Hypo/Hyperpigmentation
Differential Overview
Hyperpigmented Macules
❑ Nevus
❑ Seborrheic keratosis
❑ Post-inflammatory
❑ Solar purpura
❑ Solar lentigo
❑ Schamberg purpura
❑ Fixed drug eruption
❑ Melasma
❑ Atypical nevus
❑ Melanoma
❑ Cafe-au-lait
Generalized Hyperpigmentation
❑ Drugs
❑ Heavy metals
❑ Addison disease
❑ Ectopic ACTH syndrome
❑ Hemochromatosis
❑ Porphyria cutanea tarda
❑ Pellagra
❑ Whipple disease
❑ Primary biliary cirrhosis
❑ Metastatic melanoma
Hypopigmentation
❑ Tinea versicolor
❑ Vitiligo
❑ Halo nevus
❑ Postinflammatory
❑ Chemical
❑ Piebaldism
❑ Tuberous sclerosis
Diagnostic Approach
ABCDE criteria and their histopathological counterparts are: Asymmetry—If the lesion bisected in half is not identical to the other half, consistent with asymmetrical architecture at scanning magnification. Border—Border is uneven or ragged as opposed to smooth and straight; consistent with poor lateral circumscription (single cell extension along junction). Color—More than one shade of pigment is present; consistent with atypical melanocytes at various levels of the epidermis (brown/black) and thickening and fibrosis of the papillary dermis with loss of melanin from the epidermis (white-regression). Diameter—.6 mm; consistent with broad extension of melanocytes along
the junction. Evolving—Changed with respect to size, shape, symptoms (e.g., itching or tenderness), surface (e.g., bleeding) or shades of color. This will pick up 78% of nodular melanomas, which present at a more advanced stage but do not have the other signs.
Clinical Findings
Nevus A uniformly round brown lesion, either flat or raised, with smooth borders.
Seborrheic keratosis Typically, it is a brown plaque with a “stuck-on” appearance and a rough, greasy surface. A sudden increase in number with inflammation may be seen in association with internal malignancy (Leser-Trelat syndrome).
Post-inflammatory Particularly common to appear in darker skin when inflammation of acne, psoriasis, or eczema is resolving.
Solar purpura Occurs on the forearms of older patients taking warfarin, aspirin, or prednisone. Purpura from local trauma heals with hyperpigmentation due to hemosiderin deposition.
Solar lentigo “Liver spots” are melanocytic proliferation due to chronic sun damage. The lesions are flat, oval, evenly pigmented, and liver brown.
Schamberg purpura Brownish hemosiderin staining of the lower legs and ankles is due to capillary leakage of blood and subsequent breakdown.
Fixed drug eruption Acutely the lesion is erythematous and edematous with a grayish center or frank bullae, but chronically it has dark pigmentation. The hallmark is reoccurrence at the same location on re-exposure, as the name suggests. Common sites include the lips, face, genitalia, and acral areas. Common agents include NSAIDs, sulfonamides, tetracyclines, salicylates, barbiturates, and phenolphthalein laxatives.
Melasma A mask-like pigmentation made of splotchy macules in a photodistribution, accentuated on the upper lip. It develops during pregnancy or with oral contraceptives.
Atypical nevus Larger than common moles, these nevi have borders that are irregular and ill-defined. The color is variegated, tan to dark brown, often on a pink background. Atypical nevi are at increased risk for subsequently developing into melanoma.
Melanoma Hallmarks are an irregular border that sometimes has a notch and variegation in color and pigmentation pattern. The background color is usually jet black instead of brown. Admixed red, blue, gray, pink, and purple colors help to differentiate them from benign nevi. A previous blistering sunburn (episodic intense sun exposure), red hair with fair skin, and a family history of melanoma are important risk factors.
Cafe-au-lait Lesions are 0.5 to 12 cm in diameter, flat, uniformly brown, and have an irregular border like a coastal map. Patients with type I neurofibromatosis usually have 6 or more spots, with associated findings of axillary freckling, pigmented iris hamartomas (Lisch nodules), and flesh-colored neurofibromas.
Drugs Busulfan, cyclophosphamide, and arsenic can induce melanin formation. Arsenic produces a “raindrop” appearance and hyperkeratosis of the palms. Long-term chlorpromazine, minocycline, or amiodarone can produce blue-gray discoloration in sun-exposed skin and conjunctivae. Chloroquine complexes with melanin to produce a gray to blue-black discoloration of the shins, face, and hard palate.
Heavy metals Gold (chrysiasis) produces a brown to blue-gray discoloration, accentuated in sun-exposed areas, which may also deposit in the sclera. Silver (argyria) produces a blue-gray color. Heavy metals do not cause mucosal hyperpigmentation.
Addison disease Diffuse hyperpigmentation is found, with accentuation in the palmar and plantar creases, oral mucosa, and around scars.
Ectopic ACTH syndrome Hyperpigmentation develops in association with medullary carcinoma of the thyroid and small cell carcinoma of the lung.
Hemochromatosis The skin becomes a bronze color in patients with diabetes, congestive heart failure, or liver dysfunction.
Porphyria cutanea tarda Hyperpigmentation occurs in sun-exposed areas and is associated with vesicles and erosions.
Pellagra A dirty brownish discoloration, with a varnish-like scale, develops in sun-exposed areas.
Whipple disease Generalized hyperpigmentation is associated with diarrhea, weight loss, arthritis, and lymphadenopathy.
Primary biliary cirrhosis Photoaccentuated dark brown skin is associated with pervasive pruritus, jaundice, and tendon xanthomas.
Metastatic melanoma Slate-blue color and black urine occasionally develop with advanced disease.
Tinea versicolor Patches are sprinkled over the trunk like snow, appearing hypopigmented compared with melanotic skin. Examination via Wood lamp reveals a golden fluorescence, and a KOH prep is positive for yeast and pseudohyphae.
Vitiligo Symmetric areas of complete pigment loss appear around orifices and on flexor and extensor surfaces. Other autoimmune diseases are often present, such as pernicious anemia, thyroid disease, or Addison disease.
Halo nevus A depigmented macule around a pre-existing pigmented nevus, it represents a T-cell–mediated immune reaction to melanocytes. The rest of the skin should be examined for a possible melanoma elsewhere stimulating an immune response.
Postinflammatory Hypopigmentation occurs following a dermatitis and in active discoid lupus lesions.
Chemical Hypopigmentation usually begins on the hands and is a result of contact with phenols, rubber derivatives, or germicides.
Piebaldism Congenital hypopigmentation of the trunk and midextremities, with a white forelock, is characteristic.
Tuberous sclerosis An ash leaf spot measuring 1 to 3 cm in size is present at birth. Other findings include adenoma sebaceum adjacent to the nasal alae and ungual fibromas.
Pictures
Book Source Details
- Book Title: Field Guide to Bedside Diagnosis
- Author(s): David S. Smith
- Year of Publication: 2007
- Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.
Other Book Chapters Related to Hyperpigmentation
Read excerpts from these other book chapters related to Hyperpigmentation:
Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2008 Williams & Wilkins.
More About Causes of Hyperpigmentation
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More About This Book:
Title: Field Guide to Bedside Diagnosis
Authors: David S. Smith
Publisher: Lippincott Williams & Wilkins
Copyright: 2007
ISBN: 0-78178-165-5
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» Next page: SKIN PIGMENTATION AND OTHER PIGMENTARY CHANGES (Differential Diagnosis in Primary Care)
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