section name header

Info


A. Derivation of Tumors navigator

  1. Keratinocyte
    1. Squamous Cell
    2. Basal Cell
  2. Melanocyte
  3. Vascular (hemangiomas, others)
  4. Connective Tissue

B. Definitions navigator

  1. Acanthosis
    1. Increased thickness of epidermis
    2. Caused by hyperplasia or hypertrophy of the spinous layer
  2. Horn Cyst: intraepidermal, keratin-filled space similar to cyst
  3. Hyperkeratosis
    1. Increase in thickness of stratum corneum; seen as a scale
    2. May retain basketweave pattern, or become dense and compact
  4. Parakeratosis: retention of keratinocytic nuclei in stratum corneum
  5. Squamous eddies (pearls): concetric layers of squamous cells with increasing central keratinization
  6. Verrucous (Verrucose): resembling a wart
  7. Plaque: raised or depressed lesion >0.5cm diameter

C. Description of Skin Tumors navigator

  1. A: Asymmetry
  2. B: Border
  3. C: Color
  4. D: Diameter
  5. E: Elevation

D. Seborrheic Keratosisnavigator

  1. Common benign cutaneous lesion
    1. Single isolated lesion or numerous lesions
    2. Most common in older persons, both sexes
    3. Also called sebeorrheic wart
    4. Dermatosis papulosa nigra is similar lesion seen on dark-skinned people
  2. Appearance
    1. Well demarcated nodules, usually 1-3mm (up to ~3cm)
    2. Color: flesh, dirty-yellow, tan, brown, or black
    3. Elevated nodule with "stuck-on" appearance
    4. Warty surface
    5. Seborrheic (greasy texture)
    6. Small papules within lesion called horn cyst help to make diagnosis
    7. May become inflamed (often confused with malignancy)
  3. Presentation
    1. Initially on head, neck and upper trunk
    2. Increasing incidence with age
  4. Histopathlogy
    1. Hyperplasia of keratinocytes: squamous and basal cells (hyperkeratosis)
    2. Papillomatosis, acanthosis, keratin-filled horn cysts (helps make diagnosis)
    3. Lower border of tumor is level with base of normal epidermis
    4. Inflamed SK may show squamous cell proliferation, infiltrating leukocytes
  5. Differential Diagnosis
    1. Lentigo
    2. Wart
    3. Nevus cell nevus
    4. Pigmented basal cell carcinoma
    5. Squamous cell carcinoma
  6. Sign of Leser-Trelat
    1. Sudden appearance of multiple seborrheic keratosis
    2. May signify presence of visceral carcinoma
  7. Treatment
    1. Curettage is most common
    2. Electrodesiccation is usually unnecessary, may cause scarring
    3. Small lesions: cryotherapy, topical 50% trichloroacetic acid

E. Actinic (Solar) Keratosis (AK) [3] navigator

  1. Pre-malignant lesion usually on sun-damaged skin
  2. Macule or slightly elevated papule, often covered with scales
  3. Color: erythematous or brownish in color
  4. Untreated Lesions
    1. 0.25-1.0% progress to squamous cell cancer (SCC) each year
    2. Overall ~2% progress to SCC in lifetime
    3. Invasive SCC is relatively uncommon except with genetic defects
    4. Markedly increased incidence in xeroderma pigmentosum (XP)
  5. Histopathology
    1. Atypical keratinocytes replace normal layer of basal epidermis
    2. Atypical cells have hyperchromatic nuclei, prominent nucleioli, vacuolated cytoplasm
    3. Frequent mitoses often seen
  6. Treatment [3,9]
    1. Cryosurgery - liquid nitrogen most common technique to destroy AK
    2. Chemical Peels - for diffuse AK damage
    3. Tretinoin (Retin-A®)
    4. 5-Fluorouracil (see below)
    5. Diclofenac Gel (Solaraze®) - 3% gel apply bid for 60-90 days (30-50% response rate)
    6. Imiquimod (Aldara®)
    7. Masoprocol (Actinex®)
    8. Aminolevulinic Acid + Blue Light
    9. Amongst creams, generic fluorouracil is least expensive, imiquimod is most expensive
  7. 5-FU [3,5]
    1. For diffuse AK damage
    2. Effective in >90% of patients who can tolerate it
    3. Common moderate to severe inflammatory reaction (usually temporary)
    4. Carac® 0.5% cream applied once daily
    5. Efudex® - 5% cream, 2% solution, 5% solution; applied qd or bid
    6. Fluoroplex® - 1% cream, 1% solution; applied qd or bid
  8. Imiquimod (Aldara®) [9]
    1. Immunostimulant approved for genital warts
    2. Efficacy demonstrated in small number of patients with AK
    3. Apply cream 2-3X per week for 16 weeks
    4. Little systemic absorption with minimal side effects
    5. Fatigue and influenza-like illness has been reported [10]
  9. Masoprocol (Actinex®)
    1. Potent inhibitor of 5-lipoxygenase (anti-proliferative for keratinocytes)
    2. Side effects common itching, erythema, flaking, burning, mild edema
    3. About 85% of patients studied in trials had moderate to complete improvement
  10. Aminolevulinic Acid + Blue Light (Levulan Kerastick®) [3]
    1. Topical 5-aminolevulinic acid followed by blue-light irradiation
    2. Effective or non-hypertrophic actinic keratosis and basal cell carcinomas
  11. Topical Liposomal T4 endonuclease V prevents AK and skin cancers in XP patients [4]
  12. Prevention with use of sun screen [6,7]

F. Verrucous Epidermal Nevusnavigator

  1. Lesions develop during gestation or in early childhood
  2. Skin-colored or hyperpigmented papules
  3. Two presentations
    1. Localized to one side of body in linear fashion (nevus unius lateris)
    2. Widespread (systematized nevus)
  4. No malignant potential
  5. Epidermal hyperplasia
    1. Systematized nevi often show granular degeneration of hyperkeratosis
    2. Inlammatory verrucous epidermal nevus shows psoriatiform hyperplasia
    3. Dendritic cells may play a role in the inflammatory type
  6. Surgical excision may be warrented for cosmetic reasons

G. Tumors of Epidermal Appendagesnavigator

  1. Sebaceous Hyperplasia
    1. Enlarged sebaceous gland lobules with central dilated duct
    2. Usually occur after age 40
    3. Plaques or papules, usually on forehead, nose or cheeks
    4. Cryotherapy or 1% bichloroacetic acid has been used
    5. Torres' Syndrome - sebaceous gland neoplasms with visceral carcinoma or colonic polyps
  2. Trichoepithelioma
    1. Often inherited as episomal dominant trait
    2. Begin at puberty, grow slowly
    3. Multiple yellowish-pink, translucent papules on cheeks, eyelids, nasolabial areas
    4. May differentiate towards hair follicles
    5. Electrodesiccation and curettage may be used
  3. Syringoma
    1. Multiple small papules
    2. Symmetric distrubtion over face, especially lower eyelids
    3. Benign proliferation of eccrine ducts
  4. Epidermoid Cyst ("Wens")
    1. Single or multiple slow growing, elevated, firm nodules
    2. Often with central pore, diameter of lesions 0.2-5.0 cm
    3. Cyst lining resembles epidermis, and appears to derive from hair follicles
    4. Cyst contents are thick keratinous material
    5. Entire cyst should be dissected out being sure to remove all cyst wall
    6. Consider topical antibiotic to prevent infection
    7. Systemic antibiotic (covering staphylococcus and streptococcus) if infection occurs
    8. Apply warm-water compresses 3-4 times per day fo infected cysts

H. Melanocytic Nevinavigator

  1. Clinical features
    1. Benign cutaneous tumors, also called Nevus Cell Nevus or Moles
    2. Occasionally present at birth, but usually appear during childhood and in young adults
    3. Most common of all skin tumors
    4. Most are < 6mm at largest diameter; can however cover large surfaces
    5. May undergo spontaneous regression, particularly after age of 30
    6. All melanocyte based growths are of neuroectodermal origin
    7. Melanocytic nevus which is present at birth or within 1 year is congenital
    8. If melanoma occurs within a Giant Nevus, then it is nearly always fatal
  2. Appearance
    1. Present as a few isolated lesions or as hundreds of tumors; average 20-30
    2. Well defined macule, papule or nodule depending on type
    3. Uniform Pigmentation
    4. Regular Borders
    5. Hair may be present or absent
    6. Atypical surface, shape, color are features of dysplastic nevi (higher melanoma risk)
  3. Histopathology
    1. Melanocytic nevus cells in epidermis and/or dermis
    2. Classified according to location of the nevus cells
    3. Specific subtypes of nevi (moles) are discussed below
  4. Lentigo
    1. flat, uniformly pigmented brown-black spot
    2. due to increased numbers of melanocytes at dermal-epidermal junction
  5. Junctional nevus
    1. cells present in well-circumscribed regular sized nests
    2. confined to lower epidermis at dermal-epidermal junction
    3. usually flat to slightly elevated, 1-10mm in size
    4. found on palms, solesand genitalia
  6. Intradermal nevus
    1. cells in nests and cords, present in dermis only
    2. elevated, flesh colored to black
    3. smooth, hairy or wart-like
  7. Compound nevus: features common to junctional and intradermal nevi
  8. Halo Nevi
    1. pigmented moles
    2. usually compound or intradermal nevi surrounded by a ring of depigmented skin
  9. Dysplastic nevus
    1. junctional or compound pattern with single cell proliferation of melanocytes
    2. occurs along basal layer (lentiginous hyperplasia)
    3. atypia, dermal inflammation and fibrosis are present
  10. Congenital Nevi Syndromes
    1. Epidermal (linear sebacous) nevus syndrome
    2. Neurocutaneous Melanosis
    3. Premature Aging Syndrome
    4. Occult Spinal Dysraphism
    5. Tethered Cord Syndrome
  11. Indications for Removal
    1. Benign moles (nevi) are extremely common
    2. Major risk is melanoma, which is relatively uncommon (but highly malignant)
    3. Any moles which change, or which the patient is worried about, should be examined with biopsy and histopathology
    4. Sudden enlargement, irregular border, changing color should prompt tissue examination
    5. Bleeding, ulceration, itching or pain are strong indications for biopsy examination
    6. Wide primary excision is inappropriate prior to identification of melanoma
    7. Simple exision or biopsy does not increase metastasis risk if lesion is malignant

I. Superficial Hemangioma [8] navigator

  1. Typically occur in children, often called strawberry nevi
  2. Most common soft tissue tumors of infancy, ~10% of children <1 year
  3. <30% present at birth
  4. 90% appear within 1 month
    1. Reach maximum size at 6-8 months
    2. 50% resolve by 5 years; 90% by 10 years
    3. Thus, 50% are present when child starts primary school
  5. Initial rapid phase followed by slower involutional phase
    1. Blanched macule, telangiectasia, surrounded by blanced halo or red macule
    2. Vascular tumor of variable size then develops
  6. Complications
    1. Generally mild, though very location dependent
    2. Infection, bleeding, occlusion or obstruction of vital structures can occur
    3. Eyes, nose, mojuth, auditory canal can be affected
    4. Facial lesions in particular can cause significant cosmetic disfigurement
    5. Resolution may leave ~30% of children with residual skin changes
    6. These skin changes include epidermal atrophy, telangiectasia, hypopigmentation
  7. Treatment
    1. Usually "wait-and-see" policy
    2. Intralesional or systemic glucocorticoids, particularly in rapid growth phase
    3. Pulse dye laser has also been used
    4. No overall benefit to pulse dye laser over wait-and-see policy in children []

References navigator

  1. Brodland DG. 1997. Mayo Clin Proc. 72(5):475 abstract
  2. Katz MH. 1997. Maryland Med J. 46(5):239 abstract
  3. New Treatments for Actinic Keratosis. 2002. Med Let. 44(1133):57 abstract
  4. Yarosh D, Klein J, O'Connor A, et al. 2001. Lancet. 357(9260):926 abstract
  5. Efudex. 1993. Med Let. 35(907):97
  6. Thompson SC, et al. 1993. NEJM. 329:1147 abstract
  7. Sunscreens. 1999. Med Let. 41(1052):43 abstract
  8. Batta K, Goodyear HM, Moss C, et al. 2002. Lancet. 360(9332):521 abstract
  9. Imiquimod for Actinic Keratoses. 2004. Med Let. 46(1183):42 abstract
  10. Systemic Reactions to Imiquimod. 2004. Med Let. 46(1195):89