Melasma L81.1

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 18.08.2022

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Chloasma; Chloasma cachecticorum; chloasma climacterium; Chloasma hormonal; chloasma medicamentosum; Chloasma traumaticum; Chloasma uterinum; gravidarum chloasma; pregnancy spots

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Frequent, acquired, usually sharply defined, large or small-spotted, closed or reticular hyperpigmentation(melanosis) in sun-exposed areas, which either fade completely in winter or are hardly visible, but recur in loco in the coming solar season.

Characteristic is a progression over many years with marked recurrence after the first annual sun exposure.

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Melasma (chloasma) is the fifth most common skin condition in Arabic-origin residents of the USA. In total, >5 million US citizens are affected.

Approximately 80-90% of those affected are of childbearing age.

Approximately 10% of those affected are men.

Most common visible pigmentary disorder during pregnancy or after taking contraceptives.

Preferably occurs in people with dark skin type (skin type III-IV according to Fitzpatrick).

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The pathogenesis of melasma is multifactorial. Influence of estrogens, progesterone, MSH and ACTH are postulated; furthermore modulations of melanin synthesis by influencing tyrosinase (catalyzes the conversion of L-tyrosine to L-dopa and to L-dopa-quinone), activation and proliferation of estrogen receptors in melanocytes.

In detail, the following factors can be shown to influence:

Genetics: 50% of patients with melasma have a positive family history.

Pregnancy: 20% of melasma is due to pregnancy(melasma gravidarum); accentuation of the areolae mammae, labia minora and linea alba, which becomes linea fusca or linea nigra.

Endogenous hormones: melasma climacterium or exogenously supplied hormones (melasma hormonale). Also in thyroid dysfunction (pat. with melasma suffer 4x more often from hypo- or hyperthyroidism than thyroid healthy persons).

Medications: Long-term use of hydantoin or chlorpromazine-containing medications (melasma medicamentosum). Another strong association is with the use of antidepressants and anxiolytics, and with the use of 5alpha-reductase inhibitors such as finasteride or even dusteride.

Cosmetics: skin creams containing petrolatum or photosensitizing substances (Chloasma cosmeticum).

Consumptive diseases (melasma cachecticorum).

Trauma: pressure, friction, cold, heat (melasma (chloasma) traumaticum).

Idiopathic: see also melasma (chloasma) hepaticum.

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Occurs predominantly in women, very rarely also in men. First age of onset 20 - 40, on average 35 years. Pregnancy immediately preceded the onset of the disease in 40% of patients. Familial predisposition is common (>50%).

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Forehead, cheeks (zygomatic region), upper lip, nose, temple and lower jaw region.

Clinical features
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Usually sharply or reticulated, irregularly shaped, often symmetrical, brown-grey to deep brown, areal, bizarrely shaped hyperpigmentations that can confluent to larger areas. Melasma occurs particularly after UV exposure.

Analogous to the Psoriasis Area and Severity Index (PASI) the Melasma Assessment Severity Index (MASI) was developed.

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  • Epidermal type: Melanin deposition in the basal and suprabasal layers of the epidermis, possibly up to the stratum corneum.
  • Dermal type: Melanin-laden macrophages in the superficial and middle dermis.
  • Histochemically, an increase in the number and activity of melanocytes can be demonstrated.

General therapy
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  • If necessary, discontinuation of triggering medication, e.g. hormone therapy. Check hormone status. Hyperpigmentation often gradually recedes over a period of several years after pregnancy or after discontinuing hormonal therapy.
  • Sun protection: Avoid direct exposure to the sun (especially the midday sun), textile and chemical/physical sunscreens with high sun protection factor and protection in the UVB and UVA range (e.g. Anthelios).
  • Camouflage: As a rule, over-make-up (camouflage) of disturbing hyperpigmentations (e.g. Dermacolor) is the most sensible solution. Externals with possible irritating or light sensitizing effects must be strictly avoided.

External therapy
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Therapy of 1st choice:

Hydroquinone: Depigmenting topical preparations with 2-5% hydroquinone (hydroquinone acts as a competitive substrate of tyrosinase enzymes and is to be regarded as the first-choice therapeutic agent) can lead to regression of pigmentation. However, first changes appear only after 1-2 months, success is to be assessed after 6 months. Caveat. Irregular skin pigmentation may result!

Triple cream: More effective is the combination of hydroquinone (4%) with vitamin A acid (0.05%) and a glucocorticoid to reduce irritation of the skin. This combination is available as a magistral formulation (see Hydroquinone Ointment below). Note: Instead of vitamin A acid, a 10% glycolic acid can be used (Guevara et al. 2003).

Notice. Hydroquinone treatment can lead to localized permanent depigmentation (see external ochronosis).

Rucinol: 4-n-butylresorcinol, a resorcinol derivative that targets different points of melanin synthesis.

Kojic acid is a substance naturally occurring in Aspergillus oryzae. Kojic acid inhibits the formation of free tyrosinase. It is also a free radical scavenger. Can be seen as a substitute substance to hydroquinone when the latter is not tolerated. Widely used in Asia, controversial in Europe.

Tretinoin: The efficacy of 0.05% - 0.1% tretinoin as monotherapy is proven in postinflammatory hyperpigmentation. A study is also available for chloasma, demonstrating a high likelihood of improvement.

Azelaic acid: 15-20% azelaic acid (e.g. Skinoren) can be tried for depigmentation. Results can be expected after 2-4 weeks of therapy. Currently, 20% azelaic acid is approved for the treatment of acne. Treatment of chloasma is off-label use.

Adapalene: A comparative study demonstrated superiority of 0.1% adapalene (Differin) over a 0.05% tretinoin cream.

Internal therapy
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Experimental: Glutathione oral 500mg/day over a period of 4 weeks. Effect was demonstrated in a randomized double-blind study in 60 patients.

Operative therapie
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  • Cryosurgery: In circumscribed foci in the face, good successes have been described with superficial cryosurgery using the open spray method. This method requires great clinical experience of the therapist. However, according to his own experience, it is highly efficient.
  • Laser: The use of lasers (ruby, YAG laser) is judged differently because of the often resulting irregular depigmentation.
  • Chemical peeling: In the sunless season a chemical peeling can be tried, especially on fair-skinned patients. In particular with 50-70% glycolic acid, possibly a combination of 10% glycolic acid and 2% hydroquinone, good clinical results can be achieved in the hands of the experienced.

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Very gradual (usually only after several years) regression after pregnancy or after discontinuation of hormonal therapy.

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Liquorice extract: A locally applied liquorice extract (see belowGlycyrrhiza glabra) is commonly used in Egypt. The active agent glabridin (0.4% oily preparation) has been proven to inhibit the tyrosinase activity of the melanocytes.

Arbutin (hydroquinone-beta-D-glucopyranoside) is a plant substance from Uvae ursi folium (Bearberry plant). Chemically, arbutin is a compound belonging to the group of aryl-beta-glucosides and hydroquinones. Arbutin is less toxic than hydroquinone. Evidence of inhibition of tyrosinase has been demonstrated in one study.

Deoxyarbutin: The synthetic deoxyarbutin leads to a dose-dependent reduction of tyrosinase activity and melanin content in melanocytes.

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A 10 - 20% hydroquinone monobenzylether should not be used in this disease, as there is a risk of irreversible depigmentation.

The terms chloasma and melasma are used synonymously, with the term "melasma" becoming increasingly common in the English-speaking world.

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  2. Balina LM et al (1991) The treatment of melasma. 20% azelaic acid versus 4% hydroquinone cream. Int J Dermatol 30: 893-895
  3. Balkrishnan R et al (2003) Development and validation of a health-related quality of life instrument for women with melasma. Br J Dermatol 149: 572-577
  4. Becker S et al (2017) Melasma: An update on the clinical picture, treatment, and prevention. Dermatologist 68:120-126.
  5. Boukari F et al (2014) Prevention of melasma relapses with sunscreen combining protection against UV and short wavelengths of visible light: A prospective randomized comparative trial. J Am Acad Dermatol 72:189-190
  6. Çakmak SK et al (2015) Etiopathogenetic factors, thyroid functions and thyroid autoimmunity in melasmapatients
    . Postepy Dermatol Alergol 32:327-330.
  7. Famenini S et al (2014) Finasteride associated melasma in a Caucasian male. J Drugs Dermatol 13:484-486
  8. Guevara IL et al (2003) Safety and efficacy of 4% hydroquinone combined with 10% glycolic acid, antioxidants, and sunscreen in the treatment of melasma. Int J Dermatol 42: 966-972
  9. Trade AC Risk factors for facial melasma in women: a case-control study. Br J Dermatol 171:588-594
  10. Hegyi V et al (2010) Methods and means for pigmentation and depigmentation. dermatologist 61: 586-592
  11. Kang WH et al (2002) Melasma: histopathological characteristics in 56 Korean patients. Br J Dermatol 146: 228-237
  12. Sardana K et al (2015) Rationale of using hypopigmenting drugs and their clinical application in melasma. Expert Rev Clin Pharmacol 8:123-134
  13. Stern RS et al (1994) Laser Therapy versus cryotherapy of lentigines. J Am Acad Dermatol 30: 985-987
  14. Yokota T et al (1998) The inhibitory effect of glabridin from licorice extracts on melanogenesis and inflammation. Pigment Cell Res 11: 355-361


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Last updated on: 18.08.2022