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I Primary cutaneous disorders

II. Systemic diseases

A. Diffuse

A. Diffuse

1. Generalized vitiligo

1. Oculocutaneous albinism


a. Hermansky-Pudlak syndrome


b. chediak-Higashi syndrome


2. Phenylketonuria


3. Homocystinuria

B. Localized

B. Localized

1. Idiopathic guttate Hypomelanosis


2. Postinflammatory

2 .Scleroderma

3. Tinea (pityriasis) Versicolor

3. Melanoma-associated Lukoderma

4. vitiligo

4. Tuberous sclerosis

5. Chemical leukoderma

5. Hypomelanosis of Ito/mosaicism

6. Nevus depigmentosus

6. Incontinentia pigmenti (stage IV)

7. Piebaldism

7. Sarcoidosis


8. Tuberculoid and indeterminate Leprosy


9. Cutaneous T cell lymphoma


10. PKDL (Post kalazar dermal leishmauiasis)

  1. A Congenital Or Acquired Decrease In Melanin Production.
    The three main types of hypopigmentation are vitiligo, albinism, and postinflammatory hypopigmentation.​
    1. Vitiligo affects: The cause is unknown; although usually acquired, vitiligo is sometimes familial (autosomal dominant, with incomplete penetrance and variable expression). It may follow unusual physical trauma, especially of the head. The association of vitiligo with Addison's disease, diabetes mellitus, pernicious anemia, and thyroid dysfunction, as well as a high incidence of serum antibodies to thyroglobulin, adrenal cells, and parietal cells, has led to a postulated immunologic and neurochemical basis of disease. Some patients have antibodies to melanin.
      1. Vitiligo is characterized by depigmented areas, usually sharply demarcated and often symmetric, caused by a lack of melanocytes). Depigmentation may involve one or two spots or may cover most of the skin surface.
      2. Leukotrichia - Hair in vitiliginous areas is usually white. Skin lesions are accentuated under Wood's light. Lesions are prone to sunburn, requiring use of protective clothing, sun avoidance.
      3. Treatment is for the cosmetic disfigurement. Topical corticosteroids and topical tacrolimus occasionally help. Oral and topical psoralens with ultraviolet A (PUVA) have been used, but treatment is protracted and results vary. Khellin, a furanochrome, can be used in combination with UVA. However, 100 to 200 treatments are required to achieve a satisfactory result.
      4. Melagenena, an extract of human placenta, has had variable success in India and the Far East.
      5. Cover-up cosmetics are much more satisfactory for most when cure is doubtful.
      6. Small lesions may be camouflaged with cosmetic creams or tanning solutions that do not wipe off on clothing and last several days.
  1. Summary
    acquired loss of melanocytes characterized by sharply marginated off white macules or patches
    1. sites: extensor surfaces and periorificial areas (mouth, eyes, anus, genitalia)
    2. associated with streaks of depigmented hair, chorioretinitis
    3. 30% with +ve family history
    4. associated with autoimmune disease especially thyroid
    5. do blood work to rule out thyroid dysfunction, pernicious anemia, Addison’s disease, diabetes
    6. Wood’s lamp to detect lesions in fair-skinned patients
      1. Albinism is a rare autosomal recessive inherited disorder in which melanocytes are present but do not form melanin. There are various forms. In tyrosinase-negative albinism, the hair is white, the skin pale, and the eyes pink; nystagmus and errors of refraction are common. Albinos sunburn easily and frequently develop skin cancers. They should avoid sunlight, use sunglasses, and during daylight hours use a sunscreen with an SPF of >= 15.
      2. Postinflammatory hypopigmentation follows healing of certain inflammatory disorders (especially bullous dermatoses), burns, and skin infections and appears in scars and atrophic skin. Although pigmentation is reduced, the skin may not be ivory-white as in vitiligo, and spontaneous repigmentation may occur. Cover-up cosmetics are most satisfactory
  2. Hyperpigmentation
    1. Primary cutancous disorders
      1. Localized
        1. Epidermal alteration
        2. Seborrheic keratosis
        3. Acanthosis nigricans (Obesity)
        4. Pigmented actinic keratosis
      2. Proliferation of melanocytes
        1. Lentigo
        2. Nevus
        3. Melanoma
      3. Increased pigment production
        1. Ephelides (freckles)
        2. Café au lait macule
        3. Localized and diffuse
        4. 1.Drugs
    2. Systemic diseases
      1. Localized
      2. Epidermal alteration
        1. Seborrheic keratoses (sign of Leser-Trelat)
        2. Acanthosis nigricans (endocrine disorders, paraneoplastic)
    3. Proliferation of melanocytes
      1. Lentigines (Peutz-Jeghers and LEOPARD syndromes: xeroderma pigmentosum)
      2. Nevi [Carney complex (LAMB and NAME syndromes)]a
    4. Increased pigment production
      1. Café au lait macules (neurofibromatosis, McCune-Albright syndromeb)
      2. Urticaria pigmentosac
    5. Dermal pigmentation
      1. Incontinentia pigmenti (Stage III)
      2. Dyskeratosis congenital
      3. Diffuse
        1. Endocrinopathies
          • Addison’s disease
          • Nelson syndrome
          • Ectopic ACTH syndrome
        2. Metabolic
          • Porphyria cutanea tarda
          • Hemochromatosis
          • Vitamin B12 folate deficiency
          • Pellagra
          • Malabsorption, Whipple’s Disease
        3. Melanosis secondary to metastatic melanoma
        4. Autoimmune
          • Biliary cirrhosis
          • Scleroema
          • POEMS syndrome
          • Eosinophilia-myalgia syndromed
Drugs Type of pigmentation
•  Clofazimine
•  Psoralens
•  Minocycline
•  Bleomycin
•  Busulfan
•  Cyclophosphamide
•  Dapsone
•  Arsenic
Orange pigmentation
Brown pigmentation
Blue black discoloration in healing acne lesions, shins & mucosa
Generalized hyperpigmentation
Generalized hyperpigmentation
Generalized hyperpigmentation
Rain drop pigmentation
  1. Abnormally Increased Pigmentation.
    Increased melanin deposition resulting in hyperpigmentation may be caused by hormonal changes (eg, in Addison's disease, pregnancy, or anovular pill use). Hyperpigmentation may also result from iron deposition in hemochromatosis or from silver deposits (eg, in argyria). Long-term application (years) of hydroquinone is a rare cause of local ochronosis. Exposure to sunlight accentuates skin pigmentation.
  2. Melasma (Chloasma) consists of dark brown, sharply marginated, roughly symmetric patches of hyperpigmentation on the face (usually on the forehead, temples, and malar prominences). Melasma occurs mainly in pregnant women (melasma gravidarum, the mask of pregnancy) and in women taking anovular hormones. It may also occur idiopathically in nonpregnant women and in dark-skinned men. Hyperpigmentation related to pregnancy fades slowly and incompletely after childbirth or when related to estrogen use or cessation of hormone production or use.
  3. Treatment with 2 to 4% hydroquinone in an alcoholic glycol or cream base applied twice daily combined with rigorous photoprotection (sunscreen with an SPF of >= 15, avoidance of excessive sun exposure) may decrease the hyperpigmentation. Hydroquinone should be tested behind one ear or on a small patch on the forearm for 1 wk before being used on the face because it may cause dermatitis. Topical 0.1% tretinoin will enhance the effect of hydroquinone. Epidermal melanosis and, to a lesser degree, dermal pigmentation may be reduced.
  4. Drug-Induced Hyperpigmentation: Postinflammatory hyperpigmentation may follow various drug-induced and non-drug-related inflammatory dermatoses. Hyperpigmentation frequently follows lichen planus and lichenoid drug reactions. Fixed drug eruptions typically leave annular foci of hyperpigmentation. drugs that can cause hyperpigmentation.
    1. Amiodarone,
    2. Tetracycline,
    3. Minocycline,
    4. Bleomycin,
    5. cyclophosphamide,
    6. Antimalarials chloroquine and quinacrine,
    7. Chlorpromazine and other phenothiazines,
    8. Discoloration of skin due to heavy-metal deposition may occur when therapeutic drugs containing silver (argyria), gold (chrysiasis), mercury (hydrargyrosis), and bismuth are used.

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