Incidence of malignant melanoma, a neoplasm that arises from melanocytes, has increased by 50% in the past 20 years. In particular, an increase in incidence of melanoma in situ suggests earlier detection. The disorder varies in different populations but is about 10 times more common in white than in nonwhite populations. The four types of melanomas are superficial spreading melanoma, nodular malignant melanoma, lentigo maligna melanoma, and acral-lentiginous melanoma.
Melanoma spreads through the lymphatic and vascular systems and metastasizes to the regional lymph nodes, skin, liver, lungs, and central nervous system (CNS). Its course is unpredictable, however, and recurrence and metastasis may occur more than 5 years after resection of the primary lesion. If it spreads to regional lymph nodes, the patient has a 50% chance of survival.
The prognosis varies with tumor thickness. Generally, superficial lesions are curable, whereas deeper lesions tend to metastasize. The Breslow Level Method measures tumor depth from the granular level of the epidermis to the deepest melanoma cell. Melanoma lesions less than 0.76 mm deep have an excellent prognosis, whereas deeper lesions (more than 0.76 mm deep) are at risk for metastasis. The prognosis is better for a tumor on an extremity (which is drained by one lymphatic network) than for one on the head, neck, or trunk (which is drained by several networks).
Several factors may influence the development of melanoma:
❑ Excessive exposure to ultraviolet light. Melanoma is most common in sunny, warm areas and commonly develops on parts of the body that are exposed to the sun. A person who has a blistering sunburn before age 20 has twice the risk of developing melanoma.
❑ Skin type. Most persons who develop melanoma have blond or red hair, fair skin, and blue eyes; are prone to sunburn; and are of Celtic or Scandinavian descent. Melanoma is rare among blacks; when it does develop, it usually arises in lightly pigmented areas (the palms, plantar surface of the feet, or mucous membranes).
❑ Autoimmune factors. Genetic and autoimmune effects may be causes.
❑ Hormonal factors. Pregnancy may increase risk and exacerbate growth.
❑ Family history. A person with a family history of melanoma has eight times the risk of developing the disorder.
❑ History of melanoma. A person who has had one melanoma has 10 times the risk of developing a second.
Common sites for melanoma are on the head and neck in men, on the legs in women, and on the backs of people exposed to excessive sunlight. Up to 70% arise from a preexisting nevus. They rarely appear in the conjunctiva, choroid, pharynx, mouth, vagina, or anus.
Suspect melanoma by using the ABCD Rule of Melanoma:
Asymmetry of borders
Bleeding or crusting
Color blue/black or variegated
Diameter greater than 2¼" (5.7 cm).
Each type of melanoma has special characteristics:
❑ Superficial spreading melanoma arises on chronically sun-exposed areas, such as the legs and upper back. Characteristically, it has a red, white, and blue color over a brown or black background and an irregular, notched margin. Its surface is irregular, with small, elevated tumor nodules that may ulcerate and bleed. Horizontal growth may continue for many years; when vertical growth begins, the prognosis worsens.
❑ Nodular malignant melanoma occurs more commonly in men and can be located anywhere on the body. It’s the most frequently misdiagnosed melanoma because it resembles a blood blister or polyp.
❑ Lentigo maligna melanoma commonly develops under the fingernails, on the face, and on the backs of the hands. This lesion looks like a large (1" to 2" [2.5- to 5-cm]), flat freckle of tan, brown, black, whitish, or slate color, and has irregularly scattered black nodules on the surface. It develops slowly, usually over many years, and eventually may ulcerate.
❑ Acral-lentiginous melanoma is more common in Asian and Black individuals.
A skin biopsy with histologic examination can distinguish malignant melanoma from a benign nevus, seborrheic keratosis, and pigmented basal cell epithelioma; it can also determine tumor thickness. Physical examination, paying particular attention to lymph nodes, can point to metastatic involvement.
Baseline laboratory studies include a complete blood count with differential, erythrocyte sedimentation rate, platelet count, liver function studies, and urinalysis. Depending on the depth of tumor invasion and metastasis, baseline diagnostic studies may also include a chest X-ray and computed tomography (CT) scan of the chest and abdomen. Signs of bone metastasis may call for a bone scan; CNS metastasis, a CT scan of the brain.
A patient with malignant melanoma requires surgical resection to remove the tumor. The extent of resection depends on the size and location of the primary lesion. Closure of a wide resection may require a skin graft. Surgical treatment may also include regional lymphadenectomy. Cutaneous melanoma is nearly 100% curable by excision if diagnosed when malignant cells are confined to the epidermis.
Deep primary lesions may merit adjuvant chemotherapy and biotherapy or immunotherapy to eliminate or reduce the number of tumor cells. Radiation therapy is usually reserved for metastatic disease; gene therapy may also be a treatment option.
Regardless of the treatment method, melanomas require close, long-term follow-up to detect metastasis and recurrences.
UNDER STUDY: Nerve fiber loss may provide an explanation for the invisible neurologic deficits experienced by many patients with MS. The axons decide the presence or absence of function. Loss of myelin doesn’t correlate with loss of function.
The prognosis varies. MS may progress rapidly,. It can disable the patient by early adulthood, and it also holds the potential to cause death within months of onset. However, 70% of patients lead active, productive lives with prolonged remissions.
Terms to describe MS forms include:
❑ relapsing-remitting — clear relapses (or acute attacks or exacerbations) with full recovery or partial recovery and lasting disability. Between the attacks, there’s no worsening of the disease. This type accounts for up to 90% of all cases.
❑ primary progressive — steady progression or worsening of the disease from the onset with minor recovery or plateaus. This form is uncommon and may involve different brain and spinal cord damage than other forms.
❑ secondary progressive — begins as a pattern of clear-cut relapses and recovery but becomes steadily progressive and worsens between acute attacks.
❑ progressive relapsing — steadily progressive from the onset but also has clear acute attacks. This form is rare.
The exact cause of MS is unknown, but current theories suggest a slow-acting or latent viral infection and an autoimmune response. Other theories suggest that environmental and genetic factors may also be linked to MS.
Emotional stress, overwork, fatigue, pregnancy, and acute respiratory tract infections may precede the onset of this illness.
MS usually begins between ages 20 and 40 (average age of onset is 27). It’s more common in women than in men. Incidence is low in Japan; it’s generally higher among urban populations and upper socioeconomic groups. A family history of MS and living in a cold, damp climate increase the risk.
Signs and symptoms of MS depend on the extent and site of myelin destruction, the extent of remyelination, and the adequacy of subsequent restored synaptic transmission.
Signs and symptoms in MS may be transient, or they may last for hours or weeks. They may wax and wane with no predictable pattern, vary from day to day, and be bizarre and difficult for the patient to describe.
In most patients, visual problems and sensory impairment — such as burning, pins and needles, and electrical sensations — are the first signs that something may be wrong.
Other characteristic changes include:
❑ ocular disturbances — optic neuritis, diplopia, ophthalmoplegia, blurred vision, and nystagmus
❑ muscle dysfunction — weakness, paralysis ranging from monoplegia to quadriplegia, spasticity, hyperreflexia, intention tremor, balance problems, and gait ataxia
❑ urinary disturbances — incontinence, frequency, urgency, and frequent infections
❑ bowel disturbances — involuntary evacuation or constipation
❑ fatigue — typically the most debilitating symptom.
Associated signs and symptoms include poorly articulated or scanning speech and dysphagia. Signs and symptoms may be so mild that the patient is unaware of them or so intense that they’re debilitating.
Because early symptoms may be mild, years may elapse between onset of the first signs and the diagnosis. Diagnosis of this disorder requires evidence of two or more neurologic attacks. Periodic testing and close observation of the patient are necessary, perhaps for years, depending on the course of the disease.
The following tests may be performed:
❑ Magnetic resonance imaging may detect MS lesions.
❑ EEG is abnormal in one-third of patients.
❑ Lumbar puncture shows an elevated gamma globulin fraction of immunoglobulin G but normal total cerebrospinal fluid (CSF) protein levels. An elevated CSF gamma globulin level is significant only when serum gamma globulin levels are normal; it reflects hyperactivity of the immune system due to chronic demyelination. In addition, the white blood cell count in CSF may be elevated.
❑ Electrophoresis can detect oligoclonal bands of immunoglobulin in CSF. Present in most patients, they can be found even when the percentage of gamma globulin in CSF is normal.
A differential diagnosis must rule out spinal cord compression, foramen magnum tumor (which may mimic the exacerbations and remissions of MS), multiple small strokes, syphilis or another infection, thyroid disease, and chronic fatigue syndrome.
The aim of treatment is threefold: to treat the acute exacerbation, the disease process, and the related signs and symptoms.
I.V. methylprednisone followed by oral prednisone has been shown to be effective for speeding recovery for acute attacks. Antispasmolytics may be used to reduce muscle spasticity. Cholinergics are effective for urinary problems, antidepressants for mood and behavior symptoms, and amantadine for fatigue.
Interferon and glatiramer (a combination of four amino acids) may reduce the frequency and severity of relapses and slow central nervous system damage. These medications, which are available for relapsing-remitting MS, are used to delay disability and decrease injury to the nervous system.
❑ Spasticity occurs as a result of opposing muscle groups relaxing and contracting at the same time. Stretching and range-of-motion exercises, coupled with correct positioning, are helpful in relaxing muscles and maintaining function.
UNDER STUDY: Immunologic and molecular biological techniques now available in specialized medical centers facilitate accurate prenatal and postnatal diagnosis of Duchenne’s and Becker’s muscular dystrophies. These techniques also help to identify a person as a carrier. In addition, these newer techniques are replacing muscle biopsy and serum creatine kinase tests as diagnostic procedures.
To date, scientists have found no treatment that can stop the progressive muscle impairment of muscular dystrophy. However, orthopedic appliances as well as exercise, physical therapy, and surgery to correct contractures can help preserve the patient’s mobility and independence. Treatment for myotonia congenita includes symptomatic relief with mexiletine, phenytoin, procainamide, and quinine.
Family members who are carriers of muscular dystrophy should receive genetic counseling regarding the risk of transmitting this disease.
❑ Comprehensive long-term care and follow-up, patient and family teaching, and psychological support can help the patient and family deal with this disorder.
❑ When respiratory involvement occurs in Duchenne’s muscular dystrophy, encourage coughing, deep-breathing exercises, and diaphragmatic breathing. Teach parents how to recognize early signs of respiratory complications.
❑ Encourage and assist with active and passive range-of-motion exercises to preserve joint mobility and prevent muscle atrophy.
❑ Advise the patient to avoid long periods of bed rest and inactivity; if necessary, limit his TV viewing and other sedentary activities.
❑ Refer the patient for physical therapy. Splints, braces, surgery to correct contractures, trapeze bars, overhead slings, and a wheelchair can help preserve mobility. A footboard or high-topped sneakers and a foot cradle increase comfort and prevent footdrop.
❑ Because inactivity may cause constipation, encourage adequate fluid intake, increase dietary bulk, and obtain an order for a stool softener.
❑ Because such a patient is prone to obesity because of reduced physical activity, help him and his family plan a low-calorie, high-protein, high-fiber diet.
CLINICAL TIP: Always allow the patient plenty of time to perform even simple physical tasks because he’s likely to be slow and awkward.
❑ Encourage communication among family members to help them deal with the emotionalstrain this disorder produces. Provide emotional support to help the patient cope with continual changes in body image.
❑ If necessary, refer adult patients for sexual counseling.
❑ Refer those who must acquire new job skills for vocational rehabilitation. (Contact the Department of Labor and Industry in your state for more information.)
❑ For information on social services and financial assistance, refer patients and their families to the Muscular Dystrophy Association.
❑ Refer family members for genetic counseling.
Review other book chapters online related to Melanoma:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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