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SPOTLIGHT ON VITILIGO RESEARCH |
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| Year : 2013 | Volume
: 58
| Issue : 6 | Page : 433-438 |
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| Segmental and generalized vitiligo: Both forms demonstrate inflammatory histopathological features and clinical mosaicism |
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Venkat Ratnam Attili1, Sasi Kiran Attili2
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 Publication | 17-Oct-2013 |
Correspondence Address:
Venkat Ratnam Attili
Visakha Institute of Skin and Allergy, Marripalem, Visakhapatnam - 530 018, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
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 2023 Sep 21];58:433-8. Available from: https://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 | |  |
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 | | |
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)
Click here to view |
 | 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)
Click here to view |
| Results | | |
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
Click here to view |
 | 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]. | 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)
Click here to view |
 | 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)
Click here to view |
| Discussion | | |
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
Click here to view |
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.
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[PUBMED]  |
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.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11]
[Table 1] |
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