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Vascular response in halo of recent halo nevus
Vascular response in halo of recent halo nevus Alexander Berman, M.D., and Sidney Herszenson, M.D. Milwaukee, WI The depigmented halo of a recently acquired halo nevus showed prominent erythema. Microscopic examination of a specimen from the halo showed dilatation of the dermal blood vessels, thickening of the vessel walls, and swelling of the endothelial cells; cellular infiltration was totally absent. Direct immunofluorescent studies on skin from the halo failed to show vessel, basement membrane, or intercellular fluorescence with IgG, IgM, IgA, C3 • and fibrin. We conclude that the erythema in the skin of the depigmented halo is the result of dilated dermal blood vessels and that the mechanism of vascular dilatation is not associated with direct infiltration by inflammatory cells nor with immune complex formation. Erythema in the skin of the depigmented halo has not, to our knowledge, been studied previously. (J AM ACAD DERMATOL 4:537-540, 1981.)
A halo of depigmentation appearing around a melanocytic nevus is recognized as halo nevus or leukoderma acquisitum centrifugum and often indicates the onset of involution and subsequent regression of the nevus. 1.2 Histologically, a dense lymphocytic infiltrate is found invading and apparently destroying the nevus cells in the central nevus; skin from the depigmented halo appears normal except for the absence of melanin in the epidermis and the replacement of epidermal melanocytes by Langerhans' cells. 3 The mechanism by which the halo of depigmentation is produced is not known. After regression of the central nevus, the depigmented skin may repigment or may remain permanently leukodermatous. Recently acquired halo nevi occasionally show erythema in the depigmented halo. The erythema is temporary, disappearing after a period of weeks or a few months. Though the occurrence of such erythema is familiar to clinicians of experience, From the Milwaukee Skin Center. Reprint requests to: Dr. Alexander Berman, Milwaukee Skin Center, 7400 W. Brown Deer Road, Milwaukee, WI 53223.
0190-9622/81/050537+04$00.40/0 © 1981 Am Acad Dermatol
not a single reference to it could be found in the English literature. This report documents the occurrence of erythema in the depigmented halo of a recent halo nevus and describes clinical and histopathologic findings that suggest the mechanism of production of the erythema. CASE REPORT A 33-year-old white man was seen with a halo nevus over the left scapula (Fig. 1). The central nevus was present since childhood, but the depigmented halo appeared less than 2 months earlier; the halo was 1.8 x 1.4 em in diameter and was markedly erythematous. The erythema blanched on pressure. The skin immediately surrounding the depigmented halo washyperpigmented. The patient denied the possibility that the erythema might be related to application of topical medications or to exposure to sunlight. Six weeks after the initial observation, the erythema in the halo could no longer be perceived and the hyperpigmented skin surrounding the halo had faded. Histopathologic findings. Skin from the depigmented halo. The specimen showed normal skin but with dilated and prominent dermal blood vessels (Fig. 2), The walls of the blood
537
Journal of the
538
Berman and Herszenson
American Academy of
Dermatology
Fig. 1. Halo nevus of recent appearance. Erythema is seen in the skin of the depigmented halo.
Fig. 2. Skin of halo showing dilatation of dermal blood vessels, thickening of the vessel walls, and swelling of the endothelial cells. (Hematoxylin-eosin stain; X70.) vessels in the papillary dermis appeared thickened and the endothelial cells appeared swollen. Cellular infiltration was totally absent. There was no extravasation of red blood cells. Fontana stain showed complete absence of melanin in the cells of the basal layer of the epidermis. Central nevus. The specimen showed a compound nevus infiltrated by mononuclear cells (Fig. 3). Theques
of pigmented nevus cells at the dermoepidermal junction and nests of nonpigmented nevus cells in the upper corium were invaded from below by a dense mononuclear cell infiltration. The blood vessels in the most heavily infiltrated deeper portion of the lesion were widely dilated and engorged, and foci of extravasated red blood cells were common. Pigment incontinence in the upper dermis was prominent.
Volume 4 Number 5 May, 1981
Vascular response in halo nevus
Fig. 3. Central nevus infiltrated by mononuclear cells. (Hematoxylin-eosin stain; x90.)
Fig. 4. Beyond the margin of the central nevus (right) clumps of nevus cells in the upper corium are not infiltrated by mononuclear cells (left). (Hematoxylin-eosin stain; x 125.)
539
Journal of the American Academy of Dermatology
540 Berman and Herszenson
Beyond the margins of the central nevus and the mononuclear cell infiltrative process, theques of nevus cells in the upper corium were not infiltrated by mononuclear cells (Fig. 4). Vacuolated cells were plentiful in the overlying epidermis, but pigment was absent. The papillary dermis was edematous, the small blood vessels were engorged, and only scattered mononuclear cells were present. Deeper, the blood vessels were widely dilated and engorged. Immunofluorescent studies. Direct immunofluorescent studies on skin from the halo failed to demonstrate blood vessel, basement membrane, or other specific structural deposition of IgG, IgM, IgA, C3 , and fibrin. COMMENT
Vascular alterations in the skin of the depigmented halo of halo nevus have not been described previously. The occurrence of erythema in the depigmented halo is not mentioned in textbooks of dermatology, and we could not find a single reference to erythema in the depigmented halo of halo nevus in the English literature. Clinicians with interest and experience in the halo nevus confirm the occurrence of transient erythema in the depigmented halo of early halo nevi. We presume that the omission in the literature reflects the fact that the erythema is of short duration, is seen only in early lesions, has usually disappeared by the time the patient seeks medical attention, and is of less concern than other aspects of the phenomenon. Microscopic examination of a specimen of skin
from the erythematous depigmented halo in our patient showed dilatation of the dermal blood vessels, thickening of the vessel walls, and swelling of the endothelial cells. These findings explain the clinically evident erythema. The occurrence of erythema only in recent halo nevi suggests that the injury responsible for the vascular alterations occurs early and is probably of limited duration. The nature of the vascular injury is not apparent from the histology, but the absence of cellular infiltration indicates that the injury is not mediated by direct infiltration of inflammatory cells. Failure to demonstrate blood vessel fluorescence in direct immunofluorescent studies indicates also that immune complex formation is not involved. Vascular injury, mediated by a diffusible substance toxic to small blood vessels, liberated in the area of the central nevus, might best account for the transient erythema in the depigmented halo of recent halo nevI. We thank Dr. Robert O. Jordon, Medical College of Wisconsin, for performingthe immunofluorescentstudies and Dr. R. K. Winkelmann, Mayo Clinic, for many helpful suggestions. REFERENCES 1. Sutton RL: Unusual variety of vitiligo, leukoderma acquisitum centrifugum. J Cutan Dis 34:797-800, 1916. 2. Kopf AW, Morrill SD, Silberberg I: Broad spectrum of leukoderma acquisitum centrifugum, Arch Dermatol 92: 14-35, 1965. 3. Swanson JL, Wayte DM, Helwig BB: Ultrastructure of halo nevi. J Invest Dermatol 50:434-437, 1968.
A halo of depigmentation appearing around a melanocytic nevus is recognized as halo nevus or leukoderma acquisitum centrifugum and often indicates the onset of involution and subsequent regression of the nevus. 1.2 Histologically, a dense lymphocytic infiltrate is found invading and apparently destroying the nevus cells in the central nevus; skin from the depigmented halo appears normal except for the absence of melanin in the epidermis and the replacement of epidermal melanocytes by Langerhans' cells. 3 The mechanism by which the halo of depigmentation is produced is not known. After regression of the central nevus, the depigmented skin may repigment or may remain permanently leukodermatous. Recently acquired halo nevi occasionally show erythema in the depigmented halo. The erythema is temporary, disappearing after a period of weeks or a few months. Though the occurrence of such erythema is familiar to clinicians of experience, From the Milwaukee Skin Center. Reprint requests to: Dr. Alexander Berman, Milwaukee Skin Center, 7400 W. Brown Deer Road, Milwaukee, WI 53223.
0190-9622/81/050537+04$00.40/0 © 1981 Am Acad Dermatol
not a single reference to it could be found in the English literature. This report documents the occurrence of erythema in the depigmented halo of a recent halo nevus and describes clinical and histopathologic findings that suggest the mechanism of production of the erythema. CASE REPORT A 33-year-old white man was seen with a halo nevus over the left scapula (Fig. 1). The central nevus was present since childhood, but the depigmented halo appeared less than 2 months earlier; the halo was 1.8 x 1.4 em in diameter and was markedly erythematous. The erythema blanched on pressure. The skin immediately surrounding the depigmented halo washyperpigmented. The patient denied the possibility that the erythema might be related to application of topical medications or to exposure to sunlight. Six weeks after the initial observation, the erythema in the halo could no longer be perceived and the hyperpigmented skin surrounding the halo had faded. Histopathologic findings. Skin from the depigmented halo. The specimen showed normal skin but with dilated and prominent dermal blood vessels (Fig. 2), The walls of the blood
537
Journal of the
538
Berman and Herszenson
American Academy of
Dermatology
Fig. 1. Halo nevus of recent appearance. Erythema is seen in the skin of the depigmented halo.
Fig. 2. Skin of halo showing dilatation of dermal blood vessels, thickening of the vessel walls, and swelling of the endothelial cells. (Hematoxylin-eosin stain; X70.) vessels in the papillary dermis appeared thickened and the endothelial cells appeared swollen. Cellular infiltration was totally absent. There was no extravasation of red blood cells. Fontana stain showed complete absence of melanin in the cells of the basal layer of the epidermis. Central nevus. The specimen showed a compound nevus infiltrated by mononuclear cells (Fig. 3). Theques
of pigmented nevus cells at the dermoepidermal junction and nests of nonpigmented nevus cells in the upper corium were invaded from below by a dense mononuclear cell infiltration. The blood vessels in the most heavily infiltrated deeper portion of the lesion were widely dilated and engorged, and foci of extravasated red blood cells were common. Pigment incontinence in the upper dermis was prominent.
Volume 4 Number 5 May, 1981
Vascular response in halo nevus
Fig. 3. Central nevus infiltrated by mononuclear cells. (Hematoxylin-eosin stain; x90.)
Fig. 4. Beyond the margin of the central nevus (right) clumps of nevus cells in the upper corium are not infiltrated by mononuclear cells (left). (Hematoxylin-eosin stain; x 125.)
539
Journal of the American Academy of Dermatology
540 Berman and Herszenson
Beyond the margins of the central nevus and the mononuclear cell infiltrative process, theques of nevus cells in the upper corium were not infiltrated by mononuclear cells (Fig. 4). Vacuolated cells were plentiful in the overlying epidermis, but pigment was absent. The papillary dermis was edematous, the small blood vessels were engorged, and only scattered mononuclear cells were present. Deeper, the blood vessels were widely dilated and engorged. Immunofluorescent studies. Direct immunofluorescent studies on skin from the halo failed to demonstrate blood vessel, basement membrane, or other specific structural deposition of IgG, IgM, IgA, C3 , and fibrin. COMMENT
Vascular alterations in the skin of the depigmented halo of halo nevus have not been described previously. The occurrence of erythema in the depigmented halo is not mentioned in textbooks of dermatology, and we could not find a single reference to erythema in the depigmented halo of halo nevus in the English literature. Clinicians with interest and experience in the halo nevus confirm the occurrence of transient erythema in the depigmented halo of early halo nevi. We presume that the omission in the literature reflects the fact that the erythema is of short duration, is seen only in early lesions, has usually disappeared by the time the patient seeks medical attention, and is of less concern than other aspects of the phenomenon. Microscopic examination of a specimen of skin
from the erythematous depigmented halo in our patient showed dilatation of the dermal blood vessels, thickening of the vessel walls, and swelling of the endothelial cells. These findings explain the clinically evident erythema. The occurrence of erythema only in recent halo nevi suggests that the injury responsible for the vascular alterations occurs early and is probably of limited duration. The nature of the vascular injury is not apparent from the histology, but the absence of cellular infiltration indicates that the injury is not mediated by direct infiltration of inflammatory cells. Failure to demonstrate blood vessel fluorescence in direct immunofluorescent studies indicates also that immune complex formation is not involved. Vascular injury, mediated by a diffusible substance toxic to small blood vessels, liberated in the area of the central nevus, might best account for the transient erythema in the depigmented halo of recent halo nevI. We thank Dr. Robert O. Jordon, Medical College of Wisconsin, for performingthe immunofluorescentstudies and Dr. R. K. Winkelmann, Mayo Clinic, for many helpful suggestions. REFERENCES 1. Sutton RL: Unusual variety of vitiligo, leukoderma acquisitum centrifugum. J Cutan Dis 34:797-800, 1916. 2. Kopf AW, Morrill SD, Silberberg I: Broad spectrum of leukoderma acquisitum centrifugum, Arch Dermatol 92: 14-35, 1965. 3. Swanson JL, Wayte DM, Helwig BB: Ultrastructure of halo nevi. J Invest Dermatol 50:434-437, 1968.