INTRODUCTION
Skin color is genetically determined and is caused by the total amount of melanin pigment in the skin. Normal constitutive melanin pigmentation determines skin type, which is classified by the Fitzpatrick skin phototypes as follows:
| Skin Phototypes | Ability to Tan | Susceptibility to Burns |
|---|---|---|
|
SPT I |
Never tans, white skin |
Sunburns easily |
|
SPT II |
Tans with difficulty |
Sunburns easily |
|
SPT III |
Can tan with time |
Occasionally burns |
|
SPT IV |
Tans easily |
Rarely burns |
|
SPT V |
Tans easily, brown skin |
Rarely burns |
|
SPT VI |
Tans easily, black skin |
Rarely burns |
Disorders of hypopigmentation are caused by decreased melanin content in the skin owing to decreased or absent melanin production or melanocytes (specialized cells of the epidermis that produce and store melanin). Disorders of hyperpigmentation are caused by increased melanin content in the skin owing to an increase in melanin production or melanocytes.
DISORDERS OF HYPOPIGMENTATION
Decreased or absent melanin in the skin can lead to hypomelanosis and can occur by two main mechanisms.
-
Melanocytopenic hypomelanosis: absent or decreased number of melanocytes (e.g., vitiligo).
-
Melanopenic hypomelanosis: absent or decreased melanin production, but normal number of melanocytes [e.g., oculocutaneous albinism (OCA)].
PITYRIASIS ALBA
Pityriasis alba is a common asymptomatic, sometimes scaly, hypopigmentation of the face, neck, and body.
INSIGHT 
Pityriasis alba entails both mild dermatitis and pigment alteration; generally, the former responds quickly while the latter continues to be an issue for many months or years.
AGE Young children, often between the ages of 3 and 16 years.
GENDER M = F.
RACE All races, more noticeable in darker skin types.
PREVALENCE Common.
ETIOLOGY Likely a form of atopic dermatitis.
Pityriasis alba is thought to be an eczematous dermatosis, with hypomelanosis resulting from postinflammatory changes and ultraviolet screening effects of the hyperkeratotic (increased thickness) and parakeratotic (inappropriately maturing) epidermis.
Hypopigmented areas are usually stable then gradually disappear with age. Some lesions may persist into adulthood. The areas are typically asymptomatic, but can sometimes burn or itch.
TYPE Macules, may have slight scale.
NUMBER One to twenty lesions may be present.
COLOR Pink, then off-white to tan-white. Can repigment over time.
SIZE AND SHAPE 5 to 30 mm or larger.
DISTRIBUTION Face (malar region), neck, trunk, extremities.
SITES OF PREDILECTION Face, especially the cheeks (Fig. 12-1), midforehead, and around the eyes and mouth.
May be associated with atopy (eczema, allergies, hay fever, asthma).
Pityriasis alba can be confused with other hypopigmented skin disorders such as vitiligo, tinea versicolor, tinea corporis, pityriasis lichenoides, and postinflammatory hypopigmentation.
DERMATOPATHOLOGY Histology reveals hyperkeratosis, parakeratosis, moderately dilated vessels of the superficial dermis, slight perivascular infiltrate, and edema of the papillary dermis.
On electron microscopy or immunohistochemistry, the number of melanocytes is normal or slightly reduced and those melanocytes present contain fewer and smaller melanosomes.
WOOD’S LAMP Accentuates hypopigmentation. Lesions are NOT depigmented.
Pityriasis alba is a benign condition and often is self-limited, clearing at puberty. It is usually asymptomatic, but can be itchy or have a burning sensation.
Treatment is unnecessary. The condition improves with age. For cosmetic reasons, emollient creams (hydrated petrolatum, Vaseline, mineral oil, moisturizers) may be useful to diminish the dry scales and ambient UV exposure can help repigment the area. In severely symptomatic cases of pityriasis alba, a mild topical steroid can be used sparingly in appropriate strengths for short durations (bid for 2 weeks). Topical calcineurin inhibitors and topical vitamin D analogs have also been reported to offer some relief for individuals with pityriasis alba and can be used for longer durations.
POSTINFLAMMATORY HYPOPIGMENTATION
A common cause of benign hypopigmentation characterized by decreased melanin formation following cutaneous inflammation.
SYNONYM Postinflammatory hypomelanosis.
AGE Any age.
GENDER M = F.
ETIOLOGY Usually follows involution of any inflammatory skin disorders (e.g., eczematous or psoriatic lesions, pityriasis rosea, burns, bullous disorders, infections, etc.).
Inflammatory conditions of the epidermis may result in transient alterations in melanosome biosynthesis, melanin production, and transport. Keratinocyte injury may render them temporarily unable to accept melanin from melanocytic dendrites. Severe inflammation or cutaneous injury (e.g., freezing) may even lead to a complete loss of melanocytes or melanocyte function.
SKIN SYMPTOMS None.
TYPE Macules, patches.
COLOR Off-white.
SHAPE Linear, oval, round, punctate depending on primary process (Fig. 12-2).
DISTRIBUTION Localized or diffuse depending on primary process.
WOOD’S LAMP Accentuates hypopigmentation. Lesions are NOT depigmented.
A clinical history of an antecedent inflammatory dermatosis is helpful to differentiate postinflammatory hypopigmentation from tinea versicolor, tuberous sclerosis, vitiligo, albinism, or infectious disease (e.g., leprosy). A careful clinical examination can also aid in distinguishing hypopigmented areas from entirely depigmented lesions.
DERMATOPATHOLOGY Skin biopsy may show decreased melanin in keratinocytes; inflammatory infiltrate may or may not be present depending on the etiologic primary process.
WOOD’S LAMP Accentuates hypopigmentation. Lesions are NOT depigmented.
Hypopigmentation gradually self-resolves over a period of months provided that the affected areas are kept disease-free. Common inflammatory conditions that lead to postinflammatory hypopigmentation include psoriasis, seborrheic dermatitis, atopic dermatitis, lichen sclerosus, lichen striatus, lupus, and pityriasis lichenoides chronica.
Postinflammatory hypopigmentation is a benign reactive condition, thus no treatment is necessary. Prevention would focus on eliminating the primary inflammatory process, allowing the melanocytes to recover and the hypopigmentation to slowly self-resolve. Patients should be counseled that hypopigmentation may take weeks to months of inflammation-free periods to improve. Judicious ambient UV exposure may be helpful in repigmenting affected areas.
VITILIGO
Vitiligo is an acquired pigmentary disorder characterized clinically by the development of completely depigmented macules, microscopically by the absence of melanocytes, and medically by the increased risk of autoimmune mediated disease (e.g., thyroid disorders).
INSIGHT 
Visible depigmentation carries deep cultural and religious stigma for many and, while not life-threatening, vitiligo should be approached with this understanding.
AGE Any age, 50% begin between ages 10 and 30 years.
GENDER M = F.
RACE All races. More noticeable in darker skin types.
INCIDENCE Common. Affects up to 2% of the population.
GENETICS Up to 30% of patients have a first-degree relative with vitiligo. Families with thyroid disease, Type 1 diabetes, and other autoimmune processes are at increased risk of developing vitiligo. Several genetic loci have been implicated: AIS1 (FOXD3), PTPN22, VIT1 (FBXO11), CTLA4, MITF, MHC (HLA-DRB1, HLA-DRB4, HLA-DQB1), ESR1, AIS2, AIS3, MLB2, CAT, VDR, MYG1, GCH1, NALP1 (SLEV1), ACE, AIRE, COMT.
ETIOLOGY Likely autoimmune mediated.
In lesions of vitiligo, there is a decrease or absence of functional melanocytes in the skin. Numerous pathophysiologic mechanisms for vitiligo have been proposed: an autoimmune destruction of melanocytes, a defect in the structure and function of melanocytes, defective-free radical defenses, decreased melanocyte survival, autocytotoxic metabolites, faulty membrane lipid proteins in the melanocyte, defective melanocyte growth factors, neurochemical destruction of melanocytes, and viral etiologies.
Both genetics and environment play a role in vitiligo. Many patients attribute the onset of their vitiligo to trauma, as with cuts, suture sites, etc. (Koebner or isomorphic phenomenon). Emotional stress (e.g., grief over lost partner) is also mentioned by patients as a cause. The depigmented areas gradually appear and 30% or more of individuals with vitiligo can undergo spontaneous repigmentation.
TYPE OF LESION Macule, patch.
SIZE Variable presentation from 1- to 5-mm confetti macules, to large several centimeter confluent patches.
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