Clinical features of vitiligo

Clinical

Features of Vitiligo

SEUNG-KYUNG HANN, MD YOON-KEE PARK, MD WOO HYUNG CHUN, MD

V

itiligo is a relatively common depigmentary disorder occurring in approximately 1% of the general population without racial, sexual, or regional differences. 1 The classification of vitiligo into localized, generalized, and universal types according to distribution is widely used.’ Localized type includes focal, mucosal, and segmental. The generalized type includes acrofacial, vulgaris, and mixed type. The universal type is defined as complete or nearly complete depigmentation. Vitiligo can also be classified into two major clinical types, segmental and nonsegmental.“+ Lesions distributed along the ipsilateral dermatome, whose central part does not cross the midline, constitute segmental vitiligo. In segmental vitiligo, depigmented patches are confined to a particular dermatome, the patients are generally young, and disease activity usually ceases after one to two years of rapid spread over the particular dermatome. Nonsegmental vitiligo includes all cases not classified as segmental, such as localized, generalized, and acrofacial. It can occur at any age, and new depigmented patches continue to appear throughout the patient’s life; and it is frequently associated with a poor prognosis.’

Progression

Pattern

of Vitiligo

The course of vitiligo on a case-by-case basis is unpredictable. Vitiligo spreads either by appearance of new depigmented macules or by centrifugal enlargement of preexisting lesions, or both. The natural course of the disease is usually one of slow progression, but it may stabilize or exacerbate rapidly. In our study, vitiligo was progressive in 73.6% of patients at the time of visit, and onlv 1.3% showed regression of disease.5 Segmental vitili& usually spreads over the affected dermatoma1 area, so the progression pattern can be easily predicted; however, nonsegmental vitiligo spreads progressively over the whole body, without any known specific pattern. Our study revealed the progression pattern of nonsegmental vitiligo and its implications on prognosis.; In this study, the body surface was divided

into nine topographical areas to record the distribution of lesions. They were face, neck, anterior trunk, posterior trunk, genital area, upper extremities, lower extremities, hands, and feet. The activity, or progression, of vitiligo was defined as the development of new lesions or the extension of old lesions during the 3 months prior to examination. Successive progression of the lesions was recorded when vitiligo lesions had spread from the initial site to other s&es in number and/or in size. The progression rate was assessed by applying the following formula: Progression

rate =

(Number of patients whose vitiligo started from a particular site but progressed to another site) (Number of all patients whose vitiligo started from a particular site)

x 100.

The progression pattern of vitiligo from the initial sites was analyzed when the vitiligo started from the face, neck, anterior trunk, posterior trunk, and hands. The progression rate of nonsegmental vitiligo according to the initial sites is shown in ‘T;?blc 1. The terms one site and two sites are used in ‘Tabi? 1 to refer to the involvement of at least one or two body-surface areas respectively, in addition to the initial site. When the face was the initial site, the progression of vitiligo was k?dSt with 64.8% and 52.4%. The average rate of progression for more than one and two sites were 75.8% and 65.1%,, respectively. When the posterior trunk, hands, or feet were the initial sites, there was progression of vitiligo in over 90% of the patients. The progression pattern of nonsegmental vitiligo starting from the face, neck, anterior trunk, posterior trunk, and hands is shown in 7’nbk 2. The percentages indicate the respective progression rates from the initial sites to other specific body-surface areas. Body surface areas contiguous to the initial sites usually showed the highest percentage rates of progression; however, when the hands were the initial site, vitiligv most commonly progressed to the face. The progression of nonsegmental vitiligo had significant differences according to the site of the initial lesions. When the initial sites were the posterior trunk, hands, or feet, there was more widespread progression to other body area%; there was less progression when the initial sites wt*re the face and

HANN

892

Table 1. Vitilixo

Clinics in Dermatology

ET AL.

Initial Sites and Progression

Rates of Nonsegmental Progression

Initial

Sites

Incidence ?%)

Face Neck Anterior trunk Posterior trunk Genitalia Upper extremity Lower extremity Hands Feet Total

124 33 75 31 5 10 18 20 2 318

(39.0) (10.4) (23.6) (9.1) (1.6) (3.1) (5.7) (6.3) (0.6)

rate (%)

One Site*

Two Sitest

81 28 61 28 4 6 12 19 2 241

65 22 55 25 3 6 12 17 2 207

(64.8) (84.8) (81.3) (90.3) (80.0) (60.0) (66.7) (95.0) (100.0) (75.8)

(52.4) (66.7) (73.3) (80.6) (60.0) (60.0) (66.7) (85.0) (100.0) (65.1)

* One site = involvrmmt of atleast one body surface nrea in addition to the initial site. t Two sites = involvement of at least two body surface mm in addition to the initial site.

upper or lower extremities. These results indicate that the prognosis of vitiligo may be predicted by the location of the initial lesions. The progression pattern of nonsegmental vitiligo was usually contiguous from the initial site regardless of the location. This was interesting, because nonsegmental vitiligo is usually associated with autoimmune diseases,6,7and one would expect a generalized haphazard progression if autoimmune mechanisms were involved in its pathogenesis. When the hands were the initial site, vitiligo most commonly progressed to the face. This could be explained clinically by the fact that one-third of the patients whose vitiligo started from the hands were of the acrofacial type. In summary, the progression rate and pattern of nonsegmental vitiligo can be predicted to some extent Table 2.

The Proaression

Pattern of Nonseamental

Vitiliao

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1997;15:891-897

according to the initial sites of involvement. When the posterior trunk, hands or feet were initial sites, there was more widespread progression of vitiligo.

Factors Affecting

Vitiligo

Progression

It is important to assay the prognosis or progression of vitiligo based on commonly available clinical parameters. Definitive factors that predict progression of vitiligo are speculative, although emotional shock, physical illness, sunburn, and pregnancy are often mentioned as initiating or aggravating factors by patients. These subjective experiences vary from one patient to another and cannot be used by the dermatologist to advise new patients. Objective clinical characteristics such as sex, family history, clinical type, onset age, duration, Koebner’s phenomenon, leukotrichia, and mucous membrane involvement may be relevant in predicting the progression of vitiligo. Various clinical characteristics and their significance in the progression of vitiligo were evaluated in a report by a group of investigators.8 The summary of clinical characteristics of progressive and nonprogressive vitiligo is presented in Table 3. Vitiligo affects both sexes equally, but a higher proportion of women can be attributed to the fact that female patients are more sensitive cosmetically; however, there is no difference between the sexes where progression of vitiligo is concerned.8 Vitiligo is probably an inherited condition, with melanocytes of some individuals being genetically abnormal and predisposed to destruction and development of vitiligo. The prevalence of a positive family history of

from Initial Sites Initial Sites

Face Spreading

Neck

Anterior

Trunk

Posterior Trunk

Hands

Sites

Face (25:%) Neck

25t (30.9%)

Anterior

trunk

Posterior

trunk

(29Z%)

(5Ofi%)

(114x)

(4.h)

(7.Y%) 0 0 0 0

(1175%)

(7.i%)

(3.i%)

(1175x)

(9.&) 0 0

(14f3%) 0 0

(4.i%) 0 0

Genitalia (6.;%) Upper

extremity

Lower

extremity

(29:!%) (9.E%)

Hands Feet

*The number t The number

of patients of patients

whose initial site is the face. whose second involved site is the neck.

(lOi%)

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De~matofo~yy

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Table 3. Summa y of Clinical Characteristics Nonprogressive Vitiligo

Clinical

Parameter

of Progressive and

Progressizlf Vitiligo (N = 355)

Nonprogressive Vitiligo (N = 45)

137 218

15 30

VLLe >0.05

Sex

Men Women Family history Present Absent Clinical type Segmental Nonsegmental Onset age (years) Duration (years) Koebner phenomenon Present

Absent Leukotrichi,> Present

Absent Mucosal involvement Present Absent

co.05 51

304

44 co.05

66 289 20.2

X.1 80

16 29 16.5 4.2

275

4 41

158 197

16 29

255 100

41 4

>0.05 co.05 co.05

>0.05

10.05

vitiligo has been reported in the literature to be from 6.25% to 38%.“J” The incidence for family history of vitiligo was 13% in our study. Patients with positive family histories showed a higher degree of progression statistically;8 to our knowledge this fact has not been previously substantiated. Segmental and nonsegmental vitiligo differ substantially in their pathogenesis and clinical aspects. The activity of segmental vitiligo usually ceasesafter a short period; however, nonsegmental vitiligo generally spreads progressively over the whole body throughout the patients’ lives.8Jl Our results statistically verified that nonsegmental vitiligo is associated with a worse clinical prognosis. The mean age of onset was not important in predicting the progression of vitiligo. Patients with no progression were relatively younger, and this could be expected, because childhood vitiligo is associated with a high incidence of segmental vitiligo and a consequently better prognosis, .lz however, there was no statistical evidence to confirm that an early onset portends less progression. The duration of the disease was important in evaluating the progression of vitiligo. Patients with longer duration demonstrated a significant progression of vitiligo. This point was emphasized previously, but corroborative data was lacking.13 Koebner’s phenomenon refers to the development of vitiligo or other skin diseases after a physical injury, such as a cut, burn, or abrasion; and it is present in at least one-third of vitiligo patients.’ Our study demonstrates that patients with Koebner’s isomorphic phenomenon are more likely to have progressive vitiligo. Leukotrichia is commonly observed in vitiligo, and it has been reported in 9 to 45%

Figure 1.

Generaked

zlifiligo distrihuki

oil the hod!/

of vitiligo patients. 13~4Leukotrichia may be a marker for poor prognosis in repigmentation.’ 1 Nearly 442/oof our patients had leukotrichia, but their vitiligo did not progress more significantly than patients without leukotrichia. Mucosal involvement occltrs rather frequently around body orifices such as the lips, genitals, gingiva, areolae, and nipples. Significant progression of vitiligo in patients with mucosal involt.emen t indicates that it is a poor prognostic factor. In summary, certain clinical characteristics such as presence of family history, clinical type, duration of disease, Koebner’s phenomenon and mucosal involvement may be relevant in predicting the progression or prognosis of vitiligo.

Clinical

Features

of Nonsegmental

Vitiligo

Nonsegmental vitiligo comprises all types of vitiligo other than segmental, such as localized, generalized (Fig 2) and acrofacial vitiligo. In a recently reported study, there were 63 (19.8%) localized, 248 (78.0%) genpatients5 Altoeralized, and 7 (2.2%) acrofacial VitiligcJ gether 289 (90.9%) patients showed progression, while 29 (9.1%) patients did not show progression. The most common initial lesion site was the face (39.0%), followed by the anterior trunk (23.6%), neck (,10.4%), and posterior trunk (9.1%). It is somewhat difficult to generalize the results of this study to the w,hole population of vitiligo patients, because our patients had visited a tertiary vitiligo clinic and were therehrre likely to represent a more sexwe/chronic subset.’

894

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1997;15:891-897

Figure 3. Sepnental vitilizo cfistributerf in ophtlmlruic of trigeminal dermatowe.

Figure 2. Segmental vitiligo righf thovacic dernzatome.

Clinical

Features

distributed

of Segmental

in linear puffer?z

011

Vitiligo

In 1977, an investigator divided vitiligo into segmental (type B) and nonsegmental types (type A).3 He described segmental vitiligo as depigmented patches confined to a definite dermatome, akin to herpes zoster (Figs 2 and 3). He proposed that the pathogenesis and clinical manifestation of the two types were different from each other, based on his experiment in which sweat secretion was stimulated by local injection of physiostigmine. The segmental type results from dysfunction of the sympathetic nervous system in the affected skin area, while nonsegmental type results from immunologic mechanisms. The clinical features of vitiligo have been reported by many investigators;9J3J-r9 however, the study of segmental vitiligo has rarely been reported, and the numbers of patients studied limited. The incidence of segmental type is variable; one group of investigators reported 5%,20 another group reported 27.9%,4 and previous Korean studies show a range between 5.5-16.1%.i”J9 Vitiligo develops at all ages, but it usually occurs in young people between the ages of 10 and 3O;l3,15,21 however, according to an epidemiologic study reported

branch

in 1977,22about half of the patients developed vitiligo after 40 years of age, which was very different from other clinic-based studies. On the other hand, one group reported that onset of nonsegmental vitiligo could occur at any age, whereas segmental vitiligo generally affected the young.4 In our report,‘l segmental vitiligo developed before 30 years of age in 87.0% of the patients, and 41.3% were younger than 10 years. This is in accord with the report that segmental vitiligo occurs in young people before they are 30.” The commonly involved sites of vitiligo are exposed areas, such as the face and dorsum of the hand. In our study of segmental vitiligo,l’ the involved sites were the face, trunk, neck, extremities, and scalp, in descending order (Table 4). An older study reported that vitiligo occurs as single lesions in 75% of cases,23which was the situation with 87.0% of the patients in our study. Table 4.

Site of Segmental Vitiligo Men (%)

Head & Face Neck Scalp Trunk Chest Back Extremities Upper Lower Total

Neck

and abdomen

extremities extremities

57 49 7 1 21 17 4 13 7 6

(62.6) (53.8) (7.7) (1.1) (23.1) (18.7) (4.4) (14.3) (7.7) (6.6) 91

Women (%) 87 65 20 2 34 31 3 11 7 4

(65.9) (49.2) (15.2) (1.5) (25.8) (23.5) (2.3) (8.3) (5.3) (3.0) 132

Total (%) 144 114 27 3 55 48 7 24 14 10

(64.6) (51.1) (12.1) (1.4) (24.7) (21.5) (3.1) (10.8) (6.3) (4.5) 223

Table 5.

Vermatomal

Distribution

Deumatome Trigeminal Cervical Thoracic Lumbar Sacral Tota I ---

49 (53.9) 12 (13.2) 19 (20.9) IO (1 1.1)) l(1.1) Yl

of Segmental Vitilipo Women (%)

Total (%J

65 (50.8) 26 (20.3) 31(24.2) 4 (3.1) 2 (1.6) 128

114(52.1) 38 (17.4) 50 (22.8) 14 (6.4) 3 (1.4) 219

Dermatomal distribution revealed that the trigeminal nerve was most frequently involved, followed by the thoracic, cervical, lumbar, and sacral nerves (Table 5). There were five cases with segmental vitiligo that occurred bilaterally, following the same and different dermatomes in our recent study (data unpublished). Like herpes zoster,?-‘J5 segmental vitiligo rarely appears bilaterally. We appraised whether hand dominancy has any relation with vitiligo involving the right or left side of the body, but there was no significant relationship between these two factors. The left side was slightly more involved, regardless of the dominant hand. Poliosis, known to be associated with vitiligo in 8.9-45% of cases,‘?I7 occurred in 48.6”/0in our study. The eyebrows and scalp hair were mostly involved (46.7%); this is because when vitiligo involves the face, neck, and scalp, poliosis of the eyebrows and scalp hair is commonly present (67.4%). Physical trauma, sunburn, psychological stress, inflammation, pregnancy, contraceptives, and others are known to be the precipitating factors of vitiligo. But unlike other reports,15.18,” there was nothing particularly worth mentioning except for sunburn, trauma, and pregnancy. Family history was present in 11.5%, similar to the 7.4% reported by one group’9 and 12% by another.“,“ A pair of investigators claimed that segmental vitiligo is not associated with other autoimmune diseases,20 but another group found that they were associated in about 9.5% of their cases.ly There was one group of investigators who asserted that an autoimmune disease occurred more significantly in nonsegmental vitiligo than in segmental vitiligo, and that this difference was due to different pathogenetic mechanisms.” In our report, association with thyroid diseases, diabetes mellitus, pernicious anemia, and halo nevus, which frequently accompany vitiligo, was seen in 3.4%;” and this was lower than in other reports;‘sJH however, that could not justify the conclusion that autoimmune mechanisms are restricted to nonsegmental vitiligo, because systemic and topical steroid treatment and psoralen and ultraviolet A (PUVA) therapy can inhibit spreading and induce repigmentation of new lesions of segmental vitiligo, especially on the face?’

Figure 4. Bilateral segmental oitiligo distributed in lirrval pattern on both right and left thoracic dermatome. l’he right side lesions are located at the shoulder and arm, the i$/ silfe kions are located at the IouTer chest anti upper alvforr?~~:~.:vhi~.lt (ii? no/ cross the midline.

Bilateral

Segmental

Vitiligo

The depigmented lesions of segmental vitiligo do not always assume a true dermatomal pattern according to the peripheral nervous system; Not all the patterns of segmental vitiligo follow dermatomal distribution, unlike herpes zoster.‘” Blaschko’s lines or acupuncture lines can be applied to the pattern of segmental vitiligo.2’ From our recent study, five cases of bilateral segmental vitiligo were found among 240 casebof segmcntal vitiligo, in which the vitiligo lesions appeared on the same or different dermatomes on both sides of the body (Fig 4). The clinical characteristics of bilateral segmental vitiligo are shown in Table 6. PUVA therapy and steroid treatment could induce repigmentation or stop progression of vitiliginous lesions in bilateral segmental vitiligo. Because segmental vitiligo has clinical features that differ from nonsegmental vitiligo, it is quite important to classify the type of vitiligo. The depigmented patches of segmental vitiligo usually remain unchanged for the rest of the patient’s life. Therefore, stable segmental vitiligo is a good candidate for epidermal grafting and can be cured almost completely without recurrence.28,2y On the other hand, if segmental vitiligo occurs bilaterally, following the same or different dermatomes, it may cause confusion in defining the type of Gtiligo. As segmental vitiligo can rarely appear bilaterally follow-

896

HANN

Table 6.

Clinics in Dermatology

ET AL.

Clinical Characteristics

of Bilateral

Distribution

F/4 F/6

F/8 F/27 F/12

Duration 2 4 2 3 2

months years years years years

Right

Left Chest, Chest, Chest, Chest, Chest,

back, back, back, back, arm

arm arm arm arm

ing dermatomal distribution such as in herpes zoster,25 it may mimic some other type of nonsegmental vitiligo. The clinical course of bilateral segmental vitiligo seems to be the same as unilateral segmental vitiligo.

Trichrome

1997;15:891-897

Segmental Vitiligo

Patient Sex/Age

l

Vitiligo

Trichrome vitiligo is a rare type of vitiligo, in which an intermediate hue of varying width exists between the normal and totally depigmented skin (Fig 5).30,31 The term “trichrome vitiligo” was suggested by Fitzpatrick, who observed this gradual change of color from milkwhite in the center through light tan to normal brown at the periphery of the lesion.30 In our patients, we observed that the intermediate hue, light brown broad band was surrounded peripherally by a dark brown border.32 Thus we prefer the name “quadrichrome vitiligo” rather than trichrome vitiligo. This intermediate hue is often found on the trunk, and it is accentuated in those who have dark skin. The significance of trichrome is unknown; but it is a transitional pigmentary state, though it may persist for months to years with little change. Several authors interpreted trichrome as suggestive of a gradual centrifugal spread of hypomelanosis or stepwise depigmentation,30,33 but other authors pointed out that the sharp demarcation between the three areas in their cases, as well as the lack of gradual changes of color and the stability of the lesions, is

Chest, Buttock, Chest, Chest, Chest,

arm thigh back, arm back, arm back, arm

Treatment Systemic steroid Topical steroid Topical steroid Systemic PUVA Systemic PUVA

Response to Treatment No progression No change Repigmentation Repigmentation Repigmentation

inconsistent with the interpretation of trichrome vitiligo as an active, centrifugally spreading lesion.s4Our recent study showed that trichrome vitiligo is an active, centrifugally spreading lesion through clinico-histopathological studies.32 Trichrome vitiligo occurred mostly on the trunk in active vitiligo vulgaris. Vacuolar degeneration and inflammatory-cell infiltration were more prominent in light brown skin and dark brown perilesional normal skin than in vitiliginous skin and normal skin of trichrome vitiligo.

Leukoderma

Mimicking

Vitiligo

Differentiation of vitiligo from other hypopigmentary disorders is important. These include nevus depigmentosus, pityriasis alba, tinea versicolor, piebaldism, lichen sclerosus et atrophicus (LSA), idiopathic guttate hypomelanosis, scleroderma, nevus anemicus. Nevus depigmentosus is the most often encountered differential diagnosis in vitiligo clinics. Nevus depigmentosus is a congenital, and stable, localized leukoderma that has discrete, regular, or often serrated margins.35 Nevus depigmentosus is often discovered within several months after birth, so most infant patients having clinically apparent vitiligo actually have nevus depigmentosus. Tinea versicolor of children often appears as white macules on the face, which often shows negative potassium hydroxide (KOH) examination and clinically resembles vitiligo. Early lesions of LSA resemble vitiligo, because there is no atrophy with the characteristic violaceous or hyperpigmented border. Piebaldism without a white forelock can appear as white patches on the flexural parts of both legs (Fig 6), which is easily misdiagnosed as vitiligo. Normal skin islands in the white patch with a positive family history can give differential points from vitiligo.

Conclusions

Figure 5. Trichrome vitiligo showing light brown broad band betweenvitiliginous and dark brown perilesional skin.

Vitiligo has various clinical features. Understanding these characteristics can give us some valuable information in differentiating vitiligo from other hypopigmentary disorders, in treating vitiligo with the proper method, and to predict the prognosis of vitiligo to some extent.

Clinks

iir D~w~atolo,~y

Figure 6. (!f 77ornml

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7997;1.5:897-897

Piebnldism, skowin,y wkite pat&es with some islmds Skiff

077 flrc

f7t?Yrrr-al

p7'fS

(f

lmth

lqs.

References 1. Moscher DB. Vitiligo: Etiology, pathogenesis, diagnosis, and treatment. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, editors. Dermatology in general medicine. 4th ed. New York: McGraw-Hill, 1993;923-33. 2. Nordlund JJ, Lerner AB. Vitiligo: It is important. Arch Dermatol 1982;118:5-8. 3. Knga M. Vitiligo: A new classification and therapy. Br J Dermatol 1977;97:255-61. 4. Koga M, Tango T. Clinical features and course of type A and type B vitiligo. Br J Dermatol 1988;118:223-8. 5. Hann SK, Chun WH. The progression of nonsegmental vitiligo: Clinical analysis of 318 patients. Int J Dermatol (in press). 6. Norris DA, Kissinger RM, Naughton GM. Evidence for immunologic mechanisms in human vitiligo: Patients’ sera induce damage to human melanocytes in vitro by complement-mediated damage and antibody-dependent cellular toxicitv. J Invest Dermatol 1988;90:783-9. 7. Harning R, C;i J, Bystryn JC. Relation between the incidence and level of pigment cell antibodies and disease activity in vitiligo. J Invest Dermatol 1991;97:1078-80. 8. Harm SK, Chun WH, Park YK. Clinical characteristics of progressive vitiligo. lnt J Dermatol 1997;36:353-5.

9. Lerner AB. Vitiligo. J Invest Dermatol 1959;32:285-310. 10. Song MS, Harm SK, Ahn PS, et al. Clinical study of vitiligo: Comparative study of type A ,md type R vitiligo. Ann Dermatol (Seoul) 1994;6:22-30. 11. Hann SK, Lee HJ. Segmental vitiligo: Clinical findings in 208 patients. J Am Acad Dermatol 1996;35:671--3. 12. Halder RM, Grimes PE, Cowan CA, itt al. Childhood vitiligo. J Am Acad Dermatol 1987;16.948--54. 13. Seghal VN. A clinical evaluation of 202 cases or vitiligo. cutis 1974;14:439-45. 14. Dutta AK, Mandal SB. Clinical stud! \)t 6.50 vitiligo cases and their classification. Indian J Dermatol iY69;14:103-15. 15. Park SY, Youn JI, Lim SD. A clinical study of ? i 7 case> of vitiligo. Korean J Dermatol 1981;lc): 145-X?. 16. Lee HS, Harm SK, Park YK. Clinical shlciy of 1% patients occurred after puberty. J Wonju Chill Mt>d 1990;3:168-73. 17. Harm SK, Park YK, Whang KC, et al. Clinical study of I74 patients with generalized vitiligo. KOX+II~ 1 Dcrmatol 1986;24:798-805, 18. Harm SK, Song MS, Park YK, et ,ll. Childhood vitiligo: Clinical study compared with adult \~itili~~. .Ann Derrnato1 (Seoul) 1991;3:112-8. 19. Park KC, Youn Jl, Lee YS. Clinical study ot 3% cases of vitiligo. Korean J Dermatol 1988;26:20!) ---5. 20. El Mofty AM, El Mofty M. Vitiligo: A s~,mptom complex. Int J Dermatol 1980;19:238-47. 21. Behl PN, Bhatia RK. 400 cases of vitiiigik--ts &wan 1 Derof oral corticosteroids matol 1995;33:880-,5. 27. Bolognia JL, 0rlow SJ, Gilck SA. iLmc>s {\f 13iaschko. J Am Acad Dermatol 1994;31: 157-90. 28. Hann SK, Im S, Park YK, et al. Repigmwtaticvl of Ieukotrichia by epidermal grafting ,md syskwic psoraleii plus L’V-A. Arch Dermatol 1992;128:09S--cl. 29. Harm SK, Im S, Bong HW, rt al. ‘r’r
J Dermatol

1996;2.3:

IX7--cjll