlobes. These changes had begun in her earlobes 4 years earlier and gradually extended to the upper eyelids and facial skin. She denied preceding erythema, pruritus, or infection. She suffered from seasonal hayfever, and from 1942 through 1952 she had had generalized hives. The records did not include information regarding head and neck involvement with the episodes of
Journal of the American Academy of Dermatology
Fig. 2. Case 2. Lax skin of the ears, face, and neck of 3 to 4 years' duration in a 29-year-old woman. hives she had experienced. Her general health was otherwise good, and her family history was negative for similar skin changes. Her appearance was that of a woman much older than her stated age. The skin of her face, eyelids, and earlobes was wrinkled and lax (Fig. 2), with drooping of the upper lip, elongation of the earlobes, and pendulous skin folds hanging below the mandible. The upper aspect of the neck was involved minimally, but the remainder of her skin appeared to be normal. The remainder of the results of physical examination were negative. The following laboratory studies gave negative or normal results: hemoglobin, leukocyte count, erythrocyte sedimentation rate, urinalysis, and automated reagin test. Histologic evaluation (elastin Giemsa stain) of skin from the upper aspect of the neck revealed total loss of middermal elastic tissue. The elastic tissue within the papillary dermis and the deep dermis and about vascular structures appeared to be normal. There was no ceIIular infiltrate. Discussion. These two cases represent an acquired form of cutaneous elastolysis that presented as droopy and wrinkled earlobes. These patients have in common episodes of urticaria for several years prior to the onset of elastic tissue changes, although in neither were the urticarial lesions present at the sites of subsequent elastic tissue changes.
Volume 14 Number I January, 1986
Cunliffe' stated that blepharochalasis may include involvement of both upper and lower eyelids and, rarely, the earlobes. Personal communication* revealed that the earlobe changes occurred in a single personal case in which follow-up information was not available. Whether Case 1 represents a variety of blepharochalasis or an early stage of acquired cutis laxa will become more clear with time. In Case 2, the skin laxity began in the earlobes and then gradually spread, during 3 to 4 years, to involve the eyelids, facial skin, and neck. The clinical presentation was similar to that in a 20-year-old man with acquired cutis laxa localized to the face, as reported by Reed et aF in 1971. Diseases involving elastic tissue abnormalities present with a wide range of clinical variability. These two cases are examples of elastolysis presenting as wrinkling and drooping of the earlobes.
SusanM. Barker, M.D., and Charles H. Dicken, MD. Department of Dermatology Mayo Clinic and Mayo Foundation Rochester, MN 55905 *Cunliffe WJ, April 30, 1984. REFERENCES 1. Cunliffe WI: Disorders of connective tissue, in Rook AJ,
Wilkinson OS, Ebling FJG, editors: Textbook of dermatology, vol 2, cd. 3. Oxford, England, 1979, Blackwell Scientific Publications, pp. 1611-1653. 2. Reed WB, Horowitz RE, Beighton P: Acquired cutis laxa: Primary generalized elastolysis. Arch Dermatol103:66l669, 1971.
The linear progression of malignant melanoma: A false premise? To the Editor: In a recent editorial (J AM ACAD DERMATOL 12: 115116, 1985) Ackerman stated, "It probably takes many months of proliferation of these melanocytes before the smallest and flattest of malignant melanomas can be visualized by inspection with the naked eye. Itprobably takes years before such a flat lesion of melanoma is broad enough (5 or 6 mm) to be diagnosed as a malignant melanoma with reasonable certainly .... In short, time is on the side both of patients with malignant melanomas and of physicians charged with detecting and removing them." Unfortunately, there is no evidence that melanomas do progress consistently in a linear fashion. In fact, clinical experience points entirely to the contrary. There still appear to be "good melanomas and bad melano-
Correspondence
147
mas. " Melanomas continue to be capricious, wanton, and unpredictable. We all hope that early recognition reduces the spread and mortality, but' there is still no proof that early recognition results in dramatic cures. Malignant melanoma is not alone in its unpredictable behavior. In spite of early recognition, the results from breast carcinoma treatments are nearly as disappointing now as they were 40 years ago. Our statistical cure rates for melanoma do seem to have improved in recent years. Perhaps, and hopefully, some of this may result from earlier detection. However, most of it results from the fact that we are now reading pathologically some lesions as malignant melanoma that appear as such under the microscope but do not behave so biologically. This spectrum of cutaneous pseudomalignancy was recently reviewed by Sina. 1 This would be consistent with the data recently presented by Greene et al. 2 They stated that the National Cancer Institute surveillance epidemiology studies revealed an 80% increase in the incidence of malignant melanoma in the United States between 1973 and 1980. However, during this same time of increased recognition we have been claiming a significantly increased cure rate. Fitzpatrick et aP recently made the same assumption of linear progression of malignant melanoma. We would all like to believe this but, unfortunately, there is still no hard evidence to back up our hopes. We should all strive to recognize melanomas as early as possible, but there still seem to be good melanomas and bad melanomas. The secret probably lies in the individual's immune response to the malignant cells.
Robert N. Richards, M.D., 4800 Leslie St., Ste. 305 Willowdale, Toronto, Ontario M2J 2K9 Canada REFERENCES I. Sina B: The spectrum of cutaneous pseudo malignancy. Cutis 34:381-384, 1984.
2. Greene MH, Clark WH Jr, Tucker MA, et a1: Acquired precursors of cutaneous malignant melanoma. The familial dysplastic nevus syndrome. N Engl J Med 312:91-97, 1985. 3. Fitzpatrick TB, Rhodes AR, Sober AI: Prevention of melanoma by recognition of its precursors. N Engl J Med 312:115-116,1985.
Seborrheic dermatitis and acquired immunodeficiency syndrome To the Editor: Eisenstat and Wonnser reported an increased occurrence of seborrheic dermatitis in acquired immunodeficiency syndrome (AIDS) patients. I We have been able to confirm that observation. Our own studies,2,3 as well as those from Newcastle,4 point to the role of Malas-
Treatment of pilar cyst with solcoderrn solution To the Editor: The treatment of a pilar cyst with a solution of Solcodenn is described. Solcodenn solution has been used in Israel for some years for the treatment of skin lesions. The method and follow-up of this treatment are well established. A trial treatment of a pilar cyst with Solcoderm was undertaken successfully. Case report. A healthy 40-year-old woman came to our dennatologic clinic because of a scalp lesion of several years' duration that had recently started to grow. On examination the lesion was about 5 Cm in diameter, 3 cm in depth, and yellow in color. Histologic examination from a punch biopsy showed the lesion to have a wall composed of epithelial cells. The peripheral layer of cells had a palisade arrangement, and the cyst contained a homogeneous eosinophilic material. The patient refused an operation because she was afraid of the surgical procedure but was willing to try conservative treatment. Treatment twice monthly with an application of the Solcodenn*" material (0.05 mlJtimc) was started. There was a delayed reaction ending with a scab formation, which detached by itself. Fourteen days later the patient underwent a second application of Solcodenn, and these applications were continued in the same way for about 4 months. The lesion disappeared without any scar formation. Discussion. Solcoderm as compared to plain nitric acid has shown its superior effect in mummification of tumors and skin lesions. 2 The treatment has proved to be successful in eradicating the tumor without causing any injury to the surrounding normal tissue and without damaging the hair around the lesion when it is located on the scalp. To our knowledge, Solcoderm has been tried on various skin tumors, among them, seborrheic keratosis, compound nevus, common warts, condyloma acuminatum, basal cell epithelioma, trichoepithelioma, solar keratosis, Dubreuilh melanosis, fibroma, and papilloma. 3-s While only one application is usually needed to treat a lesion such as solar keratosis, in this case several applications were needed because of the depth of the tumor (3 cm). As far as we know this is the first attempt to treat a pilar cyst with Solcoderm. The uneventful follow-up *Solcoderm as currently marketed is a specially prepared and packaged solution of organic acids (lactic, oxalic, acetic) and copper ions in moderately strong (6 to 7 normal) nitric acid. The exact composition is: copper ions, 15 ppm; oxalic acid, 40 mg/ml; lactic acid, 3 mg/ml; nitrate, 410 mg/ml; acetic acid, 40 mg/ml.
Correspondence
145
and avoidance of surgery make trying again worthwhile.
S. Brenner, M.D., Department of Dermatology Ichilov Municipal-Governmental Center Weizmann St., Tel Aviv 61 239, Israel REFERENCES 1. Weiner M: In vitro models reflecting the action of strong acids on integumental tissue. Dermatologica 168(suppl 1): 7-11, 1984. 2. Weiner M, Semah D, Schewach-Millet M, Cesarini J: Preclinical and clinical evaluation of topical acid products for skin tumors. Clin Pharmacol Ther 33:77-83, 1983. 3. Haim S, Cohen A: Solcoderm treatment of epidennal growth including intradermal nevi. Dermatologica 168 (suppl 1):46-48, 1984. 4. Feuerman EJ, Katzenelson W, Halevy S: Solcoderm in the treatment of solar and seborrheic keratoses. Dennatologica 168(suppl 1):33-35, 1984. 5. Weiner M, Semah D, Schewach-Millet M: Double-blind study of variables influencing the clinical effect of 801coderm. Dennatologlca 168(suppl 1):26-30, 1984.
Elastolysis of the earlobes To the Editor: A mother brought her 15-year-old daughter in to be seen for droopy earlobes. She had noted that her daughter's earlobes were "flapping in the breeze" during a drive in their car with the windows down. The mother is a hairdresser and began to observe earlobes. She thought that her daughter's earlobes were similar to those of clients 80 to 90 years old. We report this unusual presentation of acquired elastic tissue loss (Case 1) and a similar case brought to our attention by review of our photographic files (Case 2). Case 1. A healthy 15-year-old girl presented with wrinkling and drooping of her earlobes. These changes had occurred gradually over 18 months and were not preceded or accompanied by swelling, erythema, infection, or pruritus. Her ears had been pierced many years earlier, but she denied any adverse reactions or wearing large, heavy earrings. She described recurrent urticarial lesions over the preceding 3 to 4 years but denied involvement of the head and neck. Her history was negative for easy bruising, abnormal scarring, or musculoskeletal symptoms, and her family history was negative for similar skin changes_ The skin of the ears was lax and wrinkled (Fig. 1), and the earlobes were elongated. The upper and lower eyelids were mildly atrophic and wrinkled. Striae were present over both breasts. The remainder of her skin was nonnal in appearance except for mild acne vulgaris. There was diffuse
146
Correspondence
Fig. 1. Case 1. Fine wrinkling and drooping of earlobes of 1 V2 years' duration in a IS-year-old girl. Laxity of the upper and lower eyelids also was present but it was less obvious. hypermobility of the joints that was thought to represent the benign hypennobility syndrome. Otherwise, the results of physical examination were unremarkable. The following laboratory studies gave negative or normal results: complete blood cell count, urinalysis, thyroid studies, erythrocyte sedimentation rate, serum protein electrophoresis, sodium, potassium, calcium, phosphorus, chloride, glucose, alkaline phosphatase, aspartate aminotransferase (AST; SOOT), lactate dehydrogenase (LDH), bilirubin (total and direct), creatinine, uric acid, CH~o, antinuclear antibodies, anti-deoxyribonucleic acid (DNA), antitrypsin, and direct immunofluorescence study of a skin biopsy specimen from the earlobe. Histologic study (elastin Giemsa stain) of skin from the earlobe showed a marked decrease in elastic tissue throughout the dermis and a mild perivascular and periappendageal mononuclear cell infiltrate. Case 2. A 29-year-old woman presented in 1955 with relaxed, wrinkled skin of the face and earlobes. These changes had begun in her earlobes 4 years earlier and gradually extended to the upper eyelids and facial skin. She denied preceding erythema, pruritus, or infection. She suffered from seasonal hayfever, and from 1942 through 1952 she had had generalized hives. The records did not include information regarding head and neck involvement with the episodes of
Journal of the American Academy of Dermatology
Fig. 2. Case 2. Lax skin of the ears, face, and neck of 3 to 4 years' duration in a 29-year-old woman. hives she had experienced. Her general health was otherwise good, and her family history was negative for similar skin changes. Her appearance was that of a woman much older than her stated age. The skin of her face, eyelids, and earlobes was wrinkled and lax (Fig. 2), with drooping of the upper lip, elongation of the earlobes, and pendulous skin folds hanging below the mandible. The upper aspect of the neck was involved minimally, but the remainder of her skin appeared to be normal. The remainder of the results of physical examination were negative. The following laboratory studies gave negative or normal results: hemoglobin, leukocyte count, erythrocyte sedimentation rate, urinalysis, and automated reagin test. Histologic evaluation (elastin Giemsa stain) of skin from the upper aspect of the neck revealed total loss of middermal elastic tissue. The elastic tissue within the papillary dermis and the deep dermis and about vascular structures appeared to be normal. There was no ceIIular infiltrate. Discussion. These two cases represent an acquired form of cutaneous elastolysis that presented as droopy and wrinkled earlobes. These patients have in common episodes of urticaria for several years prior to the onset of elastic tissue changes, although in neither were the urticarial lesions present at the sites of subsequent elastic tissue changes.
Volume 14 Number I January, 1986
Cunliffe' stated that blepharochalasis may include involvement of both upper and lower eyelids and, rarely, the earlobes. Personal communication* revealed that the earlobe changes occurred in a single personal case in which follow-up information was not available. Whether Case 1 represents a variety of blepharochalasis or an early stage of acquired cutis laxa will become more clear with time. In Case 2, the skin laxity began in the earlobes and then gradually spread, during 3 to 4 years, to involve the eyelids, facial skin, and neck. The clinical presentation was similar to that in a 20-year-old man with acquired cutis laxa localized to the face, as reported by Reed et aF in 1971. Diseases involving elastic tissue abnormalities present with a wide range of clinical variability. These two cases are examples of elastolysis presenting as wrinkling and drooping of the earlobes.
SusanM. Barker, M.D., and Charles H. Dicken, MD. Department of Dermatology Mayo Clinic and Mayo Foundation Rochester, MN 55905 *Cunliffe WJ, April 30, 1984. REFERENCES 1. Cunliffe WI: Disorders of connective tissue, in Rook AJ,
Wilkinson OS, Ebling FJG, editors: Textbook of dermatology, vol 2, cd. 3. Oxford, England, 1979, Blackwell Scientific Publications, pp. 1611-1653. 2. Reed WB, Horowitz RE, Beighton P: Acquired cutis laxa: Primary generalized elastolysis. Arch Dermatol103:66l669, 1971.
The linear progression of malignant melanoma: A false premise? To the Editor: In a recent editorial (J AM ACAD DERMATOL 12: 115116, 1985) Ackerman stated, "It probably takes many months of proliferation of these melanocytes before the smallest and flattest of malignant melanomas can be visualized by inspection with the naked eye. Itprobably takes years before such a flat lesion of melanoma is broad enough (5 or 6 mm) to be diagnosed as a malignant melanoma with reasonable certainly .... In short, time is on the side both of patients with malignant melanomas and of physicians charged with detecting and removing them." Unfortunately, there is no evidence that melanomas do progress consistently in a linear fashion. In fact, clinical experience points entirely to the contrary. There still appear to be "good melanomas and bad melano-
Correspondence
147
mas. " Melanomas continue to be capricious, wanton, and unpredictable. We all hope that early recognition reduces the spread and mortality, but' there is still no proof that early recognition results in dramatic cures. Malignant melanoma is not alone in its unpredictable behavior. In spite of early recognition, the results from breast carcinoma treatments are nearly as disappointing now as they were 40 years ago. Our statistical cure rates for melanoma do seem to have improved in recent years. Perhaps, and hopefully, some of this may result from earlier detection. However, most of it results from the fact that we are now reading pathologically some lesions as malignant melanoma that appear as such under the microscope but do not behave so biologically. This spectrum of cutaneous pseudomalignancy was recently reviewed by Sina. 1 This would be consistent with the data recently presented by Greene et al. 2 They stated that the National Cancer Institute surveillance epidemiology studies revealed an 80% increase in the incidence of malignant melanoma in the United States between 1973 and 1980. However, during this same time of increased recognition we have been claiming a significantly increased cure rate. Fitzpatrick et aP recently made the same assumption of linear progression of malignant melanoma. We would all like to believe this but, unfortunately, there is still no hard evidence to back up our hopes. We should all strive to recognize melanomas as early as possible, but there still seem to be good melanomas and bad melanomas. The secret probably lies in the individual's immune response to the malignant cells.
Robert N. Richards, M.D., 4800 Leslie St., Ste. 305 Willowdale, Toronto, Ontario M2J 2K9 Canada REFERENCES I. Sina B: The spectrum of cutaneous pseudo malignancy. Cutis 34:381-384, 1984.
2. Greene MH, Clark WH Jr, Tucker MA, et a1: Acquired precursors of cutaneous malignant melanoma. The familial dysplastic nevus syndrome. N Engl J Med 312:91-97, 1985. 3. Fitzpatrick TB, Rhodes AR, Sober AI: Prevention of melanoma by recognition of its precursors. N Engl J Med 312:115-116,1985.
Seborrheic dermatitis and acquired immunodeficiency syndrome To the Editor: Eisenstat and Wonnser reported an increased occurrence of seborrheic dermatitis in acquired immunodeficiency syndrome (AIDS) patients. I We have been able to confirm that observation. Our own studies,2,3 as well as those from Newcastle,4 point to the role of Malas-