depends on different factors:
a more effect than the number of melanocyte density in the skin.
of melanocytes in Negroes is not more than that available in the
deposition of melanosomes.
pigment to the keratinocytes.
of melanin is mainly
responsible for skin coloration.
in skin color is either:
which is mainly after, sunbathing, post inflammatory, hormonal or
associated with different diseases.
follows certain skin diseases.
loss of pigment:
such as in vitilligo and albinism.
is due to melanin, which is synthesized by the melanocytes in the
epidermis and hair follicles, from phenylallanin through
transformation of tyrosine to dopa or dopamine and to dopaquine by
the action of tyrosinase enzyme.
beings there are three types of melanin:
insoluble brown pigment, which gives the skin its brown color,
synthesized from phenylallanin.
gives the red hair synthesized from cystine and tyrosine.
the pigment of substantia nigra.
The color of
the skin depends on other factors mainly:
affecting melanocytes and melanin synthesis.
number of melanocytes in the skin.
of the pigment to the keratinocytes.
deposition of melanosomes.
305. Hyperpigmentation (Nevus of Ota)
Fig. 306. Hyperpigmentation
Fig. 307. Hyperpigmentation
Fig. 308. Hyperpigmentation
Fig. 309. Hyperpigmentation (Cosmetic)
Fig. 310. Hyperpigmentation
Fig. 312. Hyperpigmentation
Fig. 311. Hyperpigmentation (Metallic)
Affecting Skin Color
factors: the number of melanocytes in Negroes and
Caucasians are the same but melanin synthesis and
melanin deposition in Negroes
much more than other
inflammatory - Different skin diseases after healing
Thiazides may lead
to generalized skin hyperpigmentation. Drug reactions, especially to
sulfonamides, Minocycline may cause hyperpigmented patches, on feet, legs,
thighs and buttocks.
photosensitizers such as Psoralenes and cosmetic preparations containing
certain ingredients such as almonds and others may cause hyperpigmentation.
disease and Cushing‘s syndrome cause hyperpigmentation while
hypopituitrism cause hypopigmentation.
pigmentation: occurs after skin tanning due to exposure to ultraviolet
radiation, and cloasma in pregnancy.
Vitilligo is a pigmentary
skin disorder, characterized by sharply defined depigmented patches
due to deficiency or destruction of melanocytes.
Fig. 313. Vitilligo
Fig. 314. Vitilligo
Fig. 315. Vitilligo
Fig. 316. Vitilligo (Postinflammatory)
Fig. 317. Vitilligo
Psoralenes and PUVA)
Fig. 318. Vitilligo and Alopecia
Fig.318b. Vitilligo& Atopic dermatitis
Fig. 319. Vitilligo and Psoriasis
(Immunologic) (Psoriasis and vitilligo
besides psoriasis of his sister)
factors are considered in the etiology of vitilligo and there is
herido-familial occurrence of the disease.
appear usually on the exposed body surface such as the face and
sharply demarcated milky white, depigmented patches, which may show
hyperpigmented edges, especially with the progress of treatment.
may be idiopathic or secondary to certain factors.
systemic diseases may be associated with vitilligo: thyrotoxicosis,
anemia, gastric carcinoma, diabetes and Addison‘s disease.
may repigment spontaneously or as a result of treatment, become
stationary for a long period, or become very extensive covering the
whole body with complete change of all skin surface color and hair.
lines of treatment are used.
and PUVA: are the
mostly used since longtime till now, using trisoralen tablets and
exposure to sun or PUVA after two hours from taking the medications.
effects may occur as photosensitivity or sometimes exacerbation of
Fig.318c. Photosensitization due to topical psoralene (Oxysoralene
**Care should be considered especially when treating mucocutaneous
are not indicated in children, where these age groups can be treated
by topical 15-20 per cent oil of pergamount or Oxysorolene topical
preparation and sun exposure before three o‘ clock in the after
noon, preferred in the morning.
of any abnormality:
such as anemia or associated diseases.
topically or systemically:
in form of long acting steroid such as (Depot medrol, 40 mgm) given
weekly or oral Prednisolone tablets give good results in some cases.
children we use the following methods of treatment:
per cent oil pergamount twice daily in the morning, and topical mild
steroid cream at night.
cases, in older children we give Depot medrol 40mgm every two weeks
for a total of four injections, for two months.
good results, where repigmentation begins usually in the second week
on the family of the child not to discontinue treatment, where we
found that when repigmentation begins and stopping treatment,
progressive repigmentation is very difficult. The patches seem to
get resistance with little or no response to treatment.
and other camouflage locally:
are used for patches of the face or fingers and areas, which
sometimes resist treatment.
and melanocytes implantation are expensive and not always
I had in my
mind an old experience concerning using plant photosensitizers for
treatment of leucoderma and vitilligo.
This was an
important note I have to remember since a long time and to tell now
50 years ago, when the natives of our village used to instruct
patients having leucoderma or vitilligo to go to the farms in the
morning and to injure the stem or remove the leaves of a fig tree,
and apply the milky secretion on their skin lesions before exposure
It is a
primitive experience but it could do a lot for the patients who were
satisfied with the erythema and regimentation of their lesions.
a long time, I could find an explanation to that type of primitive
natural dermatological practice. By experience, which may be
inherited from grandfathers, they could find something to treat such
skin problems in the time where there were no any alternative means.
Narrow band laser
treatment for vitilligo and psoriasi has been considered recently as
an effective line of therapy for psoriasis especially cases which
don't respond to the traditional methods of treatment.Although this
type of treatment is expensive,yet it is the line of choice for
those who can afford paying for narrow band costs.
Narrow-band UVB refers to a
specific wavelength of ultraviolet (UV) radiation, 311 to 312 nm.
This range has proved to be the most beneficial component of natural
sunlight for vitilligo and Psoriasis and is promising in the
treatment of some other skin conditions including atopic eczema and
Compared with broadband UVB, in the treatment of psoriasis, Narrow
band UVB treatment has the following features:
* Exposure times are shorter
but of higher intensity.
* The course of treatment is
* It is more likely to clear
* Longer periods of
remission occur before the psoriasis reappears
For patients with psoriasis severe enough to require phototherapy,
narrow-band UVB offers efficacy superior to conventional UVB and
appears intrinsically safer than PUVA. However, because it produces
more epidermal damage than wideband UVB, the narrowband treatment
must be used with careful individualization of dosage and patient
monitoring, according to James G. Krueger, MD, PhD.
a partial or complete congenital absence of color of skin, hair and
eyes due to decrease or absence of melanization. Albinism is usually
associated with other defects and syndromes. Albinism is transmitted
as a simple recessive trait, where there is a genetic absence of
tyrosinase enzyme essential for oxidation of tyrosine to
dihydroxyphenylalanin. Melanocytes are active, but melanin cannot
deposit upon the premelanosomes. The defect is in the transfer of
pigment to the keratinocytes in spite that tyrosinase activity is
Fig. 320. Albinism
Fig. 321. Piebaldism
(Localized depigmentation of skin & Hair)
cases there is no tyrosinase activity and melanin synthesis, which
ead to milky white dry skin, white hair, pink iris. Photophobia,
skin atrophy and cancer due to loss of the protection ability of
skin from the effect of sunlight.
be complete or partial, involving localized area of the skin
manifestations appear at birth where, there is a localized
depigmented patch that may have a progressive course to total
depigmentation in older infants and children.
The skin is
paler instead of white, where islands of regimentation appear later
on and the iris is light blue due to partial melanization.
The hair is
golden instead of white as in the complete albinism.
ASSOCIATED WITH ALBINISM
pigmentary disorders of melanocytes of skin and hair presenting with
patchy depigmentation of the skin and a white forelock.
lesions may appear at birth, where the lesions remain unchanged
throughout life. The disorder is transmitted as an autosomal
forelock and the associated triangular patch of depigmentation on
the forehead are diagnostic.
depigmentation is in the form of islands of residual pigmentation in
the lesions and a line of pigmentation in the mid-line on the back
and front of the legs, face and the back of the trunk.
phenylketonuria: there is pallor of the skin due to decrease of
phenylanaline oxidase, which impairs hepatic formation of tyrosine
causing inflammation resulting in destruction of the basal layer of
the epidermis, such as discoid lupus erythematosus or in fungal
infections of skin which act as melanocytes-destructive agents.
manifestations of this syndrome are piebaldism, pallor of the iris,
wide epicanthic folds and nerve deafness.
disorder almost in females characterized by skin manifestation
appearing after birth, usually in the first, month in the form of
small vesicles or blisters, nodules and later warty lesions followed
by bizarre, linear or whorled pigmentation in the second year of
life. Other manifestations of incontinentia pigmenti are absent
teeth, epilepsy, mental retardation, spastic paresis, microcephaly,
eye abnormalities such as nystagmus, pappilitis, choroidoretinits,
alopecia and nail dystrophy.
DISEASES AND SYNDROMES
WITH SKIN COLOR CHANGES
factors can produce local or generalized skin color changes and the
differential diagnosis is often difficult.
is a characteristic feature of urticaria pigmentosa.
childhood type: the
light brown macules often exceed 2 cm in diameter and the lesions
are frequently nodular.
In the adult
type: the smaller
and more numerous macules are purplish brown in color and not
palpably infiltrated, and often fail to urticate on friction.
usually widely distributed over the trunk and limbs.
associated with hypermelanosis in biliary cirrhosis.
discoloration of the skin that is more common in children and
vegetarians, where excessive carotene can be demonstrated in blood
result from excess ingestion of certain foodstuffs rich in vit. A
such as carrots, spinach, beans, yellow corn, sweet potato, and
orange. Yellow coloration appears mainly on the palms, soles
forehead and the nasolabial folds.
The yellow coloration in diabetes may be due to hyperlipemia or
dinitrophenol, picric acid, trinitrotoluene, santonin, acriflavine,
Mepacrine may cause hyperpigmentation.
Dark red or
red-brown, often with hypermelanosis of the lowers legs in stasis
dermatitis, Sickle-cell anemia, congenital hemolytic anemia,
Schamberg‘s disease and Majocchi‘s disease.
excoriation and rubbing of the clothes against the skin causes
localized hyperpigmentation corresponding to the affected areas.
silver causes blue-gray hyperpigmentation, which is most intense on
exposed areas of skin.
causes blue-gray hyperpigmentation resembles argyria but bismuth
line on gums is more common than skin pigmentation.
causes gray-brown discoloration of the skin, which is limited to
sites of repeated application of mercurial ointments - especially on
the eyelids and skin creases
The skin pigmentation depends on the type of topical preparation.
hyperpigmented, benign, discrete macules that occur mostly on the
sun exposed areas due to increased activity of epidermal
may be multiple, appearing in early life and continue till puberty
mainly on the upper part of the body and may be associated with
pulmonary and aortic stenosis, skeletal abnormalities and genitalia
Fig. 322. Lentigo (Treated by laser)
Fig. 323. Lentigo
ruby laser is recently used as an effective device to clear lentigo.
can also give good results for ablation and resurfacing of lesions.
phenol neutralized with alcohol is an old treatment.
bleaching creams such as 4% Eldoquine may give some effect.
Busulphan, Inorganic arsenic, and ACTH causes generalized
pigmentation and remains unchanged through out life, where there is
patchy depigmentation of the skin and white forelock with diagnostic
triangular patch of depigmentation on the forehead.
may be induced by a wide variety of other drugs. Several mechanisms
are involved in the drug-induced changes of pigmentation of the
heavy metals may be deposited in the dermis in sufficient quantity
to bring about a distinctive change in skin color without any
significant increase in melanin.
eruptions hyperpigmentation occurs due to damage of cells in the
basal layer such as with Sulfonamides.
baby‘ syndrome is due to chloramphenicol overdose.
photosensitizers may cause localized skin hyperpigmentation.
This is a
rare inherited disease, affecting children, characterized by
generalized dusky or olive-brown pigmentation, congenital defects
and usually accompanied by hematological abnormalities.
commonest sites involved are lower trunk, flexures and the neck.
dusky hypermelanosis, appear with scattered over the dusky areas,
depigmented macules of raindrop type and macules of darker
pigmentation. Rarely, only café-au-lait macules are present.
children are mentally retarded, slender built with short, broad
hands with tapering fingers and thumbs which are rudimentary.
and hypogonadism are frequent besides other developmental defects.
changes are hypoplastic anemia, thrombocytopenia, neutropenia and
fatal pancytopenia with hemorrhages are usually fatal in infants and
There is an
increased incidence of acute leukemia and other neoplasms.
The cause of
this syndrome is unknown. The full syndrome with precocious puberty
occurs only in girls.
pigmentation usually develops between the ages of 4 months and 2
years, but may be present at birth.
light-brown patches, often with an irregular or serrated margin,
occur mainly on the trunk, buttocks and thighs, but may rarely
involve the face and neck. They tend to be asymmetrical and to be
most extensive on the sides.
are severe such as aching pain, pathological fractures and secondary
and defective vision are due to overgrowth of bone at the base of
calcium and phosphorus are normal, but alkaline phosphatase may be
elevated if the bone lesions are numerous.
precocious puberty, breast enlargement, vaginal bleeding and growth
of pubic hair, occur below the age of 5 in about 50% of cases and
between 5 and 10 in 30%.
childhood is accelerated but the epiphyses unite prematurely.
developmental abnormalities may be associated with the syndrome.
prognosis for life is good and the pathological fractures unite
There is no
single clinical feature of the pigmented lesions which reliably
differentiates Albright‘s syndrome from neuro fibromatosis in
which bone lesions and endocrine disturbances may also occur.
of many cafe-au-lait macules freckles in the axillae and Lisch
nodules on the iris are diagnostic for neuro fibromatosis. Giant
pigmented granules may also rarely be found in Albright‘s
can be considered as photodermatitis.
appear as an erythematous, pruritic pigmentation, which is more
intense on the sun-exposed areas, mainly on the forehead, neck,
behind the ears and areas of friction such as the axilla.
characteristic features are spotty pigmentation, light to dark brown
hyperemia and telengectasia may be other manifestations.
should be differentiated from berloque dermatitis, which is
hyperpigmentation due to photosensitization, by certain types of
syndrome is inherited as an autosomal dominant, that affects young
is of the reticulate type of pigmentation that develops on the neck
and axillae during the second or third year in a previously normal
child. It may become very extensive and is not preceded by any
of the palms and soles is usual.
with intolerance to heat is common.
nails are normal.
Teeth may be
normal or defective, with yellow discoloration of the enema.
physical development is normal.
syndrome is inherited as a sex-linked that affects young children
between 5 and 13 years of age.
Skin has a
poikilodermatous appearance with atrophy and prominent
hyperpigmentation is most conspicuous on the neck, chest and thighs.
membranes: leucoplakia of the oral, ocular and anal mucous
abnormalities are common.
syndrome begins in early life. This is different from Becker‘s
confluent brown macules appear on the neck and forearms.
areas may develop later. Small white macules appear in the pigmented
pigmentation with conspicuous macular depigmentation appears on the
trunk, associated with macular and reticulate pigmentation of the
hyperpigmentation of the dorsal aspects of fingers and toes is not
uncommon in individuals of dark complexion. The pigmentation begins
in infancy or childhood and increases in depth and in extent. There
may be increased pigmentation in the flexures of the finger joints
and in the larger joint flexures. The condition must be
differentiated from hyperpigmentation induced by repeated trauma.
Fig. 324. Acromelanosis
is usually present from early infancy but it may be progressive. It
is often diffuse and generalized but may later become rather
macules and plaques are present in 90% of cases of neuro
fibromatosis and may appear early. They are round or oval patches of
light brown pigmentation.
of one or two macules is not diagnostic in the absence of other
signs of the disease, but if six or more are present the probability
of neuro fibromatosis is high.
melanotic macules can also occur and resemble those seen in
Albright‘s syndrome; however, these tend to be confined to a
particular site and are on either side of the mid-line.
freckling is common in neuro fibromatosis and is an aid to the
nodules and iris hamartomas are present in most patients over the
age of 6.
In the acute
infantile form of Gaucher‘s disease, the skin is not pigmented but
in Niemann-Pick disease, there is diffuse brown pigmentation, most
marked on the face.
of two types occurs in adults with Gaucher‘s disease. Brown
patches of cloasma type appear on the face, neck and hands.There are
pigmentation of the lower legs with a sharp lower margin and an
irregular upper margin.
There may be
a brown wedge-shaped thickening of the bulbar conjunctiva.
pigmentosum (XP) is a rare autosomal recessive disease characterized
by photosensitivity, pigmentary changes, premature skin aging,
neoplasia and abnormal DNA repair. Some patients with xeroderma
pigmentosum have, in addition, neurological complications.
retinoids can reduce the occurrence of skin cancer in XP.
disease is characterized by diffuse pigmentation on the sun exposed
areas, flexures, sites of pressure or friction and mucous membranes
due to increased secretion of melanotrophic hormones by the
pituitary and elevated plasma levels of beta-MSH-. Nipples,
genitalia, buccal mucosa and conjuctiva become deeply pigmented.
lesions may also occur in Addison‘s disease.
of Addisonian pattern has been noted in 10% of reported patients
with Cushing‘s syndrome. It is an indication of increased
secretion of ACTH and beta-MSH by the pituitary, which may be due to
a pituitary tumor.
adrenalectomy a progressive hypermelanosis may develop in spite of
adequate hormone replacement therapy. Only in half of these
patients, the sella turcica is enlarged.
patients show marked hypermelanosis of the skin and mucous
of the skin and mucous membranes.
The hair is
sometimes multiple lentigines and longitudinal pigmented bands.
levels of both beta-MSH and ACTH are found in the plasma.
Fig. 325. Generalized
Hyperpigmentation (Cushing"s Disease)
Fig. 326. (After treatment)