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Melasma
Melasma

Chloasma, medically referred to as melasma, is a chronic, relapsing disorder of melanogenesis, which is the process of melanin production. It manifests as the formation of symmetrical, irregular patches ranging in color from light brown to brownish-gray, primarily on the forehead, cheeks, nose, temples, and above the upper lip. It most commonly affects women of reproductive age and individuals with intermediate and darker skin phototypes. Ultraviolet radiation, visible light, hormonal factors, genetic predisposition, oxidative stress, and chronic skin photoaging contribute to the development of chloasma. Effective therapy requires a combination of year-round photoprotection, treatment that inhibits pigment production, proper skin care, and carefully selected dermatological or cosmetological procedures.

Melasma - what is it

Melasma is one of the acquired skin hyperpigmentations. Melanocytes, the cells responsible for melanin production, maintain a normal count but exhibit excessive activity. They produce a greater amount of pigment, which then reaches the keratinocytes that form the epidermis. The process can also involve the dermis, which is why some lesions are characterized by high persistence.

Most commonly, three patterns of melasma distribution are distinguished:

  • centrofacial – covers the forehead, cheeks, nose, upper lip area, and chin;
  • malar – concentrates on the lateral parts of the cheeks and the nose;
  • mandibular – runs along the lower part of the face.

Based on the depth of pigment accumulation, epidermal, dermal, and mixed types are described. In practice, the presentation of melasma often turns out to be heterogeneous, and different parts of the same patch may contain melanin at different levels of the skin.

Diagnosis is based primarily on the clinical presentation, dermoscopy, and Wood's lamp examination. Differential diagnosis includes, among others, post-inflammatory hyperpigmentation, lentigines, drug-induced melanoderma, phototoxic dermatitis, lichen planus pigmentosus, and pigmented contact dermatitis. A lesion with an atypical shape, unilateral location, irregular coloration, rapid growth, or a changing surface requires dermatological evaluation.

Melasma - why it develops

Melasma has a multifactorial etiology. Its development results from the interplay of genetic predisposition, the environment, hormonal balance, and disturbances in the skin microenvironment.

The most important mechanisms include:

  • UVA and UVB radiation – activates the melanocortin receptor, increases tyrosinase expression, and stimulates melanin synthesis. UVA radiation penetrates through window glass and participates in the persistence of lesions.
  • Visible light – particularly blue-violet light can exacerbate pigmentation in individuals with higher phototypes. For this reason, tinted formulations containing iron oxides provide broader protection than untinted sunscreens.
  • Genetic predisposition – a family history of melasma is observed in a significant proportion of patients.
  • Oxidative stress – reactive oxygen species activate pathways leading to increased melanogenesis and sustain microinflammation.
  • Photoaging of the dermis – solar elastosis, basement membrane disruption, an increased number of mast cells, and impaired fibroblast function are observed within melasma.
  • Vascular component – greater expression of proangiogenic factors and increased vascularity can support melanocyte activity.
  • Heat and infrared radiation – prolonged overheating of the skin can be an exacerbating factor.
  • Certain photosensitizing drugs and cosmetics – can increase skin reactivity to light and promote hyperpigmentation.

Melasma is chronic in nature and tends to recur. Lightening visible spots represents one stage of therapy, and long-term control of factors that stimulate melanocytes is equally important.

Melasma and hormonal hyperpigmentation

Melasma is the most important example of hyperpigmentation whose activity can be influenced by hormones. Estrogen and progesterone receptors are present in melanocytes, keratinocytes, and other skin cells. Their stimulation can increase the expression of melanogenesis enzymes, including tyrosinase, and enhance the transfer of melanosomes to epidermal cells.

Hormonal dependence is particularly visible:

  • during pregnancy, when melasma is sometimes referred to as chloasma of pregnancy;
  • during the use of hormonal contraception;
  • during menopausal hormone therapy;
  • in the coexistence of thyroid axis disorders or other endocrine disorders.

Hormones usually act as a modulating factor, while light exposure remains the most important stimulus activating hyperpigmentation. Melasma can also occur in women without diagnosed hormonal disorders as well as in men.

The persistence of lesions, their sudden aggravation, or the coexistence of menstrual disorders, symptoms of hyperandrogenism, body weight changes, fertility problems, or thyroid complaints constitutes an indication for medical consultation. The scope of tests is determined by the doctor based on the medical history and clinical symptoms. The presence of melasma alone does not constitute a basis for performing an extensive hormonal panel in every person.

Melasma - how to lighten

The foundation of treatment is broad-spectrum daily photoprotection, applied year-round. The product should provide very high protection against UVB and UVA. In melasma, tinted cosmetics containing iron oxides are beneficial, as they also limit the impact of part of visible light. Protection is complemented by a wide-brimmed hat, shade, and reapplying the product throughout the day.

Topical treatment may include substances acting at different stages of melanogenesis:

  • hydroquinone – a potent tyrosinase inhibitor, used in controlled dermatological treatments;
  • triple therapy – a combination of hydroquinone, a retinoid, and a corticosteroid, considered one of the best-studied methods for treating melasma;
  • azelaic acid – reduces tyrosinase activity and has anti-inflammatory properties;
  • retinoids – accelerate epidermal renewal, facilitate pigment dispersion, and support the penetration of other substances;
  • tranexamic acid – affects the plasminogen pathway, melanocyte signaling, and the vascular component of melasma;
  • cysteamine, kojic acid, arbutin, thiamidol, and niacinamide – inhibit melanin synthesis or reduce melanosome transfer;
  • vitamin C and other antioxidants – reduce oxidative stress and help even out skin tone.

Oral tranexamic acid is sometimes used in refractory melasma as an off-label treatment. It requires medical qualification and a thorough assessment of thromboembolic risk. Pregnancy and breastfeeding significantly limit the choice of active ingredients, especially retinoids and hydroquinone.

The effects develop gradually. Excessively aggressive exfoliation, skin irritation, and intensive thermal procedures can trigger inflammation and subsequently increase melanogenesis. Maintenance therapy and consistent light protection reduce the frequency of relapses.

Treatments for melasma

The selection of the procedure should take into account the phototype, pigment depth, melasma activity, the condition of the epidermal barrier, vascularity of the lesions, and previous skin reactions. The treatments complement topical treatment and photoprotection.

The offer of Ambasada Urody Clinic & SPA includes the following procedures applicable in the therapy of melasma:

  • Cosmelan and Dermamelan – multi-stage depigmentation treatments that limit the activity of melanogenesis enzymes. They include professional mask application and continuation of home therapy. They are used for melasma, hormonal hyperpigmentation, and lesions of mixed etiology.
  • Peels with tranexamic, azelaic, mandelic, lactic, and glycolic acid, and retinol – accelerate epidermal renewal, reduce melanin accumulation, and affect melanocyte activity. The offer includes, among others, Mandelac, Azelac, and individually tailored resurfacing blends.
  • Perfect Peel and VI Peel – complex medical peels used for hormonal hyperpigmentation, photoaging, and uneven skin tone. The intensity of the therapy requires prior qualification and strict photoprotection.
  • TCA Peel – controlled exfoliation with adjustable depth. It can support the reduction of hyperpigmentation, although melasma and darker phototypes require particularly cautious determination of concentration and exposure time.
  • ClearLift with Q-Switch Nd:YAG laser – utilizes short pulses producing a photoacoustic effect. A wave with greater penetration depth is used in melasma and persistent hormonal discoloration. Low-energy protocols limit the thermal load on the skin.
  • Alma Dye-VL PRO photorejuvenation – emits light absorbed by melanin and hemoglobin. It can act on the pigmentary component, vascular component, and signs of photoaging. Qualification takes into account the phototype and the risk of reactive hyperpigmentation.
  • iPixel fractional ablative laser, laser peeling, and laser resurfacing – create controlled micro-injuries, accelerate the turnover of pigment-containing cells, and stimulate dermal remodeling. In active melasma, ablative procedures require conservative parameters and an experienced operator.
  • Hybrid laser lift – combines action on superficial and deeper skin layers, thereby helping reduce melasma coexisting with photoaging.
  • Microneedle mesotherapy with tranexamic acid or depigmenting preparations – creates microchannels that increase the absorption of active ingredients and stimulates controlled skin regeneration.
  • LED therapy with red or yellow light – serves a supportive function, soothes the inflammatory response, and promotes regeneration after exfoliating procedures.
  • Intraceuticals oxygen infusion with Rejuvenate complex and Vitamin C Booster – supports hydration, antioxidant activity, and barrier restoration after depigmentation therapy.
  • Dermaquest treatments targeting hyperpigmentation – complement the treatment by combining exfoliation, antioxidants, and ingredients regulating melanogenesis.

The safest model of management is staged: calming active melanogenesis, restoring the skin barrier, gradual lightening, possible inclusion of procedures, and multi-month maintenance therapy. The result means a reduction in the visibility and activity of melasma, while the durability of improvement depends primarily on consistent protection against radiation and visible light.

 

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