Table 3.

Acquired pigmentation disorders and the therapy options.

Disease	Type of Pigmentation Disorder	Molecular Basis of Disease Development	Symptoms	Affected Part of the Body	Occurrence	Treatment Possibilities
Melasma	Hyperpigmentation	The detailed pathogenesis is currently not fully elucidated. Risk factors are frequent UV exposure, genetic predispositions, and female hormone stimulation	Asymmetric irregular brown spots and patch	Mainly face (forehead, cheeks, and chin); rarely arms, chest, or neck	The areas with more intensive UV exposure (Asia, Africa, and Latin America) have significantly higher incidence rates	Topical steroids, chemical peels, dermabrasion, and microdermabrasion
Riehl melanosis	Hyperpigmentation	Allergic contact dermatitis to cosmetic product ingredients such as fragrance	Reticulate gray-brown to black spots	Face, neck, and upper chest	The vast majority of cases are found in the Asian population	Topical agents including hydroquinone, corticosteroids, retinoids, vitamin C, azelaic acid, chemical peels (trichloroacetic acid, glycolic acid), intense pulsed-light therapy, and low-fluence Q-switched lasers
Post-inflammatory hyperpigmentation	Hyperpigmentation	Inflammation leads to increased level of mediators, i.e., IL-1, IL-6, LT-C4, LT-D4, PGE2, and PGD2, whichstimulate melanogenesis process	Flat, tan, brown, or black spots on the skin	The areas exposed to UV radiation	PIH affect all skin types; however, a higher incidence is found in dark-skinned individuals	Topical agents including hydroquinone, corticosteroids, azelaic acid, vitamin C, tretionoin, and glycolic acid peels
Lentigo sensilis	Hyperpigmentation	Paracrine stimulation of melanogenesis by factors that include HGF, EDN1, KGF/FGF7, and SCF/KITL	Beige or brown spots	UV-exposed areas, i.e., face, neckline, hands, and shoulder	Mainly elderly population	Cysteamine, cryotherapy, and laser treatment
Cronkhike–Canada syndrome	Hyperpigmentation	Autoimmune disease associated with inflammation and increased IgG4 levels	Skin hyperpigmentation, numerous gastrointestinal polyps, weight loss, and alopecia	Hypopigmented lesions may involve the whole body	Rare disease; 450 cases described so far	Treatment of skin lesions is not required
Idiopathic guttate hypomelanosis	Hypopigmentation	Reduction in the total number of melanocytes, structural abnormalities of melanocytes, such as reduced tyrosinase activity, reduction in the number of melanosomes, or adjacent keratinocyte defects	Numerous oval, small, discrete, and porcelain-white macules	Sun-exposed areas, i.e., forearms	Available data show that IGH is present in approximately 80% of the population by the age of 70	Topical steroids, tacrolimus, retinoids, cryotherapy, chemical peel, excimer laser, and skin grafting
Leucoderma punctata	Hypopigmentation	Rare side effect of UVA and UVB phototherapy in patients with psoriasis or Q-switched and carbon dioxide lasers	Numerous, distinct, and round or oval depigmented spots	Chest and back, occasionally on the face	Usually occurs in fair-skinned females before the age of 40	Laser therapy narrow-band ultraviolet B (NB-UVB) and the 308 nm excimer laser
Vitiligo	Hypopigmentation	The etiopathology of vitiligo has not been elucidated, but the progressive loss of melanocytes has been linked to a number of factors: metabolic abnormalities, oxidative stress, inflammation, and autoimmunity	White macules in the skin and/or hair	There are two main types of vitiligo: generalized, a common symmetrical form, and segmental, affecting only one side of the body	Vitiligo affects 0.5–2% of the global population	Topical or systemic corticosteroids as monotherapy (in localised vitiligo), or in combination with phototherapy or other topical agents (in generalised vitiligo), calcineurin inhibitors (tacrolimus, pimecrolimus), topical vitamin D3 analogues (calcipotriol), antioxidants, and phototherapy