Skin Disorders in Older Adults: Age-Related Pigmentary Changes

ABSTRACT: Pigmentary changes occur in the skin with aging. During adulthood, the number of melanocytes decreases by about 10% to 20% per decade and the development of new melanocytic nevi also declines. Aging skin becomes more avascular and thus more marked by pallor. Long-term sun exposure produces a number of pigmentary changes, including idiopathic guttate hypomelanosis (which manifests as angular or circular, usually well-circumscribed, white or gray macules) and lentigines (commonly referred to as “liver spots”). The signs of cumulative photodamage include wrinkling, irregular thinning of the epidermis, blotchy hyperpigmentation, and telangiectasia formation. Drug-induced alterations in pigmentation are probably more common in the elderly because they take more medications than younger adults and they usually have had more protracted exposure to causal medications as a result of prolonged duration of use.

Key words: hyperpigmentation, hypo­pigmentation, yellow skin, yellow nail syndrome, gray hair, idiopathic guttate hypomelanosis, drug-induced hyperpigmentation, dermatoheliosis, Favre-Racouchot syndrome, lentigo, poikiloderma of dermatomyositis, poikiloderma of Civatte, Futcher line
_________________________________________________________________________________________________________________________________

A variety of changes occur in the skin as we age. The collagen content of the skin decreases by 1% per year after age 20, and the collagen fibers become more thick and brittle.¹ Ground substance and elastin fibers also decrease with aging. Changes in the dermal layer give the characteristic wrinkled, atrophic appearance of aging skin.

The number of melanocytes producing melanin per unit surface area of the skin decreases by about 10% to 20% per decade.² The development of new melanocytic nevi also declines, from a peak between ages 20 and 40 to near zero after age 70. Aging skin also becomes more avascular, making the skin of the elderly more marked by pallor.
__________________________________________________________________________________________________________________________________
Related Content
Skin Disorders in Older Adults: Eczematous and Xerotic Inflammatory Conditions, Part 1
Skin Disorders in Older Adults: Benign Growths and Neoplasms
__________________________________________________________________________________________________________________________________

In this 2-part article, I will review changes in the color and texture of the skin of the elderly that are normal and those that are pathologic. Here I discuss changes in skin pigmentation. In a coming issue, I will address changes in skin texture and quality.

YELLOW SKIN
With aging, the skin becomes paler and often more yellow. This yellowish cast to the skin occurs as a result of the optical effects of light on a thin epidermis, which more prominently reveals the yellow fat layer below (Figure 1). The yellowing of the skin is especially pronounced in persons with diabetes (perhaps because of glycosylation products) and is most noticeable on the palms and soles as a result of sparse competition with melanocytic pigment in these areas.

YELLOW NAILS
Yellow nail syndrome is most commonly associated with lung disorders and with lymphedema; it can also be related to lymphatic obstruction in cardiopulmonary disease. In yellow nail syndrome, nails are usually entirely yellow but occasionally only part of the nail plate is involved. Sometimes the nails lack a cuticle, grow slowly, and demonstrate onycholysis (Figure 2). Improvement in pulmonary function may improve the appearance of the nails.³

GRAY HAIR
Hair substantially grays in about 50% of persons by age 50, apparently because of the loss of melanocytes. Typically, the hair does not turn gray all at once but initially has a mix of black and gray hairs (“salt and pepper” hair) (Figure 3).

With aging, stem cells in the hair follicles stop making new melanocytes. Since there are no more melanocytes to create melanin, the hair turns gray (Figure 4). Studies have shown that the follicles in young adults have a high number of immature melanocytes, while those in middle-aged persons have fewer immature melanocytes. In the elderly, the follicles have no immature melanocytes.⁴

IDIOPATHIC GUTTATE HYPOMELANOSIS
Idiopathic guttate hypomelanosis (IGH) manifests as angular or circular, usually well-circumscribed, white or gray macules with a diameter of 1 to 3 mm; however, macules as large as 1 cm in diameter not infrequently occur. Typically, this very common, acquired, and benign eruption first manifests in middle age, but its incidence seems to increase with advancing age. It is associated with long-term sun exposure.

IGH is found almost equally in elderly men and women. It usually initially manifests on the legs of white women in early adult life. Later, IGH appears on other sun-exposed areas, such as the arms and the upper part of the back and chest (Figure 5). Histological examination reveals epidermal atrophy of the actinic type, a patchy decrease in or absence of melanocytes and melanin, flat rete ridges, and basket-weave hyperkeratosis. While there are reports that corticosteroids (either topical or intralesional), topical tretinoin, cryosurgery, and dermabrasion can “normalize” the hypopigmentation of IGH,⁵ I do not find treatment to be effective.

MEDICATION-INDUCED PIGMENTATION
Medication use can result in changes in skin pigmentation. Most of the pigmentation occurs in sun-exposed areas, which suggests an interaction between UV light and oral medications. Drug-induced skin pigmentation is a well-recognized effect of many different types of medications, including antimalarials, amiodarone, clofazimine, cytotoxic drugs, tetracyclines, psychotropic drugs, and minocycline.6 Photodistributed hyperpigmentation is associated with amiodarone, clofazimine, minocycline, phenothiazines, and imipramine, which produce similar patterns of progressive blue-gray pigmentation in sun-exposed areas. The blue-black hyperpigmentation caused by minocycline most commonly appears on the nose, sclera, and knees (Figure 6).

The pathogenesis of drug-induced hyperpigmentation depends on the causative medication and may involve an accumulation of melanin, accumulation of the drug or its metabolites, deposition of a drug-melanin complex, or deposition of iron following damage to the dermal vessels. Ingestion of heavy metal preparations that contain mercury, silver, bismuth, arsenic, lead, or gold can also contribute to hyperpigmentation.

Drug-induced alterations in pigmentation are probably more common in the elderly because they take more medications than younger adults and they usually have had more protracted exposure to causal medications as a result of prolonged duration of use. The treatment of medication-related pigmentation involves the discontinuation of the causal medication and the tincture of time. Sometimes the pigmentation does not disappear, which can be greatly distressing to patients.

DERMATOHELIOSIS
The signs of cumulative photodamage—also known as dermatoheliosis or photoaging—include wrinkling, irregular thinning of the epidermis, blotchy hyperpigmentation (Figure 7), and telangiectasia formation (Figure 8). Dermatoheliosis can also be marked by elastosis in plaques or nodules (nodular elastomas), colloid milia, and nodules on the helices of the ears in elderly men (weathering nodules), which on histological examination demonstrate a spur of fibrous tissue with a focus of cartilage metaplasia. Weathering nodules are associated with age and chronic UV exposure.⁷
Another manifestation of dermatoheliosis is Favre-Racouchot syndrome, an eruption consisting of multiple open and closed comedones that is associated with actinically damaged skin. Other clinical manifestations of solar elastosis include cutis rhomboidalis nuchae (Figure 9), actinic comedonal plaques, elastotic bands, and collagenous plaques of the hand. These yellow thickened plaques, nodules, and papules result from tangled masses of damaged elastin protein in the dermis.

LENTIGINES
Lentigines, commonly referred to as “liver spots,” manifest as brown macules (see Figure 5). The UV exposure that generates lentigines is cumulative and is not directly related to sunburn on a specific day. These benign lesions are attributable to the increased production of melanin as a consequence of long-standing sun exposure. The most common areas of involvement are the face, neck, upper chest, and arms. The number and extent of lentigines tend to increase with age.

POIKILODERMA
Poikiloderma is characterized by epidermal atrophy, hyperpigmentation, hypopigmentation, and telangiectasia, which produce a “mottled” appearance of the skin. It is most commonly associated with the following conditions:

• Mycosis fungoides (cutaneous T-cell lymphoma), also referred to as poikiloderma atrophicans vasculare (Figure 10).

• Dermatomyositis (Figure 11).

• Photodamage, usually but not always in the form of the poikiloderma of Civatte (Figure 12).

• Graft versus host disease.

• Radiation dermatitis (which often features only the presence of atrophy and telangiectases).

Rarer causes of poikiloderma that are not common in the elderly and thus will not be discussed in this article are topical corticosteroid overuse, arsenic toxicity, lupus erythematosus, hereditary sclerosing poikiloderma, Bloom syndrome, Cockayne syndrome, Goltz syndrome, Kindler syndrome, congenital dyskeratosis, congenital poikiloderma, Weary syndrome, and xeroderma pigmentosum.

Poikiloderma of dermatomyositis. Poikiloderma associated with dermatomyositis may occur on exposed skin, such as the extensor surfaces of the arm, the V of the neck, or the upper part of the back (the shawl sign). The erythema of poikiloderma of dermatomyositis is more marked than that of the poikiloderma of Civatte. It is also referred to as poikilodermatomyositis and is thought to be a later cutaneous sign of dermatomyositis. Other skin manifestations of dermatomyositis are described in my article “Skin Disorders in Older Adults: Papulosquamous and Bullous Diseases, Part 2” (CONSULTANT, April 2011, page 234).

Poikiloderma of Civatte. This eruption consists of cutaneous atrophy, erythema, and telangiectases. It is associated with brown and white macules and prominent hair follicles, which sometimes appear in a rippled array on the sides of the neck. The photo-protected regions of skin on the neck and upper chest under the chin are usually spared. Rarely, affected patients report mild burning, itching, and hyperesthesia.

Poikiloderma of Civatte is most common in middle-aged and elderly women, but it can also occur in men. The etiology appears related to UV light, photosensitizing chemicals in perfumes or cosmetics and, possibly, hormonal changes related to menopause or low estrogen levels.8 Histological examination reveals solar elastosis. I do not treat poikiloderma of Civatte; however, it has been effectively treated by intense pulsed-light, which is broad spectrum and noncoherent.⁹

FUTCHER LINES
About 25% of dark-skinned persons of African descent exhibit sharply demarcated pigmentary lines either at the anterolateral upper arm or posteromedial part of the lower limbs.¹⁰ These are known as Futcher lines (Figure 13). These lines seem to become less pronounced with age but can still be noted in the elderly.