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Contents | Director | One | Two | Article | Topic 1 | Topic 2 | EKG | Rad 1 | Rad 2 Albany Medical Review - May 2002 |
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Ahmer Younas , MD
The incidence of malignant melanoma has been increasing dramatically, largely due to an increase in recreational sun exposure. If the incidence continues to increase at the present rate projections suggest that by the year 2000, 1 in 75 Americans will develop melanoma. Risk factors include fair complexions, red or blond hair, blue eyes, freckles, sunlight (ultraviolet B range) particularly sunburns in early life, as well as precursor lesions such as clinically atypical mole or dysplastic nevi. A familial pattern of inheritance has been demonstrated (1 in 10 melanoma patients have an affected family member). A mutation in the CDKN2 gene on chromosome 9 can underlie susceptibility to melanoma. There are four types of melanomas. More specifically: superficial spreading melanoma, lentigo maligna melanoma, acral lentiginous melanoma and nodular melanoma. The first three have a radial growth phase in which there is an increase in size superficially with minimal penetration or so called vertical growth. This stage is amenable to cure by surgery. Nodular melanoma does not have a recognizable radial growth phase and usually presents as a deeply invasive lesion, capable of early metastasis. Melanoma lesions can be remembered by the ABCD'S of melanoma. Asymmetry is a common feature of melanoma, whereas most benign tumors tend to be symmetric in shape. Border irregularity, although not pathognomonic for melanoma, is a typical finding. Color variegation is an important diagnostic feature. Black, blue, and red hues are commonly present. Colors of the brown spectrum (tan to dark brown) are characteristic of benign lesions (nevi, seborrheic keratoses) and are rarely part of a melanoma unless it arises from a preexisting nevus of that color. Diameter of melanoma tends to enlarge with time, whereas benign lesions remain stable. Any lesion that enlarges significantly over a period of 1 to 3 months should be evaluated. Symptoms, such as bleeding and ulceration, may be present in larger lesions. The most important prognostic factor is the stage at the time of presentation. Five-year survival for clinical stages I and II (primary tumor; no clinical evidence of disease elsewhere) is about 85%. For clinical stage III (clinically palpable regional nodes that contain tumor), the 5-year survival is about 50% when only one node is involved and about 15 to 20% when four or more nodes are involved. The 5-year survival for clinical stage IV (disseminated disease) is <5%. Most tumors are diagnosed in the stage I and II stage and the patients' prognosis will depend on the thickness of the primary tumor (Breslow's staging). Another prognostic scheme for clinical stages I and II melanoma, is Clark's staging, which is based on the anatomic level of invasion in the skin. Level I is intraepidermal (in situ); level II penetrates the papillary dermis; level III spans the papillary dermis; level IV penetrates the reticular dermis; and level V penetrates into the subcutaneous fat. The 5-year survival for these stages averages 100, 95, 82, 71, and 49%, respectively. Melanoma spreads via both lymphatic channels and the blood stream, with early regional lymph node involvement. Ironically, elective lymph node dissection of draining lymph node basins has not showed any overall survival benefit in four large, randomized, prospective studies.[1] Its routine use exposes patients to the morbidity of lymphedema and nerve injury. Currently lymphatic mapping with sentinel node biopsy (the identification of the theoretical first node involved) and subsequent lymph node dissection of all the nodes has been widely practiced but remains a topic of controversy. Proponents state that a positive sentinel node biopsy identifies patients who would benefit from an elective lymph node dissection and correlates well with the prognosis. Opponents of the procedure agree with the procedure's prognostic value but point to studies that refute the utility of sentinel node biopsy in every patient. For example, a study by Nieweg[2] demonstrated that 80 percent of patients would not benefit from a sentinel node biopsy because they have no node metastasis to begin with. Metastasis is present in the other 20 percent but 10 percent already had distant metastasis. This group would not benefit from a complete lymph node dissection. Therefore, it is ten percent of patients with disease limited to the regional lymph node that may be cured with an elective lymph node dissection. One third of this group can still be cured at a later date when the node becomes clinically palpable. If we assume no false negatives no greater than 7 percent increase in survival benefit is possible.[3] The false negative rate for sentinel node biopsy is 11-12%. Opponents of sentinel node biopsy state the procedure is based on certain presumptions. First, not all melanoma spreads exclusively through the lymphatic channels. Patients may have distant metastasis and be falsely reassured by a negative sentinel node biopsy. Also, the consistency of lymphatic drainage is unreliable on the head and neck, midline of the trunk and in the inguinal node.[4] Patients with lesions <1 mm thick have an excellent prognosis and need no node dissection; at the other extreme, patients with lesions >4 mm thick have such a high risk for distant metastases that elective node dissection may not alter the ultimate clinical outcome. It is the subset of patients with intermediate thickness who stand to benefit most from the procedure. Currently there are large randomized trials underway of elective lymph node dissection after a positive sentinel node biopsy that will shed more light on the utility of sentinel node biopsy.
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30.01.2002 |
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