Kaur et al Journal of Drug Delivery & Therapeutics; 2012, 2(3): 53-59 53

Available online at http://jddtonline.info

REVEIW ARTICLE
A REVIEW ON LEUCODERMA AND REPORTED HERBS FOR ITS TREATMENT
Kaur Navneet* , Kaur Sukhbir, Sharma AK
CT Institute of Pharmaceutical Sciences, Jalandhar, Punjab, India-144020
Corresponding author’s Email ID: [email protected]
Received 24 M arch 2012; Revised 20 April 2012; Accepted 24 April 2012, Available online 15 M ay 2012

ABS TRACT:
Leucoderma is an acquired cutaneous disorder of pigmentation, with an incidence of 1% to 2% worldwide. There
are many hypotheses for the pathogenesis of leucoderma. Recent data provide strong evidence supporting an
autoimmune pathogenesis of leucoderma. Leucoderma can have major effect on quality of life. Topical therapy is
employed as first-line treatment in localized leucoderma. Plants have been the basis of many traditional medicines
throughout the world for thousands of years and continue to provide new remedies to mankind. The recent
resurgence of plant remedies resulted from several factors, such as effectiveness of plant medicines and lesser side
effects compared with modern medicines. Psoralen containing plants have been used for centuries in popular
medicine to treat leucoderma. Further advancement in treatments using different derivatives of psoralen molecules
may result in decrease possibility of long-term side effects such as cutaneous malignancies. In this review we wish
to present a detailed investigation on various herbs that can be used for the treatment of leucoderma.
Keywords: Leucoderma, melanin, psoralen, herbs, furanocoumarins

INTRODUCTION:
Leucoderma is the most common chronic depigmentation Bilateral or Generalized Leucoderma can begin at any age
disorder or hypopigmentation disorder affecting 1-2% of and tends to progress intermittently over the life of the
the world population 1 . It includes the loss of functioning patient. It produces depigmentation which is remarkably
melanocytes which causes the appearance of white patches symmytrical in distribution. A patch on the right side of
on the skin 2 . These white patches tend to become the body is matched by a patch in a similar location on the
progressive with time 3 . Any location on the body can be left side of the body. The entire body can depigment
affected and the people with leucoderma have white although it rarely does so.
patches in many areas of the body 4 . The disorder affects all
2).Unil ateral (or Segmental):
the races and both the sexes equally; however, it is more
noticeable in people with dark skin 5 . Unilateral or Seg mental Leucoderma co mmonly begins in
childrens and young adults and progresses for a limited
Although leucoderma is usually not harmfu l medically and
period, usually 1-2 years, and then remains static for the
causes no physically pain, its emot ional and psychological
rest of the life of the individual. It affects just one side of
effects can be devastating6 . Infact, in India, those with the
the body contrast to Bilateral Leucoderma, the distribution
disease, especially wo men, are sometimes discriminated
is asymmetrical on the skin.
against in marriage. Developing leucoderma after marriage
can be ground for divorce. Regardless of person’s race and MELANIN PIGMENT:
culture, wh ite patches of leucoderma can affect emotional
and psychological well-being and self-esteem. People with Melanins are polymorphous and multifunctional
biopolymers. It includes eumelanin, pheomelanin,
leucoderma can experience emotional stress, particularly if
neuromelan in and mixed melan in pig ment (shown in
the condition develops on the visible areas of the body
(such as face, hands, arms and feet) or on the genitals. figure 1)10 .
Adolescents, who are part icularly concerned about their Intact mature melanosomes pass from basal melanocytes
appearance, can be devastated by widespread leucoderma. into keratinocytes and their lysosomal compart ment to
Some people who have leucoderma feel embarrassed, become melanin dust in the upper nonviable layers of the
ashamed, depressed or worried about how others will skin 11 . Melanin is synthesized by melanocytes within
react 7 . melanosomes that are transferred into the surrounding
Leucoderma can be classified into two types 8, 9 : keratinocytes12 . The keratinocytes transport the melanin
and melanosomes from the basal layer of the epidermis to
1).Bilateral (or Generalized): the stratum corneu m where they are desquamated into the
environment (as shown in figure. 2)13 .

© 2011, JDDT. All Rights Reserved ISSN: 2250-1177 CODEN: JDDTAO

Kaur et al Journal of Drug Delivery & Therapeutics; 2012, 2(3): 53-59 54

Figure 1: Biosynthesis of Mel anin Pigment10

Figure 2: Factors Reg ulating Mammali an Melanogenesis 13

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Kaur et al Journal of Drug Delivery & Therapeutics; 2012, 2(3): 53-59 55

PATHOPHYS IOLOGY OF LEUCODERMA:

There are two basic mechanisms whereby the skin can destruction of melanocytes during postnatal life.
become white 14 . Some disorders inhibit or retard the Piebald ism affects the migration of melanocytes during
production of melan in formation and the skin develops embryogenesis and the infant is born with depig menattion
hypopigmentation 15 . Such disorders include, among many of the hair and skin. The et iology of leucoderma is poorly
others, oculocutaneous albinism, pityriasis alba, tinea understood. Various factors (stress, trauma, exposure to
vesicolor and nevus depigmentosus16 . In these disorders, sunlight, infections, malignancies, neural abnormalit ies,
melanocytes are present in normal nu mbers in the melatonin, receptor dysfunction, impaired melanocyte
epidermis but produce less than normal amounts of migrat ion, some drugs, endocrine disease and cytotoxic
melanin. Typically the skin exhib its mild to marked compounds) have been implicated in the development of
hypopigmentation. leucoderma. Despite these various factors the exact cause
of leucoderma remains unclear. Many theories 17
In contrast, other types of leucoderma are characterized by
(biochemical theory, cytotoxic theory, oxidant-antioxidant
the absence of melanocytes and therefore, complete
theory, neural theory, viral theory, autoimmune theory, self
absence of melan in. Such d isorders include piebaldis m, the
destruct theory, growth factor theory and convergence
leucoderma of lupus erythematosus and other scarring
theory) have been proposed to explain this disorder along
disorders and vitiligo. These types of leucoderma typically
with factors (as shown in table 1).
are totally depigmented. Vitiligo and lupus cause a

Table 1: Research Work on Leucoderma Skin

S .NO S TUDY ON VITILIGO S KIN S HOWS REFERNCE
1 Decreased Level of VIT1 mRNA 18
Elevated Level of M SH-6
2 Increased Area of Rough Endoplasmic Reticulum 19
3 Increased Level of T Cells 20
Increased Level of M acrophages
4 Presence of High Frequency of Skin-homing M elanocyte-specific Cytotoxic T Lymphocytes(CTL’s) 21
5 Increased Level of Th 17 Cells 22
Increased Level of Activated Dendritic Cells

TREATMENT AVAILAB LE FOR LEUCODERMA: b).Oral Psoralen Photochemotherapy: Oral PUVA

involves the admin istration of psoralens orally followed by
In general topical monotherapy is indicated for mild to
exposure to long-wavelength UVA irradiat ion.
moderate vitiligo 23,24 . Current treatment options for vitiligo
include med ical, surgical and additional treatments 25,26 . 3).Depig mentation: Dep ig mentation is a more drastic
Medical treat ment targets the immune system and helps to form of treatment, when leucoderma is extensive i.e.
arrest the spread of depigmentation 27,28 . In cases of stable leucoderma universalis. Depig mentation involves fading
vitiligo, repig mentation can be achieved by the rest of the skin on the body to match the already white
dermatosurgical techniques and additional includes use of areas by using permanent melanocytotoxic agents such as
cosmetics 29,30 . Both surgical and med ical t reatment have Monobenzyl ester of hydroquinone cream (Benzoquin), 4-
their own limitations. Additional can only cover the patch metho xyphenol (4-MP).
and can be used along with surgical and medical
B).Surgical Therapies
treatments 31 .
1).Autologous Skin Grafts: In this technique grafts are
A).Medical Therapies
implanted into perforations prepared at the recipient sites.
1).Topical Steroi d Therapy: Topical steroids are useful Pig ment spread leading to repigmentation can be
for the treatment of localized leucoderma. Marked or stimulated by phototherapies.
almost complete repig mentation can be obtained with
2).Skin Grafts Using Blisters : In this technique blisters
potent corticosteroids (betamethasone, valerate,
can be induced by different ways such as vacuum or liquid
triamcinolone) and very potent corticosteroids (clobetasol,
nitrogen. The mechanical split occurs at the
fluticasone propionate).
dermoepidermal junction. The recipient site is prepared by
2).Psoralen Photochemotherapy dermabrasion. The graft is applied and secured on the
recipient site.
a).Topical Psoralen Photochemotherapy: Topical PUVA
(Psoralen Plus UltraVio let light A) includes lower 3)Micropig mentation (Tattooing): In this technique
cumulat ive UVA doses than oral PUVA and lack of ocular permanent dermal micropig mentation is done by using a
and systemic to xicity. Low concentrations of psoralens nonallergic iron o xide pig ment to camouflage recalcitrant
should be used. The patient should be exposed to UVA areas of leucoderma.
approximately 20 to 30 minutes after application of the
4).Autologous Melanocyte Trans plant: In th is technique
topical preparation. Following treatment the area is
noncultured keratinocyte-melanocyte suspensions obtained
washed, a broad-spectrum sunscreen is applied and
fro m a shave biopsy of the buttock or full-thickness biopsy
excessive sun exposure is avoided for at least 24 hours.
© 2011, JDDT. All Rights Reserved ISSN: 2250-1177 CODEN: JDDTAO
Kaur et al Journal of Drug Delivery & Therapeutics; 2012, 2(3): 53-59 56

of the scalp and Melanocytes obtained from the hair 2).Cosmetic: Camouflage is often used to cover affected
follicles and interfollicu lar epidermis and keratinocytes are areas. This may be practical for patients that have minimal
placed into a suspension for direct applicat ion to the disease or segmental disease.
recipient site without expansion in culture.
NATURAL FURANOCOUMARINS AS
C).Additional Therapies TREATMENT FOR LEUCODERMA:
1).Sunscreen: Leucodermic skin is more susceptible to Psoralens belong to a group of heterocyclic compounds,
sunburn and long term photodamage. To prevent sun- the furanocoumarins, which are found in four or five major
induced darkening of the surrounding normal skin, broad plant families. The umbelliferae and rutacae are the largest
spectrum high protection factor sunscreens (SPF 15-30 ) and most important of these; the leguminosae and
which provide protection fro m UVB and UVA light should moraceae include few but widely distributed species.
be used. Chemical structures of Psoralen and Isopsoralen are
described (as shown in the figure. 3)59

Psoralen Isopsoralen
Figure 3: Chemical structures of Psoralen and Isops oralen 59
Many familiar edible plants as celery, figs, caraway, 1). Through the increased tolerance to sun, and ultraviolet
lemon, etc., contain psoralens. As such, psoralens are rays psoralens permit much longer solar or ultraviolet light
components, in normal d iet, and they may even play a role irradiation and thus allow stronger stimu lation to th e
in the physiology and biochemistry of normal hu man skin. melanocytes.
It is of interest to mention that psoralens are found in many
2). Dopa positive melanocytes have been claimed to be
herbal remedies that have been employed for centuries32,33 .
present in the so-called relative leucoderma.
Furanocoumarins are synthesized when the furan ring is
Repig mentation may occur in areas having melanocytes
built on a suitably substituted coumarin derivative. A furan
that still retain, although slightly, dopa positively but not in
ring can be condensed with a coumarin mo lecule in 12
areas having no dopa positive melanocytes. Psoralens may
different ways and each of the resulting compounds can
bring about stimu lation of these weak dopa positive
become the parent of a family of psoralen-like derivatives.
melanocytes to be actively engaged in melanogenesis.
Only those with a linear tricyclic structure resembling that
of psoralen are active, potent photosensitizers. Those with 3). Psoralens may induce migrat ion of active melanocytes
a non-linear structure (angular nodes) like that of iso- fro m the surrounding normal epidermis or hair
psoralen and iso-pseudo-psoralen are inactive34,35 . The melanocytes, lead to colonization of the depigmented areas
mechanis m of repig mentation of leucoderma patches under by the melanocytes of the pigmented hair bulb.
psoralen therapy cannot be clearly defined in the light of
the available knowledge of the cause of leucoderma. 4). Psoralens may correct the ultrastructural abnormalit ies
of the leucoderma melanocytes.
However, it may be justifiab le to suggest that one or more
of the following mechanis ms may operate in the process of
repig mentation of leucoderma 36,37 :
Table 2: Reported Herbs that are cl ai med to be used in the condi tion of Leucoderma
S.No Biological Name of The Family Common Name Acti ve Chemical Constituent Ref
Plant
1 Albizzia lebbek Black ebony Fabaceae Saponins, stigmastadienone 58
2 Aloe barbadensis Aloes Aloeaceae Antraquinone glycosides 55
3 Alstonia scholaris Indian devil t ree Apocyanaceae Hallucinogenic indole alkalo ids 55
4 Althaea officinalis Marshmallow Malvaceae Altheacoumarin g lycosides 42
5 Ammi majus Ammi Umbelliferae Furanocoumarins 41,52
6 Ammi visnaga Khella Umbelliferae Furanocoumarins 52
7 Angelica sinensis Dong quai Umbelliferae Ferulic acid 57
8 Apium graveolens Celery Umbelliferae Furanocoumarins 43
9 Arisaema amurense Tian nan xing Araceae Diacy lglycerlgalactoside 57
10 Aristolochia bracteata Bracteated Aristolochiaceae Anthraquinones 56
birthwort
11 Astragalus membranaceus Astragalus Fabaceae Saponins, flavonoids 57
12 Atractylodes japonica Japanese Co mpositae Patchoulene 57
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Kaur et al Journal of Drug Delivery & Therapeutics; 2012, 2(3): 53-59 57

atractylodes
13 Azadirachta indica Neem Meliaceae Azadirachtinol, nimbosterol 51,52
14 Bambusa arundinaceae Bamboo Bambusaceae Polyuronides, pentosans 53
15 Bituminaria bituminosa Arabian pea Fabaceae Furanocoumarins 44
16 Carthamus tinctorius Safflower Co mpositae Phenols, flavonoids 57
17 Cassia angustifolia Senna leaf Legu minosae Anthraquinone glycosides 42
18 Cassia occidentalis Coffee senna Caesalpiniaceae Anthraquinone glycosides 57
19 Citrullus colocynthis Wild gourd Cucurbitaceae Saponins, phytosterol glycosides, 58
alkaloids
20 Citrus limonia Rangpur Rutaceae Furanocoumarins 43
21 Cnidium officinale Chunkung Umbelliferae Butlyidenephthalide 57
22 Codonopisis pilosula Dang shen Campanulaceae Hesperidin, alpha spinosterol, 57
beta spinosterol
23 Cuscuta chinensis Chinese dodder Fabaceae Quercetin, kaemferol, hyperos ide 57
24 Dalbergia sissoo Dalberg ia Fabaceae Isoflavones, stigmasterols 53,58
25 Daucus carota Wild carrot Umbelliferae Furanocoumarins 38
26 Diplotaenia damavandica Kozal Umbelliferae Furanocoumarins 43
27 Eclipta alba Bhringraj Asteraceae Steroids, flavonoids 43
28 Elaeagnus bockii ------------ Elaegnaceae Furanocoumarins 43
29 Ficus carica Co mmon fig Moraceae Furanocoumarins 45
30 Foeniculum vulgare Fennel Umbelliferae Furanocoumarins 39
31 Gentiana scabra Chinese gentian Gentianaceae Xanthones, picroside 57
32 Ginko biloba Gingko Gin kgoaceae Furanocoumarins 46,52
33 Glycyrrhiza glabra Liquorice Fabaceae Glycyrrh itin ic acid, flavonoids 42
34 Helectoris isora Indian screw fruit Sterculiaceae Sitosterols, flavonoids 56
35 Lawsonia inermis Henna Lythraceae Xanthones, glycosides 53
36 Liquidambar formosana Formosan gum Hamamelidaceae Beta-sitasterol, oleanolic acid 56
37 Lyceum Chinese Wolfberry Solanaceae Beta-sitosterol,ferulic acid 56
38 Malva sylvastris Tall mallow Malvaceae Flavonoids, carotenoids, phenols 42
39 Melia azadirach Kattu vembu Meliaceae Vanillic acid, melianol 55
40 Milk thistle Marian thistle Asteraceae Flavanolignan, triterpene 52
glycosides
41 Mimosa pudica Lajwanti Fabaceae Alkaloids, tannins 53
42 Murraya koenigii Curry leaf tree Rutaceae Terpines 53
43 Nigella sativa Kalonji Ranunculaceae Glucoside melanthin metarb in 52
44 Ocimum sanctum Tulsi Lamiaceae Eugenol, o leanolic acid 53
45 Operculina turpenthum Trivruth Convolvulaceae Cou marin, beta sitosterol 42
46 Paeonia lactiflora Garden peony Ranunculaceae Monoterpene glycoside, albiflo rin 57
47 Pastinaca sativa Parsnip Umbelliferae Furanocoumarins 43
48 Petroselinum crispum Parsley Umbelliferae Furanocoumarins 41
49 Picorrhiza kurroa Kutki Scrophulariaceae Picrosides 47,52,
57
50 Plumbago indica Fire plant Plu mbaginaceae Plu mbagin, vanillic acid, beta 50
sitosterol
51 Polygala tenuifolia Chinese senega Polygalaceae Presengenin, xanthones 57
52 Polypodium leucotomos Go lden polypody Polypodiaceae Furanocoumarins 48
53 Prunella vulgaris Selfheal Lamiaceae Phenols, tannins, saponins 57
54 Prunus persica Peach Rosaceae Glycerides, sterols 57
55 Psoralea corylifolia Babchi Fabaceae Furanocoumarins 40
56 Ruta graveolens Herb of g race Rutaceae Furanocoumarins 49
57 Semecarpus anacardium Bhilwa Anacardiaceae Sterols, flavonoids, glycosides 50,52
58 Solanum nigrum European black Solanaceae Phenols, anthocyanidins 57
nightshade
59 Swertia chirata Indian gentian Gentianaceae Xanthones, oleanolic acid 57
60 Tecomella undulata Roheda Bignoniaceae Stig masterol 54

© 2011, JDDT. All Rights Reserved ISSN: 2250-1177 CODEN: JDDTAO

Kaur et al Journal of Drug Delivery & Therapeutics; 2012, 2(3): 53-59 58

CONCLUS ION: characterized by lack of pig mentation. Further

advancement in treatments using different derivatives of
Furanocoumarins are biologically active natural
psoralen molecu les should strive to decrease the possibility
compounds found main ly in p lants belonging to the
of long term side effects such as cutaneous malignancies.
Umbelliferae, Rutaceae, Apiaceae, Asteraceae, Fabaceae,
Oleaceae, Moraceae, Thymeleaceae Families. ACKNOWLEGD EMENTS :
Furanocoumarins forms monofunctional adducts which
Authors wish to acknowledge Drug Info rmation Centre of
would less likely pro mote cutaneous malignancies as
CT Institute of Pharmaceutical Sciences, Shahpur Campus,
compared to bifunctional adduct. The application of
Jalandhar, Punjab, India, for provid ing literature facilit ies
psoralens and different derivatives of psoralens with
during the preparation of this review article.
potentially fewer acute side effects has been one of the
most recent advancements in the treatment of leucoderma. CONFLICTS OF INTER ES T: The authors declare no
Psoralen containing plants have been used for centuries in conflicts of interest.
popular medicine to treat leucoderma, a skin disease

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