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General Reference ⬇

Nejm 2003;349:2233; 1991;325:171; Ann IM 1985;102:546; Jama 1984;251:1864

Pathophys and Cause ⬆ ⬇

Cause:

UV irradiation damage esp. in childhood, even in cases of ocular melanoma (Nejm 1985;313:789); high-intensity burns that reach melancocytes worse than chronic sun exposure (Nejm 1999;340:1341)

Congenital nevi: melanoma occurs w highest frequency in those >20 cm diameter at birth; most feel risk to some degree even <2 cm but some say no risk there (Jama 1997;277:1439)

Atypical mole syndrome (AMS) (NIH Consensus Statement 1992;10:1) or older term, dysplastic nevus syndrome (DNS) (Nejm 1985;312:91; Ann IM 1985;102:458—both with pictures); on short arm of chromosome 1 (Nejm 1989;320:1367)

Epidemiology ⬆ ⬇

8th most common cancer in US (20th in 1985) (Ann IM 1996;125:369); 1/80 lifetime risk in US

Increased in Celts, especially those with red hair

Congenital nevi occur in ~1% of pop, though rarely >20 cm diameter

AMS can be autosomal dominant or sporadic; 2-5% prevalence; of familial type, 100% will get in lifetime and account for 10% of all melanoma; 18% of sporadics will get in lifetime and account for 30-50% of all melanomas; increased prevalence in Hodgkin's patients (Ann IM 1985;102:37); but a few atypical nevi do not imply AMS although incidence of melanoma is may be higher (Jama 1997;277:1439)

Signs and Symptoms ⬆ ⬇

Sx:Black, blue, or gray lesions increasing in size; pain; pruritus; bleeding; notched borders; asymmetric

Si: Central black (or blue-gray, "hurricane gray") papule or nodule in center of lentigo, dysplastic nevus; disorderly color, surface, and edges; inflamed; occasional satellites; does not dimple if squeezed unlike dermatofibromas (Nejm 1976;294:1511). Amelanotic melanomas most often on soles

ABCDE criteria (Jama 2004;292:2771): Asymmetry, Borders irregular, Color variable, Diameter >6 mm, Evolving over time; each has a sens and specif of 60-90%

Course ⬆ ⬇

Stage I: survival by thickness, <0.75 mm has a 96% 5-yr survival, >4 mm has a 47% 5-yr survival

Stage II: nodal mets, 36% 5-yr survival

Stage III: distant mets, 5% 5-yr survival

Complications ⬆ ⬇

2nd or 3rd primary melanoma, especially in AMS (DNS)

r/o other melanotic lesions including TINEA NIGRA PALMARIS(Nejm 1970;283:1112), junctional, compound, or dermal nevi which may have halos; LENTIGO MALIGNA(only a few bizarre melanocytes), seen most often in elderly, in sun-exposed areas, good prognosis; NEVUS OF OTA, benign melanosis of eye and surrounding skin in 1st and 2nd branches of trigeminal nerve, seen in 1/200 Asians, rx w laser (Nejm 1994;331:1745)

Lab and Xray ⬆ ⬇

Lab: Path:Excisional (or incisional or punch if too large; never curette) biopsy; melanoma is staged by thickness of tumor. Reverse transcriptase PCR study of sentinel nodes find tumor in 1/2 of nodes neg by standard path techniques and recurrence rates are higher in those pts (Jama 1998;280:1410)

Xray:CT and gallium scanning especially good for metastases (Ann IM 1982;97:694)

Treatment ⬆

Rx:(Nejm 2004;351:998; NIH Consensus Statement 1992;10:1)

Prevent by excision of congenital nevi, at least those >20 cm or those that are changing; and of changing atypical moles; photographs can help to follow both

of lesions, excision with 1-2+ cm margins (Nejm 2004;350:757, 823; Jama 2001;285:1819) though 1-2 mm adequate for diagnostic excisions. If positive, then sentinel node bx (Nejm 2006;355:1307, 1370)

of metastatic disease: follow w hx, PE and chest xray to monitor for mets (Jama 1995;274:1703)

  • Interferon alpha.gif 2 iv may help (Ann IM 1985;103:32)
  • Radiation helps palliate local lesions
  • Chemotherapy by isolated perfusion of extremities being tried
  • Adoptive immunotherapy with tumor-infiltrating lymphocytes (lymphocyte-activated killer cells) + interleukin 2 helps 5-10% to remission when widely metastatic disease (Nejm 1990;323:570; Med Let 1990;32:85)
  • dacarbazine + tamoxifen (Nejm 1992;327:516)