DISSERTATION

ON
LEUCODERMA

SUBMITTED BY: SUBMITTED TO:

RAMESH KUMAR SAROJ DR.MANOJ YADAVA
BATCH 2003 PROFESSOR
(MATERIA MEDICA)
N.H.M.C.LUCKNOW
 ACKNOWLEDGEMENT

This is great honour to offer my sincere thanks to

DR.MANOJ YADAVA, PROFESSOR, (MATERIA
MEDICA), N.H.M.C, Lucknow under whose able
guidance I completed this dissertation.

I also offer my sincere

thanks to PROFESSOR DR. A.N. MISHRA,
PRINCIPAL who extended his help in every
possible way.

I also offer my thanks to Dr. R.S.

Jaiswal, incharge I.P.D. and Dr.Sangeeta Bhatia,
intern incharge, who extended their kind help in
every possible way, whenever required.

NAME OF INTERN :Ramesh Kumar Saroj

BATCH: 2003
 CERTIFICATE

This is to certify that INTERN DR. RAMESH

KUMAR SAROJ of Batch-2003 has completed his
dissertation titled Leucoderma and its
Homoeopathic Treatment, under my guidance.
He has worked hard.

DR. MANOJ YADAVA

PROFESSOR(MATERIA MEDICA)
NATIONAL HOMOEOPATHIC MEDICAL
COLLEGE AND HOSPITAL
 CERTIFICATE

This is to certify that INTERN DR. RAMESH

KUMAR SAROJ of Batch-2003 has completed his
dissertation titled Leucoderma and its
Homoeopathic Treatment, under my guidance. He
has worked hard.

PROFESSOR DR. A.N. MISHRA

PRINCIPAL
NATIONAL HOMOEOPATHIC
MEDICAL COLLEGE AND
HOSPITAL
 INDEX

1. INTRODUCTION
2. AIMS AND OBJECTIVES
3. REVIEW OF LITERATURE
A. Skin components
B. Functions
C. Skin types
D. Skin layers
E. Pigmentation of skin
F. Skin tone variability
G. Genetics of skin colour variation
4. EPIDEMOLOGY AND GENETICS
5. CLINICAL COURCE AND PROGNOSIS
6. MATERIAL AND METHODS OF INVESTIGATION
7. MEDICAL AND SURGICAL THERAPIES
8. DISCUSSION: MIASMATIC EVOLUTION
9. HOMOEOPATHIC APPROACH FOR THE TREATMENT
10.HOMOEOPATHIC THERAPEUTICS
11.AUXILLARY TREATMENT
12.BIBLIOGRAPHY
13.ANNEXURES
A. Case Proforma
B. Graphics
C. Master Charts
D. Synopsis of Cases
INTRODUCTION:

Leucoderma is an acquired disease in which the melanocytes

in localized areas of the body stop producing
melanin.Clinically it manifests as macular areas of
depigmentation.Occassionally,the skin in certain areas may
only be hypopigmented.There is no other change in the skin.In
some lesions,hair may also become depigmented.This is
called leucotrichia.The lesions vary in shape and size and
may appear on any part of the skin and mucous
membranes.the extent of involvement may vary from a single
macule to involvement of almost the entire skin and mucous
membranes.The progression of disease is variable.The
disease may show a gradual extension or remain static for
prolonged periods with occasional exacerbations.

Leucoderma is a chronic skin disease that causes loss of

pigment, resulting in irregular pale patches of skin. It occurs
when the melanocytes, cells responsible for skin
pigmentation, die or are unable to function. The precise cause
of vitiligo is complex and not fully understood. There is some
evidence suggesting it is caused by a combination of auto-
immune, genetic, and environmental factors. The population
incidence worldwide is considered to be between 1% and 2%.
According to Diseases Database: "A disorder consisting of
areas of macular depigmentation, commonly on extensor
aspects of extremities, on the face or neck, and in skin folds.
Age of onset is often in young adulthood and the condition
tends to progress gradually with lesions enlarging and
extending until a quiescent state is reached."
 AIMS AND OBJECTIVES

1. To see the pace of deep acting and short acting medicines

in treatment.

2. To see homoeopathic dosage and directions.

3. To see the miasmatic and constitutional background in the

treatment.

4. To see the auxiliary management in the treatment.

REVIEW OF LITERATURE:

The skin is the outer covering of the body, also known as the
epidermis, of an animal.It is the largest organ of the
integument system made up of multiple layers of epithelial
tissues, and guards the underlying muscles, bones, ligaments,
internal organs. The adjective cutaneous literally means "of
the skin" (from Latin cutis, skin).

Because it interfaces with the environment, skin plays a very

important role in protecting (the body) against pathogens.Its
other functions are insulation, temperature regulation,
sensation, synthesis of vitamin D, and the protection of
vitamin B folates. Severely damaged skin will try to heal by
forming scar tissue. This is often discolored and depigmented.

The environmental agents that can influence the skin can be

categorized into:

Physical agents- trauma, friction, extremes of heat and cold,

radiation etc.

Chemical agents- strong acids and alkalis that may burn or

lead to irritation.

Biological agents- include variety of infecting/infesting

organisms which can thrieve on skin.
Skin components

Skin has pigmentation, or melanin, provided by melanocytes,

which absorb some of the potentially dangerous ultraviolet
radiation (UV) in sunlight. It also contains DNA-repair
enzymes that help reverse UV damage, and people who lack
the genes for these enzymes suffer high rates of skin cancer.
One form predominantly produced by UV light, malignant
melanoma, is particularly invasive, causing it to spread
quickly, and can often be deadly. Human skin pigmentation
varies among populations in a striking manner. This has led to
the classification of people(s) on the basis of skin color.The
skin is often known as the largest organ of the human body.
This applies to exterior surface, as it covers the body,
appearing to have the largest surface area of all the organs.
For the average adult human, the skin has a surface area of
between 1.5-2.0 square meters (16.1-21.5 sq ft.), most of it is
between 2-3 mm (0.10 inch) thick. The average square inch
(6.5 cm²) of skin holds 650 sweat glands, 20 blood vessels,
60,000 melanocytes, and more than a thousand nerve
endings.
Cross-section of skin showing different layers
Functions

Skin performs the following functions:

1. Protection: an anatomical barrier from pathogens and

damage between the internal and external environment
in bodily defense; Langerhans cells in the skin are part
of the adaptive immune system.
2. Sensation: contains a variety of nerve endings that react
to heat and cold, touch, pressure, vibration, and tissue
injury; see somatosensory system and haptics.
3. Heat regulation: the skin contains a blood supply far
greater than its requirements which allows precise
control of energy loss by radiation, convection and
conduction. Dilated blood vessels increase perfusion
and heat loss while constricted vessels greatly reduce
cutaneous blood flow and conserve heat. Erector pili
muscles are significant in animals.
4. Control of evaporation: the skin provides a relatively dry
and impermeable barrier to fluid loss. Loss of this
function contributes to the massive fluid loss in burns.
5. Aesthetics and communication: others see our skin and
can assess our mood, physical state and attractiveness.
 6. Storage and synthesis: acts as a storage center for
lipids and water, as well as a means of synthesis of
vitamin D by action of UV on certain parts of the skin.
7. Excretion: sweat contains urea, however its
concentration is 1/130th that of urine, hence excretion
by sweating is at most a secondary function to
temperature regulation.
8. Absorption: Oxygen, nitrogen and carbon dioxide can
diffuse into the epidermis in small amounts, some
animals using their skin for their sole respiration organ.
In addition, medicine can be administered through the
skin, by ointments or by means of adhesive patch, such
as the nicotine patch or iontophoresis. The skin is an
important site of transport in many other organisms.
9. Water resistance: The skin acts as a water resistant
barrier so essential nutrients aren't washed out of the
body.

Skin types

Skin can be classified based on its reaction to ultraviolet

radiation:

Type Definition Description

Always burns but never
I Pale skin, red hair, freckles
tans
Usually burns,
II Fair Skin
sometimes tans
III May burn, usually tans Darker Skin
IV Rarely burns, always Mediterranean
 tans
Moderate constitutional Latin American, Middle Eastern,
V
pigmentation Maori and Polynesian
Marked constitutional
VI Black
pigmentation

Skin layers

Skin is composed of three primary layers:

 The epidermis, which provides waterproofing and serves

as a barrier to infection;
 The dermis, which serves as a location for the
appendages of skin; and
 The hypodermis (subcutaneous adipose layer).

1.EPIDERMIS

Epidermis, "epi" coming from the Greek meaning "over" or

"upon", is the outermost layer of the skin. It forms the
waterproof, protective wrap over the body's surface and is
made up of stratified squamous epithelium with an underlying
basal lamina.

The epidermis contains no blood vessels, and cells in the

deepest layers are nourished by diffusion from blood
capillaries extending to the upper layers of the dermis. The
main type of cells which make up the epidermis are Merkel
cells, keratinocytes, with melanocytes and Langerhans cells
also present. The epidermis can be further subdivided into the
following strata (beginning with the outermost layer): corneum,
lucidum (only in palms of hands and bottoms of feet),
granulosum, spinosum, basale. Cells are formed through
mitosis at the basale layer. The daughter cells (see cell
division) move up the strata changing shape and composition
as they die due to isolation from their blood source. The
cytoplasm is released and the protein keratin is inserted. They
eventually reach the corneum and slough off (desquamation).
This process is called keratinization and takes place within
about 27 days. This keratinized layer of skin is responsible for
keeping water in the body and keeping other harmful
chemicals and pathogens out, making skin a natural barrier to
infection.

Components

The epidermis contains no blood vessels, and is nourished by

diffusion from the dermis. The main type of cells which make
up the epidermis are keratinocytes, melanocytes, Langerhans
cells and Merkels cells. The epidermis helps the skin to
regulate body temperature

Layers

Epidermis is divided into several layers where cells are formed

through mitosis at the innermost layers. They move up the
strata changing shape and composition as they differentiate
and become filled with keratin. They eventually reach the top
layer called stratum corneum and are sloughed off, or
desquamated. This process is called keratinization and takes
place within weeks. The outermost layer of the epidermis
consists of 25 to 30 layers of dead cells.

Sublayers

Epidermis is divided into the following 5 sublayers or strata:

 Stratum corneum
 Stratum lucidum
 Stratum granulosum
 Stratum spinosum
 Stratum germinativum (also called "stratum basale")

The deeper most part of the epidermis is called basal cell

layer or stratum germinativum and consists of a single
layer of columnal cells. The cells in this layer keep dividing
at a fixed rate and progressively move towards the surface.

The layer superficial to the basal cell layer is called the

prickle cell layer or the malphigian cell layer. This is
made up of several layers of cells which are polygonal in
shape and attached to each other as well as to the cells of
basal cell layer by means of specialized cell-wall structures
called desmosomes. In addition, these cells are covered
with a proteinous substance called the intercellular cement.
The cytoplasm of the basal cells as well as prickle cells
contain very fine filamentous structures called
tonofilaments which consists of long chain of aminoacids.
These filaments are attached to the desmosomes and form
a criss-cross pattern in the cytoplasm of the cells.
Tonofilaments do not cross from one cell to the other but
constitute a sort of skeleton for the cell. The cells in the
most superficial layer of the prickle cell layer develop small
circular organelle called membrane coating granules or
odland bodies which progressively move towards and fuse
with the cell membrane and discharge their content in the
intercellular space. Superficial to the prickle cell layer lies
the granular layer which consists of two layers of
rhomboid shaped cells which are flatter than cells of the
prickle cell layer. These cells characteristically contain
irregular shaped masses of dark-staining material lying in
between the tonofilaments. The tonofilaments progressively
become parallel to each other, develop interfilamentous
bonds and together with the cement substance constitute
larger fibrils called tonofibrils. It takes 14 days for a
daughter cell of the basal layer to evolve into a granular cell
and another 14 days before that cell is exfoliated as a
mature horny cell.

The most superficial layer of epidermis is called corneal

cell layer or the stratum corneum. It is composed of
stratified layers of horn cells and forms a tough elastic and
supple surface to the skin. These cells have lost their nuclei
and other cellular inclusions but contain a protein called
keratin which consists of bundles of tonofibrils embedded in
the interfibrillar cement substance. The deeper layers are
compact while superficial layers are loose. Thus there is a
continuous outward movement of the epidermal cells, new
 cells being generated in the basal cell layer and the old
cells falling off from the surface. This process is called
epidermopoiosis which continue at a fixed rate and is under
a local control.

The continuous outward movement of the epidermal cells

constitute a barrier for the agents which tend to penetrate
the skin from outside. The stratum corneum constitutes a
mechanical barrier against invading organisms as well as a
very highly selective barrier for chemicals.

Blood capillaries are found beneath the epidermis, and are

linked to an arteriole and a venule. Arterial shunt vessels may
bypass the network in ears, the nose and fingertips.

2.DERMIS

The dermis is the layer of skin beneath the epidermis that

consists of connective tissue and cushions the body from
stress and strain. The dermis is tightly connected to the
epidermis by a basement membrane. It also harbors many
mechanoreceptor/nerve endings that provide the sense of
touch and heat. It contains the hair follicles, sweat glands,
sebaceous glands, apocrine glands, lymphatic vessels and
blood vessels. The blood vessels in the dermis provide
nourishment and waste removal to its own cells as well as the
Stratum basale of the epidermis.
The major component is the collagen fibres which lie singly or
in smaller bundles in the papillary dermis, while the lower part
contains thick and larger bundles lying in criss-cross pattern.
Another important component of the dermis is the elastic
fibres which form a horizontal network at the junction of
papillary dermis with reticular dermis. The collagen and elastic
fibres are embedded in a ground substance made up of water,
electrolytes and proteoglycans. In addition, dermis contains
the cellular elements which are mainly of three types:

1.Fibroblasts which are spindle shaped cells with a central

oval nucleus. The cells are concerned with the formation of
collagen and elastic fibres.

2.Histiocytes which are amoeboid in shape and concerned

with phagocytosis and immunologic functions.

3.Mast cells which contain the mast cell granules and can
release histamine and several other substances with potent
biologic functions. These cells have a role in inflammatory,
immunologic and repair mechanisms.

The dermis is structurally divided into two areas: a superficial

area adjacent to the epidermis, called the papillary region, and
a deep thicker area known as the reticular region.
Papillary region

The papillary region is composed of loose areolar connective

tissue. It is named for its fingerlike projections called papillae,
that extend toward the epidermis. The papillae provide the
dermis with a "bumpy" surface that interdigitates with the
epidermis, strengthening the connection between the two
layers of skin.

In the palms, fingers, soles, and toes, the influence of the

papillae projecting into the epidermis forms contours in the
skin's surface. These are called friction ridges, because they
help the hand or foot to grasp by increasing friction. Friction
ridges occur in patterns (see: fingerprint) that are genetically
and epigenetically determined and are therefore unique to the
individual, making it possible to use fingerprints or footprints
as a means of identification.

Reticular region

The reticular region lies deep in the papillary region and is

usually much thicker. It is composed of dense irregular
connective tissue, and receives its name from the dense
concentration of collagenous, elastic, and reticular fibers that
weave throughout it. These protein fibers give the dermis its
properties of strength, extensibility, and elasticity.
Also located within the reticular region are the roots of the
hair, sebaceous glands, sweat glands, receptors, nails, and
blood vessels.

Tattoo ink is held in the dermis. Stretch marks from pregnancy

are also located in the dermis.

3.HYPODERMIS

The hypodermis is not part of the skin, and lies below the
dermis. Its purpose is to attach the skin to underlying bone
and muscle as well as supplying it with blood vessels and
nerves. It consists of loose connective tissue and elastin. The
main cell types are fibroblasts, macrophages and adipocytes
(the hypodermis contains 50% of body fat). Fat serves as
padding and insulation for the body.

Microorganisms like Staphylococcus epidermidis colonize the

skin surface. The density of skin flora depends on region of
the skin. The disinfected skin surface gets recolonized from
bacteria residing in the deeper areas of the hair follicle, gut
and urogenital openings.
PIGMENTATION OF SKIN

Normal skin color is composed of a mixture of four

biochromes,namely- 1.Reduced hemoglobin (blue)

2.Oxyhemoglobin(red)

3.Carotenoids (yellow,exogenous from diet)

4.Melanin (brown)

The principal determinant of the skin colour is melanin

pigment,and variations in the amount and distribution of
melanin in the skin are the basis of the three principal human
skin colours:black,brown and white.These three basis colours
are genetically determined and are called constitutive melanin
pigmentation.The normal basic skin colour pigmentation can
be increased deliberately by exposure to ultraviolet radiation
or pituitary hormones,and this is called inducible melanin
pigmentation.The combination of the constitutive and inducible
melanin pigmentation determines what is skin phototype and it
is a marker for skin cancer risk and should be recorded at first
patient visit.

The major pigmentation of skin i.e. melanin is produced

inside special cells called melanocytes which are located
along the basal cells along epidermis and contain small
granules called melanosomes.The fully melanised
melanosomes are called melanin granules which are then
transferred to the epidermal cells.Melanin granules inside the
keratinocytes account for the skin colour.The melanin is shed
off with the shedding of epidermal cells.Melanin is synthesized
from the amino acid tyrosine by the action of an oxidizing and
copper containing enzyme tyrosinase.This enzyme converts
tyrosine into dihydroxyphenylalanine (DOPA) and further into
melanin through a series of non enzymatic steps.

Increase of melanin in the epidermis results in a state

known as hypermelanosis.This reflects one of the two types of
changes:

1.An increase in the number of melanocytes in the epidermis

producing increased levels of melanin,which is called
melanocytotic hypermelanosis (an example is lentigo).

2.No increase of melanocytes but an increase in the

production of melanin only,which is called melanotic
hypermelanosis (an example is melasma).

Hypermelanosis of both types can result from three

factors: genetic, hormonal(as in Addison’s disease),when it
is caused by an increase in circulating pituitary melanotropic
hormone and ultraviolet radiation as in tanning).

A decrease of melanin in the epidermis is called

hypomelanosis.This reflects mainly two types of changes:

1.A decrease in the number or absence of melanocytes in the

epidermis producing no or decreased levels of melanin .This
is called melanocytopenic hypomelanosis (an example is
Leucoderma).

2.No decrease of melanocytes but a decrease in the

production of melanin only that is called melanophinic
hypomelanosis (an example of albinism).

Hypomelanosis also results from genetic (as in albinism),from

autoimmune(as in vitiligo) or other inflammatory processes
(as in postinflammatory leukodermia in psoriasis.)

Human skin color can range from almost black

(due to very high concentrations of the dark brown pigment
melanin) to nearly colorless (appearing reddish white due to
the blood vessels under the skin) in different people. Skin
color is determined by the amount and type of melanin, the
pigment in the skin. Variation in skin color is largely due to
genetics. As a general pattern people with ancestors from
tropical regions (hence greater sunlight exposure) have darker
skin than people with ancestors from subtropical regions. This
is far from a hard and fast rule however, because many light
skinned groups have managed to survive at the equator by
way of social adaptation. The same can be said of dark
skinned groups living at subtropical latitudes. Melanin comes
in two types: pheomelanin (red) and eumelanin (very dark
brown). Both amount and type are determined by four to six
genes which operate under incomplete dominance. One copy
of each of those genes is inherited from each parent. Each
gene comes in several alleles, resulting in the great variety of
different skin tones.

SKIN TONE VARIABILITY:

The tone of human skin can vary from a dark brown to nearly
a colorless pigmentation, which may appear reddish due to
the blood in the skin. Europeans generally have lighter skin,
hair, and eyes than any other group on Earth, although this is
not always the case. For practical purposes, such as exposure
time for sun tanning, six skin types are distinguished following
Fitzpatrick (1975), listed in decreasing lightness.

Von
Tanning Hair and eye
Type Also called Luschan
behavior color
scale
Tends to have
freckles, red
Very light, also Often burns,
I or blond hair, 1-5
"Nordic" rarely tans.
blue or green
eyes.
II Light, or light- Usually Tends to have 6-10
 burns, light hair,
skinned European sometimes blue/green or
tans brown eyes.
Light intermediate,
or dark-skinned Sometimes Tends to have
III European or burns, brown hair 11-15
"average usually tans. and eyes.
Caucasian"
Dark intermediate,
Sometimes Tends to have
also
IV burns, often dark brown 16-20
"Mediterranean" or
tans. eyes and hair.
"Olive"
Naturally Often has
Dark or "Brown"
V black-brown dark brown 21-28
type
skin eyes and hair.
Naturally Usually has
Very dark, or
VI black-brown black-brown 29-36
"Black" type
skin eyes and hair.

Genetics of skin color variation

Several genes have been invoked to explain variations of skin

tones in humans, including SLC45A2, ASIP, MATP, TYR, and
OCA2. A recently discovered gene, SLC24A5 has been shown
to account for a substantial fraction of the difference in the
average of 30 or so melanin units between Europeans and
Africans.

Wide variations in human skin tones have been correlated

with mutations in another gene; the MC1R gene]. The "MC1R"
label for the gene stands for melanocortin 1 receptor, where:
  "melano" refers to black,
 "melanocortin" refers to the hormone stimulant produced
by the pituitary gland that stimulates cells to produce the
melanin that makes skin cells black,
 the "1" in the MC1R gene name specifies the first family
of melanocortin genes, and
 "receptor" indicates that the protein from the gene
serves as a signal relay from outside the cell membrane
to inside the cell—to the place in the cell where the
black melanin is synthesized.

Accordingly, the MC1R gene specifies the amino acid

sequence in the receptor protein that relays through the cell
membrane the hormone signal from the pituitary gland to
produce the melanin that makes human skin very dark. Many
variations in the amino acid sequence of this receptor protein
result in lighter or darker skin.
LEUCODERMA: INTRODUCTION

Leucoderma is also known as Vitilago, which simply means

white (leuco) skin (derma), i.e. a disorder where the skin loses
its normal color. Estimated 1.2% of American and world
population, about 8% of Indian and Mexican population suffer
with this disorder.

Largely, there are two process at work towards producing

vitiligo.

a. Destruction of melanin (color pigment)

b. Lack of formation of melanin

Leucoderma can hardly be called as a disease but a skin-

disorder that has more social than medical significance,
especially amongst the dark skinned people. Due to
destruction of the melanin (pigment) cells due to lesser known
processes (largely what is called as an auto-immune disorder)
the normal skin starts loosing pigments from various parts of
the skin, in a varying speed and extent. Our clinical
experience based on the treatment of over 4500 cases,
suggests that there is a strong genetic factor in the
background of most cases, especially those who have
extensive leucoderma or those who have leucoderma
affecting the finger-tips, toes, lips or the genitals. The
indication of strong genetic factor is observed in the form of
family history of one or more of the auto-immune diseases
such as vitiligo, diabetes, hypothyroid, alopecia areata,
cancer, rheumatoid arthritis or allergies.

EPIDEMOLOGY AND GENETICS:

The leucoderma sufferers are observed all over the world,

including the white skin communities. However,
epidemiologically most cases are recorded in India (8.8%) and
Mexico. Estimated 1-2% of the Americans have leucoderma
as per the survey made by the American Academy of
Dermatology. Males and females are affected equally,
inclusive of children age group. It may begin at any age.
Childhood vitiligo is common.

Factors affecting the occurance of disease are given as:

1.SEX-Equal in both sexes.The predominance in women

suggested by the literature likely reflects the greater concern
of women about cosmetic appearance.

2.AGE OF ONSET-May begin at any age,but in 50%of cases

it begins between the age of 10 and 30 years.

3.INCIDENCE-Common.Affects upto 1% of population.

4.RACE-All races.The apparently increased prevalence
reported in some countries and among darker-skinned
persons results from a dramatic contrast between white vitiligo
macules and dark skin and from marked social stigma in
countries such as India,where even today the oppourtunities
for advancement or marriage among affected individuals are
limited.

5.INHERITANCE-Leucoderma has a genetic background

;>30% of affected individuals have reported vitiligo in a
parent ,sibling or child, leucoderma in identical twins has been
reported.Transmission is most likely polygenic with variable
expression.The risk of vitiligo for children affected individuals
is unknown but may be <10%.Individuals from families with an
increased prevalence of thyroid disease, diabetes mellitus,
and leucoderma appear to be at increased risk for
development of leucoderma.

AETIOLOGY-Melanocytes in areas of depigmented skin are

destroyed and the cause is unknown. However both genetic
and immunological factors are considered responsible for
vitiligo. Anti-melanocytic antibodies directed against
intracellular components of melanocytes have been shown.
The presence of organ specific autoimmune disease occurs in
about 19% of patients. Such conditions are more common in
their families than in a normal population. A neurogenic defect
has been postulated for the rare dermatomal pattern of
leucoderma which affect principally the limbs.

HISTORY-Many patients attribute the onset of their

leucoderma to physical trauma (where leucoderma appears at
the site of trauma, it is called Koebner phenomenon),illness,or
emotional stress. Onset after the death of a relative or after
severe physical injury is often mentioned. A sunburn reaction
may precipitate vitiligo.

PATHOGENESIS-

Three physical theories have been presented about the

mechanism of destruction of melanocytes in leucoderma:

1.THE AUTOIMMUNE THORY that selected melanocytes are

destroyed by certain lymphocytes that have somehow been
activated.

2.THE NEUROGENIC HYPOTHESIS is based on an

interaction of the melanocytes and nerve cells.

3.THE SELF-DESTRUCTIVE HYPOTHESIS suggests that

melanocytes are destroyed by toxic substances formed as
part of normal melanin biosynthesis.
CLINICAL COURSE AND PROGNOSIS

Half of people with leucoderma develop patches of de-

pigmented skin appearing on extremities before their 20s. The
patches may grow, shrink, or remain constant in size.The
disease is slowly progressive,but sometimes can progress
rapidly.Segmental leucoderma has a stable course. Patches
often occur symmetrically across both sides on the body.
Occasionally small areas may repigment as they are
recolonised by melanocytes. The location of vitiligo affected
skin changes over time, with some patches re-pigmenting and
others becoming affected.Acrofacial vitiligo is more resistant
to treatment.

Leucoderma may also be caused by stress that affects the

immune system, leading the body to react and start
eliminating skin pigment.

Leucoderma on the scalp may affect the color of the hair

(though not always), leaving white patches or streaks. It will
similarly affect facial and body hair.

People who develop vitiligo usually first notice white patches

(depigmentation) on their skin. These patches are more
commonly found on sun-exposed areas of the body, including
the hands, feet, arms, face, and lips. Other common areas for
white patches to appear are the armpits and groin, and around
the mouth, eyes, nostrils, navel, genitals, and rectal areas.
Leucoderma generally appears in one of three patterns:

1.Focal pattern-the depigmentation is limited to one or only a

few areas.May be slowly or rapidly progressive.Family history
is frequently present.

2.Segmental pattern-Depigmented patches develop on only

one side of the body.Has a stable course and remain static.

3.Generalized pattern-The most common pattern.

Depigmentation occurs symmetrically on both sides of the
body.Variants of generalized leucoderma are:

Acrofacial leucoderma–leucoderma present periorificially

(around eyes and on lips on the face) and acral
parts(periungal area and palms and soles).This type is more
resistant to therapy due to absence of hair in the affected
parts.

Lip-tip leucoderma-when lips, tip of penis and nipples are

involved.

Lucoderma universalis-widespread leucoderma, only few

areas of normal pigmentation.

Leucoderma In addition to white patches on the skin, people

with may have :
1.Premature graying of the scalp hair, eyelashes, eyebrows,
and beard.

2.Uveitis.
3.Sun sensitivity.

ACROFACIAL LEUCODERMA

ACROFACIAL LEUCODERMA
GENERALISED PATTERN LEUCODERMA
GENERALISED PATTERN LEUCODERMA

FOCAL PATTERN LEUCODERMA

SEGMENTAL PATTERN LEUCODERMA

Spread of leucoderma:

The spread of leucoderma is governed by various factors such

as :1.Genetic activity
2.Hormonal factors
3.Continued stress factors
4. Exposure to chemicals

Many patients may start with just a single spot and

may not get more spots for many years or for throughout life
time. Some patients may show rapid spread, as fast as from
one spot to hundreds, in a few months time. It is not possible
to predict the pace of spread. Also, some patients may show
intermittent spread. It may be noted form experience that
those who pace certain body areas affected such a finger tips,
are at higher risk of having an aggressive spread; it is not a
rule though. Some patients may present with grey hair,
suggesting loss of pigment in the hair.

Prognostic factors

Though there are no indicators of good prognosis,the

following factors indicate poor prognosis for therapy:

Long standing disease.

Leucotrichia.

Acrofacial lesions.

Lesions on resistant areas :ankles,wrists,elbows,peri-ungual

areas,nipples and areolae,lips and genitalia (i.e.,lesions on
bony prominences,non-fleshy areas,non-hairy areas and
mucosae.)

Associated Skin Disorders:

At times, you may find leucoderma associated with one or

more of the following conditions:

1. Alopecia Areata (Loss of hair)

2. Premature graying of the hair

3.Lichen Planus

4. Lichen sclerosus

5. Psoriasis

6. Halo Naevus

7.Ichthyosis

Associated Systemic Disorders:

There are several systemic diseases (affecting the entire body

system), which are at times associated with leucoderma:

1. Thyroid Disorders (Hypo and Hyperthyroidism)

2. SLE (Systemic Lupus Erythematosus)

3. Pernicious Anemia

4.Addison's Disease

5. Collagen Diseases

6.Grave's Disease
7. Diabetes Mellitus

Diagnosis

The diagnosis of leucoderma is made based on physical

examination, medical history, and laboratory tests.

A doctor will likely suspect leucoderma if you report (or the

physical examination reveals) white patches of skin on the
body-particularly on sun-exposed areas, including the hands,
feet, arms, face, and lips.It shows progressive,acquired,chalk-
white,bilateral (usually symmetrical),sharply defined macules
in typical sites (periorbital,perioral,neck,penis,perineum,axillae
and points of pressure such as the
elbow,malleoli,knees,lumbosacral areas). If leucoderma is
suspected, the doctor will ask about your medical history.
Important factors in the diagnosis include a family history of
leucoderma; a rash, sunburn, or other skin trauma at the site
of leucoderma 2 to 3 months before depigmentation started;
stress or physical illness; and premature (before age 35)
graying of the hair. In addition, the doctor will ask whether you
or anyone in your family has had any autoimmune diseases,
and whether you are very sensitive to the sun.

To help confirm the diagnosis, the doctor may take a small

sample (biopsy) of the affected skin to examine under a
microscope. In leucoderma, the skin sample will usually show
a complete absence of pigment-producing melanocytes. On
the other hand, the presence of inflamed cells in the sample
may suggest that another condition is responsible for the loss
of pigmentation.

Because leucoderma may be associated with pernicious

anemia (a condition in which an insufficient amount of vitamin
B12 is absorbed from the gastrointestinal tract) or
hyperthyroidism (an overactive thyroid gland), the doctor may
also take a blood sample to check the blood-cell count and
thyroid function. For some patients, the doctor may
recommend an eye examination to check for uveitis
(inflammation of part of the eye), which sometimes occurs with
leucoderma. A blood test to look for the presence of
antinuclear antibodies (a type of autoantibody) may also be
done. This test helps determine if the patient has another
autoimmune disease.

LABORATORY EXAMINATIONS

Wood’s Lamp Examination-It is required to evaluate

macules,particularly in lighter skin types,and to identify
macules,in sun-protected areas in all but the darkest skin
types.

Dermatopathology-In certain difficult cases,a skin biopsy

may be required.Established leucoderma macules show
normal skin except for an absence of melanocytes.Use
special stains to identify melanocytes.There may be mild
lymphocytic response.These changes are not diagnostic for
leucoderma,however,only consistent with it.
Electron Microscopy-Absence of melanocytes and of
melanosomes in keratinocytes ;also changes in
kertinocytes;spongiosis,exocytosis,basilar vacupathy,and
necrosis. Lymphocytes have been seen in the epidermis.

Laboratory studies-T4, TSH, fasting blood sugar, complete

blood count with indices, ACTH, stimulation test for Addison’s
disease, if suspected.

Disease mechanism

Leucoderma is associated with autoimmune and inflammatory

diseases, commonly thyroid overexpression and
underexpression. Jin in the New England Journal of Medicine
reported a study comparing 656 people with and without
leucoderma in 114 families, which found several mutations
(single-nucleotide polymorphisms) in the NALP1 gene. The
NALP1 gene, which is on chromosome 17 located at 17p13, is
on a cascade that regulates inflammation and cell death,
including myeloid and lymphoid cells, which are white cells
that are part of the immune response. NALP1 is expressed at
high levels in T cells and Langerhan's cells, white cells that
are involved in skin autoimmunity.

Among the inflammatory products of NALP1 are caspase 1

and caspase 5, which activate the inflammatory cytokine
interleukin-1β. Interleukin-1β is expressed at high levels in
patients with leucoderma. There are compounds which inhibit
caspase and interleukin-1β, and so might be useful drugs for
leucoderma and associated autoimmune diseases.
Of the 656 people, 219 had leucoderma only, 70 had
leucoderma with autoimmune thyroid disease, and 60 had
leucoderma and other autoimmune diseases. Addison's
disease (typically an autoimmune destruction of the adrenal
glands) may cause vitiligo.

In one of the mutations, the amino acid leucine in the NALP1

protein was replaced by histidine (Leu155->His). The original
protein and sequence is highly conserved in evolution, and
found in humans, chimpanzee, rhesus monkey, and bush
baby, which means that it's an important protein and an
alteration is likely to be harmful. The following is the normal
DNA and protein sequence in the NALP1 gene:

TCA CTC CTC TAC CAA

Ser Leu Leu Tyr Gln

S L L Y Q

In some cases of vitiligo the first leucine is altered to histidine,

by a Leu155→His mutation:

TCA CAC CTC TAC CAA

Ser His Leu Tyr Gln

S H L Y Q

(Leucine is nonpolar and hydrophobic; histidine is positively

charged and hydrophilic, so it is unlikely both serve the same
function. The normal sequence of the DNA code for NALP1 of
TCACTCCTCTACCAA is replaced in some of these
leucoderma families by the sequence TCACACCTCTACCAA,
which respectively code for the amino acid sequence of the
normal NALP1 protein SLLYQ being replaced by SHLYQ.

Emotional and Psychological aspects of Leucoderma :

While leucoderma is usually not harmful medically, its

emotional and psychological effects can be devastating. In
fact, in India, women with the disease are sometimes
discriminated against in marriage. Developing leucoderma
after marriage can be grounds for divorce.

Regardless of a person's race and culture, white patches of

leucoderma can affect emotional and psychological well-being
and self-esteem. People with leucoderma can experience
emotional stress, particularly if the condition develops on
visible areas of the body, such as the face, hands, arms, and
feet; or on the genitals. Adolescents, who are often particularly
concerned about their appearance, can be devastated by
widespread vitiligo. Some people who have leucoderma feel
embarrassed, ashamed, depressed, or worried about how
others will react.

Fortunately, there are several strategies to help people cope

with leucoderma. Also, various treatments-which we will
discuss a bit later-can minimize, camouflage, or, in some
cases, even eliminate white patches. First, it is important to
find a doctor who is knowledgeable about the disorder and
takes it seriously. The doctor should also be a good listener
and be able to provide emotional support. You must let your
doctor know if you are feeling depressed, because doctors
and other mental health professionals can help people deal
with depression. You should also learn as much as possible
about the disorder and treatment choices so that you can
participate in making important decisions about medical care.

Talking with other people who have leucoderma may also

help. The National leucoderma Foundation can provide
information about leucoderma antiligod refer you to local
chapters that have support groups of patients, families, and
physicians; improve their appearance and help them feel
better about themselves. You may need to experiment with
several brands of concealing cosmetics before finding the
product that works best.

Treatment

There are a number of ways to alter the appearance of

leucoderma without addressing its underlying cause. In mild
cases, leucoderma patches can be hidden with makeup or
other cosmetic camouflage solutions. If the affected person is
pale-skinned, the patches can be made less visible by
avoiding sunlight and the sun tanning of unaffected skin.
However, exposure to sunlight may also cause the
melanocytes to regenerate to allow the pigmentation to come
back to its original color.

The traditional treatment given by most dermatologists is

cortico steroid cream.
Phototherapy may also be beneficial. Using exposure to long-
wave ultraviolet (UVA) light from the sun or from UVA,
together with Psoralen, called "PUVA", Or with UVB
Narrowband lamps (without Psoralen), can help in many
cases. Psoralen can be taken in a pill 1-2 hours before the
exposure or as a Psoralen soaking of the area 1/2 hour before
the exposure. Lately, PUVA is being more and more replaced
with exposure UVB Narrowband light at a wavelength of 311-
313 nanometers. This treatment does not involve Psoralen
since the effect of the lamp is strong enough. The source for
the UVB Narrowband UVB light can be special fluorescent
lamps that treat large areas in a few minutes, or high power
fiber-optic devices in a fraction of a second.

Studies have also shown that immunomodulator creams such

as Protopic and Elidel also cause repigmentation in some
cases, when used with UVB Narrowband treatments.

Alternatively, some people with leucoderma opt for chemical

depigmentation, which uses 20% monobenzone
(monobenzylether of hydroquinone). This process is
irreversible and generally ends up with complete or mostly
complete depigmentation.

In late October 2004, doctors successfully transplanted

melanocytes to leucoderma affected areas, effectively
repigmenting the region. The procedure involved taking a thin
layer of pigmented skin from the patient's gluteal region.
Melanocytes were then separated out and used to make a
cellular suspension. The area to be treated was then ablated
with a medical laser, and the melanocyte graft applied. Three
weeks later, the area was exposed to UV light repeatedly for
two months. Between 73 and 84 percent of patients
experienced nearly complete repigmentation of their skin. The
longevity of the repigmentation differed from person to person.

In early 2008 scientists at King's College London discovered

that piperine, a chemical derived from black pepper can aid
repigmentation in skin, especially when combined with UV
therapy produces a longer lasting and more even
pigmentation than previous treatments .

A study has shown that orally-taken Ginkgo biloba can be

effective in arresting the progression of slowly-spreading
leucoderma.

APPROACH TO THE PATIENT WITH VITILIGO:

The main goal of treating vitiligo is to improve appearance.

Therapy for leucoderma takes a long time-it usually must be
continued for 6 to 18 months. The choice of therapy depends
on the number of white patches; their location, sizes, and how
widespread they are; and what you prefer in terms of
treatment. Each patient responds differently to therapy, and a
particular treatment may not work for everyone. Current
treatment options for leucoderma include medical, surgical,
and adjunctive therapies (therapies that can be used along
with surgical or medical treatments).
Medical therapies

A number of medical therapies, most of which are applied

topically, can reduce the appearance of white patches with
leucoderma. These are some of the most commonly used
ones:

Topical steroid therapy—steroid creams may be helpful in

repigmenting (returning the color to) white patches,
particularly if they are applied in the initial stages of the
disease. Corticosteroids are a group of drugs similar to
hormones such as cortisone, which are produced by the
adrenal glands. Doctors often prescribe a mild topical
corticosteroid cream for children under 10 years old and a
stronger one for adults. You must apply the cream to the white
patches on the skin for at least 3 months before seeing any
results. Corticosteriod creams are the simplest and safest
treatment for leucoderma, but are not as effective as psoralen
photochemotherapy.Yet, like any medication, these creams
can cause side effects. For this reason, the doctor will monitor
you closely for skin shrinkage and skin striae (streaks or lines
on the skin). These side effects are more likely to occur in
areas where the skin is thin, such as on the face and armpits,
or in the genital region. They can be minimized by using
weaker formulations of steroid creams in these areas.

Psoralen photochemotherapy—also known as psoralen and

ultraviolet A therapy, or PUVA therapy, this is probably the
most effective treatment for vitiligo available in the United
States. The goal of PUVA therapy is to repigment the white
patches. However, it is time-consuming, and care must be
taken to avoid side effects, which can sometimes be severe.
Psoralen is a drug that contains chemicals that react with
ultraviolet light to cause darkening of the skin. The treatment
involves taking psoralen by mouth (orally) or applying it to the
skin (topically). This is followed by carefully timed exposure to
sunlight or to ultraviolet A (UVA) light that comes from a
special lamp. Typically, you will receive treatments in your
doctor's office so you can be carefully watched for any side
effects. You must minimize exposure to sunlight at other
times. Both oral and topical psoralen photochemotherapy are
described below.

Topical psoralen photochemotherapy—often used for

people with a small number of depigmented patches affecting
a limited part of the body, it is also used for children 2 years
old and older who have localized patches of leucoderma.
Treatments are done in a doctor's office under artificial UVA
light once or twice a week. The doctor or nurse applies a thin
coat of psoralen to your depigmented patches about 30
minutes before exposing you to enough UVA light to turn the
affected area pink. The doctor usually increases the dose of
UVA light slowly over many weeks. Eventually, the pink areas
fade and a more normal skin color appears. After each
treatment, you wash your skin with soap and water and apply
a sunscreen before leaving the doctor's office.

There are two major potential side effects of topical PUVA

therapy: (1) severe sunburn and blistering and (2) too much
repigmentation or darkening (hyperpigmentation) of the
treated patches or the normal skin surrounding the
leucoderma. You can minimize your chances of sunburn if you
avoid exposure to direct sunlight after each treatment. Usually,
hyperpigmentation is a temporary problem that eventually
disappears when treatment is stopped.

Oral psoralen photochemotherapy—used for people with

extensive leucoderma (affecting more than 20 percent of the
body) or for people who do not respond to topical PUVA
therapy, oral psoralen is not recommended for children under
10 years of age because it increases the risk of damage to the
eyes caused by conditions such as cataracts. For oral PUVA
therapy, you take a prescribed dose of psoralen by mouth
about 2 hours before exposure to artificial UVA light or
sunlight. If artificial light is used, the doctor adjusts the dose of
light until the skin in the areas being treated becomes pink.
Treatments are usually given 2 or 3 times a week, but never 2
days in a row.
For patients who cannot go to a facility to receive PUVA
therapy, the doctor may prescribe psoralen that can be used
with natural sunlight exposure. The doctor will give you careful
instructions on carrying out treatment at home and monitor
you during scheduled checkups.
Known side effects of oral psoralen include sunburn, nausea
and vomiting, itching, abnormal hair growth, and
hyperpigmentation. Oral psoralen photochemotherapy may
also increase the risk of skin cancer, although the risk is
minimal at doses used for leucoderma. If you are undergoing
oral PUVA therapy, you should apply sunscreen and avoid
direct sunlight for 24 to 48 hours after each treatment to avoid
sunburn and reduce the risk of skin cancer. To avoid eye
damage, particularly cataracts, you should also wear
protective UVA sunglasses for 18 to 24 hours after each
treatment.

Depigmentation—This treatment involves fading the rest of

the skin on the body to match the areas that are already white.
For people who have leucoderma on more than 50 percent of
their bodies, depigmentation may be the best treatment
option. Patients apply the drug monobenzylether of
hydroquinone (monobenzone or Benoquin) twice a day to
pigmented areas until they match the already-depigmented
areas. You must avoid direct skin-to-skin contact with other
people for at least 2 hours after applying the drug, as transfer
of the drug may cause depigmentation of the other person's
skin. The major side effect of depigmentation therapy is
inflammation (redness and swelling) of the skin. You may
experience itching or dry skin. Depigmentation tends to be
permanent and is not easily reversed. In addition, a person
who undergoes depigmentation will always be unusually
sensitive to sunlight.

Surgical therapies
All surgical therapies must be considered only after proper
medical therapy is provided. Surgical techniques are time-
consuming and expensive and usually not paid for by
insurance carriers. They are appropriate only for carefully
selected patients who have vitiligo that has been stable for at
least 3 years.

Miniature punch grafting

Multiple thin grafts of 2 - 2.5 mm diameter are taken from the

donor site by special punches and grafted on to the diseased
area. Once the grafts are 'taken up' the patient is advised to
take PUVA or PUVA SOL. Re pigmentation occurs in 3 - 6
months and good cosmetic result is obtained.

Ultra thin skin grafting

A very thin skin graft (ultra thin) consisting of epidermis is

grafted onto the dermabraded or laser ablated part of stable
leucoderma. The graft falls off by 8 -10 days but there takes
place a cellular uptake of melanocytes on to the abraded skin
which gradually starts pigmenting, it takes 2 - 3 months for the
pigmentation to merge and match with the surrounding skin
color.

Suction blister grafting

A prolonged suction (negative pressure) is applied to the
donor site this raises a large bleb and a thin graft containing
only the epidermis is obtained. This is grafted on to the
dermabraded recipient surface. This technique is time
consuming but gives good cosmetic results.

Melanocyte transplantation

Melanocytes are cultured in artificial culture media. The de

pigmented recipient site is dermabraded or laser ablated and
the melanocyte suspension is applied to it. The area is
covered with a collagen dressing and immobilized. Large
areas can be covered with this method and excellent cosmetic
results obtained.

Tattooing

Tattooing is injecting artificial pigment into the depigmented

area. After selecting the pigment shade which matches the
surrounding skin color, the pigment granules are implanted
into the depigmented patch either with a manual or electrically
driven needles.
Though the patch resembles the surrounding normal skin, it
may permanently fade or acquire a bluish hue after 1 - 2
years which is distinctly noticeable and may become
unacceptable. Hence, tattooing is usually not advised unless
the patch is in an inoperable site.
The tattooed area will not change in color when exposed to
sun, while the surrounding normal skin will. So even if the
tattooed area matches the surrounding skin perfectly at first, it
may not later on. Tattooing tends to fade over time. In
addition, tattooing of the lips may lead to episodes of blister
outbreaks caused by the herpes simplex virus.

MIASMATIC EVOLUTION:

The manifestations of chronic disease conditions which

Hahnemann called miasm,can be defined as polluting
exhalations or malarial poisons.

In a letter to Dr. Friederich Golthelf Baugmaster,

Hahnemann wrote in 1820…..”In the homoeopathic writings
as yet published,there is still lacking a great keystone
which binds together all that has been so far published so
that we may be able to improve the treatment of chronic
diseases.”He further writes:by thousands of experiments,I
have at last attained my object.None of my pupils as yet
know anything of this ‘invaluable discovery’,the work of
which to mankind exceeds all else that I have ever
discovered and without which all existing homoeopathy
remains defective or imperfect.The keystone which solved
the mystery of incurable diseases is in aphorism 74.The
keystone which revealed that the organism revolts in only
three different ways to give rise to three different types of
diseases at the base of which are 3 miasms-Psora ,Sycosis
,Syphilis.

Every living cell or a living organism, which is atleast

deductively its descendant, also possesses the following
‘three’ basic functions which can be used to defend itself.

1.Using or sacrificing the primary or first function of nutrition

and respiration the cell brings about the ‘physiologic
defense’ or psora.

This response starts with hypoxia and ischemia leading to

depletion of energy generation.This in turn affects the cell
functioning and health.

2.Using or sacrificing the second basic function of

generation,the cell brings about the morphological
‘constructive defense’ by sacrificing functions of ‘mitosis’
etc which corresponds to sycosis.

3.Using or sacrificing the third basic function of

immunity,the morphological ‘destructive defense’ is brought
about .This corresponds to syphilis.

There are three basic functions of a cell.Therefore only

three defence processes exist.Therefore only three types of
chronic diseases exist,hence there can be only three
miasms.All others are pseudo-miasms.
Pathogenesis of sycosis-Sycosis is secondary response
to cell injury brought about by using or sacrificing second
function of reproduction or generation.

We know that reproduction in a cell occurs due to many

processes.For cell division there is a process called
‘mitosis’.This process of division is so perfect and so
meticulous that a cell can give birth to two of its own kind
that exactly resembles the parent cell.That means the cell
divides in ratio of 1:2.

Now the secondary defensive response sacrifices this

second function of cell.This means something has to go
wrong with generation, production, or reproduction by 1:2.If
the reproduction ratio of 1:2 is changed, it could be either
more or less.The cell can thus start multiplying in ratio of 1:
more than 2 or 1: less than 2.The first can be ‘sycosis
excess’ and the second condition can be ‘sycosis less’.

Hence sycosis can be expressed in all ways and in all

systems and tissues in two forms-excess and less.The
diseases or pathological states both on physical as well as
mental level will be expressed as ‘excess’ or ‘less’.

Examples of ‘sycosis excesss’are:

warts,polyps,ascitis,cysts,hyperproteinemia
,gout,fibrosis,arteriosclerosis,strictures,stenosis,calculi,hyp
ermelanosis, calcanean spur etc.
Examples of ‘sycosis less’ are: hypoproteinemia, laxity of
muscles, prolapse, ptosis, osteoporosis, hypo-
pigmentation, anaemia etc.

The same sycosis miasm is responsible for

hypopigmentation of leucoderma which is caused due to
less production of melanin pigment.

Sycotic constitutions-Individuals born with predominantly

sycotic constitution have an innate and predominant
tendency to fight all the invasions whether they are
pathogens,toxins or on mental plane the ‘emotions’ by
constructive defensive responses of the cells and
tissues.These people are bound to get easy
constructions ,easy growths, thickenings, tumours,chronic
non-resolving inflammations.Insidious diseases like
diabetes,high blood
pressure,anaemia,hyperlipidemias,ischaemias,are common
at an early age.Warts,moles,keloids thrown up externally
gives us an indication that the patient has entered the
sycotic defence stage.

Patients get primary inflammation and go into constructive

pathology easily.Wounds and injuries are deceptive ,never
clean-cut nor do they heal neatly and cleanly like psoric
constitutions.They are deep inside and concealed with
yellow or green colour discharges.Deposition of
 pigments,hence blackening of skin or wounds is a rule in
this miasm.These diseases predominate middle age
groups.

HOMOEOPATHIC APPROACH FOR TREATMENT OF

LEUCODERMA:

Homoeopathy treats the patient as a whole, not the liver,

not the ulcer, not the particular part of body.Homoeopathic
prescription for vitiligo is based on two modes depending
on the severity and course of disease:

1.Chronic medicine as per totality and constitution.

2.Therapeutic medicine.

Chronic medicine as per totality - The “totality of

symptoms” means a good deal.It is all that is visible and
represents the disease in the natural world to the eyes, the
touch and external understanding of man.It is all that
enables the physician to individualize between diseases
and remedies;the entire representation of a disease is the
totality of the symptoms.It does not mean independent
symptoms,but it means that which will bring to the mind a
clear cut idea of the nature of thee sickness.

“From this indubitable truth, that besides the totality of

symptoms, nothing can by any means be discovered in
diseases where with they could express their need of aid, it
follows undeniably that the sum of all the symptoms in each
individual case of disease must be the sole indication, the
sole guide to direct us in the choice of a remedy.”

But it is not enough to consider the totality as a grand

whole, besides considering all the symptoms collectively,
each individual symptom must be considered.Every
symptom must be examined to see what relation it sustains
to and what position it fills in that totality in order that we
may know its value, whether it is common symptom, a
particular symptom, or a peculiar characteristic symptom.

As stated in aphorism 19,diseases are nothing more than

alterations in the state of health of the healthy
individual,which expresses themselves by morbid signs
and the cure is only possible by a change to the healthy
condition of the state of health of the diseased individual.It
is very evident that medicines could never cure diseases if
they do not possess the power of altering man’s state of
health ,which depends on sensation and function;indeed
that their curative power must be owing solely to this power
they possess of altering man’s state of health.

The statement is that medicines must be capable of

affecting changes in the economy.The potency must be
consistent with the degree of susceptibility that calls for the
medicine.This susceptibility includes a wide range of
potency,so that from 30 to the CM there is.

In aphorism 20 Hahnemann says:”This spirit like power to

alter man’s state of health (and hence to cure diseases)
which lies hidden in the inner nature of medicines can
never be discovered by us by a mere effort of reason; it is
only by experience of the phenomena it displays when
acting in the state of health of man that we can come
clearly cognizant of it.”

Every medicine that a homoeopath uses should have been

thoroughly proven upon the healthy so that its symptom
image shall have been thoroughly brought into.

Thus to summarize,the importance of totality of symptoms

are:

1. Sole guide in the choice of homoeopathic medicine, as it

is the outwardly reflected picture of the internal essence of
the diseases.

2.Totality of symptoms is to be recovered in affecting the

cure.

Now with the totality of symptoms we can apply ever

guiding law ‘similia similibus curanter’ intelligently for the
benefit of the suffering humanity.

Chronic medicine as per constitution-According to

Stuart Close,”Constitution is that aggregate of hereditary
characters, influenced more or less by environment,which
determines the individual’s reaction,successful or
unsuccessful,to the stress of environment.”

Dr.Kent says ,”Physical constitution is the external disorder

following disorder in the man,the vital force.”

An individual consists of a ‘psychobiological

apparatus”(biological intelligence,intellect, emotion, spirit).
Working towards homoeostasis and is concerned with the
individuals biological,emotional and spiritual needs.This
evolves in accordance with a codified genetic plan that
unfolds progressively as the individual ages,in response to
environmental factors.It acquires (through the immune
system PNIE Axis i.e. Psycho-Neuro-Immuno-Endocrine
Axis)a potential to fight its way through adverse conditions
and to reach an adaptive balance for survival.This fight is
expressed by external physical signs and symptoms as
well as through the mental symptoms.A homoeopathic
physician is concerned with understanding the
characteristic individuality of this expression for the
purpose of finding the similimum remedy.

Constitution has two basic factors:

Endogenous factor

Exogenous factor

Endogenous factors are innate in the individual incurred

from the heredity and endow the organism with various
types of tendencies, susceptibilities, reactions to the stress
of the environment etc.
Exogenous factors are incurred gradually and steadily
since birth from the various intimate details of the
environmental factors.

Ultimately these endogenous and exogenous factors may

become intimately mingled up that they form a new type of
constitution of the particular organism.From this approach it
is clear that each individual has a distinctly characteristic
constitution of his/her own.

Types of constitution:There are different types of

constitution which are carried into homoeopathic parlance
from old time pathology.

1.Scrofulous constitution-Glands remain swollen,general

weakness,lack of reaction,tardy to heal.Considered to be
the result of hereditary combinations of psora and syphilis.

2.Hydrogenoid constitution-Increased susceptibility to

humidity,even to aquatic vegetables,where all the
symptoms are aggravated by everything which in any way
increases the atoms of water in the organism.Considered
to be the result of intimate combination of psora and
sycosis.

3.Leucophlegmatic constitution-Catarrhal,flabby,water-
bagged constitution, with pale loose skin,sluggish in all
movements and activities,chilly and susceptible to cold.

Factors related to constitution:

Constitution consists chiefly of the following factors-

(a)Physical make-up of the body

(b)Temperament

(c)Heat and cold relation

(d)Desire,aversion and intolerance to food

(e)Miasm

(f)Diathesis

(g)Susceptibility and responses

(h)Addiction,habits etc.

It also includes all other factors that work in his framing

and that make him distinct, definite and thus separate from
other persons.

Thus constitutional medicine means the medicine which

can correct the constitutional defects-inherent or acquired.

Therapeutic medicines-Therapeutic approach is guided

by the dynamic concept of disease,and the homoeopathy
treats deranged vital force to restore the healthy state.

The homoeopathic law of nature or the therapeutic law of

nature states,”A weaker dynamic affection is permanently
extinguished in the living organism by a stronger one; if the
later is very similar to the former in its manifestations.

As vital force is dynamic,hence to correct it,homoeopathy

uses potentised medicine which causes total annihilation of
the disease.Potentisation brings medicine to dynamic plane
so that it acts on dynamic vital force which is dynamically
deranged.
Therpeutic curative mode depends upon the size and
strength of the dose,and susceptibility of the patient.The
homoeopathic cure is obtained without suffering,without
production of any drug symptom,in a positive and direct
manner by the minimum dose,which is a dose so small that
it is not capable of producing symptoms when used
therapeutically.Homoeopathy requires that the therapeutic
dose must be capable only of producing a slight temporary
aggravation,or intensification of already existing symptoms,
never producing new symptoms.Only the similar remedy in
the smallest possible dose is capable of bringing about this
highly desirable result.By this means the patient’s strength
and vitality are concerned,his suffering quickly reduced to
the lowest possible degree,and a true cure is brought
about.We cannot ignore that homoeopathic drug is always
given singly,so that its action is complete and unmodified
by other drugs.

Choosing the potency is another cumbersome process.Is

there any teaching which will help us to choose the best
potency for a given case?There is little teaching but many
opinions.Five considerations influence us in choice of dose:

1.The susceptibility of the patient-It varies in different

individuals according to age, temperature, constitution,
habits, character of diseases and environment.

The more similar the remedy ,the more clearly and

positively the symptoms of the patient take on the peculiar
and characteristic form of the remedy;the greater the
susceptibility to that remedy ,the greater is the potency
required.

2.The seat of the disease

3.The nature and intensity of the disease-Certain malignant

and rapidly fatal diseases like cholera may require material
doses or low potencies of the indicated drug.

4.The stage and duration of the disease

5.The previous treatment of the disease.

HOMOEOPATHIC THERAPEUTICS:

Arsenicum sulfuratum flavum- Head remedy for

leucoderma.It is to be given for a very long time in varying
dilutions.

Arsenicum album- White skin in scrofula.

Apis mellifica- White skin accompanied by ovarian

dropsy.Infantile derangement.Patches have surrounding
redness

Kali carbonicum- When the skin is milky.

Hydrocotyle- Great thickening of epidermoid layer and

exfoliation of scales.
 Borax- White skin with red patches.

Psorinum- Spot of white skin with white lock of hair

becomes natural colour under this remedy.

AUXILLARY TREATMENT:

In addition to medical and surgical therapies, there are many

things you can do on your own to protect your skin, minimize
the appearance of white patches, and cope with the emotional
aspects of vitiligo:

Sunscreens—People who have leucoderma, particularly

those with fair skin, should minimize sun exposure and use a
sunscreen that provides protection from both the UVA and
UVB forms of ultraviolet light. Sunscreen helps protect the
skin from sunburn and long-term damage. Sunscreen also
minimizes tanning, which makes the contrast between normal
and depigmented skin less noticeable.

Cosmetics—Some patients with leucoderma cover

depigmented patches with stains, makeup, or self-tanning
lotions. These cosmetic products can be particularly effective
for people whose leucoderma is limited to exposed areas of
the body. Dermablend, Lydia O'Leary, Clinique, Fashion Flair,
Vitadye, and Chromelin offer makeup or dyes that you may
find helpful for covering up depigmented patches. Selftanning
lotions have an advantage over makeup in that the color will
last for several days and will not come off with washing.

Counseling and support groups-Many people with

leucoderma find it helpful to get counselling from a mental
health professional. People often find they can talk to their
counsellor about issues that are difficult to discuss with
anyone else. A mental health counselor can also offer support
and help in coping with leucoderma. In addition, it may be
helpful to attend a leucoderma support group.

Dietary instruction in Vitiligo:

There are a few instructions for patients regarding their diet in
vitiligo especially with mention of what they should avoid
during the treatment of leucoderma.

:: Foods that are excessively sour should

be avoided. Vitamin C (ascorbic) is known
to inhibit the production of the melanin, the
color pigment. Patients with leucoderma
are suggested to refrain from citrus fruits,
sour yogurt, sour pickles, etc.
Non vegetarian foods are also to be
avoided as they act as a foreign body to
pigment cells.

:: Artificial colors used in various food

preparations should also be avoided.

BIBLIOGRAPHY

1. Harrison’s Principles of Internal Medicine

2. J.S. Pasricha,Illustrated textbook of dermatology

3. Fitzpatrick’s,Synopsis of clinical dermatology

4. Neena Khanna,Illustrated Synopsis of dermatology

5. Hahnemann,Organon of Medicine

6. Hahnemann,The Chronic Diseases

7. Stuart Close,The Genius of Homoeopathy

8. Allen’s keynotes

9. Kent’s Lectures on Homoeopathic Materia Medica

10. Kent’s Lectures on Homoeopathic Philosophy

11. Kent’s Repertory

12. Boericke Materia Medica

13. Millington GW, Levell NJ "Vitiligo: the historical curse of
depigmentation”

14. Taraborrelli, J. Randy The Magic and the Madness

15. George, Nelson Michael Jackson: The Ultimate Collection

booklet.

CASE PROFORMA

CASE NO.: …………………………………………….

DATE:………

PHYSICIAN’S NAME:………………………….. OPD NO……..

ACUTE/CHRONIC:……………………………………
IPD/WARD NO.:………..

RESIDENT/STUDENT:……………………………….
DOA…………

DOD…………
PATIENT’S NAME:……………………………………

AGE/SEX/RELIGION:……………………………

ADDRESS:………………………………………..

OCCUPATION:……………………………………………………

MARITAL STATUS:
……………………………………………………………

DIAGNOSIS CONSTITUTION
PROVISIONAL D……………………………
…………………………………………..
MIASMATIC D……………………………
…………………………………………..
THERAPEUTIC D…………………………… .
…………………………………………
FINAL D………………………….. ..
……………………………………….

CLINICAL HISTORY

CHIEF COMPLAINTS(including
causation,duration,location,character,sensation, extension or
radiation,modalities and concomitant)

………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………

HISTORY OF PRESENT ILLNESS:

………………………………………………………………………
………………………………………………………………………
……………………………………………....

PHYSICAL EXAMINATION
GENERAL EXAMINATION
A. 1.Inspection……………………………………………………
………………..
2.Palpation……………………………………………………
…………………
3.Percussion…………………………………………………
…………………..
4.Auscultation…………………………………………………
………………...

B. Pulse……………..B.P………………Tempt……………………..
R.R……………..
Pallor……………. Cyanosis………...Oedema ………………….
Anaemia……….

SYSTEMIC REVIEW

GENERAL: (weight,height,gait)
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
Eye………………
Conjunctiva…………………….Pupil…………….Vision…………
….
Oral cavity (mouth,gums,teeth,tongue,throat)
……………………………………………...
Ear (pain,discharge,hearing,sound)
…………………………………………………………
………………………………………………………………………
………………………
GIT,ABDOMEN,PELVIS……………………………………………
………………………………………………………………………
………………………………………………………………………
……………………………………………………………………
UPPER ALIMENTARY TRACT(pain,vomiting,flatulence,water
brash,heart burn, dysphagia)
………………………………………………………………………
………………………………………………………………………
……………………………….
LOWER ALIMENTARY
TRACT(stool,diarrhea,constipation,pain,etc)
………………………………………………………………………
………………………………………………………………………
………………………………………………
LIVER AND GALL BLADDER(jaundice,pain,calculi)
………………………………………………………………………
………………………………………………………………………
………………………………………………
GENITAL SYSTEM
MALE(spermatorrhoea,urethral discharge,s.t.d.s,sexual
behaviour,secondary sex characters)
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
…………………………………………………………
FEMALE(vaginal discharge,s.t.d.s,sexual behaviour,secondary sex
characters)
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………

CVS(dysponea,pain,palpation,cough,oedema,etc)
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
…………………
BLOOD(lassitude,infections,blood loss,etc)…
………………………………………………………………………
………………………
………………………………………………………………………
………………………
ENDOCRINE
SYSTEM……………………………………………………………
………
………………………………………………………………………
………………………
RESPIRATORY
UPPER RESPIRATORY LOWER
RESPIRATORY
NASOPHARYNGEAL CAVITY
NASAL DISCHARGE COUGH
Acrid/Bland Colour
Colour Consistency
Thick/Thin Odour
Smell Taste
Sneezing Characters
BREATHING
WHEEZE
CHEST PAIN
URINARY SYSTEM(pain,micturition,colour,smell)
………………………………………………………………………
………………………………………………………………………
………………………………………………
NERVOUS SYSTEM(reflexes,fits,strokes,gait,power)
………………………………………………………………………
………………………………………………………………………
………………………………………………
LOCOMOTOR SYSTEM(pain,articular affection,gait etc)
………………………………………………………………………
………………………………………………………………………
………………………………………………
SKIN
APPEARANCE……………………………….
ITCHING………………………
DISCOLOURATION…………………………
SUPPRESSION………………..
ERUPTIONS………………………………….
ULCERATIONS…………………
DISCHARGE………………………………… WARTS OR
MOLES……………

OBSTETRIC/GYANIC HISTORY

No. of previous pregnancies……………………

Normal…………..Abnormal……………
Abortions………………No. of children living………….Born
alive……………………..
Still born……………… Date of last delivery or
abortion…………………………………

MENSTRUAL HISTORY

Menarche………………………………Duration
/cycle………………Flow……………..
Dysmen………………………………...L.M.P………………………
..E.D.D…………….

PAST HISTORY(Including mile stones)

………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
……………………………………………………………………....
PERSONAL HISTORY
CONSTITUTION…………………………………
FOOD HABIT…………………………………….
ADDICTION(if any)……………………………..
HABITS…………..(Sedentary/Active/Hard Labour)
EXTRA MARITAL RELATION…………………

FAMILY HISTORY
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
………………………………………………………………………
SOCIAL STATUS…………………………………..
NUTRITIONAL STATUS………………………….

GENERAL SYMPTOMS

PHYSICAL GENERALS
Appetite
Thirst
Desires
Aversions
Sleep
Dreams
Perspiration

Effect on Patient and his complaints of:

Time
Weather
Hot/Cold
Rest/Motion
Position
External stimuli (Touch,Light,Sound,Odour)
Eating and Drinking

MENTAL GENERALS

WILL(love,hate,emotion,perversion)………………………………
UNDERSTANDING(delusion,hallucination, illusion)…………….
INTELLECT(memory,concentration)……………………………..

INVESTIGATIONS

URINE BLOOD
Reaction Blood Group
Sp.Gr. Hb%
Albumin T.L.C.
Sugar D.L.C.
Acetone E.S.R.
Microscopic Blood Urea
Culture & Sensitivity Bl.Sugar
STOOL EXAMINATION T3,T4,TSH
Serum creatinine
SPECIAL INVESTIGATIONS
S.G.P.T.
S.G.O.T.
CHOLESTEROL
AUSTRALIA ANTIGEN

EVALUATION OF SYMPTOMS
MENTAL……………………………………………………………
……………………………………………………………………..
GENERAL…………………………………………………………
……………………………………………………………………..
PARTICULAR………………………………………………………
……………………………………………………………………..
CONSULTATION FROM MATERIA
MEDICA/REPERTORY……………………………………………
……………………………………………………………………….
THERAPEUTIC FINAL
DIAGNOSIS…………………………………………………………
……………………………………………………………………….
SURGICAL/MANUAL INTERVENTION(if any)………………….
………………………………………………………………………..

FINAL PRESCRIPTION ……………………………………………………….

…………………………………………………………………………………..

PROGRESS REPORT

DATE PROGRESS TREATMENT

SIGNATURE SIGNATURE
PHYSICIAN INTERN

GRAPHICS

Age group
 Graph showing the prevalence of disease (leucoderma)
in different age groups,showing the highest risk between
10-20 yrs. Of age.Both sexes are equally affected.

MASTER CHART

S. NAME AG P/C Prescription Medici Result

N E/S basis ne
O. EX
1 Jabir 35/ Complaint of bilaterally Constitution Sulph improved
M symmetrical moderate size al 200/3
white spots on legs, dose
knees,ankles with
constipation

2 Hashee 18/ Complaint of Constitution Carcin improved

n Bano F bilaterally symmetrical al ocin
depigmented spots on 200/3d
legs, ankles, knees, ose
upper legs,groin &
lower back along with
menstrual complaintsof
dysmenorrhoea &
profuse flow

3 Pradeep 28/ Complaint of Constitution Kali improved

Kumar M depigmented patches al Ars.
on chest and lower 200/3d
back,also suppering
 from chronic
constipation and
attacks of frequent cold

4 Anjali 7/F Complaint of small Constitution Lyco.1 Further

patches on left upper al M/3d progress
eyelid,right retro- was
auricular region which stopped
was gradually
increasing.Eczema on
back,cubital fossa and
popliteal fossa
aggravating in winter
5 Ravindr 28/ Complaint of Constitution Carcin improveme
a Singh M depigmented patches al ocin nt noted
on back and thigh 1M/3d
region.Patient had
family history of
Cancer. and tendency
of catching cold easily.
6 Vijay 62/ Complaint of white Constitution Nat. Improved
Pratap M patches on al mur
toe,ankle,knees since 3 1M/3d
years,without any
further complaint.
7 Rahul 13/ Complaint of Constitution Vert. Slight
M depigmented bilateral al alb improveme
large patches on 200/3d nt
knees.Patient is highly
irritable and had a
desire for ice and cold
things ,general
aggravation after
anger.
8 Manor 21/ Complaint of constitution Sulph. improveme
ma F depigmented patch on al 1M /3 nt noted
 lower lip & d
chin.Patient has history
of evening fever &
marked fear of animals

9 Kalim 18/ Complaint of milky constitution Ars. Improveme

M white patches on lower al sulph.f nt noted
abdomen & inner parts lav .30
of thighs.patient has /BD
personal& family
history of eczema & is
sensitive to change of
weather

10 Kalpan 26/ Complaint of constitution Ars. Slight

a F depigmented patch on al Alb improveme
Pandey arms,shoulders &back, 200/3d nt
bilaterally symmetrical
along with menstrual
troubles
11 Monu 21/ Complaint of white constitution Tuberc No
M patches on nape of al ulinum improveme
neck with recurrent 1M /3 nt noted
cold & cough d
12 Shalu 13/ Complaint of milky constitution Sulph No
F white patches on ear al 1M improveme
lobes,around lips,great / 3d nt noted
toe and excessive
offensive perspiration.
13 MN 43/ Complaint of constitution Laches improveme
Tripathi M depigmented patch on al is.200/ nt noted
dorsal side of hand BD
14 Uma 50/ Complaint of constitution Acid improveme
F depigmented patch on al sulp nt noted
inner parts of thighs 200/3d
and lower back and
 had sour belching
15 Yogesh 21 Complaint of white constitution Sulph Slight
Verma M patches on finger al 200/3d improveme
joints,elbow,knees,ankl ose nt noted
es.Also suffering from
joint pain and difficult
respiration.
16 Durges 45/ Complaint of Therapeutic Ars. Slight
h M depigmented patch on sulp. improveme
both legs,symmetrical Flavu nt noted
below knees m
200 /
3d
17 Mansi 7 Complaint of white Therapeutic Ars. improveme
mo patches on face,near alb.30/ nt noted
n/F right corner of lips and BD
on cheeks.Child was
moderately active and
have thrist for little
quantity of water.

18 Balcha 37/ Complaint of Therapeutic Apis. No

ndra M depigmented patches mel. improveme
on abdomen and 30/TD nt noted
back.Patches S
surrounded by slight
redness.

19 Fatima 11/ Complaint of constitution Merc. improveme

F depigmented patches al sol. nt noted
on both fore arms 200/3d
along with bowel
trouble.Stool
accompanied with
mucus and slight
blood.
20 Pawan 11/ Complaint of milky Therapeutic Ars. improveme
M white patches on sides sulp. nt noted
of neck ,behind right flavum
ear lobe,left shoulder 30/TD
and chest. S

SYNOPSIS OF CASES

CASE 1:
Patient A,35 year old male reported us with a complaint of
bilaterally symmetrical moderate size spots of leucoderma
present on his legs,ankles and knees since 2.5 years.Patient
was treated with steroid with no changes in the size of
spots..
Along with his skin complications,he suffered from painful
defecation due to hard stool.His appitite was normal and he
used to crave for sweet and fatty food.He had profuse
perspiration and disturbed sleep patterns.
He had prolonged depression which had been caused due to
grief of fathers death,the stress of his mother’s illness and
his elder brother separation from family.He was very
chearfull but dull and lazy .
Based on detailed case study he was prescribed Sulph 200
for his complaints.After 1 month his leucoderma patches
over knees and ankles were better.His bowel symptoms
were relieved to a certain extent.After 3 months his
leucoderma was better by 30%.

CASE 2:
Patient B ,a 18 years old female,reported with bitaterally
symmetrical,moderately depigmented patches on
legs,ankles,knees and upper legs,groin and lower back.
She also suffered from menstrual complaints.She had
dysmenorrhoea with profuse flow.She was of social
nature,hardly get angry and if did mostly left
unexpressed.She have family history of cancer.
She had craving for cold drinks and ice creams.She had a
calm and sound sleep and usually on right side.
Based on the history she was prescribed Carcinocin
200.After 15 days she reported with relief in menstrual
complaints and disappearance of spots later on.

CASE 3:
Patient C ,a 28 years old male had depigmented pathes on
chest and lower back since 2 years.he was also suffering
from loss of appetite and chronic constipation.he had
suffered from frequent cold in his childhood.
He had marked weeping tendencies,especially if could not
perform well in competitions.He used to get hurt easily.He
hated partiality of any kind.
His father was hypersensitive and mother suffered from
cervical spondilitis.His parental grandmother suffered from
lung cancer and maternal grandparents suffered from
Ischaemic heart diseases.
Based on the history he was prescribed Kali ars.200 and
after 4 months,leucoderma patches had faded up upto 15%.

CASE 4:

Patient D ,a 7 years old girl reported with vitiligo on her

left upper eyelid ,right retro-auricular region since 6
months.Hypo pigmented spots were noticed to be increasing
gradually.
She was also suffering from eczema on her back,cubital
fossa and popliteal fossa since 3 months of age,usually
aggravated during winters.
Her father was hypertensive & mother had suffered from
vitiligo in the past.She was very friendly but quite short-
tempered.She didn’t like to be alone to the point that she
can’t sleep alone in a room.She had a good memory &
concentration.
She was hot patient,having normal thirst & desire for hot
food.On detailed case history she was prescribed
Lycopodium 1M & slight improvement was seen for 4
months that stopped further.

CASE 5:

Patient E,a 28year male came with depigmented patches on

back and thigh region since 1 year.He was sensitive to
change of weather & and had tendency of catching cold
easily.His appetite was normal with craving for
spicy,sweet ,salt and cold food .He was a hot patient & had
fear of dogs.Detailed case history revealed family history of
Canaer.On constitutional basis he was prescribed
Carcinocin 1M & was reported with good improvement
within 2 months.

CASE 6:

Patient F,a 62 year male reported with white patches on

toe,ankle,knees since 3 years.He had taken steroids without
any improvement.His appetite,thirst,bowel habits were
normal.He desire for salt and aversion to fatty food. Patches
were stable,not increasing. He was very depressed and
dwelling about past.He was prescribed Nat.mur 200 on
constitutional basis & the patches started fading after 5
months.

CASE 7:

Patient G,a 18 year male came with complaint of

depigmented patches (bilateral, large)on knees since 8
months.He was very friendly,mix up with people easily but
make only superficial relations.Patient was highly
loquacious and was very distructive in natureHe had
craving for ice,cold drinks and salty things.Complaint
started from left side 7 proceeded to right.Memory &
concentration was average but he had general aggravation
after anger.Based on general and mental symptoms he was
given Verat.alb 200.Even after 6 months the case was stand
still with no progression or regression of patches.

CASE 8:

Patient H,a 21 year female reported with complaint of

depigmented patch on lower lip & chin since 1.5 year.She
had history of evening fever & debility.She was intelligent
wjth sharp memory.She had poor appetite,thirst increased.
But desire for sweets and fat was very marked.She had
marked laziness& dullness.Based on the case taking she
was prescribed Sulph 200.After 3 months the patches on
lips started fading.

CASE 9:

Patient I, a 18 year male reported with complaint of milky

white patches on lower abdomen & inner parts of thighs .
Patient has personal & family history of eczema & is
sensitive to change of weather.Based on the detailed case
history he was givenArs.sulph.flav30/bd.Within 45 days
eczema was totally cured & slight improvement was noted
in patches.

CASE 10:

Patient J ,a 26 year female reported with complaint of

depigmented patch on arms,shoulders & back, bilaterally
symmetrical,since 10 months along with menstrual troubles.
She had painful and irregular menses.Patient was calm bit
very emotional.She had desire for fatty food although it
aggravates.Sleep was sound and on back.She feel
suffocation in closed room.She was very sympathetic and
use to weep easily.based on the case taking she was given
Arsenic alb 200/3d.In follow ups,menses became regular
and patches were 30 % improved .
CASE 11:

Patient K, a 21 year male came with the complaint of white

patches on nape of neck since 2 year.He was a sensitive
person with recurrent cold & cough.Patient was intelligent
and active.He had changeability regarding job.He can’t
remain in one job for longer period.He had fear of dark.At
age of 7 years he suffered from Tuberculosis & had taken
allopathic treatment.After detailed case history he was
prescribed Tuberculinum 1M but no remarkable
improvement was noted.

CASE 12:

Patient L, a 13 year female have complaint of milky white

patches on ear lobes,around lips,great toe since 5 years.He
was highly hot patient.He had past history of typhoid and
still having diabetes.He had desire for cold food &
sweets.He was usually constipated.He had excessive,
offensive perspiration especially on feet,hands & axillae.On
constitutional basis he was given Sulph 200/3d.His
constipation was relieved but no change in the depigmented
patches.

CASE 13:

Patient M, a 43 year male reported with small,depigmented

patches on the dorsal side of hand since 7 months. Patient
was very restless with physical debility.He was very
loqacious,and had tight cloathing aggravation.Sometimes he
has burning in extremities, which was relieved by cold
application.On the basis of presenting complaints he was
prescribed Lachesis.200/3d.After 2.5 months he was
reported with 10% improvement.

CASE 14;

Patient N, a 22 year female have complaint of depigmented

patches on inner parts of thighs and lower back since 2
years.Skin seems to be dry and thick with pealing off of
skin in winters.Patient was chilly and all her discharges like
sweat,nasal discharge,stool were foul smelling.Appetite was
good.Patient has past history of skin eruptions which were
suppressed by allopathic treatment.She has sever sour
belching.On the basis of case history she was givenAcid
sulph 200/3d.After 1 month of treatment skin eruptions
reappeared.She was strictly told not to use any ointment and
after next 1 month eruptions disappeared.Later on patches
also improved upto 15%.

CASE 15:

Patient O,21 year male reported with complaint of white

patches on finger joints,elbow,knees,ankles since 6 years.He
was also suffering from joint pain and difficult
respiration.His appetite was normal and have craving for
sweets,fat and cold drinks.He was artistic in nature,having
hobbies like painting,embroidery etc.He was hot
patient,wants to be in open air,loves natural beauty.He had
past history of uterine tumour and was operated for it.Based
on the detailed case history he was prescribed Sulphur 200
and slight improvement was noted in white patches,joint
pain was also 40% relieved.

CASE 16:

Patient P, 45 year male reported with complaint of

depigmented patch on both legs,(symmetrical) below knees
since 18 months.His appetite was normal.Patient was
friendly and quiet in nature.He doesn’t have any specific
desire or aversion.On therapeutic basis he was given
Ars.sulph.fla.200/3d.After 7 months of treatment the
patches started fading.

CASE 17:

Patient Q,7 months female child reported with complaint of

white patches on face,near right corner of lips and on
cheeks.Child was moderately active and have thrist for little
quantity of water.On therapeutic basis she was given
Arsenic alb. 30 and after 25 days 10% improvement was
seen.

CASE 18:
Patient R,37 year male reported with complaint of
depigmented patches on abdomen and back since 1 year.
Patches were surrounded by slight redness. He was short
tempered, punctual and fastidious.He was prescribed Apis
mel. 30 on therapeutic basis but no improvement was noted
even after 2 months.

CASE 19:

Patient S, 11 year female reported with complaint of

depigmented patches on both fore arms along with bowel
trouble since 1.5 years. She had normal appetite with desire
for milk and sweets and intense thrist. Stool was
accompanied with mucus and slight blood. She had profuse
and offensive perspiration. Patient was impulsive in
nature .Based on her constitution she was given Merc.sol
200.Within 3 months the patches started getting lighter and
improved upto 20%.

CASE 20:

Patient T, 11 year male reported with complaint of milky

white patches on sides of neck ,behind right ear lobe,left
shoulder and chest since 13 months.He was moderately
active child having average performance in his
studies.Father was suffering from arthiritis and mother was
hypertensive He was given Ars.sulph.fla.30 and after 3
months 10% improvement was noted.