In elderly Americans, most changes in the skin's appearance are the result of chronic UV radiation from sunlight and occur most prominently on exposed areas. This process, known as photoaging, differs clinically, histologically, and physiologically from intrinsic aging, although most patients and many physicians do not make the distinction. Elderly persons whose pigmentation or lifestyle protects them from sun damage often look younger than their chronologic age.
Some geriatric skin diseases, such as skin cancer, occur almost exclusively in photoaged skin.
Fine and coarse wrinkling, irregular mottled pigmentation, lentigines (brown macules), roughness, sallowness, and telangiectases characterize photoaged skin. Poorly defined rough, red dysplastic areas of actinic keratoses are associated with more severe damage and a higher risk of skin cancer. (see page 1276) The overall picture may be hypertrophic or atrophic, depending on the patient's complexion and the severity of the sun damage. Actinic purpura (also called Bateman's, solar, or senile purpura) appear as nonpalpable ecchymotic areas usually on the extensor forearms of the elderly and are thought to represent extravasation of red blood cells from friable vessels in sun-damaged connective tissue. Thrombocytopenia is often suspected, but platelet function and quantity are not altered. Depigmented stellate pseudoscars on the extremities also indicate photoaging. Cigarette smoking exacerbates the coarse wrinkling of photoaging.
Histologically, photoaged skin changes include epidermal dysplasia and atypia, decreased numbers of Langerhans' cells, and striking dermal elastosis (deposits of abnormal elastic fibers). Loss of immunologic and inflammatory responsiveness is greater than that caused by intrinsic aging alone.
Because damage due to photoaging is cumulative, preventive measures are most successful if begun during childhood. However, evidence strongly suggests that avoiding sun exposure and regularly using sunscreen, even after marked actinic damage, achieves considerable clinical improvement.
Patients of all ages should be encouraged to wear hats, keep their shoulders covered, and apply sunscreen before going out, as part of their daily routine. Sunscreens with a sun protection factor (SPF) of >= 15 should be applied liberally over all exposed areas and reapplied after swimming or washing. Patients should especially avoid going outdoors unprotected when UV radiation is strongest, around midday. Because sunscreens also block UV-induced vitamin D formation in the skin, elderly patients should be advised to consume vitamin D-fortified milk or vitamin D supplements to safeguard against osteomalacia. Moreover, cigarette smoking should be discouraged for dermatologic reasons: smoking exacerbates photoaging in a dose-related fashion.
Topical retinoin (all-trans-retinoic acid) is useful in treating photoaging. Improvements in global appearance, fine and coarse wrinkling, roughness, mottled hyperpigmentation, and lentigines occur within 4 to 6 months. New capillary formation, collagen synthesis, anchoring fibril formation, and regularization of epidermal melanin distribution and disappearance of premalignant actinic keratoses may also occur.
Initial treatment consists of applying tretinoin cream 0.05% once daily at bedtime. The patient should be warned that mild erythema and peeling (retinoid dermatitis) will occur, although older adult skin is usually less prone to this problem than younger adult skin. If necessary, the regimen can be changed to every other day until tolerance improves. After 8 to 12 months, a maintenance regimen of one to three applications a week may be instituted.
A dermatologist or plastic surgeon may surgically treat photoaging with collagen injections, chemical peels, rhytidectomy (face-lift), and various forms of laser surgery. Before undergoing such elective surgery, elderly patients should be thoroughly screened for cardiovascular, renal, and pulmonary diseases that might increase the risk of complications. Patients should also be advised that the healing time for procedures such as dermabrasion and chemical peels tends to be longer than that for younger adults.
Laser removal of vascular ectasias or benign pigmented lesions is usually very well tolerated, and medical evaluation is rarely indicated before undertaking these procedures.
In general, medical and surgical treatments for photoaging are not covered by third-party payers.
FROM THE MERCK MANUAL OF GERIATRICS
(Gravitational Eczema; Varicose Eczema)
Inflammation associated with venous hypertension in the lower legs.
The pathogenesis is unknown. Stasis dermatitis may be exacerbated by edema, contact dermatitis due to use of topical medications, and scratching. Continued venous hypertension, even in the absence of stasis dermatitis, is a risk factor for venous ulceration.
Affected skin in the lower legs is eczematous and usually is edematous, with hemosiderin pigmentation and dilatation of superficial venules around the ankles.
The affected limb must be elevated at least to heart level to facilitate venous return. Compression can be continuous or intermittent and should be increased over days to weeks to 30 to 40 mm Hg of pressure with use of surgical tube stockings and elastic bandages. Compression therapy may need to be continued even if the condition appears to have improved. However, aggressive compression may lead to ischemia in patients with arterial insufficiency, particularly diabetics. Thus, if arterial insufficiency is likely, ankle-brachial indexes and other vascular studies should be performed before initiating compression therapy.
A low- to mid-potency topical corticosteroid (eg, hydrocortisone 1% ointment or triamcinolone 0.1% ointment) may help relieve pruritus, scaling, and inflammation. Any possible contact allergen (eg, bacitracin, neomycin, fragrance) should be avoided.
Bowen's Disease (C'est probablement pas ton cas)
(Squamous Cell Carcinoma In Situ)
Premalignant lesions, often due to arsenic exposure, that may give rise to squamous cell carcinomas.
These lesions predominantly affect the elderly. Sun exposure is a probable contributing cause in many patients, although some patients may have a history of arsenic exposure (either medicinal or occupational). Human papillomavirus (HPV) may also play an etiologic role.
Symptoms and Signs
Lesions consist of persistent, erythematous, scaly plaques with well-defined margins. Lesions can occur anywhere on the skin or mucous membranes and may be single or multiple.
Prognosis and Treatment
Multiple lesions are associated with an increased incidence of internal malignancies and mandate close follow-up. Treatment options include excision, cryotherapy with liquid nitrogen for 15 to 20 seconds, curettage and cautery, and topical 5-fluorouracil.
(Hutchinson's Freckle)
Premalignant lesions that may give rise to lentigo maligna melanoma.
These lesions are pigmented macules, often > 1 cm in diameter with an irregular border, occurring mainly on sun-exposed areas, particularly the cheeks and forehead. Lesions characteristically have brown, black, red, and white areas and become more irregularly pigmented over time. Gradually, lesions expand in a prolonged radial (superficial) growth phase. Nodule development, with or without bleeding, signifies invasion and conversion to lentigo maligna melanoma. (see page 1282)
Risk of conversion to melanoma by age 75 is estimated at 1 to 2%.
Patients should undergo regular follow-up examinations for signs of conversion to melanoma. Some authorities suggest cryotherapy or argon laser therapy to decrease the number of abnormal melanocytes and thus, theoretically, to reduce the risk of developing melanoma. However, both of these procedures have a high recurrence rate. Because conversion to melanoma is usually relatively slow, the decision to excise lentigo maligna should be based on several factors, including the size and location of the lesion, which determines the complexity of the procedure required, and the patient's life expectancy and comorbidities.
When too many mast cells exist in a person's body, the additional chemicals can cause: •Bone or muscle pain •Abdominal discomfort •Nausea and vomiting •Stomach ulcers •Diarrhea •Skin lesions •Episodes of very low blood pressure and faintness •Shock
Doctors can diagnose urticaria pigmentosa by seeing the characteristic lesions which are dark-brown and fixed. A small skin sample may help confirm the diagnosis. By taking a tiny piece of tissue from a different organ, such as the bone marrow, the doctor can diagnose systemic mastocytosis. Using special techniques on a bone marrow sample, the doctor looks for an increase in mast cells. Another sign of this disorder is high levels of certain mast-cell chemicals and proteins in a person's blood and sometimes in the urine.
Several medicines help treat the symptoms of mastocytosis.: 1) Antihistamines to work against mast cell chemicals 2) Medicines to relieve cramping in the intestines 3) Medicines help treat other signs and symptoms of mastocytosis, including: •itching and other skin reactions •ulcer-like symptoms •low blood pressure •inability to take up nutrients from food
In rare cases in which mastocytosis is cancerous or associated with a blood disorder, the patient may have to use steroids and/or chemotherapy.
Research
National Institute of Allergy and Infectious Diseases (NIAID) scientis