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Perilesional linear atrophy and hypopigmentation after intralesional corticosteroid therapy
A d v e r s e reaclions II
I
II
I
Perilesional linear atrophy and hypopigmentation after intralesional corticosteroid therapy Report o f two cases and review of the literature Stephen J. Friedman, MAJ, MC, USA,*.** David F. Butler, MAJ, MC, USA,** and Mark R. Pittelkow, M.D.*** El Paso, TX, and Rochester, M N We report on the eases of two patients in whom linear perilesional hypopigmentation and atrophy developed after intralesional injection of corticosteroids for treatment of keloids. Evaluation of our patients and the previously reported cases showed that perilesional linear atrophy or hypopigmentation (or both) is a distinct complication after intralesional or intraarticular administration of corticosteroids and is probably due to lymphogenous spread of the steroid suspension. (J A~4 ACADDERMATOL 1988;19:537-41.)
Many complications are associated with systemic and local administration of corticosteroids. '3 Local injections of corticosteroids have been associated with septic arthritis, tendon rupture, bowstring digital deformity, carpal tunnel infection, and pronounced flushing of the face. 3 Cutaneous changes after local corticosteroid administration include dermal or subcutaneous atrophy," 4-9hyperpigmentation, 1,7 alopecia, 7 and hypopigmentation. l, 5, 8-12 A specific pattern of perilesional linear, streaklike atrophy4-6,8.9 or hypopigmentations-'2 identified after intralesional 4-6,9.,2 and intraarticular 8, ~0.1~corticosteroid therapy has been designated "perilymphatic atrophy" or "hypopigmentation" (or both). We report on the development of perilesional linear
From the Department of Internal Medicine, Dermatology Service, William Beaumont Army Medical Center,** and the Department of Dermatology, Mayo Clinic and Mayo Foundation.*** The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Defense. Reprint requests to: Dr. M. R. Pittelkow, Department of Dermatology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. *Present address: Skin Therapeutics Institute, 16260 Ventura Blvd., Suite 300, Encino, CA 91436.
atrophy and hypopigmentation in two black patients after intralesional corticosteroid therapy for keloids. CASE REPORTS
Case 1 A 6-year-old black girl was admitted in October 1985 for treatment of two keloids on the left calf, 2.5 X 1.4 cm and 5.0 • 1.5 cm. The lesions developed during the healing of a burn sustained in April 1984. In December 1984 and January 1985, she received corticosteroids intralesionally at another clinic, and the lesions temporarily resolved. In October and November 1985, the lesions were treated intralesionally with triamcinolone, 10 mg/ml, one with 0.3 ml and the other with 0.4 mL When the patient returned in December, there was an approximate 80% reduction in the thickness of the lesions; lesional hyperpigmentation remained. In February 1986 mottled lesional hyperpigmentation and hypopigmentation of both keloids were present. Also, perilesional streaks of atrophy and hypopigmentation radiating primarily cephalad were apparent (Fig. 1). There were no areas of atrophy or hypopigmentation elsewhere. A 4-ram punch biopsy specimen obtained from a streaklike hypopigmented lesion revealed epidermal atrophy, flattening of the rete ridges, basket-weave hyperkeratosis, and a single-cell layer of a stratum 537
538
Journal of the American Academyof Dermatology
Friedman et al.
Fig. 2. Case 1. Melanocyte (M) containing few mature melanosomes and condensed pyknotic nucleus. Few organeUes are present. (Uranyl acetate and lead citrate; •
Fig. 1. Case 1. Streaklike atrophy and hypopigmentation radiating primarily .cephalad from keloid on left calf. Arrows indicate cephalad margins of linear streaklike hypopigmentation.
contained numerous mature melanosomes, and others contained few melanosomes. Melanophages were present in the dermis of the hypopigmented skin (Fig. 3). After about 10 weeks the atrophy and hypopigmentation resolved.
Case 2 granulosum. The number of melanin-containing cells was reduced, as shown by silver nitrate staining. In the dermis, homogenization of the collagen fibers and a perivascular mononuclear cell infiltrate were evident. A specimen of hypopigmented skin was submitted for electron microscopic examination. The tissue was fixed in 2% gluteraldehyde, processed in osmium tetroxide, and embedded in Spun" resin. Grids were stained with uranyl acetate and lead citrate. They were examined with a Zeiss 109 electron microscope. Melanocytes were less numerous in the hypopigmerited area. Those present often appeared vacuolated. Cytoplasmic organeUes were poorly visualized, although melanosomes were present (Fig. 2). Some keratinocytes
An 8-year-old black boy was admitted in February 1985 for treatment of numerous keloids that had developed 6 months earlier during the healing of some varicella lesions. Larger lesions involved the right postauricular (15 mm), right clavicular (6 • 4 ram), and right presternal (10 • 5 mm) regions. In March 1985 the fight postauricular lesion was excised and 0.5 ml of triamcinolone, 10 mg/ml, was injected intralesionaUy. The other lesions each received 0.5 ml triamcinolone, 10 mg/ml, by intralesional injection. The patient returned in June, October, November, and December 1985 and in January 1986, and the right IX~stauricular, right clavicular, and right presternal lesions cumulatively received 1.2, 1.5, and 2.4 ml,
Volume 19 Number 3 September 1988
Linear atrophy and hypolgigmentation after corticosteroid therapy 539
Fig. 3. Case 1. Melanophage (MP) within dermis. Keratinocyte (K) contains melanosomes, and melanocyte dendritic process (arrow) is visualized. (Uranyl acetate and lead citrate; •
Table I. Reported cases of perilesional linear atrophy or hypopigmentation associated with intralesional injection of corticosteroid First author
Age (yr), sex
myres4
55, F
KJ.kuchi6
34, F
Kikuchi5
12, F
Gottlieb8 Goldman ~~ McCormack" Litt ~ Gupta 9 Friedman* Friedman*
68, 55, 51, 26, 15, 6, 8,
F F F F F F M
Location
Forehead, left side Forehead, right side Upper part of left arm Knees Left thumb Left 2MTP Left hand Left foot Left calf Sternal
Diaguosls
i I I
Drug, route
Dose
AA
Triam, IL
NR
AA
Triam, IL
Keloid RA RA Pain Ganglion Psoriasis Keloid Keloid
First noted
A/H
NR
+/-
16 mg
59 days
+/-
Triam, IL
70 mg
5 mo
+/-
Triam, IA Triam, IA Triam, IA Pred, IL Triam, IL Triam, IL Triam, IL
1 gm 8 mg 40 mg I0 mg NR 7 mg 24 mg
NR Weeks 1 mo 2-3 wk Weeks Weeks Months
+/+ -/+ -/+ -/+ +/+ +/+ +/+
AA, Alopecia areata; A/H, atrophy/hypopigmentation; /'A, intraarticular; IL, intralesional; 2MTP, second metatarsophalangeal joint; NR, recorded; pred, prednisolone tebutate; RA, rheumatoid arthritis; triam, triamcinolone acetonide. *Present cases.
respectively, of triamcinolone, I0 mg/ml, given intralesionally. In February 1986 the fight postauricular and fight clavicular lesions had flattened and contained residual hyperpigmentation. The right presternal lesion was reduced about 80% in thickness; although it was hyper-
not
pigmented, perilesional streaks of atrophy and hypopigmentation radiated cephalad and caudad (Fig. 4). There were no areas of atrophy or hypopigmentation elsewhere. The intralesional injections were discontinued. Consent to perform a biopsy was not granted. Three months later, the hypopigmentation had resolved.
540
Friedman et al.
i .5: !,~
i.i/ii:~i
Fig. 4. Case 2. Streaklike atrophy and hypopigmentation radiating caudad and cephalad from keloid on presternal area.
DISCUSSION Review of the clinical manifestations of our patients and the previously reported cases in the English literature (Table I) revealed that perilesional linear atrophy or hypopigmentation (or both) is a distinct adverse effect of intraarticular or intralesional corticosteroid therapy. Perilesional linear atrophy or hypopigrnentation occurred after the administration of a corticosteroid--after a single injection, ~-I~ a few injections .6,9 (case 1), or months of therapy 8 (case 2). The latency period was long: several weeks to months 5,6,9-t2 (case 2). Resolution of hypopigmentation 5' 9,~0 (cases 1 and 2) or atrophy ~'6"9 (case 1) was noted in some
Journal of the American Academy of Dermatology
patients; however, linear hypopigrnentation was reported to be persistent almost 1 year later in one patient. ~~ Follow-up was not mentioned in some reports.4, 8,~2 The exact pathogenesis of perilesional linear atrophy or hypopigrnentation is unknown. The probable cause is lymphogenous spread of the corticosteroid suspension that results in overlying epidermal and dermal changes from the pharmacologic effects of excessive corticosteroid. .6,8-~2 After injecting Evans blue dye or alphazurine 2G (patent blue) into atrophic lesions, Kikuchi and Horikawa 5,6 concluded that the lesion was related to lymphatic vessels. They noted that the atrophy occurred over areas not subject to movement; however, subsequent reports of intraartieular therapy disproved their conclusion?, 10,~ The cutaneous changes associated with intraarticular corticosteroid therapy are difficult to explain 8, m.~ because ideally no medication is introduced into the dermis or subcutaneous tissue. Possible factors are that medications injected into the intraarticular space are removed mainly by the lymphatic system and that the lymphatic plexus in the synovial membrane is adjacent to the joint cavity. 8 Other contributing factors may be the proximity to the overlying skin, leakage from the joint space, inadvertent extraarticular injection, certain inherent characteristics of the patient's skin, and an aberrant superficial lymphatic drainage) The histologic evaluation of a perilymphatic hypopigmented lesion from one of our patients (case l) and two previously reported cases 5,6 revealed findings similar to those resulting from chronic use of topical steroid, ~3,~4 including disappearance of the rete ridges, degeneration of the appendages, degeneration of the blood and lymphatic vessels, and homogenization of the collagen fibers. Hyl~rpigmentation t,7, ~4 and hypopigmentation 1,8-ta have been associated with local corticosteroid use. The mechanism for the development of these changes is unknown. Perhaps postinflammatory hyperpigmentation or hypopigmentation is associated with the dermatitis that follows the discontinuation of chronic administration of steroid) 3,~4 Interestingly, no instances have been
Volume 19 Number 3 September 1988
Linear atrophy and hypopigrnentation after corticosteroid therapy 541
reported of streaklike perilesional hyperpigmentation with or without atrophy associated with local injection of corticosteroid. In the silver nitrate staining of the biopsy specimen obtained from a hypopigmented lesion from one patient (case 1), the decrease in melanin staining implied a corticosteroid-induced reduction in the number or activity of the melanocytes. Ultrastructural findings support this mechanism as the cause of the transient hypopigrnentation. Interestingly, only one of the patients was male (case 2). The clinical significance of this occurrence is not clear. He was, however, prepubertal. Perhaps the effect of estrogen and progesterone is combined with that of the corticosteroid in the pathogenesis of perilesional linear atrophy or hypopigmentation. Evaluation of more patients with this complication of ~rticosteroid therapy will be necessary before any definitive conclusions are made about sexual distribution. REFERENCES 1. Goldman L. Reactions following intralesional and sublesional injections of corticosteroids. J A M A 1962;182: 613-6. 2. Gallant C, Kenny P. Oral glucocorticoids and their complications: a review. J AM AcAI~ D~RMA'roL 1986; 14:161-77.
3. Gottlieb NL, Riskin WG. Complications of local corticosteroid injections. JAMA 1980;243:1547-8. 4. Ayres S Jr. Alopecia areata with associated subcutaneous atrophy. Arch Dermatol 1964;90:242. 5. Kikuchi I, Horikawa S. Perilymphatic atrophy of the skin: a side effect of topical corticosteroid injection therapy. Arch Dermatol 1974;109:558-9. 6. Kikuchi I, Horikawa S. Perilymphatic atrophy of the skin [letter]. Arch Dermatol 1975;111:795-6. 7. Cassidy JT, Bole GG. Cutaneous atrophy secondary to intra-articular corticosteroid administration. Ann Intern Med 1966;65:1008-18. 8. Gottlieb NL, Penneys NS, Brown HE Jr. Periarticular perilymphatic skin atrophy after intra-articular corticosteroid injections. JAMA 1978;240:559-60. 9. Gupta A, Rasmussen J. Perilesional linear atrophic streaks associated with intralesional corticosteroid injections in a psoriatic plaque. Pediatr Derrnatol 1987;4:25960. 10. Goldman L, AbrarrL~N, Goldman J. Linear hypopigmenration after digital intra-articular injection of corticosteroid [letter]. Arch Dermatol 1981;117:605. 11. McCormack PC, Ledesma GN, Vailtant JG. Linear hypopigmentation after intra-articular eorticosteroid injection [letter]. Arch Dermatol 1984;120:708-9. 12. Litt JZ. Linear hypopigmentation [letter]. Arch Dermatol 1985;121:26. 13. Lehmann P, Zheng P, Lavk~r RM, et al. Corticosteroid atrophy in human skin: a study by light, scanning, and transmission electron microscopy. J Invest Dermatol 1983;81:169-76. 14. Zheng P, Lavker RM, Lehmann P, et al. Morphologic investigations on the rebound phenomenon after corticosteroid-induced atrophy in human skin. J Invest Dermatol 1984;82:345-52.
BOUND VOLUMES AVAILABLETO SUBSCRIBERS Bound volumesof the JOtJRN~ OVa'HEAMERICANACADEMYOFDERMATOLOGYare availableto subscribers (only) for the 1988 issues from the Publisherat a cost of $49.00 ($62.00 international) for volume 18 (January-June) and volume 19 (July-December). Shipping charges are included. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 60 days after publication of the last issue in the volume.The bindingis durable buckram with the journal name, volume number, and year stamped in gold on the spine. Payment must accompany all orders. Contact The C. V. Mothy Company, Circulation Department, 1!.830 Westline Industrial Drive, St. Louis, Missouri 63146-3318. USA: phone (800) 325-4177, ext. 351. Subscriptions must be in force to qualify. Bound volumes are not available hl place of a regular journal subxcription.
I
II
I
Perilesional linear atrophy and hypopigmentation after intralesional corticosteroid therapy Report o f two cases and review of the literature Stephen J. Friedman, MAJ, MC, USA,*.** David F. Butler, MAJ, MC, USA,** and Mark R. Pittelkow, M.D.*** El Paso, TX, and Rochester, M N We report on the eases of two patients in whom linear perilesional hypopigmentation and atrophy developed after intralesional injection of corticosteroids for treatment of keloids. Evaluation of our patients and the previously reported cases showed that perilesional linear atrophy or hypopigmentation (or both) is a distinct complication after intralesional or intraarticular administration of corticosteroids and is probably due to lymphogenous spread of the steroid suspension. (J A~4 ACADDERMATOL 1988;19:537-41.)
Many complications are associated with systemic and local administration of corticosteroids. '3 Local injections of corticosteroids have been associated with septic arthritis, tendon rupture, bowstring digital deformity, carpal tunnel infection, and pronounced flushing of the face. 3 Cutaneous changes after local corticosteroid administration include dermal or subcutaneous atrophy," 4-9hyperpigmentation, 1,7 alopecia, 7 and hypopigmentation. l, 5, 8-12 A specific pattern of perilesional linear, streaklike atrophy4-6,8.9 or hypopigmentations-'2 identified after intralesional 4-6,9.,2 and intraarticular 8, ~0.1~corticosteroid therapy has been designated "perilymphatic atrophy" or "hypopigmentation" (or both). We report on the development of perilesional linear
From the Department of Internal Medicine, Dermatology Service, William Beaumont Army Medical Center,** and the Department of Dermatology, Mayo Clinic and Mayo Foundation.*** The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Defense. Reprint requests to: Dr. M. R. Pittelkow, Department of Dermatology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. *Present address: Skin Therapeutics Institute, 16260 Ventura Blvd., Suite 300, Encino, CA 91436.
atrophy and hypopigmentation in two black patients after intralesional corticosteroid therapy for keloids. CASE REPORTS
Case 1 A 6-year-old black girl was admitted in October 1985 for treatment of two keloids on the left calf, 2.5 X 1.4 cm and 5.0 • 1.5 cm. The lesions developed during the healing of a burn sustained in April 1984. In December 1984 and January 1985, she received corticosteroids intralesionally at another clinic, and the lesions temporarily resolved. In October and November 1985, the lesions were treated intralesionally with triamcinolone, 10 mg/ml, one with 0.3 ml and the other with 0.4 mL When the patient returned in December, there was an approximate 80% reduction in the thickness of the lesions; lesional hyperpigmentation remained. In February 1986 mottled lesional hyperpigmentation and hypopigmentation of both keloids were present. Also, perilesional streaks of atrophy and hypopigmentation radiating primarily cephalad were apparent (Fig. 1). There were no areas of atrophy or hypopigmentation elsewhere. A 4-ram punch biopsy specimen obtained from a streaklike hypopigmented lesion revealed epidermal atrophy, flattening of the rete ridges, basket-weave hyperkeratosis, and a single-cell layer of a stratum 537
538
Journal of the American Academyof Dermatology
Friedman et al.
Fig. 2. Case 1. Melanocyte (M) containing few mature melanosomes and condensed pyknotic nucleus. Few organeUes are present. (Uranyl acetate and lead citrate; •
Fig. 1. Case 1. Streaklike atrophy and hypopigmentation radiating primarily .cephalad from keloid on left calf. Arrows indicate cephalad margins of linear streaklike hypopigmentation.
contained numerous mature melanosomes, and others contained few melanosomes. Melanophages were present in the dermis of the hypopigmented skin (Fig. 3). After about 10 weeks the atrophy and hypopigmentation resolved.
Case 2 granulosum. The number of melanin-containing cells was reduced, as shown by silver nitrate staining. In the dermis, homogenization of the collagen fibers and a perivascular mononuclear cell infiltrate were evident. A specimen of hypopigmented skin was submitted for electron microscopic examination. The tissue was fixed in 2% gluteraldehyde, processed in osmium tetroxide, and embedded in Spun" resin. Grids were stained with uranyl acetate and lead citrate. They were examined with a Zeiss 109 electron microscope. Melanocytes were less numerous in the hypopigmerited area. Those present often appeared vacuolated. Cytoplasmic organeUes were poorly visualized, although melanosomes were present (Fig. 2). Some keratinocytes
An 8-year-old black boy was admitted in February 1985 for treatment of numerous keloids that had developed 6 months earlier during the healing of some varicella lesions. Larger lesions involved the right postauricular (15 mm), right clavicular (6 • 4 ram), and right presternal (10 • 5 mm) regions. In March 1985 the fight postauricular lesion was excised and 0.5 ml of triamcinolone, 10 mg/ml, was injected intralesionaUy. The other lesions each received 0.5 ml triamcinolone, 10 mg/ml, by intralesional injection. The patient returned in June, October, November, and December 1985 and in January 1986, and the right IX~stauricular, right clavicular, and right presternal lesions cumulatively received 1.2, 1.5, and 2.4 ml,
Volume 19 Number 3 September 1988
Linear atrophy and hypolgigmentation after corticosteroid therapy 539
Fig. 3. Case 1. Melanophage (MP) within dermis. Keratinocyte (K) contains melanosomes, and melanocyte dendritic process (arrow) is visualized. (Uranyl acetate and lead citrate; •
Table I. Reported cases of perilesional linear atrophy or hypopigmentation associated with intralesional injection of corticosteroid First author
Age (yr), sex
myres4
55, F
KJ.kuchi6
34, F
Kikuchi5
12, F
Gottlieb8 Goldman ~~ McCormack" Litt ~ Gupta 9 Friedman* Friedman*
68, 55, 51, 26, 15, 6, 8,
F F F F F F M
Location
Forehead, left side Forehead, right side Upper part of left arm Knees Left thumb Left 2MTP Left hand Left foot Left calf Sternal
Diaguosls
i I I
Drug, route
Dose
AA
Triam, IL
NR
AA
Triam, IL
Keloid RA RA Pain Ganglion Psoriasis Keloid Keloid
First noted
A/H
NR
+/-
16 mg
59 days
+/-
Triam, IL
70 mg
5 mo
+/-
Triam, IA Triam, IA Triam, IA Pred, IL Triam, IL Triam, IL Triam, IL
1 gm 8 mg 40 mg I0 mg NR 7 mg 24 mg
NR Weeks 1 mo 2-3 wk Weeks Weeks Months
+/+ -/+ -/+ -/+ +/+ +/+ +/+
AA, Alopecia areata; A/H, atrophy/hypopigmentation; /'A, intraarticular; IL, intralesional; 2MTP, second metatarsophalangeal joint; NR, recorded; pred, prednisolone tebutate; RA, rheumatoid arthritis; triam, triamcinolone acetonide. *Present cases.
respectively, of triamcinolone, I0 mg/ml, given intralesionally. In February 1986 the fight postauricular and fight clavicular lesions had flattened and contained residual hyperpigmentation. The right presternal lesion was reduced about 80% in thickness; although it was hyper-
not
pigmented, perilesional streaks of atrophy and hypopigmentation radiated cephalad and caudad (Fig. 4). There were no areas of atrophy or hypopigmentation elsewhere. The intralesional injections were discontinued. Consent to perform a biopsy was not granted. Three months later, the hypopigmentation had resolved.
540
Friedman et al.
i .5: !,~
i.i/ii:~i
Fig. 4. Case 2. Streaklike atrophy and hypopigmentation radiating caudad and cephalad from keloid on presternal area.
DISCUSSION Review of the clinical manifestations of our patients and the previously reported cases in the English literature (Table I) revealed that perilesional linear atrophy or hypopigmentation (or both) is a distinct adverse effect of intraarticular or intralesional corticosteroid therapy. Perilesional linear atrophy or hypopigrnentation occurred after the administration of a corticosteroid--after a single injection, ~-I~ a few injections .6,9 (case 1), or months of therapy 8 (case 2). The latency period was long: several weeks to months 5,6,9-t2 (case 2). Resolution of hypopigmentation 5' 9,~0 (cases 1 and 2) or atrophy ~'6"9 (case 1) was noted in some
Journal of the American Academy of Dermatology
patients; however, linear hypopigrnentation was reported to be persistent almost 1 year later in one patient. ~~ Follow-up was not mentioned in some reports.4, 8,~2 The exact pathogenesis of perilesional linear atrophy or hypopigrnentation is unknown. The probable cause is lymphogenous spread of the corticosteroid suspension that results in overlying epidermal and dermal changes from the pharmacologic effects of excessive corticosteroid. .6,8-~2 After injecting Evans blue dye or alphazurine 2G (patent blue) into atrophic lesions, Kikuchi and Horikawa 5,6 concluded that the lesion was related to lymphatic vessels. They noted that the atrophy occurred over areas not subject to movement; however, subsequent reports of intraartieular therapy disproved their conclusion?, 10,~ The cutaneous changes associated with intraarticular corticosteroid therapy are difficult to explain 8, m.~ because ideally no medication is introduced into the dermis or subcutaneous tissue. Possible factors are that medications injected into the intraarticular space are removed mainly by the lymphatic system and that the lymphatic plexus in the synovial membrane is adjacent to the joint cavity. 8 Other contributing factors may be the proximity to the overlying skin, leakage from the joint space, inadvertent extraarticular injection, certain inherent characteristics of the patient's skin, and an aberrant superficial lymphatic drainage) The histologic evaluation of a perilymphatic hypopigmented lesion from one of our patients (case l) and two previously reported cases 5,6 revealed findings similar to those resulting from chronic use of topical steroid, ~3,~4 including disappearance of the rete ridges, degeneration of the appendages, degeneration of the blood and lymphatic vessels, and homogenization of the collagen fibers. Hyl~rpigmentation t,7, ~4 and hypopigmentation 1,8-ta have been associated with local corticosteroid use. The mechanism for the development of these changes is unknown. Perhaps postinflammatory hyperpigmentation or hypopigmentation is associated with the dermatitis that follows the discontinuation of chronic administration of steroid) 3,~4 Interestingly, no instances have been
Volume 19 Number 3 September 1988
Linear atrophy and hypopigrnentation after corticosteroid therapy 541
reported of streaklike perilesional hyperpigmentation with or without atrophy associated with local injection of corticosteroid. In the silver nitrate staining of the biopsy specimen obtained from a hypopigmented lesion from one patient (case 1), the decrease in melanin staining implied a corticosteroid-induced reduction in the number or activity of the melanocytes. Ultrastructural findings support this mechanism as the cause of the transient hypopigrnentation. Interestingly, only one of the patients was male (case 2). The clinical significance of this occurrence is not clear. He was, however, prepubertal. Perhaps the effect of estrogen and progesterone is combined with that of the corticosteroid in the pathogenesis of perilesional linear atrophy or hypopigmentation. Evaluation of more patients with this complication of ~rticosteroid therapy will be necessary before any definitive conclusions are made about sexual distribution. REFERENCES 1. Goldman L. Reactions following intralesional and sublesional injections of corticosteroids. J A M A 1962;182: 613-6. 2. Gallant C, Kenny P. Oral glucocorticoids and their complications: a review. J AM AcAI~ D~RMA'roL 1986; 14:161-77.
3. Gottlieb NL, Riskin WG. Complications of local corticosteroid injections. JAMA 1980;243:1547-8. 4. Ayres S Jr. Alopecia areata with associated subcutaneous atrophy. Arch Dermatol 1964;90:242. 5. Kikuchi I, Horikawa S. Perilymphatic atrophy of the skin: a side effect of topical corticosteroid injection therapy. Arch Dermatol 1974;109:558-9. 6. Kikuchi I, Horikawa S. Perilymphatic atrophy of the skin [letter]. Arch Dermatol 1975;111:795-6. 7. Cassidy JT, Bole GG. Cutaneous atrophy secondary to intra-articular corticosteroid administration. Ann Intern Med 1966;65:1008-18. 8. Gottlieb NL, Penneys NS, Brown HE Jr. Periarticular perilymphatic skin atrophy after intra-articular corticosteroid injections. JAMA 1978;240:559-60. 9. Gupta A, Rasmussen J. Perilesional linear atrophic streaks associated with intralesional corticosteroid injections in a psoriatic plaque. Pediatr Derrnatol 1987;4:25960. 10. Goldman L, AbrarrL~N, Goldman J. Linear hypopigmenration after digital intra-articular injection of corticosteroid [letter]. Arch Dermatol 1981;117:605. 11. McCormack PC, Ledesma GN, Vailtant JG. Linear hypopigmentation after intra-articular eorticosteroid injection [letter]. Arch Dermatol 1984;120:708-9. 12. Litt JZ. Linear hypopigmentation [letter]. Arch Dermatol 1985;121:26. 13. Lehmann P, Zheng P, Lavk~r RM, et al. Corticosteroid atrophy in human skin: a study by light, scanning, and transmission electron microscopy. J Invest Dermatol 1983;81:169-76. 14. Zheng P, Lavker RM, Lehmann P, et al. Morphologic investigations on the rebound phenomenon after corticosteroid-induced atrophy in human skin. J Invest Dermatol 1984;82:345-52.
BOUND VOLUMES AVAILABLETO SUBSCRIBERS Bound volumesof the JOtJRN~ OVa'HEAMERICANACADEMYOFDERMATOLOGYare availableto subscribers (only) for the 1988 issues from the Publisherat a cost of $49.00 ($62.00 international) for volume 18 (January-June) and volume 19 (July-December). Shipping charges are included. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 60 days after publication of the last issue in the volume.The bindingis durable buckram with the journal name, volume number, and year stamped in gold on the spine. Payment must accompany all orders. Contact The C. V. Mothy Company, Circulation Department, 1!.830 Westline Industrial Drive, St. Louis, Missouri 63146-3318. USA: phone (800) 325-4177, ext. 351. Subscriptions must be in force to qualify. Bound volumes are not available hl place of a regular journal subxcription.