J Cutan Pathol 2015: 42: 150–154 doi: 10.1111/cup.12437 John Wiley & Sons. Printed in Singapore
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Journal of Cutaneous Pathology
Colocalization of vitiligo and alopecia areata presenting as poliosis Vitiligo and alopecia areata are two cutaneous diseases believed to be primarily autoimmune in pathogenesis. While the coexistence of the two conditions in the same patient has been well-described, reports of the two disease processes occurring in the same location are rare. We report the case of a 10-year-old male with an unremarkable past medical history who presented with a single localized area of poliosis with depigmented underlying skin on the frontal scalp. The hair in the affected area was relatively decreased in density. A punch biopsy of the depigmented patch demonstrated features consistent with both vitiligo and alopecia areata. The decreased number of large hair follicles and a focal peribulbar lymphocytic infiltrate around an anagen follicle were suggestive of alopecia areata. A panel of melanocyte-specific stains revealed absent melanocytes in the epidermis, consistent with vitiligo. Loss of microphthalmia-associated transcription factor-positive root sheath cells was seen, suggestive of loss of melanocyte stem cells. The combination of clinical and histopathologic findings supports the theory of a common pathogenesis of alopecia areata and vitiligo. Keywords: alopecia, hair follicle, scalp Walker A, Mesinkovska NA, Boncher J, Tamburro J, Bergfeld WF. Colocalization of vitiligo and alopecia areata presenting as poliosis. J Cutan Pathol 2015; 42: 150–154. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Report of a patient A 10-year-old male presented with a localized area of poliosis and depigmentation of the underlying skin (Fig. 1). The 3 × 2 cm triangular-shaped patch was present on the left frontal scalp and had been present for at least 6 weeks. The hairs within this patch of skin were white and showed a questionable decrease in density. No other areas of poliosis or skin depigmentation were identified. There was no history of trauma to the affected area. Family history included a possible depigmentation disorder in the patient’s maternal great-grandmother and an undefined thyroid condition in the patient’s father. The patient himself had no medical
150
Addie Walker1 , Natasha Atanaskova Mesinkovska1,2 , Julia Boncher3 , Joan Tamburro2 and Wilma F. Bergfeld1,2 1
RJ Tomisch Institute of Pathology and Laboratory Medicine, Cleveland Clinic, Cleveland, OH, USA, 2 Department of Dermatology, Cleveland Clinic, Cleveland, OH, USA , and 3 Department of Pathology, University of New Mexico, Albuquerque, NM, USA
Wilma F. Bergfeld Robert J Tomisch Pathology and Laboratory Medicine Institute L25, Cleveland Clinic, Cleveland, OH 44195, USA Tel: +504 453 3349 Fax: +216 445 6967 e-mail: [email protected] Accepted for publication June 7, 2014
problems aside from a speech problem in early childhood; no abnormalities were detected on audiological testing. Thyroid-stimulating hormone, T3, free T4 and complete blood count were all within normal limits. A punch biopsy was taken from the area of poliosis. Topical clobetasol was started for treatment of the affected area. At follow-up 2 months later, the depigmented skin patch and poliosis had not improved. Additional loss of density of the white hairs in the depigmented area was observed, and a second similar-appearing 2 × 0.8 cm patch of poliosis and depigmented skin had developed. The new patch was located on the frontal scalp, separate from the initial area.
Vitiligo with alopecia areata
Fig. 1. An area of poliosis and underlying depigmented skin was observed on the patient’s left frontal scalp.
stains showed positivity in the root sheath. For comparison, when performed on a normal scalp biopsy from an age-matched patient, all four stains highlighted melanocytes in the epidermis and follicular matrix. Cells with strong Melan-A and MiTF nuclear staining were also identified within the external root sheath on the normal biopsy. Additional special stains performed included periodic acid-Schiff (PAS) with and without diastase, which showed Pityrosporum yeast forms in the stratum corneum; Gram stain which was negative for bacteria; and colloidal iron stain with and without digestion, which did not reveal increased dermal mucin.
Histopathologic examination of the punch biopsy from the initial area of poliosis demonstrated features of vitiligo and alopecia areata. Hematoxylin and eosin staining showed an unremarkable epidermis. Within the dermis, a slight decrease in large hair follicles was noted. A dense peribulbar infiltrate was present around an anagen follicle (Fig. 2). These features were suggestive of alopecia areata, which had not been clinically suspected. A panel of stains that highlight various melanocytic elements – Melan-A, microphthalmia-associated transcription factor (MiTF), Fontana-Masson and tyrosinase – was performed to assess pigmentation (Fig. 3). None of the four stains labeled junctional cells, suggesting an absence of epidermal melanocytes compatible with vitiligo (Fig. 4). Within the hair follicles, matrix melanocytes were strongly positive with tyrosinase, weakly positive with MiTF and negative with Melan-A and Fontana-Masson. Rare cells scattered throughout the external root sheath of the follicular epithelium were positive with Melan-A stain. None of the other three
Discussion While concomitant occurrence of vitiligo and alopecia areata in the same patient has been well-described, only a small number of cases of the occurrence of both disease processes at the same site have been reported. Searches for ‘vitiligo, poliosis and alopecia’ using pubmed.gov and google.com search engines yielded 10 cases of colocalization published as of April 7, 2014 (Table 1).1 – 10 Patients of both sexes, of various ethnicities and of various age groups were represented. Two of the patients had thyroid disease, and two had pre-existing areas of vitiligo or alopecia areata prior to developing colocalization. The most commonly affected area was the scalp. We present a case of poliosis with depigmentation of the underlying skin and very slightly decreased density of the white hairs in which alopecia areata was not suspected until microscopic examination of the biopsy had occurred. Vitiligo has been shown to be associated with other autoimmune disorders, particularly hyperthyroidism and hypothyroidism,
Fig. 2. The biopsy demonstrated a peribulbar lymphocytic infiltrate (hematoxylin/eosin).
151
Walker et al.
Fig. 3. Melanocyte-specific staining patterns observed in our patient (left) and in normal scalp of an age-matched patient (right).
psoriasis and hearing loss due to dysfunction of melanocyte-related cells in the stria vascularis.11 – 13 Vitiligo is also associated with several syndromes, most notably autoimmune polyendocrinopathy-candidiasis-ectodermal dysplasia, in which alopecia areata can be a feature.14 Multiple hypotheses exist for the pathogenesis of vitiligo, including the autoimmune, neurohumoral and autocytotoxic theories. Within the autoimmune theory, alterations in both humoral and cellular immunity are implicated. Antibodies to pigment cell-specific antigens and common tissue antigens have been identified in the sera of vitiligo patients.15 Epidermotropic CD8+ T cells, many of which
152
are directed against cells expressing Melan-A, have also been identified in these patients.16 An autoimmune-oriented mechanism of pathogenesis is well-supported for alopecia areata and is based upon the loss of immune privilege of the hair follicle. It is hypothesized that an increase in pro-inflammatory signals causes expression of previously sequestered major histocompatibility complex class I receptors in the follicular epithelium, which in turn attract a CD8+ T-cell lymphocytic infiltrate to attack the hair follicle.17,18 As the lymphocytic infiltrate typically affects only anagen follicles, it has been proposed that autoantigens from anagen-specific processes such as melanogenesis
Vitiligo with alopecia areata
Fig. 4. Epidermal melanocytes were not detected (Melan-A immunostain).
are targeted by the CD8+ T-cell-mediated destruction.18,19 The melanocyte staining patterns seen on our patient’s biopsy are an interesting element of our case. Absence of melanocytic staining within the epidermis of our patient’s biopsy
was not surprising, given the clinically depigmented skin. However, melanocyte staining in the follicular structure was variable. In the follicular matrix, only tyrosinase, and to a lesser extent MiTF, showed positive staining. All four stains were positive in the matrix on the control biopsy. In the external root sheath of the follicular epithelium, only Melan-A was positive in scattered cells. On the control biopsy, Melan-A and MiTF showed positive staining in the root sheath. The presence of root sheath cells expressing Melan-A with absence of Melan-A-positive cells in the epidermis may be due to the fact that epidermal melanocytes are believed to be antigenically distinct from melanocytes within follicular epithelium.20 The loss of MiTF-expressing cells in the follicular epithelium of our patient may represent loss of putative melanocyte stem cells, which have been identified as a population of MiTF-positive, Melan-A-negative non-pigment-producing melanocytes located in this portion of the hair follicle.21,22
Table 1. Clinical features of reported cases with colocalization of vitiligo and alopecia areata Age/sex/ethnicity
Location of colocalization
Clinical appearance
Treatment and follow-up
9/F/not stated None 18/F/African-American Depigmented areas on lips
Scalp, occipital Scalp, occipital
Depigmented alopecic patch Depigmented alopecic patch
17/F/Korean
None
Eyebrow and eyelashes
12/F/Indian
None
Lateral eyelid
Depigmented alopecic patch on eyebrow; poliosis and alopecia of ipsilateral eyelashes Depigmented alopecic patch
Not described1 Topical steroid; lost to follow-up2 Ultraviolet light therapy and topical minoxidil; some improvement of lesions3
60/F/not stated 53/F/Caucasian
Scalp Entire scalp
Depigmented alopecic patch Depigmented alopecic patches
8/M/Caucasian
Hypothyroidism Vitiligo of face and upper extremities (since age 10); hyperthyroidism None
Scalp, frontal
Depigmented alopecic patch
42/M/Indian
None
Scalp
Two depigmented alopecic patches
12/M/not stated
Depigmented areas on scalp, face, neck, extremities (since age 8) Alopecia of upper extremities (since age 16); widespread vitiligo (since age 30) None
Scalp, eyebrows
Alopecic patches on areas of previously depigmented skin
Upper extremities
Depigmentation of previously alopecic patches
Not described10
Scalp, frontal
Poliosis; depigmented skin
Topical clobetasol; enlargement of lesion and development of additional lesion
33/M/not stated
10/M/Caucasian
Additional findings
Prostaglandin-E2 eyedrops; complete skin repigmentation and regrowth of pigmented eyelashes4 Not described5 Not described6
Topical mometasone furoate; complete regrowth of white hairs7 Topical mometasone furoate; complete hair regrowth and repigmentation of hairs and skin8 Not described9
F, female; M, male.
153
Walker et al. While the significance of this variable melanocyte staining pattern remains uncertain, it does suggest a convergence of the pathogeneses of vitiligo and alopecia areata. Our case is unique in its clinical presentation of poliosis with alopecia areata not identified until biopsy interpretation. We feel that this
presentation, coupled with the curious immunohistochemical findings regarding melanocytes, supports an interplay of vitiligo and alopecia areata pathogenetic elements manifesting in clinically and microscopically variable stages of disease evolution.
References 1. Dhar S, Kanwar A. Colocalization of vitiligo and alopecia areata. Pediatr Dermatol 1994; 11: 85. 2. Adams B, Lucky AW. Colocalization of alopecia areata and vitiligo. Pediatr Dermatol 1999; 16: 364. 3. Cho HR, Lee MH. Colocalization of segmental vitiligo and alopecia areata. Korean J Dermatol 2007; 45: 115. 4. Yadav S, Dogra S, Kaur I. An unusual anatomical colocalizaion of alopecia areata and vitiligo in a child, and improvement during treatment with topical prostaglandin E2. Clin Exp Dermatol 2009; 34: 1010. 5. Ramot Y, Thomaidou E, Mali A, Zlotogorski A. An extraordinary colocalization of alopecia areata and vitiligo. Int J Trichology 2010; 2: 108. 6. Rodriguez-Martin M, Merino M, Contreras P, et al. Anatomical colocalization of vitiligo and alopecia areata. Open Autoimmunity J 2010; 2: 193. 7. Ozcan D, Aydogan FC. Concurrence of alopecia areata and vitiligo at the same anatomical site. Australas J Dermatol 2012; 53: 61. 8. Krishnaram AS, Saigal A, Adityan B. Alopecia areata-vitiligo overlap syndrome: an emerging clinical variant. Indian J Dermatol Venereol Leprol 2013; 79: 533.
154
9. Kumar S, Mittal J, Mahajan BB. Colocalization of vitiligo and alopecia areata: coincidence or consequence? Int J Trichology 2013; 5: 50. 10. Harris JE. Vitiligo and alopecia areata: apples and oranges? Exp Dermatol 2013; 22: 785. 11. Iacovelli P, Singara JL, Vidolin AP, Marenda S, Capitanio B, Leone G, Picardo M. Relevance of thyroiditis and of other autoimmune diseases in children with vitiligo. Dermatology 2005; 210: 26. 12. Powell FC, Dicken CH. Psoriasis and vitiligo. Acta Derm Venereol 1983; 63: 246. 13. Gopal KV, Rama Rao GR, Kumar YH, Appa Rao MV, Vasudev P. Vitiligo: a part of a systemic autoimmune process. Indian J Dermatol Venereol Leprol 2007; 73: 162. 14. Ahonen P, Myllarniemi S, Sipila I, Perheentupa J. Clinical variation of autoimmune polyendocrinopathy-candidiasisectodermal dystrophy (APECED) in a series of 68 patients. N Engl J Med 1990; 322: 1829. 15. Bystryn JC. Serum antibodies in vitiligo patients. Clin Dermatol 1989; 7: 136. 16. Ogg GS, Rod Dunbar P, Romero P, Chen JL. High frequency of skin-homing melanocyte-specific cytotoxic T lymphocytes in autoimmune vitiligo. J Exp Med 1998; 188: 1203.
17. Paus R, Slominski A, Czarnetzki BM. Is alopecia areata an autoimmune-response against melanogenesis-related proteins, exposed by abnormal MHC class I expression in the anagen hair bulb? Yale J Biol Med 1993; 66: 541. 18. Ito T, Ito N, Bettermann A, Tokura Y, Takigawa M, Paus R. Collapse and restoration of MHC class-I-dependent immune privilege: exploiting the human hair follicle as a model. Am J Pathol 2004; 164: 623. 19. Wade MS, Sinclair RD. Persistent depigmented regrowth after alopecia areata. J Am Acad Dermatol 2002; 46: 619. 20. Tobin DJ, Bystryn JC. Different populations of melanocytes are present in hair follicles and epidermis. Pigment Cell Res 1996; 9: 304. 21. Lu S, Slominski A, Yang SE, Sheehan C, Ross J, Carlson JA. The correlation of TRPM1 (Melastatin) mRNA expression with microphthalmia-associated transcription factor (MITF) and other melanogenesis-related proteins in normal and pathological skin, hair follicles and melanocytic nevi. J Cutan Pathol 2010; 37(Suppl 1): 26. 22. Cu J, Shen L, Wang G. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol 1991; 97: 410.
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Journal of Cutaneous Pathology
Colocalization of vitiligo and alopecia areata presenting as poliosis Vitiligo and alopecia areata are two cutaneous diseases believed to be primarily autoimmune in pathogenesis. While the coexistence of the two conditions in the same patient has been well-described, reports of the two disease processes occurring in the same location are rare. We report the case of a 10-year-old male with an unremarkable past medical history who presented with a single localized area of poliosis with depigmented underlying skin on the frontal scalp. The hair in the affected area was relatively decreased in density. A punch biopsy of the depigmented patch demonstrated features consistent with both vitiligo and alopecia areata. The decreased number of large hair follicles and a focal peribulbar lymphocytic infiltrate around an anagen follicle were suggestive of alopecia areata. A panel of melanocyte-specific stains revealed absent melanocytes in the epidermis, consistent with vitiligo. Loss of microphthalmia-associated transcription factor-positive root sheath cells was seen, suggestive of loss of melanocyte stem cells. The combination of clinical and histopathologic findings supports the theory of a common pathogenesis of alopecia areata and vitiligo. Keywords: alopecia, hair follicle, scalp Walker A, Mesinkovska NA, Boncher J, Tamburro J, Bergfeld WF. Colocalization of vitiligo and alopecia areata presenting as poliosis. J Cutan Pathol 2015; 42: 150–154. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Report of a patient A 10-year-old male presented with a localized area of poliosis and depigmentation of the underlying skin (Fig. 1). The 3 × 2 cm triangular-shaped patch was present on the left frontal scalp and had been present for at least 6 weeks. The hairs within this patch of skin were white and showed a questionable decrease in density. No other areas of poliosis or skin depigmentation were identified. There was no history of trauma to the affected area. Family history included a possible depigmentation disorder in the patient’s maternal great-grandmother and an undefined thyroid condition in the patient’s father. The patient himself had no medical
150
Addie Walker1 , Natasha Atanaskova Mesinkovska1,2 , Julia Boncher3 , Joan Tamburro2 and Wilma F. Bergfeld1,2 1
RJ Tomisch Institute of Pathology and Laboratory Medicine, Cleveland Clinic, Cleveland, OH, USA, 2 Department of Dermatology, Cleveland Clinic, Cleveland, OH, USA , and 3 Department of Pathology, University of New Mexico, Albuquerque, NM, USA
Wilma F. Bergfeld Robert J Tomisch Pathology and Laboratory Medicine Institute L25, Cleveland Clinic, Cleveland, OH 44195, USA Tel: +504 453 3349 Fax: +216 445 6967 e-mail: [email protected] Accepted for publication June 7, 2014
problems aside from a speech problem in early childhood; no abnormalities were detected on audiological testing. Thyroid-stimulating hormone, T3, free T4 and complete blood count were all within normal limits. A punch biopsy was taken from the area of poliosis. Topical clobetasol was started for treatment of the affected area. At follow-up 2 months later, the depigmented skin patch and poliosis had not improved. Additional loss of density of the white hairs in the depigmented area was observed, and a second similar-appearing 2 × 0.8 cm patch of poliosis and depigmented skin had developed. The new patch was located on the frontal scalp, separate from the initial area.
Vitiligo with alopecia areata
Fig. 1. An area of poliosis and underlying depigmented skin was observed on the patient’s left frontal scalp.
stains showed positivity in the root sheath. For comparison, when performed on a normal scalp biopsy from an age-matched patient, all four stains highlighted melanocytes in the epidermis and follicular matrix. Cells with strong Melan-A and MiTF nuclear staining were also identified within the external root sheath on the normal biopsy. Additional special stains performed included periodic acid-Schiff (PAS) with and without diastase, which showed Pityrosporum yeast forms in the stratum corneum; Gram stain which was negative for bacteria; and colloidal iron stain with and without digestion, which did not reveal increased dermal mucin.
Histopathologic examination of the punch biopsy from the initial area of poliosis demonstrated features of vitiligo and alopecia areata. Hematoxylin and eosin staining showed an unremarkable epidermis. Within the dermis, a slight decrease in large hair follicles was noted. A dense peribulbar infiltrate was present around an anagen follicle (Fig. 2). These features were suggestive of alopecia areata, which had not been clinically suspected. A panel of stains that highlight various melanocytic elements – Melan-A, microphthalmia-associated transcription factor (MiTF), Fontana-Masson and tyrosinase – was performed to assess pigmentation (Fig. 3). None of the four stains labeled junctional cells, suggesting an absence of epidermal melanocytes compatible with vitiligo (Fig. 4). Within the hair follicles, matrix melanocytes were strongly positive with tyrosinase, weakly positive with MiTF and negative with Melan-A and Fontana-Masson. Rare cells scattered throughout the external root sheath of the follicular epithelium were positive with Melan-A stain. None of the other three
Discussion While concomitant occurrence of vitiligo and alopecia areata in the same patient has been well-described, only a small number of cases of the occurrence of both disease processes at the same site have been reported. Searches for ‘vitiligo, poliosis and alopecia’ using pubmed.gov and google.com search engines yielded 10 cases of colocalization published as of April 7, 2014 (Table 1).1 – 10 Patients of both sexes, of various ethnicities and of various age groups were represented. Two of the patients had thyroid disease, and two had pre-existing areas of vitiligo or alopecia areata prior to developing colocalization. The most commonly affected area was the scalp. We present a case of poliosis with depigmentation of the underlying skin and very slightly decreased density of the white hairs in which alopecia areata was not suspected until microscopic examination of the biopsy had occurred. Vitiligo has been shown to be associated with other autoimmune disorders, particularly hyperthyroidism and hypothyroidism,
Fig. 2. The biopsy demonstrated a peribulbar lymphocytic infiltrate (hematoxylin/eosin).
151
Walker et al.
Fig. 3. Melanocyte-specific staining patterns observed in our patient (left) and in normal scalp of an age-matched patient (right).
psoriasis and hearing loss due to dysfunction of melanocyte-related cells in the stria vascularis.11 – 13 Vitiligo is also associated with several syndromes, most notably autoimmune polyendocrinopathy-candidiasis-ectodermal dysplasia, in which alopecia areata can be a feature.14 Multiple hypotheses exist for the pathogenesis of vitiligo, including the autoimmune, neurohumoral and autocytotoxic theories. Within the autoimmune theory, alterations in both humoral and cellular immunity are implicated. Antibodies to pigment cell-specific antigens and common tissue antigens have been identified in the sera of vitiligo patients.15 Epidermotropic CD8+ T cells, many of which
152
are directed against cells expressing Melan-A, have also been identified in these patients.16 An autoimmune-oriented mechanism of pathogenesis is well-supported for alopecia areata and is based upon the loss of immune privilege of the hair follicle. It is hypothesized that an increase in pro-inflammatory signals causes expression of previously sequestered major histocompatibility complex class I receptors in the follicular epithelium, which in turn attract a CD8+ T-cell lymphocytic infiltrate to attack the hair follicle.17,18 As the lymphocytic infiltrate typically affects only anagen follicles, it has been proposed that autoantigens from anagen-specific processes such as melanogenesis
Vitiligo with alopecia areata
Fig. 4. Epidermal melanocytes were not detected (Melan-A immunostain).
are targeted by the CD8+ T-cell-mediated destruction.18,19 The melanocyte staining patterns seen on our patient’s biopsy are an interesting element of our case. Absence of melanocytic staining within the epidermis of our patient’s biopsy
was not surprising, given the clinically depigmented skin. However, melanocyte staining in the follicular structure was variable. In the follicular matrix, only tyrosinase, and to a lesser extent MiTF, showed positive staining. All four stains were positive in the matrix on the control biopsy. In the external root sheath of the follicular epithelium, only Melan-A was positive in scattered cells. On the control biopsy, Melan-A and MiTF showed positive staining in the root sheath. The presence of root sheath cells expressing Melan-A with absence of Melan-A-positive cells in the epidermis may be due to the fact that epidermal melanocytes are believed to be antigenically distinct from melanocytes within follicular epithelium.20 The loss of MiTF-expressing cells in the follicular epithelium of our patient may represent loss of putative melanocyte stem cells, which have been identified as a population of MiTF-positive, Melan-A-negative non-pigment-producing melanocytes located in this portion of the hair follicle.21,22
Table 1. Clinical features of reported cases with colocalization of vitiligo and alopecia areata Age/sex/ethnicity
Location of colocalization
Clinical appearance
Treatment and follow-up
9/F/not stated None 18/F/African-American Depigmented areas on lips
Scalp, occipital Scalp, occipital
Depigmented alopecic patch Depigmented alopecic patch
17/F/Korean
None
Eyebrow and eyelashes
12/F/Indian
None
Lateral eyelid
Depigmented alopecic patch on eyebrow; poliosis and alopecia of ipsilateral eyelashes Depigmented alopecic patch
Not described1 Topical steroid; lost to follow-up2 Ultraviolet light therapy and topical minoxidil; some improvement of lesions3
60/F/not stated 53/F/Caucasian
Scalp Entire scalp
Depigmented alopecic patch Depigmented alopecic patches
8/M/Caucasian
Hypothyroidism Vitiligo of face and upper extremities (since age 10); hyperthyroidism None
Scalp, frontal
Depigmented alopecic patch
42/M/Indian
None
Scalp
Two depigmented alopecic patches
12/M/not stated
Depigmented areas on scalp, face, neck, extremities (since age 8) Alopecia of upper extremities (since age 16); widespread vitiligo (since age 30) None
Scalp, eyebrows
Alopecic patches on areas of previously depigmented skin
Upper extremities
Depigmentation of previously alopecic patches
Not described10
Scalp, frontal
Poliosis; depigmented skin
Topical clobetasol; enlargement of lesion and development of additional lesion
33/M/not stated
10/M/Caucasian
Additional findings
Prostaglandin-E2 eyedrops; complete skin repigmentation and regrowth of pigmented eyelashes4 Not described5 Not described6
Topical mometasone furoate; complete regrowth of white hairs7 Topical mometasone furoate; complete hair regrowth and repigmentation of hairs and skin8 Not described9
F, female; M, male.
153
Walker et al. While the significance of this variable melanocyte staining pattern remains uncertain, it does suggest a convergence of the pathogeneses of vitiligo and alopecia areata. Our case is unique in its clinical presentation of poliosis with alopecia areata not identified until biopsy interpretation. We feel that this
presentation, coupled with the curious immunohistochemical findings regarding melanocytes, supports an interplay of vitiligo and alopecia areata pathogenetic elements manifesting in clinically and microscopically variable stages of disease evolution.
References 1. Dhar S, Kanwar A. Colocalization of vitiligo and alopecia areata. Pediatr Dermatol 1994; 11: 85. 2. Adams B, Lucky AW. Colocalization of alopecia areata and vitiligo. Pediatr Dermatol 1999; 16: 364. 3. Cho HR, Lee MH. Colocalization of segmental vitiligo and alopecia areata. Korean J Dermatol 2007; 45: 115. 4. Yadav S, Dogra S, Kaur I. An unusual anatomical colocalizaion of alopecia areata and vitiligo in a child, and improvement during treatment with topical prostaglandin E2. Clin Exp Dermatol 2009; 34: 1010. 5. Ramot Y, Thomaidou E, Mali A, Zlotogorski A. An extraordinary colocalization of alopecia areata and vitiligo. Int J Trichology 2010; 2: 108. 6. Rodriguez-Martin M, Merino M, Contreras P, et al. Anatomical colocalization of vitiligo and alopecia areata. Open Autoimmunity J 2010; 2: 193. 7. Ozcan D, Aydogan FC. Concurrence of alopecia areata and vitiligo at the same anatomical site. Australas J Dermatol 2012; 53: 61. 8. Krishnaram AS, Saigal A, Adityan B. Alopecia areata-vitiligo overlap syndrome: an emerging clinical variant. Indian J Dermatol Venereol Leprol 2013; 79: 533.
154
9. Kumar S, Mittal J, Mahajan BB. Colocalization of vitiligo and alopecia areata: coincidence or consequence? Int J Trichology 2013; 5: 50. 10. Harris JE. Vitiligo and alopecia areata: apples and oranges? Exp Dermatol 2013; 22: 785. 11. Iacovelli P, Singara JL, Vidolin AP, Marenda S, Capitanio B, Leone G, Picardo M. Relevance of thyroiditis and of other autoimmune diseases in children with vitiligo. Dermatology 2005; 210: 26. 12. Powell FC, Dicken CH. Psoriasis and vitiligo. Acta Derm Venereol 1983; 63: 246. 13. Gopal KV, Rama Rao GR, Kumar YH, Appa Rao MV, Vasudev P. Vitiligo: a part of a systemic autoimmune process. Indian J Dermatol Venereol Leprol 2007; 73: 162. 14. Ahonen P, Myllarniemi S, Sipila I, Perheentupa J. Clinical variation of autoimmune polyendocrinopathy-candidiasisectodermal dystrophy (APECED) in a series of 68 patients. N Engl J Med 1990; 322: 1829. 15. Bystryn JC. Serum antibodies in vitiligo patients. Clin Dermatol 1989; 7: 136. 16. Ogg GS, Rod Dunbar P, Romero P, Chen JL. High frequency of skin-homing melanocyte-specific cytotoxic T lymphocytes in autoimmune vitiligo. J Exp Med 1998; 188: 1203.
17. Paus R, Slominski A, Czarnetzki BM. Is alopecia areata an autoimmune-response against melanogenesis-related proteins, exposed by abnormal MHC class I expression in the anagen hair bulb? Yale J Biol Med 1993; 66: 541. 18. Ito T, Ito N, Bettermann A, Tokura Y, Takigawa M, Paus R. Collapse and restoration of MHC class-I-dependent immune privilege: exploiting the human hair follicle as a model. Am J Pathol 2004; 164: 623. 19. Wade MS, Sinclair RD. Persistent depigmented regrowth after alopecia areata. J Am Acad Dermatol 2002; 46: 619. 20. Tobin DJ, Bystryn JC. Different populations of melanocytes are present in hair follicles and epidermis. Pigment Cell Res 1996; 9: 304. 21. Lu S, Slominski A, Yang SE, Sheehan C, Ross J, Carlson JA. The correlation of TRPM1 (Melastatin) mRNA expression with microphthalmia-associated transcription factor (MITF) and other melanogenesis-related proteins in normal and pathological skin, hair follicles and melanocytic nevi. J Cutan Pathol 2010; 37(Suppl 1): 26. 22. Cu J, Shen L, Wang G. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol 1991; 97: 410.
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
