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بسم هللا الرحمن الرحيم

The Challenge Of Melasma MangementNot Just Treatment

It’s A Life Style

SAMIA ESMAT

PROFESSOR OF DERMATOLOGY

CAIRO UNIVERSITY

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MELASMA

• Melasma is a tan or dark skin discoloration, usually on face. is thought to be caused by sun exposure, genetic predisposition, hormone changes, and skin irritation.is particularly common in women, especially pregnant women and those who are taking oral or patch contraceptives or hormone replacement therapy (HRT).

• “Melas”, which means black.

• cloazein: green-ish

• “mask of pregnancy”, liver spots.

Epidemiology

• The global prevalence varies according to ethnicity, skin type, and intensity of sun exposure.

• Fitzpatrick dark skin types IV, V and VI.• Latin, Asian, Indian, Middle Eastern,

Mediterranean,Hispanics, Asians, and African Americans.

• 2.88 % in Saudi Arabia,3.4 % in Lebanon and 8.2 % in United States.

• South Asian countries as seen in China (13.61% ).

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• 50% a family history of melasma in at least one family member.

• It was found that the most common precipitating factors were pregnancy (36.4%), oral contraceptives (16.2%), and sun exposure (27.2%).

• The most common time of onset of melasma was post pregnancy (42%), whereas 26% of patients developed it during pregnancy

• The onset of the disease is found to be earlier in light skin types, whereas dark skin types are usually associated with a late onset of melasma.

• The frequency of thyroid disorders is four times greater in patients with melasma.

Epidemology

• Affects women more than men.

In Caucasians: 1:9 (Vazquez et al 1988).

Epidemology

In Asian populations india 1:4(Pichardo et al, 2007& 2009),(Sarkar ,2003 &2010,).

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MALE VS FEMALE MELASMA (Sarker et el 2018)

DIAGNOSIS• Characteristic symmetric blotchy hyperpigmented patches on the

face.usually the cheeks, bridge of the nose, forehead, chin, and upper lip, mandible, and rarely upper chest and extremities.

• worsens in the summer and improves in the winter. appears during pregnancy or after starting birth control or other

hormonal treatments. Handai et al 2014

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Clinical Variants

PERIPHERAL CENTROFACIAL MIXED

IMPORTANCE OF HISTORY

Outdoors life.Make up habitsContraceptive pills / Injections/ Smart IUDPregnanciesMedications

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HISTOLOGY• Histologically, melasma is characterized by excessive melanin deposition in

the epidermis (epidermal type, 70%), dermal macrophages (dermal type, 10%), or both (mixed type, 20%).

• Compared to uninvolved adjacent skin, increased melanin deposition is observed in all layers of the epidermis.

• An increased number of melanophages may also be seen. • Epidermal melanocytes are normal to increased in number,and they are enlarged with prominent dendrites..

• Elastolytic changes of solar damage.

WOODS LIGHT EXAMINATIONEPIDERMAL VS DERMAL

USUALLY MIXED

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Accentuation of the normal pseudo‐rete ridges of facial skin

Differential diagnosis

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Gray‐brown macules in the zygomatic region, spotted with pinpoint, dark brown (caviar‐like) papules

Exogonous ochronosis

•clinical

•Histology

•Dermoscopy

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Pigmentary demarcation lines

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• Corresponded to axial lines of Sherrington and not lines of Blaschko or dermatome lines.

• These axial lines of Sherrington correspond to a subset of Voigt's lines. Voigt's lines separate dermatomes arising from nonconsecutive dorsal roots. PDL may become apparent only when subtle variation in pigmentation is apparent between two contiguous dermatomes originating from noncontiguous dorsal roots.

Pigmentary demarcation lines

FG

H H

CHIN SOMANI ET AL 2004

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PIGMENTARY DEMARCATION LINES

• Appear around puberty and may even be present from childhood persist without much change throughout life. They may have a genetic predisposition. Increase during pregnancy. Few other triggering factors for Group F PDL reported are acute illnesses such as typhoid, chickenpox, and viral hepatitis.

• Group F PDL may present as periorbital melanosis. On histopathology, both Group F PDL and periorbital melanosis have been found to have melanophages in upper dermis.

Treatment trials: disappointing results

• Pigmentary demarcation line in pregnancy may regress spontaneously after delivery and does not require treatment.

• Facial PDL has a persistent course posing cosmetic concern for the patient

• Kligman regimen along with strict photoprotection failed.

• Chemical peels for facial PDL have been reported to have some effect, but not long lasting and only 10% decrease in pigmentation. Six sittings of reverted back.

• Q switched Alexandrite laser has been tried on PDL Group A on the anterolateral aspect of both arms and had satisfactory responded.

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WORK UP?•No specific labs

•Associted thyroid abnormaltites especially in pregnant and contraceptive pills associated melasma.

•Liver functions in debilitated men excluding ovarian malignancies in females and hypogonadism in males.

ETOIPATHOGENISIS

• Melasma is caused by a complex interplay of environmental factors in a genetically predisposed individuals.

• Most common factors include, sun exposure, and hormonal dysfunctions.

• less common causes include cosmetics, photosensitizing drugs, food items, thyroid diseases, hepatopathies, ovarian tumors, parasitic infestations, and stressful events.

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PATHOGENESIS

Genetic

Environmmental Susceptible melanocytes

Hormonal dysfunctions

MELASMA

GENETIC BACKGROUD

• POSITIVE FAMILY HISTORY IN 50% OF CASES.

• REPORTED IN TWINS.

• NO GENE ASSOCIATION STUDIES.

• PROBABLY RELATED TO EPIGENETIC CONTROL OF HORMONAL FUNCTIONS.

• HYPERFUNCTIONING MELANOCYTES.

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HYPERFUNCTIONING MELASMA MELANOCYTES

• Number : normal to increased in number.

• enlarged with prominent dendrites..

• Ultrastructurally

- increased number of melanosomes.

- increased in number or amount of mitochondria,

Golgi apparatus and rough endoplasmic reticulum are LARGER.

- Imuunohistochemically: increased expression of ckit the SCF ligand

and MSH.

- Estrogen receptors???????

HYPERFUNCTIONAL MELANOCYTES,PRESUMABLY STIMULATED BY UV IRRADIATION OR HORMONES

MELASMA

NORMAL

THE HORMONAL STATUS

• The preferential development of melasma during women's reproductive age and the association of this disease with oral contraceptives.

• During pregnancy high levels of circulating sex hormones.

• Estrogens stimulate melanogenesis in cultured human melanocytes and induces synthesis of melanogenic enzymes such as tyrosinase and tyrosinase‐related proteins 1 and 2,

• Progesterone stimulates melanogenesis in the epidermal melanocytes.

BUT prevents melasma by progesterone components in oral contraceptives since progesterone can reduce melanocyte proliferation.

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• The levels of female or male sex hormones as well as pituitary hormones are controversial. Some studies show high female sex hormones (Mahmoud et al 2011) but most show lower levels of estradiol.

• Ovarian dysfunction, pituitary dysfunction (gopichandani et al 2015)

• relation to cyctic ovaries(Adalat khah, 2007) has been raised.

• Increase receptor sensitivity to estrogen has been suggested (Perez 1983).

• Higher protein expression of estrogen-β and progesterone receptors (TAMEGA ET AL 2015).

THE HORMONAL STATUS IN MELASMA FEMALES(PHILONI ET AL,2019)

THE HORMONAL STATUS IN MALE MELASMA

• HYPOGONADISM AND HISTORY OF ANTIANDROGEN OR ESTORGEN INTAKE IS REPORTED BUIT ONLY IN 10% OF CASES.

• SUN EXPOSURE AND FAMILY HISTORY SEEM TO BE MORE IMPORTANT.

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Not only in melanocytes (Kang et al 2011)

• Up‐regulation of many melanin bio‐synthesis‐related genes as well as melanocytes markers such as TYR, MITF, SILV and TYRP1 were found to be up‐regulated in melasma skin.

• Involved in other biological processes and/or expressed by other cells than melanocytes, were found to be differentially expressed as compared with the surrounding unaffected skin.

- Wnt pathway modulator genes.

- prostaglandin metabolic process.

- fatty acid metabolism

One clinical phenotype but many cellular players and pathways involved (passeron,2012)

• Not only a melanocyte defect.

• Keratinocytes and its interaction with melanocytes. • Down regulation of non coding RNA H19 gene in melasma lesions.

• increased expression of Inducible nitric oxide synthase in melasma lesions (iNOS) within keratinocytes was shown to have a role in melanogenesis process, especially after UV

• iNOS and NF‐kB pathway could thus be also implicated in melasma pathogenesis, and could be interesting targets for developing more effective treatments.

• Altered wnt pathway and barrier lipid deffect (Lee, 2015) st corneum melanin retention (Gautier 2017).

• These results also emphasize the role of keratinocytes in the pathophysiology of melasma.

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Vascular changes and elastolytic changes

• Histological studies have clearly shown a significant increase of the vascularization within melasma lesions as compared to the surrounding healthy skin. Those results were confirmed by using laser confocal microscopy examination.

• Increased expression of VEGF.

• Increasd oxidative stress

• The exact role of the vascularization in the hyperpigmentation observed in melasma still remains to be elucidated.

• UV induced aging………… A phenotype of photodamage.

UV radiation

❑Transcription of the tyrosinase gene (via MITF)❑Number or activity of MC1-R on melanocytes❑Expression of POMC and its derivative peptides by keratinocytesand other cells within the dermis❑Release of diacylglycerol from the plasma membrane, whichactivates protein kinase C❑Activation of the nitrous oxide/cGMP pathway❑Production of cytokines and growth factors (e.g. endothelin-1) ❑Induction of an SOS response to UVR-induced DNA damage❑Transactivation of the POMC promoter by p53❑ Ratio of kinesin to dynein

In general it works by

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Solar exposureIn genetically predisposed person:1)Stimulates Melanogenesis by the hyperactive

melanocytes.2)Solar damage causing elastolysis and

telangiectasia. +

HORMONAL DYSFUNCTION

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TREATMENT

Melasma is Difficult to Treat

• The pigment of melasma develops gradually, and resolution is also gradual.

•Resistance is common and

recurrence is the rule

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PROGNOSIS

• Epidermal melasma.

•Dermal melasma

• Mixed melasma

(a combination of the epidermal and dermal types).

• (LASER MIGHT BE A HOPE).

GOOD

POOR

ACCORDING

Ideal treatment (grimes etal 2019)

- a plan of an efficacious treatments that offer sustained long-term remission for patients with this frustrating and therapeutically challenging disorder.- Multimodality approach that covers the multiple pathogenic factors

- incorporates photoprotective agents, antioxidant treatments, skin lighteners, exfoliants, and resurfacing procedures.

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FIRST LINEFLUORINATED STEROID CONTAINING 2–4% HQ-BASED TRIPLE COMBINATION

FOR 12W THEN MAITAINANCE

SECOND LINE SUPERFICIAL peels if required

THIRD LINE. LASERS ARE A LAST RESORT.

MANDATORY FOR LIFE BROAD SPESTRUM SUN SCREEN AND

OPTIOINAL CAMAUFLAGING

Sun protection for melasma should not only be against UVA and B but visible light should be included• Visible blue light has been shown recently to stimulate opsin-3,

which activates the melanogenesis-associated transcription factor and other melanogenic enzymes such as tyrosinase and dopachrome tautomersae that form a protein complex that is mainly generated in the melanocytes of dark-skinned individuals, type III and above (Regazzetti et al., 2018).

• Therefore, photoprotection that incorporates visible light, such as iron oxide sunscreens, is essential as proved by RCTS. Boukari et al. 2015 Castanedo-Cazares et al 2014.

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Sun protection (FOR LIFE)

• SPF MORE THAN 30• BROAD SPECTRUM SUNSCREENS UVA, UVB, AND

VISIBLE LIGHT

• COMBINED PHYSICAL AND CHEMICAL.• IRON OXIDE FOR VISIBLE LIGHT.

Absolute light avoidance is necessary; thus,

a good sunscreen must be used during the day repeated every 2-3h,even when indoors.

• COSMETICALLY ACCEPTABLE BY THE PATIENT

• SUITABLE FOR THE SKIN TYPE.

• Makeups containing iron oxide can serve the dual purpose of covering melasma lesions that patients believe are unsightly, while also serving as protective and preventative therapy.

• Improves quality of life till effect of treatment appears.

Role of camouflage

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Oral photo protection: Polypodium leucotomos

• Polypodium is a leafy plant unique to central and south America.

• Promotion of the p53 suppressor gene expression.

• Modulation of inflammatory cytokines,

• Upregulation of endogenous antioxidant systems,

• And blockade of UV radiation-induced cyclooxygenase–2

Expression (Nestor et al., 2014, siscovick et al., 2008).

• Several recent studies have documented a beneficial effect

in patients with melasma (goh et al., 2018, martin et al., 2013).

• 240 mg twice daily versus placebo in combination with

topical ttt and sun protection.

RECURRANCE IS THE RULE

PROPHYLAXIS FOR MAINTAINANCE IS A MUST

For high risk populations including pregnant females, darker

skin types and locations with intense UV exposure.

NO ESTROGENS

NO SUN OR VISIBLE LIGHT

Prophylactic Sun protection reduced the incidence of melasma with

pregnancy from 53% to 2.5% Lkhdar et al, 2007 .

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•Alter hormone replacement therapy.

Shifting regimen to the night can help alleviate the problem.

•Creams and patches might be slightly less inclined to cause melasma than oral versions of the treatment.

Avoid or control The hormonal influence

Principles of Melasma Therapy

1-Protection from Sun exposure.

2- Preventing hormonaleffects.

3-Inhibition of melanin synthesis and transfer.

4- Enhancing Melanin elemination.

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GOAL

decrease melanin production

And transfer to keratinocytes increase elimination

..

Mechanism of action at the epidermal-melanin unit

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Before melanin synthesis

Tyrosinasetranscription

Tretinoin, c-2 ceramide

Tyrosinaseglycosylation

PaSSO3Ca

Inhibition of plasmin

Tranexamic acid**

Tranexamic acid tablets were prescribed to 74 patients at a dosage of 250 mg twice daily for 6 months. At follow-up, more than half of patients (54%) showed good results. This treatment may be effective for some patients, but further study is needed.

During melanin synthesis

Hydroquinone, mequinol, azelaicacid, kojic acid, arbutin, deoxyarbutin, licorice extract, rucinol, 2,5-dimethyl-4-hydroxy-3(2H)-furanone, N-acetyl glucosamine, resveratrol, oxyresveratrol, ellagic acid, methyl gentisate, 4-hydroxyanisole

Phenolic compounds

Ascorbic acid, ascorbic acid palmitate, thiotic acid, hydrocumarins

Tyrosinase inhibition

Peroxidase inhibition

Reactive oxygen species scavengers

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After melanin synthesis

Inhibition of melanosome transfer

Niacinamide, serine protease inhibitors, retinoids, lecithins, neoglycoproteins, soybean trypsin inhibitor

Skin turnover accelerationLactic acid, glycolic acid, linoleic acid, retinoic acid

Regulation of melanocyte environment

Corticosteroids, glabiridin

Interaction with copper Kojic acid, ascorbic acid

Inhibition of melanosome maturation

Arbutin and deoxyarbutin

Inhibition of protease activated receptor 2

Soybean trypsin inhibitor

Competitive Inhibitors Of Tyrosinase

• Hydroquinone: a phenolic compound, a potent competitive tyrosinase inhibitor. It inhibits the conversion of L- DOPA to melanin. It also induces melanosome degradation & melanocyte apoptosis.

• HQ is the prototype depigmenting agent used in melasma.

• 2%-4% formulas are commercially available.

• 5%-10% compounded by dermatologists.

• HQ alone in a concentration of 2% to 5% can be used as an effective monotherapy. It is found to be more efficacious than KA and AA.

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Complications: acute

• Acute complications include irritant or allergic contact dermatitis and postinflammatory hyper- and hypopigmentation.

• Irritant reactions are the most common. Review of the literature suggests that monotherapy hydroquinone agents cause irritant reactions in 0%-70% of patients. In combination therapy, the incidence rises to 10%-100%.

• The concentration , duration of contact and the pharmaceutical prepartions.

SHOULD BE

AVOIDED

• confetti‐like

depigmentation.

• Exogenous

ochronosis.

due to the continual and

chronic use of the

hydroquinone, not

necessarily in high

concentrations, Due to

inhibition of HGO.

CHRONIC COMPLICATIONS OF PROLONGED USE

Grey‐brown or blue‐black hyperpigmentation, as well as

pinpoint hyperchromic papules that look like caviar later

papulonodular lesions and colloid millia

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Inhibition of melanosome & melanin transfer to KCs Retinoids• Non-selective dispersion of pigment granules within

KCs.

• interferes with pigment transfer from MCs to KCs.

• Increases pigment loss from KCs by increasing its turnover.

• It inhibits tyrosinase activity.

• Tretinoin, is an effective ttt for melasma but often causes irritation & usually requires months to show improvemt as monotherapy.

• It is better combined with other topical agents (eg. Hydroquinone).

CORTICOSTEROIDS

• Corticosteroids reduce pigmentation by decreasing the epidermal turnover and its anti-metabolic effect on melanocytes.

• Anti inflammatory effects.

• Both fluorinated and nonfluorinated steroids have been used in the TCC in various formulations.

• However, their use as monotherapy is not recommended due to the plethora of AE and misuse by the patients.

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Triple Combination cream

• Kligman–Willis formula, 5% HQ, 0.1% tretinoin, and 0.1% dexamethasone.

• Tretinoin prevents the oxidation of HQ and improves epidermal penetration, it also reduces the atrophogenic effect of corticosteroids.

• While the topical corticosteroid (TCS) reduces irritation due to the other two ingredients and decreases cellular metabolism, further inhibiting melanin synthesis.

• The synergistic action of the three topical agents achieves significantly higher depigmentation and faster acting than monotherapies, thereby shortening the treatment duration and reducing the AE due to an individual drug.

•

• The original Kligman's formula (5% HQ, 0.1% tretinoin, and 0.1% dexamethasone). has been modified.

• Maximum experimentation has been done with the TCS component, namely, the addition of mid to high potent, fluorinated/non fluorinated agents and their concentration.

• Furthermore, the concentration of tretinoin and HQ has been kept low in most formulations.

• The (4% HQ, 0.05% tretinoin, and 0.01% flucinolone acetonide) is FDA approval.

Triple combination CREAM

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MAINTAINANCE WITH TRIPLE COMBINATION CREAM• fluocinolone based TCCs can be used as maintenance regimen for

more than 8 weeks up to a maximum period of 1 year in either daily/intermittent/tapering dose regimen.

• Adverse effects such as skin atrophy and telangiectasia were found to be quite low even on continuing this regimen for more than 6 months.

• Sequential rotation with other nonphenolic compounds.

Competitive inhibitors of tyrosinase

❖Competitive inhibitors of Tyrosinase activity act by direct competition with tyrosinase at various receptors sites:

1- Hydroquinone.

2- Arbutin & Deoxyarbutin.

3- Azelaic acid.

4- Mequinol.

5- Allosine.

6- Dioic acid.

7- Gentisic acid.

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Non-Competitive inhibitors of tyrosinase

Licorice extract:

➢A non- competitive tyrosinase inhibitor.

➢ It has anti-inflammatory properties.

➢Some studies claim its efficacy in melasma, but further research is required.

Copper Chelating Agents➢Kojic acid:

➢A hydrophilic fungal product.

➢A tyrosinase inhibitor, by chelating copper at the enzyme’s active site.

➢It may give modest improvement for melasma, but it often causes irritation.

➢Best results in combination with GA or HQ

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Copper Chelating Agents

➢Ascorbic acid:➢Vitamin C, it interacts with copper at the active site

of tyrosinase.

➢ inhibits melanogenesis by acting as a reducing agent at various oxidative steps in melanin synthesis.➢ However, stability is an issue with the Vitamin

C preparations due to rapid oxidation. Magnesium ascorbic phosphate is a stable esterified derivative of Vitamin C.

➢However, it is rapidly oxidized, highly unstable & does not work well alone.

➢Therefore, it is better used in combination with Licorice extracts & Soy or ferulic acid to increase its efficacy.

Inhibition of melanosome & melanin transfer to KCs

➢Soybean:

➢A trypsin inhibitor, inhibits the protease-activated receptor-2 (PAR-2) pathway that is needed for melanosome transfer by keratinocytephagocytosis of melanosomes.

➢It induces pigment loss in a dose dependent manner.

➢It provides a novel approach for ttt of melasma.

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Niacinamide

• IT IS THE ACTIVE AMIDE OF VITAMIN B3 THAT REDUCES PIGMENTATION BY INHIBITING THE TRANSFER OF MELANOSOMES TO KERATINOCYTES.

• SLIGHTLY LESS EFFECTIVE THAN HQ 4%.

• NO ADVERSE EVENTS.

• IMPROVES SOLAR DAMAGE CHANGES.

Inhibition of melanosome & melanin transfer to KCs

Reduction of MSH & Alternative pathways

• Tranexamic acid.

• Beta Carotenes.

• Topical Steroids

• Glutathione.

• N-acetyl cysteine (NAC).

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Tranexamic acid (TA)

• (Trans-4-Aminomethylcyclohexane-carboxylic acid) is a synthetic derivative of the amino acid lysine.

Tranexamic acid (TA) is a relatively new treatment for melasma .

• TA is US FDA approved as a hemostatic agent for heavy menstrual bleeding and in tooth extractions for patients with hemophilia FOR ITS ANTI FIBRINOLYTIC ACTIVITY.

• It binds reversibly to the lysine binding sites on plasminogen molecules and inhibits plasminogen activator (PA) and thus the conversion of plasminogen to plasmin.

ANTI FIBRINOLYTIC

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INHIBITION OF MELANOGENESIS

• It is through prevention of binding of plasminogen to keratinocyte, TA inhibits UV-induced plasmin activity in keratinocytes, thereby decreasing melanogenesis through reduced production of PGs.

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Vascular effects

• ANTI ANGIOGENIC EFFECT

• plasmin is thought to convert matrix-bound vascular endothelial growth factor (VEGF) into freely diffusible forms, leading to angiogenesis.

• TA may exert its effect twofold by reducing the production of pro-melanogenic factors and by decreasing erythema and vasculature.

ANTI ANGIOGENIC

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Dosage of TA (ZHU CY ETAL 2019)

• Dosing for the treatment of melasma is far lower than when indicated as an anti-fibrinolytic.

• IN MENORRHAGIA 1300MG THREE TIMES DAILY (3900 MG) FIVE DAYS FOR EVERY MONTH

• 250 MG TWICE DAILY• DOSES OF 750, 1000, AND 1500MG PROVED BETTER EFFICACY WITH

HIGHER DOSES BUT NO SIGNIFICANT DIFFERENCE• MILD SIDE EFFECTS• CAN BE TOLERATED FOR A LONG TIME UP TO 6 M

CONTRA INDICATIONS

• Needless to say, this medication should not be given to those with clotting disorders or a history of thromboembolism and should be used with caution in those using oral contraceptives and other pro-coagulants.

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Topical Tranexamic Acid• Emulsion of 2% TA applied bid and a nonwoven fabric mask

immersed in 2% TA lotion applied three times weekly. After 12 weeks

• 5% TA topical gel versus a vehicle placebo gel.

• liposomal topical 5% TA versus a topical 4% hydroquinone cream over 12 weeks.

• indicate that topical TA 3% TA suspension is as effective as topical hydroquinone/dexamethasone for melasma

Physical Methods for Delivering Tranexamic Acid

• weekly intradermal injections of TA over 12 weeks, showed a statistically significant reduction in MASI score by the fourth week of treatment and an even greater improvement after 8 and 12 weeks.

• both micro-needling and micro-injection with TA can be effective for melasma, with the greatest improvement found with micro-needling .

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COMBINATIONS of TA

Combination therapy of NIACINAMIDE and TA for the treatment of hyperpigmentation has been considered because of the synergistic effects of the two treatments.

Both agents are safe alternatives to many other skin-lightening agents that are notorious for inducing adverse effects.

Combinations handling multiple pathways involved in the induction of hyperpigmentation

MELANOCYTE ACTIVATION, MELANOSOME DEVELOP-

MENT, MELANIN SYNTHESIS, MELANOSOME TRANSFER, AND KERATINOCYTE DIFFERENTIATION AND DESQUAMATION

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PEELSIMPORTANT POINTS (SARKAR ET AL 2017) • SECOND LINE.

• PHOTOPROTECTION

• PRIMING AND EMOLLIENT .

• USE ONLY SUPERFICIAL

• COMBINATION SUPERFICIAL PEELS MIGHT BE SAFER.

• DON’T DO CASES

LONG DURATION , EXCESSIVE DERMAL AFFECTION AND UNREALISTIC EXPECTATION

Lasers and lights

• THIRD CHOICE

• HIGH RISK OF PIH

• FRACTIONAL LASERS WITH LOWFLUENCES AND SHORT PILSE DURATION

• Q SWITCHED YAG TONING LOW FLUENCE HIGH FREQUENCY LARGE SPOT SIZE,

• COMBINATIONS.

• PICO, FRACTIONAL Q SWITCHED

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FIRST VISIT OF MELASMA PATIENT

HISTORY OF PREDISPOSING FACTORS VERY IMPORTANT FOR PUTTING THE TREATMENT PLANS

CORRECTION OF MAKE UP AND DEPILATION HABITS

AVOID EXCESSIVE HEAT EXPOSUREE

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PATIENT SHOULD LEARN THAT THEY NEED STRICT SOLAR PROTECTION FOR LIFE

DON’T JUST PRESCRIBE A SUNSCREEN HELP THE PATIENT TO CHOOSE THE MOST CONVINIENT TO ENSURE COMPLIANCE

NO OR CONTROLLED HORMONAL THERAPIES

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AVOID INFLAMMATION

• IRRITATION IS A VERY COMMON COMPLCATIONS.

• DELAYS THE IMPROVEMENT AND MIGHT CAUSE PIH.

• TRY NEVER TO DEVELOP ERYTHEMA.

THE REGIMEN

• USE HYDROQUNONE ALONE OR IN COMBINATION THREE DAYS A WEEK.

• USE SHORT CONTACT THERAPY FOR HALF AN HOUR THAT CAN BE INCREAED GRADUALLY.

• GIVE NON PHENOLIC AGENTS ON ALTERNATING DAYS.

• PEELS AND LASERS ARE NOT FIRST OPTION BUT THE CHOICE OF THE INTERVENSION IS VERY IMPORTANT.

RECURRENCE IS THE RULE AFTER ALL MODALITIES SO MAINTAINANCE IS ALSO A RULEIS BEST DONE BY BROAD SPECTRUM SUN SCREENS AND NON HQ BLEACHING CREAMS

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Thank You