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SPOTLIGHT ON VITILIGO RESEARCH
Year : 2013  |  Volume : 58  |  Issue : 6  |  Page : 433-438
Segmental and generalized vitiligo: Both forms demonstrate inflammatory histopathological features and clinical mosaicism


1 Visakha Institute of Skin and Allergy, Marripalem, Visakhapatnam, Andhra Pradesh, India
2 Department of Dermatology, Dewsbury District and General Hospital, Dewsbury, WF13 4HS, United Kingdom

Date of Web Publication17-Oct-2013

Correspondence Address:
Venkat Ratnam Attili
Visakha Institute of Skin and Allergy, Marripalem, Visakhapatnam - 530 018, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5154.119949

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   Abstract 

Background: Segmental vitiligo (SV) and generalized vitiligo (GV) are perceived to evolve by different mechanisms, the former with unspecified neural mechanisms and the latter by melanocyte specific autoimmune mechanisms. However, the two diverse mechanisms are difficult to reconcile in cases of "mixed vitiligo." To test the possibility of a common pathogenesis, we reviewed clinical and histopathological features of SV and GV. Materials and Methods: As part of an ongoing histopathological study on vitiligo and vitiligo like lesions, over a 10 year period from 2002 to 2011, biopsies were taken routinely from evolving or recently evolved lesions. 50 cases of SV with quasi-dermatomal distribution and 154 cases of GV were identified and the clinical and histopathological features were compared. Results: Mild clinical inflammation was recorded in 33 of 154 GV cases but, none among 50 SV had such features. In addition to bilateral symmetrical involvement, mirror image lesions with unusual segmentation were observed in nine cases of GV. SV with a few bilateral lesions (4) and GV with quasi-dermatomal lesions (3), i.e., mixed vitiligo, were included in their corresponding groups for analytical purposes. Focal lichenoid inflammation of varying degrees around epidermal/adnexal melanocytes was identified as a common feature in evolving lesions of both SV (78%) and GV (70%). Conclusions: SV and GV demonstrated a similar inflammatory histopathological spectrum. "Segmentation/mosaicism," identified for the first time in GV is another unifying factor. Cutaneous mosaicism harboring fragile melanocyte populations, which are susceptible to external as well as auto-inflammatory mechanisms, is an attractive hypothesis to pursue in the causation of vitiligo.


Keywords: Generalized vitiligo, lichenoid inflammation, segmental vitiligo, segmentation/mosaicism


How to cite this article:
Attili VR, Attili SK. Segmental and generalized vitiligo: Both forms demonstrate inflammatory histopathological features and clinical mosaicism. Indian J Dermatol 2013;58:433-8

How to cite this URL:
Attili VR, Attili SK. Segmental and generalized vitiligo: Both forms demonstrate inflammatory histopathological features and clinical mosaicism. Indian J Dermatol [serial online] 2013 [cited 2019 Sep 23];58:433-8. Available from: http://www.e-ijd.org/text.asp?2013/58/6/433/119949

What was known?
1. Segmental vitiligo (SV) and generalized vitiligo (GV) are perceived to evolve by different mechanisms; the former with unspecified neural mechanisms and the latter by melanocyte specific autoimmune mediated inflammation.
2. Recent reports of "mixed vitiligo," with features of both SV and GV indicate common factors in the pathogenesis.



   Introduction Top


Immunological studies indicate T-cell mediated autoimmune destruction of melanocytes in vitiligo.[1],[2],[3],[4],[5],[6] Never the less, the status of vitiligo among other autoimmune inflammatory skin diseases has not been clearly established because of scanty, inconclusive histopathological studies[7],[8],[9],[10],[11],[12],[13],[14] and very few reports of associated clinical inflammation.[15],[16],[17],[18],[19] The clinical patterns of vitiligo are also diverse and therefore the disease is considered as a complex syndrome with multiple etiopathogenic factors, either singularly or in unison, being responsible for the disease.[20] Vitiligo is mainly classified into localized segmental vitiligo (SV) and non-segmental vitiligo (NSV) forms. Among the latter, generalized vitiligo (GV) cases with bilateral, symmetrical lesions constitute 50-90% and therefore considered as the prototype.[21] SV is considered different from GV in many aspects as: It preponderantly affects younger patients; stabilizes early in a limited quasi-dermatomal distribution indicating involvement of neural/developmental mechanisms; and is relatively resistant to medical treatments.[22],[23],[24],[25] Histopathological and immunological studies in SV have been few and inconclusive.[26] Therefore, the autoimmune hypothesis generally accepted in GV has not been considered in SV. Lichenoid inflammation in all clinical types of vitiligo including SV[12] and recent reports of “mixed vitiligo” combining features of both patterns[27],[28] suggest common pathogenetic mechanisms. To test this hypothesis further with a focus on SV, we reviewed biopsies taken from a large number of SV and compared the histopathological features with those seen in GV.


   Materials and Methods Top


Patients who had an unequivocal clinical diagnosis of vitiligo, seen in our clinic from 2002 to 2011 were identified from our electronic database. In all such cases, as part of a long-term study on vitiligo and vitiligoid lesions in our institute, biopsies were routinely taken from the margins of all evolving or recently (less than 3 months duration) evolved lesions. Total duration of the disease, as well as the age of the biopsied lesion was recorded. A clear diagnosis of vitiligo was made after a thorough clinical and histological review, excluding other diseases that may result in transient or persisting post-inflammatory depigmentation. Clinical features of lesions such as, macular well defined margins, trichrome or punctate extension, marginal inflammation, leucotrichia and Koebner's phenomenon (KP), were recorded. GV was diagnosed when the disease presented with generalized bilateral lesions, while unilateral lesions in a linear distribution, were considered as SV. To eliminate a possible misdiagnosis of nevus depigmentosus,[29] only SV lesions with a quasi- dermatomal distribution were selected, excluding other phenotypes and children under the age of 3 years.

In all cases, 4 mm punch biopsies were taken from the margins of evolving or recently evolved lesions. Hematoxylin and eosin, stained sections were examined systematically for signs of inflammation: Cellular infiltrates and consequent structural alterations in the epidermis and dermis. Lesions were classified as “inflammatory” when lymphocytic infiltration was seen around melanocytes either in the basal layer or in adnexal adventitium. This was graded as L1 when there were small clusters of lymphocytes observed around melanocytes [Figure 1] and L2 when focal lichenoid inflammation was observed [Figure 2]. Lesions that had no significant lymphocytic infiltration were further sub-classified as (a) “early post-inflammatory” with basement zone disarray, pigment incontinence and melanophages in the papillary dermis [Figure 3] and (b) “late post-inflammatory” with degeneration of adnexal structures and fibrosis [Figure 4] and [Figure 5]. Additional biopsies were also taken from skin expressing KP (10 cases), spontaneously repigmenting areas of skin (12 cases, all from the GV series, as these were not seen in SV) and eleven long-standing lesions of more than 5 years duration as they had textural changes of mild atrophy or thickening on clinical examination (8 lesions from the legs in GV cases; and 3 from SV involving the forehead including the eye brows).
Figure 1: (a) Evolving segmental vitiligo of 3 months duration with (b) Lymphocytic clusters around melanocytes in the basal layer (grade L1) and pigment incontinence (H and E, ×40)

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Figure 2: (a) Evolving segmental vitiligo of 2 months duration with (b) Focal lichenoid inflammation targeting melanocytes (grade L2) (H and E, ×20)

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Figure 3: (a) Fully depigmented segmental vitiligo with (b) Recent post-inflammatory changes at the interface: Thin epidermis, hazy basement zone and pigment incontinence with macrophages (H and E, ×40)

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Figure 4: (a) Persisting leucotrichia in a partially repigmented segmental vitiligo lesion (>6 years) with (b) Follicular centered lymphocytic infiltration (H and E, ×20)

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Figure 5: (a) Persisting segmental vitiligo lesion (>8 years) with partial repigmentation showing (b) Degenerating follicles, mild fibrosis and absence of eccrine units (H and E, ×20)

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   Results Top


A total of 154 cases of GV including four cases of universal vitiligo with near total body involvement and 50 cases of SV were identified from our electronic patient database. Seven cases of SV/NSV mixed pattern were identified in this series and were classified according to the major presenting pattern: SV with few bilateral lesions in four and evolving GV with quasi-dermatomal lesions [Figure 6] in three cases. Majority of SV lesions involved the head and neck (28), followed by the limbs (13) and trunk (9). In 9/154 GV cases (4 of 66 with predominant involvement of the trunk and 5 of 88 with predominant acral involvement); the lesions on both halves of the body were exact mirror images. Some had horizontal and some curved anatomical cut off lines giving an impression of unusual bilateral segmentation/mosaicism [Figure 7]a-f.
Figure 6: (a) Rapidly evolving punctate generalized vitiligo over trunk along with (b and c) concurrently evolving bilateral segmental vitiligo like lesions over lower face

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Figure 7: (a) Segmented unilateral face lesion in generalized vitiligo. (b) Trunk and bilateral limb involvement distally restricted sharply by wrist lines. (c) Progressive GV with midline restriction of fresh evolving lesions over abdomen. (d) Involvement of both palms proximally restricted by wrist lines in GV. (e) Mirror image trunk lesions in GV. (f) Unusual segmentation with curved lines over both feet in GV

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The clinical profiles and histopathological features of SV and GV are presented in [Table 1]. The sex ratios were similar in both the groups with SV affecting a slightly younger age group. Trichrome extension, marginal inflammation and KP were absent in the SV group but, leucotrichia was more frequent and appeared among early evolving lesions. Punctate evolution [Figure 2], [Figure 6] and [Figure 8] was seen among both SV (9/50) and GV (26/154) cases. Though features of clinical inflammation (Marginal scaling, erythema and hyper pigmentation are considered as mild inflammatory signs in vitiligo)[12] were significantly more common among GV, histopathological features in both groups were not very different; with lesions either demonstrating varying grades of lymphocytic infiltration targeting melanocytes in the epidermal basal layer and adnexal adventitia or post-inflammatory changes [Table 1]. Long standing lesions demonstrated structural alterations of a milder nature in SV [Figure 5] compared with those in GV reported earlier.[12] 9 out of 10 KP and 10/12 repigmenting areas demonstrated significant inflammatory features on histology [Figure 9] and [Figure 10].
Table 1: Clinical profiles of SV and GV patients

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Figure 8: (a) Punctate evolving generalized vitiligo over the back with (b) Lymphocytic clusters around epidermal melanocytes with loss of melanocytes and loss of pigment around the acrosyringium (H and E, ×20)

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Figure 9: (a) Focal lichenoid infiltrates (H and E, ×40) in (b) Skin expressing Koebner's phenomenon

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Figure 10: (a) Spontaneous repigmentation associated with (b) Focal lymphocytic infiltration around the follicular infundibulum in a case of universal vitiligo of over 20 years duration (H and E, ×40)

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   Discussion Top


A common pathogenesis and causative factors for vitiligo have eluded researchers because of the varied clinical patterns and behavior. However, our observations indicate that the two major types SV and GV share a similar inflammatory evolution and structural alterations. Punctate lesions, which we consider to be a hallmark of disease progression, were seen in both SV and GV [Figure 2] and [Figure 8] and demonstrated similar inflammatory histological features. Leucotrichia, which is generally considered as a late sign in GV, was observed in early evolving SV lesions [Figure 11]a-c and persisted for many years; in some cases, with apparent unabated follicular inflammation [Figure 4]. These observations are consistent with the opinion that follicular melanocytes can be preferentially affected in SV.[30] On the other hand, trichrome spreading margins and marginally inflamed lesions exclusively seen among cases of GV, suggest preferential involvement of epidermal melanocytes with a wave like progression, resulting in the trichrome effect. KP induced by minor trauma is an indicator of predisposition to vitiligo in apparently normal skin in GV. Absence of KP in SV is consistent with the opinion that the disease process is localized in most cases.
Figure 11: (a) Post-inflammatory changes centered over the hair follicle (H and E, ×40) in segmental vitiligo of 3 weeks duration (b and c) with leucotrichia appearing along with early depigmentation of the skin

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The histopathological spectrum of vitiligo suggests a sequence of events initiated by focal lichenoid inflammation targeting melanocytes in the epidermis [Figure 1], eccrine/follicular antra [Figure 8], followed by the dermal components of eccrine and follicular structures, leading to their gradual destruction with post-inflammatory changes [Figure 4] and [Figure 5]. Immunological studies carried out in vitiligo in the past have been selective for marginally inflamed vitiligo lesions in progressive GV. Consistent with the inflammatory features observed in this series of SV, presence of CD 8 cells was reported in a SV case associated with a halo nevus,[26] indicating a T-cell mediated immune response as observed in GV. Further elaborate immunological studies are indicated.

Our study demonstrates focal lichenoid inflammation around melanocytes and post-inflammatory sequelae with the loss of melanocytes, in both SV and GV. These features may not be absolutely diagnostic of vitiligo but help to differentiate nevoid depigmentations that may appear late at prepuberty or adolescence, from SV.[31] Mixed patterns of SV/GV seen among our patients and similar reports in literature[27],[28] lend weight to a unifying theory. Bilateral pleuri-segmental SV and mixed vitiligo cases appear to bridge the spectral gap between localized SV and GV. Further studies on such cases should help us better understand the pathogenesis of vitiligo.

Mixed patterns of vitiligo are presumed to be progression from localized SV to GV. However, a reverse phenomenon of segmentation of lesions occurring in progressive GV was observed in our series [Figure 6] and [Figure 7]. Although bilateral symmetrical involvement in GV has been well-known, this is the first time that mirror image lesions have been observed. Bilateral/pleuri-segmental lesions of SV, mirror image/sharply segmented lesions in GV and the recent discovery of “mixed vitiligo” cases, all suggest that mosaicism may be a common factor to both. The difficulty in differentiating bilateral SV from bilateral segmented GV [Figure 7]b lends further support to this hypothesis. Multiplicity of mosaics affected in GV may not be appreciated when lesions do not extend up to the pre-determined cut off lines and simply may give an impression of bilateralism. Detailed pattern analysis of bilaterally symmetrical GV cases in a large number, might help us identify and characterize these mosaic patterns. We believe that GV evolves as two basic forms: One that evolves rapidly with central body preponderance and the acral form with an insidiously slow and intermittent progression. Recognition of bilateral mosaic patterns in the former category might prove extremely difficult, as the evolution is rapid.

A consensus is emerging with vitiligo increasingly perceived as a disease affecting segments or mosaics of skin, either genetically or developmentally populated by fragile melanocytes that are vulnerable to external or internal insults (multi-hit hypothesis).[32],[33],[34],[35] It has recently been suggested that “SV pattern” probably represents a distinct and new (“type 6”) pattern of cutaneous mosaicism, that defies existing Happle type's.[35] The relationship between SV and GV can be akin to other autoimmune skin diseases with localized and disseminated forms; a good example being alopecia areata, another silent inflammatory disease. However, it remains a puzzle as to why the disease is unilaterally limited in SV, while progresses at an equal pace over the two halves of the body in GV, resulting in unique mirror image lesions. Probably yet another unknown central mechanism needs to be explored.

“Arresting disease progression and re-establishing pigmentation are conceptually different phases of the disease that may have to be addressed by separate therapeutic means because establishing pigmentation in patients with active disease is problematic.”[36] This opinion is supported by the histopathological features, which suggest the progressive phase as “inflammatory” and inactive phase as “post-inflammatory persisting depigmentation.” The latter may be sub-classified as (a) early: With minimal structural alterations and (b) late: With the absence of adnexal structures and subsequent loss of dermal melanocyte reservoirs. Such information should be useful in selecting appropriate treatment protocols: Oral/topical steroids or immune modulators/suppressants to arrest the inflammatory progressive phase and treatments aimed at upward migration of the dermal melanocytes (i.e., phototherapy) for promoting repigmentation, in the post-inflammatory phase. For longstanding lesions with adnexal destruction where melanocyte migration from the depleted dermal reservoir is unlikely, various surgical grafting techniques can be considered. The concept of stability implying a standstill in the disease activity is difficult to judge in the absence of objective parameters. Moreover, inflammatory cellular infiltration observed in spontaneously repigmenting areas in GV raises the question whether re-pigmentation can in turn reactivate autoimmune mechanisms [Figure 10]. Therefore “stability” determined by the patient's history and clinical parameters can be unreliable for planning therapy. Absence of cellular infiltrates on histopathological assessment[37] or test grafting[38] may prove to be better parameters, when contemplating surgery for “stable” or long standing focal lesions. However, caution needs to be exercised, as sustained stability cannot be guaranteed in autoimmune diseases where remissions and relapses are unpredictable.

 
   References Top

1.Bystryn J. Theories on the pathogenesis of depigmentation: Immune hypothesis. In: Hann KS, Nordlund JJ, editors. Vitiligo: A Monograph on the Basic and Clinical Science. 1 st ed. Oxford, London: Blackwell Science Ltd.; 2000. p. 129-37.  Back to cited text no. 1
    
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3.Le Poole IC, van den Wijngaard RM, Westerhof W, Das PK. Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. Am J Pathol 1996;148:1219-28.  Back to cited text no. 3
    
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5.Das PK, van den Wijngaard RM, Wankowicz-Kalinska A, Le Poole IC. A symbiotic concept of autoimmunity and tumour immunity: Lessons from vitiligo. Trends Immunol 2001;22:130-6.  Back to cited text no. 5
    
6.Ongenae K, Van Geel N, Naeyaert JM. Evidence for an autoimmune pathogenesis of vitiligo. Pigment Cell Res 2003;16:90-100.  Back to cited text no. 6
    
7.Hann SK, Park YK, Lee KG, Choi EH, Im S. Epidermal changes in active vitiligo. J Dermatol 1992;19:217-22.  Back to cited text no. 7
    
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11.Gokhale BB, Mehta LN. Histopathology of vitiliginous skin. Int J Dermatol 1983;22:477-80.  Back to cited text no. 11
    
12.Attili VR, Attili SK. Lichenoid inflammation in vitiligo - A clinical and histopathologic review of 210 cases. Int J Dermatol 2008;47:663-9.  Back to cited text no. 12
    
13.Kim YC, Kim YJ, Kang HY, Sohn S, Lee ES. Histopathologic features in vitiligo. Am J Dermatopathol 2008;30:112-6.  Back to cited text no. 13
    
14.Horn TD, Abanmi A. Analysis of the lymphocytic infiltrate in a case of vitiligo. Am J Dermatopathol 1997;19:400-2.  Back to cited text no. 14
    
15.Eng AM. Marginal inflammatory vitiligo. Cutis 1970;6:1005-8.  Back to cited text no. 15
    
16.Yagi H, Tokura Y, Furukawa F, Takigawa M. Vitiligo with raised inflammatory borders: Involvement of T cell immunity and keratinocytes expressing MHC class II and ICAM-1 molecules. Eur J Dermatol 1997;7:19-22.  Back to cited text no. 16
    
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18.Arata J, Abe-Matsuura Y. Generalized vitiligo preceded by a generalized figurate erythematosquamous eruption. J Dermatol 1994;21:438-41.  Back to cited text no. 18
    
19.Michaëlsson G. Vitiligo with raised borders. Report of two cases. Acta Derm Venereol 1968;48:158-61.  Back to cited text no. 19
    
20.Le Poole IC, Das PK, van den Wijngaard RM, Bos JD, Westerhof W. Review of the etiopathomechanism of vitiligo: A convergence theory. Exp Dermatol 1993;2:145-53.  Back to cited text no. 20
    
21.Hann KS, Nordlund JJ. Clinical features of generalized vitiligo. In: Hann KS, Nordlund JJ, editors. Vitiligo: A Monograph on the Basic and Clinical Science. 1 st ed. Oxford, London: Blackwell Science Ltd.; 2000. p. 35-49.  Back to cited text no. 21
    
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26.van Geel NA, Mollet IG, De Schepper S, Tjin EP, Vermaelen K, Clark RA, et al. First histopathological and immunophenotypic analysis of early dynamic events in a patient with segmental vitiligo associated with halo nevi. Pigment Cell Melanoma Res 2010;23:375-84.  Back to cited text no. 26
    
27.Ezzedine K, Gauthier Y, Léauté-Labrèze C, Marquez S, Bouchtnei S, Jouary T, et al. Segmental vitiligo associated with generalized vitiligo (mixed vitiligo): A retrospective case series of 19 patients. J Am Acad Dermatol 2011;65:965-71.  Back to cited text no. 27
    
28.Mulekar SV, Al Issa A, Asaad M, Ghwish B, Al Eisa A. Mixed vitiligo. J Cutan Med Surg 2006;10:104-7.  Back to cited text no. 28
    
29.Lee HS, Chun YS, Hann SK. Nevus depigmentosus: Clinical features and histopathologic characteristics in 67 patients. J Am Acad Dermatol 1999;40:21-6.  Back to cited text no. 29
    
30.Hann S. Particular clinical characteristics of Segmental vitiligo. In: Picardo M, Taïeb A, editors. Vitiligo. Berlin, Heidelberg: Springer; 2010. p. 296-8.  Back to cited text no. 30
    
31.Sheth PB. Differential diagnosis of vitiligo vulgaris. In: Hann KS, Nordlund JJ, editors. Vitiligo: A Monograph on the Basic and Clinical Science. 1 st ed. Oxford, London: Blackwell Science Ltd.; 2000. p. 101-20.  Back to cited text no. 31
    
32.Taïeb A, Morice-Picard F, Jouary T, Ezzedine K, Cario-André M, Gauthier Y. Segmental vitiligo as the possible expression of cutaneous somatic mosaicism: Implications for common non-segmental vitiligo. Pigment Cell Melanoma Res 2008;21:646-52.  Back to cited text no. 32
    
33.van Geel N, Mollet I, Brochez L, Dutré M, De Schepper S, Verhaeghe E, et al. New insights in segmental vitiligo: Case report and review of theories. Br J Dermatol 2012;166:240-6.  Back to cited text no. 33
    
34.Picardo M, Taïeb A. Editor's synthesis. In: Picardo M, Taïeb A, editors. Vitiligo. 1 st ed. London: Springer; 2010. p. 311-5.  Back to cited text no. 34
    
35.van Geel N, Speeckaert R, Melsens E, Toelle SP, Speeckaert M, De Schepper S, et al. The distribution pattern of segmental vitiligo: Clues for somatic mosaicism. Br J Dermatol 2013;168:56-64.  Back to cited text no. 35
    
36.Mosenson JA, Zloza A, Klarquist J, Barfuss AJ, Guevara-Patino JA, Poole IC. HSP70i is a critical component of the immune response leading to vitiligo. Pigment Cell Melanoma Res 2012;25:88-98.  Back to cited text no. 36
    
37.Benzekri L, Gauthier Y, Hamada S, Hassam B. Clinical features and histological findings are potential indicators of activity in lesions of common vitiligo. Br J Dermatol 2013;168:265-71.  Back to cited text no. 37
    
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[PUBMED]  Medknow Journal  

What is new?
1. Segmental vitiligo (SV) and generalized vitiligo (GV) demonstrated a similar histopathological spectrum.
2. Segmentation/Mosaicism, which is well-known in SV, is also observed in GV.
3. Cutaneous mosaicism harboring fragile melanocyte populations susceptible to external/or auto-inflammatory mechanisms is an attractive hypothesis to pursue in the causation of vitiligo.


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11]
 
 
    Tables

  [Table 1]

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