management of facial hyperpigmentation

Management of Facial HyperpigmentationAna Pérez-Bernal, Miguel A. Muñoz-Pérez and Francisco Camacho

Department of Dermatology, Faculty of Medicine, Virgen Macarena Hospital, Seville, Spain

ContentsAbstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2611. Management of Facial Hyperpigmentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2622. Riehl’s Melanosis and Related Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262

2.1 Poikiloderma of Civatte . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2622.2 Erythromelanosis Follicularis of the Face and Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2622.3 Erythrose Peribuccale Pigmentaire of Brocq . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2632.4 Linea Fusca . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263

3. Facial Hyperpigmentation Associated with Use of Cosmetics and Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2644. Melasma (Chloasma) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2645. Treatment of Facial Hyperpigmentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265

5.1 General Instructions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2655.2 Hypopigmentation Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265

5.2.1 Hydroquinone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2655.2.2 Hydroquinone and Tretinoin Combinations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2665.2.3. Other Phenolic Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2665.2.4 Azelaic Acid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2665.2.5 Tretinoin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2665.2.6 Kojic Acid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2665.2.7 Ascorbic Acid (Vitamin C) and Tocopherol (Vitamin E) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266

5.3 Chemical Peels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2665.4 Laser Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267

6. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268

Abstract Facial and neck pigmentations are the most cosmetically important. They are common in middle-agedwomen, and are related to endogenous (hormones) and exogenous factors (such as use of cosmetics and per-fumes, and exposure to sun radiation). Melasma (chloasma) is the most common cause of facial pigmentation,but there are many other forms such as Riehl’s melanosis, poikiloderma of Civatte, erythrose peribuccalepigmentaire of Brocq, erythromelanosis follicularis of the face and neck, linea fusca, and cosmetichyperpigmentations.

Treatment of melasma and other facial pigmentations has always been challenging and discouraging. It isimportant to avoid exposure to the sun or to ultraviolet lamps, and to use broad-spectrum sunscreens. Severalhypopigmenting agents have been used with differing results. Topical hydroquinone 2 to 4% alone or in com-bination with tretinoin 0.05 to 0.1% is an established treatment. Topical azelaic acid 15 to 20% can be asefficacious as hydroquinone, but is less of an irritant. Tretinoin is especially useful in treating hyperpigmentationof photoaged skin. Kojic acid, alone or in combination with glycolic acid or hydroquinone, has shown goodresults, due to its inhibitory action on tyrosinase. Chemical peels are useful to treat melasma: trichloroaceticacid, Jessner’s solution, Unna’s paste, α-hydroxy acid preparations, kojic acid, and salicylic acid, alone or invarious combinations have shown good results. In contrast, laser therapies have not produced completelysatisfactory results, because they can induce hyperpigmentation and recurrences can occur. New laser ap-proaches could be successful at clearing facial hyperpigmentation in the future.

DISEASE MANAGEMENT Am J Clin Dermatol 2000 Sep-Oct; 1 (5): 261-2681175-0561/00/0009-0261/$20.00/0

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1. Management of Facial Hyperpigmentation

Normal skin color is dependent on the quantity and type ofmelanin pigment in the melanocytes and keratinocytes. The thick-ness of the stratum corneum, the dermal vasoconstriction or vaso-dilatation and the occasional presence of endogenous or exoge-nous pigments, may also modify the skin color.

Several factors may be responsible for the numerous hyper-chromatic processes affecting the epidermis and/or dermis: he-reditary, endocrine, nutritional, neoplastic, inflammatory, drugs,physical and chemical.[1]

Due to their visibility, facial and neck pigmentations (cervico-facial pigmentations) are the most cosmetically important. Theyare more common in middle-aged women and are related to endo-genous and exogenous factors, such as use of cosmetics and per-fumes, and exposure to sun radiation.[2]

Among the most common cervicofacial hyperpigmentationsare Riehl’s melanosis, which is difficult to conceptually differen-tiate from other disorders such as poikiloderma of Civatte, ery-throse peribuccale pigmentaire of Brocq, erythromelanosisfollicularis of the face and neck, because they share clinical andetiologic factors. Currently, all of them are considered variants ofRiehl’s melanosis.[3] In addition to these forms of hyperpigmen-tations, the management of cosmetic hyperpigmentations, lineafusca, and melasma (chloasma) will also be discussed.

2. Riehl’s Melanosis and Related Conditions

Riehl’s melanosis occurs in middle-aged women. Brownishgray reticulate pigmentation develops over the face and neck, onthe temples, cheeks, chin, supraciliary, dorsum of nose, lateralsurfaces of neck, and low neck (fig. 1). It was first described inthe First World War, and endogenous factors may be involved,such as digestive disorders, neurovegetative lability, vitamin de-ficiency, and toxic factors. However, in most currently observedcases the condition has been induced by use of cosmetics contain-ing coal tar derivatives, which have a high propensity to causephotosensitivity.[4]

Histologically, there is a pigmentary overload in the dermalmelanophages, occasional epidermic edema and hyperfunction ofmelanocytes.

Riehl’s melanosis shows a long evolution over time and therecognition and removal of causal agents will lead to a gradualimprovement in the condition. The use of sunscreens, and creamscontaining hydroquinone 2 to 5% plus tretinoin or glycolic acid,also produce a slow improvement.

2.1 Poikiloderma of Civatte

Poikiloderma of Civatte is a very common disorder that

mainly affects perimenopausal women. There is an irregular darkpigmentation with a reticulate distribution over a slight erythem-atous field, located on the lateral and low neck.

Histologically, there is hyperkeratosis and epidermal atro-phy, liquefaction degeneration of the basal layer, numerous der-mal melanophages, and a perivascular or band-like lymphocyticinfiltrate. Exposure to light, photodynamic substances in cosmet-ics, and an unknown endocrine factor are important factors. It isnecessary to use sunscreens and avoid precipitating factors.[5]

2.2 Erythromelanosis Follicularis of the Face and Neck

Erythromelanosis follicularis of the face and neck is an ery-thematous and pigmentation disorder affecting the follicles. His-tologically, there is follicular dilatation with infundibular keratotic

Fig. 1. Riehl’s melanosis: brownish reticulate pigmentation on neck.

262 Pérez-Bernal et al.

© Adis International Limited. All rights reserved. Am J Clin Dermatol 2000 Sep-Oct; 1 (5)

plugging, the sebaceous glands are enlarged, and a periadnexiallymphocytic infiltrate and vasodilatation may be observed.

Clinically, there is a symmetric, well defined, reddish brownpigmentation affecting preauricular and maxillary areas, with fol-licular papules and erythema (fig.2). Using the pressure of a glassthe reddish brown area becomes pale, and then it is possible tosee brown pigmentation and some telangiectasia.

First described in Japan, cases in Caucasians have been re-ported.[6] This condition can be differentiated from ulerythemaophryogenes, erythromelanosis peribuccale pigmentaire ofBrocq and poikiloderma, due to its typical location, the presenceof pigment and telangiectasia. Of unknown etiology, some casesare inherited as an autosomal recessive disorder. No photosensi-tivity relationship has been found.

Therapy with tretinoin cream, ammonium lactate 12% lotion,metronidazole gel, or hydroquinone cream is ineffective. No effec-tive therapy is currently available.

2.3 Erythrose Peribuccale Pigmentaire of Brocq

Erythrose peribuccale pigmentaire of Brocq typically appearsas a reddish brown pigmentation around the mouth as far as thenasolabialis sulcus, and sometimes presents as a narrow perioralring.

It may be the result from the use of topical corticosteroids ofthe treatment of rosacea,[7] and from photodynamic substancespresent in cosmetics.

The pigmentation persists for a long time, even after the causeis eliminated. Elimination of the cause, camouflage, sunscreens,and depigmentation using the different techniques that will bedescribed for melasma (see section 3), have been used to treat thiscondition.

2.4 Linea Fusca

In linea fusca, brownish yellow pigmentation develops nearthe hair implantation line in an arch disposition, affecting theforehead (fig. 3) and temporal areas. Similar dark plaques can beobserved all over the face.

Histologically, there is liquefaction degeneration of the basallayer, perivascular chronic inflammatory infiltrate, follicular hy-perkeratosis and melanin deposition in dermis and melano-phages.[7]

It is necessary to rule out the possibility of exogenous factorsas a cause for the condition (e.g. use of cosmetics, hat ribbons,

Fig. 2. Erythromelanosis follicularis of the face and neck: reddish brown pigmen-tation on face and neck.

Fig. 3. Linea fusca: brownish pigmentation affecting forehead.

Management of Facial Hyperpigmentation 263


etc), because typical linea fusca can be associated to central nerv-ous system disorders such as encephalitis, tumors, and syphilis.

3. Facial Hyperpigmentation Associated with Use ofCosmetics and Drugs

Photosensitizers can act by a phototoxic, or by a photoal-lergic mechanism. Some photodynamic substances that inducephototoxic contact dermatitis can produce severe hyperpigmenta-tion. This is the case of berloque dermatitis occurring after theapplication of eau de cologne or perfumes containing bergamotoil, an ultraviolet sensitizer. Some plants containing furocou-marines may induce prairie dermatitis (phytophotodermatitis)when patients are exposed to sun after contact with the particularplant. The photosensitizer capacity of furocoumarines inducespigmentation, and this capacity is used for vitiligo repigmentationtherapy.

Other compounds act as photoallergens, although many ofthem may only develop a phototoxic action: sulfonamides, ani-lines, p-aminobenzoic acid, chlorothiazides, some oral antidia-betics, phenothiazines, chlorpromazine, hexachlorophene, andsalicylamides, are also present in some cosmetic products. Tetra-cyclines induce an erythema followed by pigmentation of un ex-posed areas by a phototoxic mechanism, as do griseofulvin andminocycline.[8]

Lichenoid toxic melanodermitis of Hoffman and Habermannis an example of occupationally-induced hyperpigmentation. Itoccurs in people whose work brings them into contact with lubri-cant oils and derivatives over a long period of time. It also mayoccur in men and women who have applied creams or prepara-tions containing petrolatum with photodynamic additives. Irreg-ular areas of brownish violet pigmentation will appear after atransitory inflammatory reaction in photoexposed areas, some-times with lichenoid papules and blisters. Histologically, there isacanthosis, perivascular inflammatory infiltrate, and melanin de-posits in upper dermis and melanophages. It will slowly disappearwhen the cause is eliminated, although the use of sunscreens andtherapy similar to that used for melasma (see section 3) may ac-celerate healing.[9]

4. Melasma (Chloasma)

Melasma is a brown or gray hyperpigmentation, with an ill-defined periphery, more or less symmetrical, and localized to theforehead, cheeks, chin, and upper lip. It is quite common in women(fig. 4), and rare in men (who comprise only 10% of the cases ofmelasma)[10] (fig. 5). It appears in people of all races, but is morecommon in people with skin phototypes IV to VI who live in areasof high ultraviolet (UV) radiation.

Although the etiology is unknown, several etiogenic factorshave been implicated, including genetic factors, UV exposure,pregnancy, oral contraceptives, hormonal replacement therapies,thyroid disturbances, cosmetics, and some photosensitizer drugs.[11]

The sun exposure is the most important factor, and is present inall patients,[12] who improve or worsen with sun exposure. Im-provements have been reported at the end of pregnancy or at theend of oral hormonal therapy, although melasma do not alwaysdisappear. It can appear during menopause or in men who takeestrogens to treat prostate cancer. Some papers show the exist-ence of a subclinical ovarian dysfunction,[13] and that it is morecommon in patients with autoimmune thyroiditis.[14] Melanocytestimulating hormone is not relevant in the etiology of melasma.[4]

There are 3 clinical models: (i) centrofacial, the most com-mon, in which the nose, chin, upper lip and forehead are affected;(ii) malar, where the nose and cheeks are affected and; (iii) man-dibular, the most rare, where the lower jaw is affected.

Using Wood’s light examination it is possible to classifymelasma into 4 types:[15]

1. Epidermal type: melanin increased in all the epidermal layerswith sparse melanophages in the upper dermis. It is the mostcommon type, and the pigmentation increases under Wood’s lightexamination.

2. Dermal type: pigmentation does not increase under Wood’slight examination. Histologically, there are many melanophagesthroughout the whole dermis.

3. Mixed type: there is an increase of melanin in epidermisand in dermal melanophages, and Wood’s light examination in-creases pigmentation only in some areas, whereas in other areasno changes are observed.

Fig. 4. Melasma (chloasma) in a woman affecting cheeks and upper lip.



4. Indeterminate type: patients with VI phototype who showno differences under Wood’s light examination.

This classification has a prognostic value: patients with epi-dermal type melasma show a better response to hypopigmentingagents. In the case of dermal pigmentation, the response tohypopigmenting agents will depend on macrophage transport andelimination.[5]

5. Treatment of Facial Hyperpigmentation

Treatment of melasma and other facial pigmentations hasalways been challenging, and at many times discouraging. It in-cludes general instructions that patients must follow exactly, andthe use of hypopigmenting agents, like hydroquinone and kojicacid, with or without the addition of exfoliative agents (tretinoin,glycolic acid or trichloroacetic acid). In addition, azelaic acid,

α-hydroxy acid preparations, chemical peels, and laser therapiesare also used.

In the following sections we will discuss the efficacy, advan-tages, and disadvantages of these different therapeutic options.

5.1 General Instructions

All women at risk of developing melasma should avoid sunexposure and not sue UV lamps. They should use appropriateclothes and broad-spectrum sunscreens.

If melasma has been induced by the use of oral contracep-tives, they must be stopped. If melasma appears during pregnancyit is necessary to use sunscreens, with an improvement seen at theend of gestation.

5.2 Hypopigmentation Agents

5.2.1 HydroquinoneHydroquinone is a hydroxyphenolic chemical classically

used in melasma treatment. It inhibits the conversion of dopa tomelanin by inhibiting the tyrosinase enzyme. Other proposedmechanisms of action are inhibition of DNA and RNA synthesis,degradation of melanosomes, and destruction of melanocytes.[16]

Hydroquinone efficacy depends on its concentration, the ve-hicle used, and the chemical stability of the final product. Com-monly used concentrations range from 2 to 5%. As a higher con-centration is used, a higher efficacy is reached, but more skinirritation is caused. In addition, concentrations higher than 5% donot produce better results.[17] Good results are obtained with aconcentration of a 3% concentration. Use of a 2% concentration,without the use of additional substances, is only useful as a main-tenance therapy, as is recommended by the US Food and DrugAdministration and European Regulation of Cosmetics Prod-ucts.[5]

Hydroquinone must not be prepared as a monobencyl-ether,because it can induce confetti-like depigmentation, and also adelayed-type hypersensitivity reaction. It must be formulated asa hydroalcoholic solution by adding an antioxidant such as so-dium bisulphite 0.1% and ascorbic acid (vitamin C) 0.1%.

Adverse effects of hydroquinone are irritative dermatitis,contact dermatitis, postinflammatory pigmentation, nail bleach-ing, and there have been some published cases of exogenous oc-hronosis, appearing as a dark and reticulated pigmentation of theface after using hydroquinone preparations,[18] although this ad-verse effect is infrequent, in relation to the common use of hy-droquinone products. Hydroquinone can provide permanent de-pigmentation if the lesion is treated with a high concentration andfor a long time.Fig. 5. Melasma (chloasma) in a man affecting the forehead and cheeks.



5.2.2 Hydroquinone and Tretinoin CombinationsHydroquinone in combination with other chemical products

has been used for many years, with more therapeutic success thanhydroquinone alone. Hydroquinone 2 to 5% plus tretinoin 0.05to 0.1% cream is commonly used, and sometimes dexamethasone0.1% or hydrocortisone 0.5% is also added. Tretinoin acts by pre-venting the oxidation of hydroquinone, improving epidermal pen-etration, allowing pigment elimination, and increasing keratin-ocyte proliferation. Corticosteroids decrease the irritative effectsof hypopigmenting agents, and also inhibit melanin synthesis bydecreasing cellular metabolism, but they must not be used for longperiods of time to avoid adverse effects. Good results are usuallyobtained with these combinations, used twice a day for 8 to 10weeks.[19]

5.2.3. Other Phenolic CompoundsIsopropylcatechol metabolites 1 to 3% induce toxic radicals

which target melanocytes. They produce confetti-like depigmen-tation, contact and allergic dermatitis. The combination of 4-hydroxyanisole 2% plus 0.01% tretinoin is better tolerated.Jimbow[20] proposed the use of a phenolic thioether (N-acetyl-4-S-cysteaminylphenol, in 4% oil/water emulsion, twice a day for6 months) for the treatment of epidermal melasmas, inducing lessirritation than hydroquinone.

5.2.4 Azelaic AcidAzelaic acid is a dicarboxylic acid (1,7-heptanedicarboxylic

acid) isolated from Pityrosporum ovale, that has been found to beeffective on hyperactive melanocytes, and was used in the 1980sas an adjuvant treatment for melanoma.[21] The antiproliferativeand cytotoxic effects of azelaic acid are mediated via inhibitionof mitochondrial oxidoreductase activity and DNA synthesis. Itis used as a cream at a concentrations of 15 to 20%, showing agreater efficacy than hydroquinone 2%,[22] but not greater thanhydroquinone 4%.[23] In addition, it only induces slight irritation,and can be used for a long time.

5.2.5 TretinoinTretinoin induces dispersion of pigment granules inside the

keratinocyte, and accelerates the turn over of epidermal cells,facilitating the elimination of dispersed pigment. It is used to treathyperpigmentation of photoaged skin, postinflammatory hyper-pigmentation, and melasma. Tretinoin 1% has been used to suc-cessfully treat melasma in Black patients; improvements of up to73% were seen after 40 weeks of treatment.[24] Erythema andpeeling in the area of application are adverse effects of tretinoin0.05 to 0.1%; postinflammatory hyperpigmentation is can alsooccur.

5.2.6 Kojic AcidKojic acid has recently been used as a 2% cream, alone or in

combination with glycolic acid or hydroquinone, due to its inhib-itory action on tyrosinase. In a comparative study in Chinesewomen with epidermal melasma, half of the face was treated withkojic acid 2% gel plus glycolic acid 10% and hydroquinone 2%,and the other half of the face with just glycolic acid 10% andhydroquinone 2%.[25] Better results were obtained on the half ofthe face treated with the cream including kojic acid.

5.2.7 Ascorbic Acid (Vitamin C) and Tocopherol (Vitamin E)Ascorbic acid and tocopherol (vitamin E) have a synergistic

action. In mild forms of melasma, ascorbic acid may be usefuldue to its ability to transform melanin to leucomelanin, which iswithout color.[14]

5.3 Chemical Peels

Chemical peels, mainly medium peels, are useful to treat melas-ma: trichloroacetic acid, Jessner’s solution, Unna’s paste, α-hydroxyacid preparations, kojic acid, and salicylic acid, alone or in com-bination are used.

Complete blanching of diffuse melasma was observed in30% of patients treated with glycolic acid 50% plus kojic acid10%, partial blanching in 60% and no effect in 10% of patients.The same results were obtained with trichloroacetic acid 15 to25%.[26]

Glycolic acid peels (50 to 70%) are becoming increasinglypopular in the treatment of melasma. They can be safely used indark skinned patients due to a quite low risk of hyperpigmenta-tion.[27]

Fig. 6. Chemical peel that contains resorcinol, kojic acid, hydroquinone and α-hydroxy acid for treating melasma (chloasma).



Grimes[28] used a series of 5 peelings with salicylic acid 20to 30% at 2 weeks intervals in dark skinned patients (phototypesV to VI), after initial treatment with hydroquinone 4% for 2weeks, obtaining good results for melasma and other types ofhyperpigmentation.

Peels are commercially available that combine resorcinol, kojicacid, hydroquinone, salicylic acid, and α-hydroxy acid prepara-tions with a pH of 2.5; peels without hydroquinone or withoutresorcinol are also available (fig. 6). Layers of solution are ap-plied on the skin every 3 weeks, and neutralisation is not required.Resorcinol, a classic therapeutic agent in dermatology, is an iso-mer of catechol and hydroquinone. It is used as Jessner’s solution,which consists of 14g resorcinol, 14g of salicylic acid, 14g oflactic acid 85%, and enough 95% ethanol to make up 10ml. Resor-cinol is also used in Unna’s paste: up to 50% resorcinol plus zincoxide and ceisatite, used for 30 minutes, making a deeper peel.[5]

The use of trichloroacetic acid 35% followed by hydroqui-none hydroalcoholic 4% solution or tretinoin 0.05% plus hydro-cortisone acetate 1% cream has produced excellent results inWhite patients with lighter complexions.[14]

5.4 Laser Therapy

Laser therapy is of little use for treating melasma and lasertherapy should only be considered when other therapeutic options

have failed. Even with the availability of more sophisticated la-sers, the results obtained are not completely satisfactory. Lasersinduce hyperpigmentation, and recurrence of melasma after lasertreatment is the usual outcome.

Several types of lasers have been used to treat pigmented le-sions: argon laser, Q-switched Nd:YAG (1064nm) laser (used toremove tattoos), Q-switched Nd:YAG (532nm) and Q-switchedruby laser.[29] These lasers have been used to treat epidermalhyperpigmentations such as ephelides, lentigo, and café-au-laitspots, but results with melasma have not been satisfactory.

The erbium-YAG laser is probably the best one to treatmelasma. Manaloto and Alster[30] treated 10 women with melasmaresistant to other forms of treatment with erbium-YAG laser re-surfacing, obtaining a good improvement of hyperpigmentationimmediately after the treatment. However, 3 to 6 weeks aftertreatment, all of them had a postinflammatory hyperpigmenta-tion, that could be resolved with glycolic acid peels every 2weeks. They concluded that laser therapy should be only used inrefractory melasmas.

Nouri et al.[31] obtained good results using a pulsed carbondioxide laser to destroy melanocytes, followed by a Q-switchedalexandrite laser to eliminate dermal melanin, in patients withdermal type melasma. In the future, the combined use of severaltypes of lasers may become the key weapon for melasma therapy.

Table I. Facial hyperpigmentation: clinical features and recommended therapy

Pigmentary condition Clinical features Recommended therapyRiehl’s melanosis Reticulate pigmentation

Neck and facePhotosensitivity?

SunscreensHydroquinone creams plus tretinoin orglycolic acid

Poikiloderma of Civatte Perimenopause womenReticulate dark pigmentationLateral and low neck

SunscreensAvoid precipitating factors (cosmetics,hormones)

Erythromelanosis follicularis of the face and neck Affecting folliculesPreauricular, maxillary areasSymmetric pigmentation

Ineffective

Erythrose peribucale pigmentaire of Brocq Around the mouthResult of corticosteroid therapy andphotodynamic cosmetics

Eliminate the causeSunscreens and melasma therapies

Linea fusca Forehead and temporal areasExogen factorsCNS disorders

If possible eliminate the cause (cosmetics,ribbons)

Cosmetic and drugs associated facial hyperpigmentation Berloque dermatitisPrairie dermatitisPhotoallergensLichenoid toxic melanodermitis of Hoffmanand Habermann

Eliminate the causeSunscreens and melasma therapies

Melasma (chloasma) Women (phototypes IV to VI)Hormonal factorsWood’s light classification

Avoid sun exposureSunscreensHypopigmentation agentsChemical peelsLasers?



6. Conclusions

The treatment of facial hyperpigmentation is still challeng-ing. The use of sunscreens is recommended in all conditions.Elimination of precipitating factors could be beneficial inpoikiloderma of Civatte, erythromelanosis follicularis of the faceand neck, erythrose peribucale pigmentaire of Brocq, linea fusca,and cosmetic- and drug-associated facial hyperpigmentation (ta-ble I). New laser approaches could be successful at clearing facialhyperpigmentations in the future, but at the present time combi-nations of hypopigmentation agents and chemical peels are themost useful therapies for melasma and other facial hyper-pigmentations.

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25. Lim JT. Treatment of melasma using Kojic Acid in a gel containing Hydroquinoneand Glycolic Acid. Dermatol Surg 1999; 25: 282-4

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31. Nouri K, Bowes L, Chartier T, et al. Combination treatment of melasma withpulsed CO2 Lase followed by Q-Switched Alexandrite Laser: a pilot study.Dermatol Surg 1999; 25: 494-7

Correspondence and offprints: Professor Francisco Camacho, Departo.Dermatología, Hospital Virgen Macarena, Avda Dr Fedriani s/n. 41009 Se-ville, Spain.



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