The prevalence has been estimated to be around 35 percent among patients with early HIV infection, and up to 85 percent among patients with AIDS Patients with Parkinson disease often have increased sebum production; in these patients seborrhea and seborrheic dermatitis improve with L-dopa therapyThe reason for the increased susceptibility of patients with HIV infection to seborrheic dermatitis is not known.
Malassezia hydrolyze human sebum, releasing a mixture of saturated and unsaturated fatty acids. They take up the required saturated FAs, leaving behind unsaturated FAs. The unsaturated FAs penetrate the stratum corneum and due to their non-uniform structure breach the skins barrier function. This barrier breach induces an irritation response, leading to dandruff and seborrheic dermatitis.The Malasseziaspp that have been most commonly associated with SD are M. globosa and M. restricta, both of which are commensal yeasts that require an exogenous source of lipids.
Solar elastosis: due to sun demage and looks like “bluish colour of the upper dermis with accumulation of irregularly thickened elastic fibers”.Increased epidermal melanin is the key feature and this requires Masson Fontana stain. This increase is seen mainly in the basal/suprabasal cells as pigmentary caps , but in a Korean study increased melanization was noted in all layers of the epidermis  Dermal melanin is observed in some cases (dermal melasma) mainly in macrophages (also called melanophages) but also as free melanin deposits around superficial and deep vascular plexuses.
The centrofacial pattern is themost common and consists of lesions on the fore-head, cheeks, nose, upper lip, or chin. The malarpattern describes lesions located primarily on thecheeks and nose. The mandibular pattern consists oflesions on the ramus of the mandible. This latterpattern may actually be a form of poikiloderma ofCivatte, because patients are often postmenopausaland biopsy specimens reveal significant actinic dam-age
Hyperpigmentation is largely epidermal, causing accentuation of the lesions under Wood's lamp. Melasma may, in some cases, present with significant dermal pigmentation, and this is clinically suggested by grayish hue and the lack of accentuation under Wood's light examination. The clinical and histopathological correlation of increased dermal melanin and negative Wood's lamp examination is controversial, Sanchez et al.  showing the correlation and Grimes  denying it.Wood lamp examination implyan increase in dermal melanin content. Lesions thathave both enhancing and nonenhancing areas aresaid to have a mixed pattern. Recent histologicstudies indicate that this construct may not beaccurate.
. Intense pulsed light (IPL) appears to be the most effective light therapy investigated so far. The topicals described above should also be used before and after treatment. Fractional lasersare preferred and have been approved by the FDA for treating melasma. Patients should be pretreated with a tyrosinase inhibitor Cosmetic camouflage :Mineral makeup which contains titanium dioxide and zinc oxide
Civatte was a French dermatologist who first described a common weathering change that affects the skin of the sides and front of the neck.
Under no circumstances should monoben-zylether of hydroquinone or the other ethers of hydroquinone (monomethyl- or monoethyl-) be used in the treatment of melasma because these drugs can lead to a permanent loss of melanocytes with the development of a disfiguring spotty leu-koderma.
Comprehensive overview of melasma
Comprehensive overview of
Wood’s lamp may not be accurate and Fligman’s formula still the best
Almansouri Daifallah MD
• Risk factors
• Local Symptoms
• Systemic symptoms:
• Investigation, and DDx,
• Psychological impact
• Priscription table of 1st line medication dose
• 2 commonest and 2 most serious side effects:
• Patient education
• Progression, severity and response assessment
• chloasma: Greek; chloázein to be green.
• Melasma: Greek; melas means black.
– French: mélasma
– Synonym: Chloasma faciei, mask of pregnancy
“melasma gravidarum”, melasma addiso´nii.
• An acquired hypermelanosis (sharply
demarcated brown macules) often secondary
to sun light and/or hormonal changes that
oxidize tyrosine to melanin.
• Possible factors:
– Sun light: most important
• LH and female sex hormones e.g. OCP and
pregnancy, HRT, menopause.
• Hypothyroidism: melasma patient 4X will have thyroid
• Addisonni melasma
– Medication: salicylic acid, oxidized linoleic
agents, antisiezure, diphenylhydantoin.
• Racial: dark skin and
black (Fitzpatrick skin
types III and V)
• Age: elderly.
• Environmental: strong
solar radiation radiation
• 14.5% in Arab-American
• In Hail 2.88% of skin diseases
• Two peaks: infant after 2 wks + 20s -30s.
• F>M: 5-9>1
• Sun-light cause
elevated levels of
nitric oxide via the
• nitric oxide
• Tyrosinase convert
Tyrosine -> melanin
NB. no increase in melanocyte number, but the melanocytes themselves were
larger and had more prominent dendritic processes.
• MSH, ACTH, lutei-nizing hormone (LH), and
follicle-stimulating hor-mone (FSH) increase
melanocyte size and tyrosinase production
• In epidermis:
• Highly dendritic melanocytes
• Melanin deposited (key feature and requires Masson Fontana stain) in basal and
• In dermis:
• Solar elastosis in dermis (Verhoeff-van Gieson stain)
(b) Perilesional normal skin, pigmented (c) Lesional: Epidermal hyperpigmentation.
Symptoms and signs
• Cosmetic concern only.
• Sun exposure
• Skin: symmetrical light or
dark brown or even black
has serrated, irregular, and
Sun exposed areas:
• Forehead, cheeks
bridge, upper lip
melasma), chin, V
• Diagnosis is clinically: pattern +risk factors.
• Wood lamps: intensification of epidermal
• TFT: to exclude hypothyrodism.
• Biopsy: rarely.
Classification 1: Area based
(commonest), malar, mandibular, brachial
(acquired brachial cutaneous dyschromatosis).
malar centrofacial mandibular brachial
Classification 2: histologically based
• by Wood’s light examination !!!/ physical examination:
I. Remove the cause:
a) Minimize sun exposure: apply sunscreen (titanium dioxide and/or zinc
oxide with hight SPF), make-up that contains sunscreen, use wide-
brimmed hat .
b) Discontinue hormonal contraception.
II. Remove the extra melanin:
a) Fist line: Bleaching agents: (Kligman’s formula= Tretinoin +
1. Hydroquinone (2-4%) “the gold standard”
2. Tretinoin cream
3. Steroid: to quickly to fade the colour and reduce the likelihood of a
contact dermatitis of previous agents e.g. hydrocortisone,
b) Second line: chemical peeling for superficial melasma ONLY and may change it
to post-inf-peg.: glycolic acid, low-concentration TCA, and salicylic acid.
c) Third: Intense pulsed light and fractional Laser: both are effective and quick
but both give inconsistent result. FL may cause complications
d) Fourth: Surgical peeling may cause scars, inflammation, pigmentation, …..etc.
III. Palliative: Cosmetic camouflage: Mineral makeup; titanium and zinc
Fligman’s formula : prepared called trimula or mix the following in hydrophilic oinyment OR
(ethanol+propylene gycol 1:1)instead.
for 6 months
6 weeksOnce daily at
left on for 30 min
Once dailycreamAscorbic acid
Life longEvery 2 hoursHigh SPF (>30)lotionSunscreen
2nd line: peeling agents
Till achievement of desired
4-6 sessions /
Till achievement of desired
Starting from 30%
up to 70%
3nd line: lights
• stinging and redness in
• Conc >4% will may
pigmentation and local
ochronosis (a bluish
Sick child or <
TC complicationsPregnancy; Cat CHydrocortisone
Stop iterythema, scaling,
dryness, stinging or
burning, edema, and hypo-
All are temporaryRedness, pain, swelling,
pigmentation and rarely
Hydroquinone Side Effect
• Exogenous ochronosis( ): Blue-gray
discoloration of the skin with characteristic
pin-point, caviar-like papules
• significant negative impact on patients’ quality
of life and assessed using MelasQoL.
Hx+ EX: diffuse and less irregularDrug-induced pigmentation; amiodarone,
Papular lesion + histologyLichen planus
Naevus of Ota
Clinical examinationEphelides (freckles)
On neck and sparing of the submental .Poikiloderma of Civatte
Amiodarone-induced pigmentation |Postinflammatory pigmentation |Pigmented contact dermatitis (Riehl's melanosis)
• clusters of concentrated melanin in fair skin.
Poikiloderma of Civatte
• thin skin with telangiectasia
• sparing of the submental area is characteristic.
Follow Up and Prognosis
• Response assessment: MASI scoring=
area*homogenicity*darkness = 0-48
• 8% of melasma gravidarum noted
• Monitor for exogenous onchronosis and skin
atrophy for long term treatment.
• Risk factors(sun/hormone/Fx) + symmetrically
distributed hyperpigmented macules on face
and neck = melasma.
• TTT: Frigman’s formula and sun protection.
• Recurrance is high
• Never use monoben-zylether of
• European Handbook of Dermatological Treatments
• Vaneeta M. Sheth, Amit G. Pandya, Melasma: A comprehensive update: Part II, Journal of the
American Academy of Dermatology, Volume 65, Issue 4, October 2011, Pages 699-714, ISSN 0190-
• Andrew's Diseases of the Skin: Clinical Dermatology
• Fitzpatrick's Dermatology in General Medicine, Eighth Edition,
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