Melasma, Chloasma

Chloasma (Greek chloazein = to be green; melasma: Greek melas = black; pregnancy spots; ICD-10-GM: L81.1: Chloasma [melasma]) refers to a circumscribed benign (benign) hyperpigmentation that occurs on the face. The condition is more common in people with dark skin type (skin type III-IV according to Fitzpatrick). Age of manifestation (first age of onset): 20-40 years; average age 35 years.

Sex ratio: Women are much more frequently affected than men. Course and prognosis: Chloasma is chronic over years to decades and has a strong tendency to recur. A chloasma occurring during pregnancy (chloasma gravidarium; chloasma uterinum; melasma gravidarium) often regresses. Otherwise, the rate of spontaneous remission (unexpected improvement) is only 8 percent overall.

Symptoms – Complaints

Skin discolorations are yellowish to brownish and of irregular shape and size; often appearing symmetrically.They usually occur symmetrically on the face, preferentially in the area of the forehead, cheeks, temples, and/or nose. Based on the pattern of distribution on the face, several manifestations can be distinguished:

  • Frontal type – hyperpigmentation on the forehead.
  • Centrofacial type – mainly affecting the upper lip, but also the nose, cheeks, and chin (most common)
  • Malar type – zygomatic arches and the cheeks.
  • Mandibular type – area of the lower jaw.

Pathogenesis (disease development)

The cause of chloasma is multifactorial. Chloasma is an epidermal (“affecting the epidermis”) hyperpigmentation (increased pigmentation) caused by hyperactive melanocytes (pigment cells of the skin). The following hormones have an influence on the development of chloasma: estrogens, progesterone, MSH (melanocyte-stimulating hormone) and ACTH (adrenocorticotropic hormone). They occur especially after UV exposure (the most important trigger). Visible light (VL, visible light) and infrared light (IR) can also trigger chloasma.The VL can trigger melanogenesis in people with skin type (skin phototype) III or higher according to Fitzpatrick. In skin phototypes III and IV, high-energy visible light (HEV or blue-violet light, 400-450 nm) can trigger pigmentation.

Etiology (Causes)

Biographic causes

  • Genetic burden – approximately 50% have a positive family history.
  • Ethnic origin – among residents of Arab descent in the U.S., chloasma is the fifth most common dermatosis (skin condition)

Behavioral causes

  • Sunlight (UV rays) [most important cofactor!]

Disease-related causes

  • Systemic diseases such as cirrhosis of the liver, tuberculosis, malaria, or sprue (diseases associated with diarrhea; one is celiac disease (synonym: gluten-sensitive enteropathy), which was formerly also called indigenous sprue in adults, and the other is tropical sprue, in which infection is thought to be the cause).
  • Consumptive diseases (melasma cachecticorum).
  • Tumors that produce estrogens

Medications (Chloasma medicamentosum).

Environmental pollution – intoxications (poisonings).

  • UV exposure (most important trigger).

Other causes

  • Gravidity* (pregnancy)
  • Chemical substances such as fragrances, perfumes, photoprotective filters, and plant juices that may cause a phototoxic reaction
  • Emergence without apparent cause (idiopathic) (idiopathic chloasma).
  • Trauma (Chloasma (Melasma) traumticum)

* Estrogens and progestins, which are also synthesized more in gravidity, are thought to be responsible for the genesis of chloasma. UV light exposure further exacerbates the discoloration.

Consequential diseases

There are no known sequelae.

Diagnostics

Chloasma is diagnosed by visual inspection.

Prevention

  • Broad spectrum light protection (UVA and UVB light protection).
  • Non-hormonal contraceptive (contraception).

Therapy

General measures

  • Light protection (high sun protection factor and protection in the UVB and UVA range).
  • Review of permanent medication due topossible effect on the existing disease.
    • Z. E.g., discontinuation of hormone therapy (possibly regression of chloasma over years).
  • Avoidance of environmental stress:
    • UV exposure (sun; solarium)

Note: First of all, it is important to clarify the cause of chloasma to prevent recurrence (recurrence of the disease) if possible. Treatment of chloasma is possible as follows:

  • Lightening of the spots locally by means of azelaic acid, hydroquinone (about 40% develop erythema (areal skin redness) under therapy!) or vitamin A acids (tretinoin).
  • Highest efficacy with the topical triple combination with hydroquinone 4%, tretinoin and fluocinolone acetonide (glucocorticoid, class 3) [gold standard].
  • Chemical peeling (chemical peeling) [second-line therapy].
    • Fruit acid peeling (e.g. glycol).
    • Trichloroacetic acid peeling
  • Tranexamic acid (TXA; antifibrinolytic agent) (in one study, oral administration and intradermal injection were comparable in terms of MASI (melasma area severity index) and response rate) [further studies await].
    • Oral administration (250 mg TXA orally twice daily for a period of twelve weeks) or
    • Intradermal injection (4 mg/ml every four weeks (weeks 0, 4, 8) intradermally by microinjection).

The use of laser, IPL technology or cryotherapy can be tried, but improvement often can not be achieved.With the help of a krypton ion laser or Nd:Yag laser may be able to remove the offending spots. However, undesirable effects (skin irritation, rebound hyperpigmentation) occur more frequently (third-choice therapy). Chloasma can also be easily covered with makeup (camouflage).Furthermore, consistent UV protection should be practiced; if necessary, hormonal stimulus (hormonal contraceptives/hormonal contraceptive medications; hormone therapy during menopause) should be interrupted.