Am J Clin Dermatol 2009; 10 (2): 73-86

REVIEW ARTICLE 1175-0561/09/0002-0073/$49.95/0

ª 2009 Adis Data Information BV. All rights reserved.

Clinical Implications of Aging Skin

Cutaneous Disorders in the Elderly
Miranda A. Farage,1 Kenneth W. Miller,1 Enzo Berardesca2 and Howard I. Maibach3
1 The Procter & Gamble Company, Winton Hill Business Center, Cincinnati, Ohio, USA
2 San Gallicano Dermatological Institute, Rome, Italy
3 Department of Dermatology, University of California, San Francisco, California, USA

Contents

Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
1. Vascular Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
1.1 Stasis Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
1.2 Pressure Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
1.3 Rosacea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
2. Cutaneous Expression of Autoimmune Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
2.1 Bullous Pemphigoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
2.2 Mucous Membrane Pemphigoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
2.3 Pemphigus Vulgaris . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
2.4 Paraneoplastic Pemphigus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
2.5 Lichen Sclerosus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
3. Viral Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
3.1 Herpes Zoster (Shingles) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
4. Inflammatory Dermatoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
4.1 Xerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
4.2 Pruritus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
4.3 Eczema. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
4.4 Contact Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
4.5 Seborrheic Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
5. Management of Cutaneous Disorders in the Elderly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
6. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

Abstract Aging skin undergoes progressive degenerative change. Structural and physiologic changes that occur as a
natural consequence of intrinsic aging combined with the effects of a lifetime of ongoing cumulative extrinsic
damage and environment insult (e.g. overexposure to solar radiation) can produce a marked susceptibility to
dermatologic disorders in the elderly. As skin ages, the vasculature progressively atrophies. The supporting
dermis also deteriorates, with collagen and elastin fibers becoming sparse and increasingly disordered. These
changes leave the elderly increasingly susceptible to both vascular disorders such as stasis dermatitis and skin
injuries such as pressure ulcers and skin tears, with a steadily decreasing ability to effect skin repair.
A parallel erosion of normal immune function produces higher levels of autoimmune skin disorders such
as bullous pemphigoid, benign mucous membrane pemphigoid, paraneoplastic pemphigoid, and pemphigus
vulgaris. Lichen sclerosus, an autoimmune disorder often occurring in the genital area in older women, is not
common but is an important development because of the potential for substantial discomfort as well as
serious complications. The prevalence of polypharmacy in this population increases the risk for autoimmune
drug reactions, and diagnosis should be undertaken with an awareness that polypharmacy in this population
creates a greatly increased susceptibility to drug eruptions that can mimic other cutaneous disorders.
74 Farage et al.

Immunologic senescence in the elderly also sets the stage for potential reactivation of the Varicella zoster
virus, in which initial dermatologic involvement expands into the major sensory ganglia. Known as shingles, this
disorder can be excruciatingly painful with the potential to cause blindness if the optic nerve becomes involved.
Dermatoses such as xerosis, pruritus, and eczema are also widespread in the elderly, create substantial
suffering in those afflicted, and often prove recalcitrant to treatment. Individual susceptibility to specific
types of contact dermatitis changes over the lifetime, and seborrheic dermatitis is substantially more prev-
alent in the elderly.
It is not uncommon for older patients to have multiple impairments, with the potential for cognitive
dysfunction as well as impaired vision, hearing, or mobility. In addition, they may not have adequate housing
or nutrition, or the financial resources necessary for adequate compliance. Physicians must take into con-
sideration the patient’s physical ability to comply with the recommended therapy as well as socioeconomic
factors that may impact on compliance. Simple topical regimens are preferable wherever possible in order to
maximize compliance and, therefore, efficacy. Extra effort may be necessary to ensure that instructions are
accurately followed and that ongoing compliance with the regimen prescribed is actually achieved.
Management of dermatologic disorders in the elderly is often less than optimal, due to the fact that the
special needs and limitations of this population are not adequately considered. Treatments should consider the
intrinsic differences between younger and older patients that may impact on diagnosis and therapy choice. The
aged patient is often afflicted with numerous co-morbidities that can influence the choice of therapy. Skin
integrity in the elderly is compromised, and safety concerns are increased with the long-term use of any
medication prescribed. In addition, the prevalence of polypharmacy in the aged population substantially
increases the risk of cutaneous drug reactions, which can profoundly complicate accurate diagnosis of der-
matologic disorders. The aged population also needs to be more closely monitored because of increased
fragility of the skin and the physical limitations that may hinder compliance with prescribed regimens.

The human integument, comprising one-sixth of the total
bodyweight, is the most visible indicator of age.[1] A sophisticated
and dynamic organ, the skin acts as a barrier between the internal
environment and the world outside, yet has numerous functions
that extend far beyond that role,[2] including homeostatic reg-
ulation; prevention of percutaneous loss of fluid, electrolytes, and
proteins; temperature maintenance; sensory perception; and
immune surveillance.[3]
Aging is a complex multifactorial phenomenon in which
progressive intrinsic changes in the skin combine synergistically
with cumulative environment insults (table I) to produce both
structural and functional disturbances. In a survey of healthy
older adults (aged 50–91 years), every individual had at least one
dermatologic complaint, with nearly two-thirds found to have a
medically significant disorder.[4] Although rarely fatal, cutaneous
diseases carry with them significant morbidity and the potential
to greatly decrease the patient’s quality of life.[5] It is estimated
that 7% of all physician visits by the elderly involve skin dis-
orders,[6] and that treatable (but often untreated) cutaneous
diseases occur in >50% of otherwise healthy older adults.[6]
Furthermore, as the proportion of the US population in their
later years continues to increase, the dermatologic problems
of this population will also continue to increase in medical
importance.[5]
The cumulative intrinsic and extrinsic effects of aging skin,
a multifunctional organ, have a wide spectrum of clinical ex-
pression. Common nonspecific and inflammatory dermatoses
such as xerosis, eczema, psoriasis, seborrheic dermatitis, and
contact dermatitis result largely from progressive intrinsic
changes in the aging skin. Xerosis and pruritus are the most
common dermatologic afflictions in the elderly, accounting for as
many as 80% of dermatologic complaints among the aged po-
pulation.[11] Inflammatory dermatoses such as eczema, psoriasis,
and seborrheic dermatitis are also very common.[11,12] Although
rarely fatal, these disorders can produce substantial morbidity in
those afflicted and significantly reduce quality of life in the latter
years of life.[12] The cumulative effects of environment insults,
particularly exposure to solar radiation, also contribute to the
marked increase in neoplastic diseases in old age, an aspect that
has been reviewed separately.[13]
The progressive deterioration of the integument that occurs
with age, however, has sequelae beyond the direct effects of
xerosis or basal cell carcinoma. As the skin ages, the number of
collagen and elastin fibers in the dermis decreases and total skin
thickness decreases,[14] a result of flattening of the dermal papillae
at the epidermal-dermal junction. These degenerative changes in
the structure of aging skin act to erode the cushioning of and
support for the dermal vasculature, giving rise to increasing

ª 2009 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2009; 10 (2)
Clinical Implications of Aging Skin 75

Table I. Clinical implications of aging skin[6-10]

Physiologic change Pathologic change
Thinning of epidermis and dermis Increased vulnerability to mechanical
trauma, especially shearing and friction
Flattening of dermal papillae Increased risk of blister formation
Slowdown in turnover rate of epidermis; decrease in ratio Delayed cellular migration and proliferation
of proliferative-to-differentiated keratinocytes Decreased wound contraction
Decrease in elastin fibers Loss of elasticity
Decrease in vascularity and supporting Fragile, easily broken blood vessels
structures in dermis Decreased wound capillary growth
Decrease in vascular plexus, blunted capillary loops Loss of thermoregulatory ability
Changes in and loss of collagen and elastin fibers Decreased tensile strength, lower layers
more susceptible to injury
Delayed collagen remodelling
Impaired immune response Impaired inflammatory response
Impaired delayed hypersensitivity reaction
Decreased production of cytokines
Decrease in numbers of Langerhans cells
Impaired neurologic responses Reduced sensation
Decreased skin thickness Loss of cushioning and support
Decreased vitamin D precursor production
Atrophy of sweat glands Decreased sweating
Reduced stratum corneum lipids Decreased ability to retain water
Structural changes in stratum corneum Altered barrier function
Reduced movement of water from dermis to epidermis Reduced epidermal hydration
Decrease in melanocytes Loss of ability to tan, greater susceptibility
to solar radiation
Graying hair
Clinical significance
Increased incidence of skin tears
Increased susceptibility to infection
Increased time to re-epithelialization
Longer healing times after injury or surgery
Lax skin and wrinkling, with loss of self-esteem
and/or depression
Skin easily bruised (senile purpura)
Increased risk of wound dehiscence
Hypothermia, heat stroke
Increased risk of pressure damage to elderly skin,
decubitus ulcers
Longer healing times after injury or surgery
Impaired wound healing
Increased risk of severe injury from irritants
Impaired immune function
Increased susceptibility to photocarcinogenesis,
false-negative delayed hypersensitivity tests
Increased risk of thermal or other accidental injury
Increased risk of pressure damage, decubitus
ulcers
Increased susceptibility to skin tears, bruising
Osteoporosis and bone fractures
Less ability to thermoregulate, hypothermia
Dry skin, xerosis
Dry skin, xerosis
Variable response to topical medications, altered
sensitivity to irritants
Dry skin, xerosis
Cutaneous neoplasms
Loss of self-esteem

susceptibility to vascular disorders of the skin,[6] such as pressure
ulcers[15] and stasis dermatitis.[16]
In addition, cutaneous immunity, with age, suffers from both
intrinsic and extrinsic degeneration of immune function. Pro-
gressive decay of normal immune function allows reactivation of
prior infection with the virus that causes chicken pox (Varicella
zoster), producing shingles, a particularly painful disease with
potentially serious complications.[17] Immune dysfunction in the
elderly encourages the development of several autoimmune dis-
orders: bullous[18] and benign mucous membrane pemphigoid,[19]
paraneoplastic pemphigus,[18] and the potentially fatal pemphi-
gus vulgaris.[20] Another possibility, rosacea, remains a myster-
ious disorder with vascular involvement but which may be
infectious in nature.[16]
Unfortunately, management of dermatologic disorders in the
elderly is often less than optimal, due to the fact that the special
needs and limitations of this population are not adequately
considered. Treatment of dermatologic disorders in elderly pa-
tients should take into the account the intrinsic differences be-
tween younger and older patients that may impact on diagnosis
and therapy choice.
This article reviews the clinical implications of aging skin, the
cutaneous disorders that occur most commonly in the elderly as a
result of intrinsic changes in the skin and cumulative extrinsic

ª 2009 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2009; 10 (2)
76
damage, the key diagnostic issues for clinicians, and the optimal
management of dermatologic disorders associated with aging skin.
1. Vascular Disorders
Aging of the skin is associated with regression and dis-
organization of capillaries and small vessels,[21] reduced vessel
density,[14] and a 30% reduction in the number of venular cross
sections per 3 mm2 of skin surface in non-exposed areas.[21] In-
travital capillaroscopy measurements in 26 individuals using
fluorescein angiography and native microscopy suggested a de-
crease in dermal papillary loops.[14] There is a reduction in the
maximum amount of blood pumped because of loss of functional
capillary plexi, although the blood flow pattern remains un-
changed in individual capillary units.[22]
In addition, a decrease in the tensile strength of the skin re-
sulting from changes in and loss of collagen and elastin fibers in
the dermis (associated with an overall derangement of organi-
zation) renders the skin more susceptible to injury (especially
involving the lower layers)[23] and results in a collapse of
structural support for the cutaneous vasculature. Where initial
skin injury occurs, impaired wound healing related to im-
munodysfunction in the elderly significantly increases the risk of
complications.[22,24,25]
1.1 Stasis Dermatitis
Arteriosclerosis and diabetes mellitus, which are common
afflictions of the elderly, can also cause vascular insufficiency and
decreased sensation in the lower extremities.[26] Chronic venous
insufficiency, defined by retrograde flow of blood in the lower
extremities, is therefore a common debilitating disorder in the
elderly population,[16] and one that is increasing in prevalence.[27]
Stasis dermatitis is a recurrent swelling of the feet and ankles
associated with chronic venous insufficiency that results in cya-
notic erythema of the distal extremities, either unilateral or bi-
lateral.[16] Lesions are characterized by poorly demarcated
erythema and possible scaling, most commonly in the medial
perimalleolar area.[16] The lesions are often pruritic and some-
times painful, and can occasionally be accompanied by aching,
heaviness, or nocturnal cramping.[18]
Untreated, stasis dermatitis can eventually result in hyper-
pigmentation with focal purpura that eventually ulcerate.[28]
Ulceration, which can be extremely painful, is characterized by
distinctly marginated erosions that heal with ivory-white plaques
called ‘atrophie blanche.’[29] Up to 6 million people have chronic
venous insufficiency in the US, and approximately 500 000 have
venous ulcers.[27]
ª 2009 Adis Data Information BV. All rights reserved.
Farage et al.
Stasis ulceration is responsible for substantial immobility
and prolonged hospitalization of many otherwise healthy
elderly people and is often chronic and refractory.[30] Although
varicose veins, another indication of venous insufficiency, are
more common in women, men are more susceptible to venous
ulceration.[27] Risk factors include a familial disposition,
prolonged standing or sitting, and concomitant vascular
disease.[31]
The pathology of stasis dermatitis is primarily related to its
characteristic edema and inflammation.[32] In an ongoing state of
venous insufficiency, impairment of the main veins and venules
causes microvascular changes wherein intermittent increases in
pressure act to dilate and elongate the capillaries, thereby da-
maging the endothelium.[33] Compromise of the endothelium
leads to increased extravasation in the interendothelial spaces
and edema in the interstitial tissue.[33]
Edema in its own right is inflammatory, perpetuating swelling
and creating pruritus as well as increasing susceptibility to
ulceration.[34] Hemoglobin from the extravasated erythrocytes
degrades, resulting in increased tissue pigmentation.[33] Micro-
thrombi in the capillaries cause microinfarctions and micro-
necrosis.[33] Cytokines are trapped in the perivascular fibrinoid
deposits with inadequate spatial distribution, leading to impaired
cytokine cascades.[35] Upregulation of transforming growth
factor-b, basic fibroblast growth factor, platelet-derived growth
factor, and the associated chronic inflammation, leads to the
development of fibrous scar tissue (made up of collagen bundles
and loss of cellular components) in the reticular dermis called
lipodermatosclerosis.[32] Chronic lipodermatosclerosis can
spread to the thighs and trunk.[36]
This scleroderma-like hardening of skin, characterized by
intense proteolytic activity, creates a breakdown in the extra-
cellular matrix that results in ulceration, a refractory condition
that represents total eradication of the epidermis with partial
degradation of matrix structures in the upper dermis.[37] At this
point, the physiologic compensatory mechanisms are no longer
able to repair damage.[33]
The initial damage in statis dermatitis is driven by micro-
vascular changes, whereas later pathology is often associated
with bacterial vasculitis.[35] The scale prevalent in this disorder
can harbor abundant microbial life and should be treated by
soaking followed by a gentle rub with emollient to soften and lift
off the scale.[38]
Since nodular squamous cell carcinoma (SCC) not infre-
quently ulcerates on the legs, it is important to ensure that a
vascular ulcer is not in fact a malignant growth. SCC ulcers on
the leg (distinguishable by a heaped-up, partially keratinized
lesion with a raised border) have a 30% metastasis rate.[34] Ulcers
Am J Clin Dermatol 2009; 10 (2)
Clinical Implications of Aging Skin
that continue to resist healing despite treatment should also be
considered suspect.[33,39]
The entire pathophysiologic process leading to venous ul-
ceration needs to be addressed if treatment is to be effective.[40]
Support stockings, which act to minimize edema, have been the
mainstay of prevention and are effective in the short term but do
not represent a long-term solution.[41] Once edema develops, it is
important to treat this promptly to prevent rapid deterioration.
The legs should be elevated and compression continued.[18] Mild-
to-moderate potency topical corticoids are commonly pre-
scribed, but topical medications should be used judiciously, as
gravitational edema is often further complicated by contact
sensitization to common constituents in moisturized, medicated
dressings, preservatives, and topical antimicrobials and anti-
bacterials.[42] Allergic reactions can give rise to diagnostic diffi-
culties.[39] Oral antibacterials are appropriate and effective when
ulceration has resulted in infection.[18] New therapies stimulate
cytokine release by dermal dendrocytes to promote healing.[35]
1.2 Pressure Ulcers
Elderly patients who lose functional mobility become sus-
ceptible to pressure (decubitus) ulcers (bedsores), which are lo-
calized areas of tissue necrosis involving the skin as well as
underlying structures, including subcutaneous tissues, muscles,
and bones. People aged 70–75 years have double the risk of
pressure ulcers compared with those aged 55–69 years.[43] Up to
14% of patients in acute care,[15] 25% of patients in skilled nursing
facilities, and 12% of patients in home care experience bed-
sores.[44] In a study published in 1997,[45] the cost of treating one
pressure ulcer was reported to be as high as $US60 000. Loss of
subcutaneous fat deposits means bony prominences are very
close to the skin, and the most frequent sites of pressure ulcera-
tion are over bony prominences: the sacrum, ischial tuberosities,
greater trochanters, heels, and lateral malleoli.[28]
With pressure damage, initial blanchable erythema indicating
the presence of a mild, perivascular, lymphocytic infiltrate and
edema in the papillary dermis are followed by non-blanchable
erythema, which indicates red blood cell engorgement of the
capillaries and venules associated with degeneration of pilose-
baceous structures and subcutaneous fat. At this stage there is
still no observable effect in the epidermis.[15] Pressure ulcer der-
matitis is subsequently revealed by marked redness with scaling
and sometimes bullae. Initial ulceration is characterized by a loss
of the epidermis and acute inflammation of the papillary and
reticular dermis; chronic ulcers comprise a diffusely fibrotic
dermis.[15] Early pressure damage may go unnoticed by care-
givers[46] because the damage results in destruction of deeper
ª 2009 Adis Data Information BV. All rights reserved.
77
structures but the localized surface displays erythema only.[15]
High interstitial pressures can occur at the bone/muscle interface,
causing substantial deep tissue injury with relatively little super-
ficial damage.[7]
Pressure combines with shear forces, moisture, prolonged im-
mobilization, sensory deficiency, vascular compromise, and nutri-
tional status to form the ulcer. Institutionalized patients are most at
risk; a constant pressure of 70 mmHg applied for a 2-hour period
will cause localized tissue necrosis, but many hospital beds generate
double that pressure.[15] It is vital, therefore, that immobile patients
be regularly repositioned. Nevertheless, one author termed it nur-
sing’s ‘‘dirty little secret’’ that many nurses document repositioning
patients when, in fact, no repositioning was attempted.[47]
Almost 2 million skin tears a year occur in institutionalized
adults.[7] Skin integrity is more fragile in the elderly because of a
decrease in elastic fibers and lower adherence between skin lay-
ers.[7] Turning and lifting can tear delicate skin when dressing the
patient or when bandages are removed,[7] while friction creates
tears during transporting and repositioning of elderly patients.[15]
Most skin tears occur on the upper extremities, nearly half with
no apparent cause, during routine activities such as dressing,
bathing, and positioning.[7]
Malnutrition delays healing.[15] Thus, it is important to ensure
consistent and adequate nutrition in patients susceptible to
pressure ulcers.[48] Pressure ulcers are about five times more likely
to occur in patients with low serum albumin levels than in those
with normal levels;[15] smoking also increases risk.[15] A meta-
analysis of nutritional influence in pressure-ulcer formation
demonstrated that pressure ulcers were significantly less likely in
at-risk patients taking oral nutritional augmentation than in a
similar population receiving appropriate routine care without
nutritional supplement.[49]
Management of pressure ulcers should focus on prevention,
with nutritional supplementation, regular pressure relief, and
fastidious hygiene in the presence of incontinence.[15] Seating
systems that provide pressure relief/blood flow stimulation and/
or passive standing capability reduce the risk of pressure ulcers
and enhance functional status.[15]
1.3 Rosacea
Rosacea is a chronic inflammatory disorder characterized by
acneiform papules, pustules, and dilation of capillaries, primarily
on the cheeks but also occurring on the nose, forehead, and chin.
Rosacea has a typical intermittent onset in middle age and then
becomes persistent with a prevalence of up to 12% in those aged >64
years.[16,50] There is also often sebaceous gland hyperplasia while
ocular involvement occurs in >90% of all patients.[16]
Am J Clin Dermatol 2009; 10 (2)
78
Histologic evaluation demonstrates telangiectasias and a
perivascular lymphocytic inflammatory infiltrate, with dermal
edema.[50] The etiology and exact mechanisms for the disorder
are still not understood, with numerous etiologies having been
proposed, including mites, vascular instability, and vitamin de-
ficiencies.[50] The pathology involves, at least in part, atrophy of
the papillary dermis, which allows easier visualization of dermal
capillaries.[50] Triggers include spicy foods, sun exposure, some
medications, and use of strong facial products.[51] A long-
standing observation that rosacea tends to be associated with
gastrointestinal disorders[50] has been strengthened recently by a
growing association of the disorder with Helicobacter pylori in-
fection[52] and confirmed by the fact that eradication therapy in
patients with H. pylori infection produced significant improve-
ment in rosacea symptoms in 66% of patients treated, and total
resolution in 33%.[53]
Rosacea, although not related to normal aging, is a chronic
condition that steadily worsens over time.[18] Treatment of the
condition is therefore necessary to avoid disfiguring skin changes,
including a particularly distressing involvement of the nose that is
particular to men.[51] Patients with rosacea should be instructed
to avoid triggers.[51] Oral antibacterials have been given first-line
preference because of their inarguable efficacy, despite the lack of
any identified causative micro-organism. Tetracyclines, doxycy-
cline, and erythromycin have proven to be effective, although
antibacterial resistance with long-term use is a concern.[54] The
onset of efficacy of isotretinoin is later than that of oral anti-
bacterials but isotretinoin nevertheless has high efficacy and is
effective against multiple rosacea subtypes.[54] Topical me-
tronidazole and azelaic acid are commonly prescribed.[51] Topical
retinaldehyde and ascorbic acid (vitamin C) have also shown
preliminary promise.[51]
2. Cutaneous Expression of Autoimmune Disorders
Senescence of the immunologic system of the skin in the el-
derly results in an increase in autoimmune disease.[55] The pre-
valence of polypharmacy in the elderly also increases the risk of
drug-induced autoimmune cutaneous eruptions.[55]
2.1 Bullous Pemphigoid
Bullous pemphigoid, typically occurring in those aged >60
years and with no ethnic or gender preference,[20] is a chronic
eruption characterized by multiple bullae on normal skin or on an
urticarial base,[56] occasionally with intense itching that may in-
itially present as hives.[57] About one-third of patients with bul-
lous pemphigoid also experience oral blisters,[18,28] and these may
ª 2009 Adis Data Information BV. All rights reserved.
Farage et al.
be exquisitely painful. The blisters are large, tense, and resistant
to minor trauma.[58] The disease may be preceded by a long
period of generalized itching or eczema; large areas of denuded
skin can result in significant loss of fluids and vital electrolytes.[36]
Bullous pemphigoid is defined by the presence of circulating
and tissue-associated[18,56] antibodies to hemidesmosomal pro-
teins present in the basement membrane of stratified squamous
epithelia.[59] The antibodies are produced specifically against a
230-kDa antigen located in the lamina lucida region of the
dermo-epidermal junction.[56] Bullous pemphigoid is confirmed
by histology, immunofluorescence immune electron microscopy,
and molecular biology techniques.[56] Ultrapotent topical corti-
costeroids are standard treatment,[18] although recent research
indicates that potent topical corticosteroids are equally effec-
tive.[56] Tetracycline alone or with nicotinamide (niacinamide) is
appropriate for patients who can not tolerate corticosteroids or
corticosteroid-sparing therapy following corticosteroid use.[56]
2.2 Mucous Membrane Pemphigoid
Mucous membrane pemphigoid occurs primarily in the el-
derly population, with erosions and blisters occurring primarily
in the mouth, on the conjunctivae, and in the nose.[19] In 20–30%
of patients, some blisters also occur on the head, neck, and upper
trunk. Left untreated, the disease will typically involve both eyes
within 3–5 years, with the potential to cause blindness, because
occlusion of the lacrimal ducts leads to optic keratitis. Patients
diagnosed with mucous membrane pemphigoid should be
promptly referred to an ophthalmologist. Topical corticosteroid-
containing artificial tears may be administered in patients with
ophthalmic involvement and mouthwashes containing topical
corticosteroids may be employed for oral lesions.[19] Ocular dis-
ease can be difficult to treat and management usually involves
systemic therapy with immunomodulators to control inflam-
mation and prevent progression to irreversible blindness, as well
as surgical intervention in advanced disease. Recent advances in
treatment, including methotrexate, mycophenolate mofetil,
monoclonal antibodies, and topical tacrolimus therapies have
been associated with promising results.[60]
2.3 Pemphigus Vulgaris
Pemphigus vulgaris is the most serious blistering disease of the
elderly, with an onset typically occurring between the ages of 50
and 65 years. Initial oral blisters are typically followed by blis-
tering of the trunk, limbs, face, and scalp. Lesions progressively
ooze, become crusted, and lichenify.[18] The condition is readily
identified by Nikolsky’s sign, in which lateral pressure with the
Am J Clin Dermatol 2009; 10 (2)
Clinical Implications of Aging Skin
thumb at the edge of the blister produces an erosion.[18] Histo-
logic evaluation reveals intra-epidermal blister formation and
acantholytic cells within the lesion. Indirect immunofluorescence
findings include an intercellular deposition of immunoglobulin
conjugates IgG and C3; other complement components as well as
immunoglobulins are also present on occasions.[18]
Pemphigus vulgaris is a serious, chronic disorder with the
potential for fatality as a result of electrolyte imbalance or sec-
ondary infection.[18] Management of pemphigus vulgaris requires
systemic therapy with corticosteroids, which should be started as
early as possible. However, as adverse effects of corticosteroid
therapy represent a significant part of the morbidity of this
disorder, lower doses (80–120 mg/day) of corticosteroids,[18]
adjunctive use of immunosuppressive drugs or tetracycline with
nicotinamide,[18] and sublesional corticosteroid injections[61] may
be preferable choices.
2.4 Paraneoplastic Pemphigus
The elderly are especially susceptible to paraneoplastic pem-
phigus.[59] This disorder occurs in conjunction with leukemia or
lymphoma, is primarily seen in patients aged >60 years and
occurs twice as often in men as in women. Paraneoplastic pem-
phigus is characterized by extensive painful mucocutaneous
erosions, typically beginning in the oral mucosa. Histologic
analysis reveals acantholysis with basal cell vacuolation,
dyskeratotic keratinocytes, and lichenoid/interface dermatitis.
Direct immunofluorescence shows intercellular and basement
membrane IgG and C3 within the epidermal spaces as well as at
the epidermal basement membrane. Indirect immuno-
fluorescence demonstrates circulating antibodies specific for
stratified squamous or transitional epidermal epithelium.[20]
2.5 Lichen Sclerosus
Although cutaneous problems involving the genitalia in men
are generally limited to the uncircumcised, genital lesions are not
uncommon among elderly women.[62] Lichen sclerosus is an ap-
parently autoimmune dermatosis with a predilection for genital
skin. Known formerly as kraurosis vulvae or leukoplakia of
the vulva, lichen sclerosus is characterized by well demarcated,
porcelain-white papules and plaques among areas of bruising;
lesions occur throughout the genital area with the exception of
the genital mucosa.[63] Itching is the principal symptom, leading
to the potential for lichenification.[63]
Lichen sclerosus is an important disease of the genital skin
because of the possibility, albeit rare, of potentially debilitating
complications. Lichenification occasionally results in significant
ª 2009 Adis Data Information BV. All rights reserved.
79
scarring or adhesions that can result in narrowing or closure of
the introitus in women, creating problems with micturition and
intercourse and (in men) occasionally requiring subtotal or total
circumcision.[63] Additionally, lichen sclerosus is associated with
an increased incidence of invasive SCC in the anogenital area.[63]
First-line therapy consists of the ultrapotent topical corticoster-
oid clobetasol,[64] although there is some concern that corticos-
teroid use may reactivate oncogenic human papillomavirus,
which is carried by 20% of lichen sclerosus patients.[63]
3. Viral Infections
3.1 Herpes Zoster (Shingles)
Herpes zoster (shingles) is a reactivation of the chicken pox
virus (V. zoster) with major sensory nerve ganglion involvement
in addition to its original involvement in the skin.[18] Two-thirds
of cases occur in patients aged >50 years,[30] and the condition is
most commonly seen in patients aged ‡60 years.[50] Shingles is
characterized by a tingling or itching sensation (sometimes pain)
that can precede the vesicular unilateral[65] cutaneous eruption by
several days.[18] Vesicles persist for up to 2 weeks, eventually
resulting in dry hemorrhagic crusts and possible scarring. Sec-
ondary bacterial infections are common.[50] Reactivation sites are
(in decreasing order of frequency): thoracic, cervical, and tri-
geminal nerves, then lumbosacral segments.[36]
Shingles is usually self-limiting,[17] and is serious only in
immunosuppressed patients (because of dissemination) or when
there is involvement of the ophthalmic nerve, a complication that
is more frequent with age.[18] Vesicles on the side of the nose are
indicative of corneal involvement.[65]
Post-herpetic neuralgia, causing acute and chronic pain along
involved nerves, is a complication in about half of patients with
herpes-zoster reactivation aged >60 years, and the risk increases
with age.[18] Although the pain gradually abates over time, it is
also frequently disabling and refractory to typical pain medi-
cations, thereby sometimes destroying an elderly patient’s re-
maining years.[36] Prompt (i.e. before the virus spreads beyond
the initially damaged nerve) and aggressive treatment of the acute
infection with oral antiviral drugs such as acyclovir (aciclovir)
significantly reduces the severity of pain during the reactivation
phase and reduces the risk and length of post-herpetic neur-
algia,[34,66] particularly in the older population.[67]
A new vaccine composed of live, attenuated V. zoster virus
and tested in a randomized, double-blind, placebo-controlled
study involving >38 000 senior adults reduced the subsequent
incidence of post-herpetic neuralgia by 66.5%.[68] However,
Am J Clin Dermatol 2009; 10 (2)
80
although the vaccine markedly reduced morbidity due to herpes
zoster with few adverse effects (principally mild dermatologic
reactions at the injection site), discussion is ongoing with regard
to the cost effectiveness of this strategy in target populations.[69]
4. Inflammatory Dermatoses
Inflammatory dermatoses are common and comprise a wide,
complex variety of clinical conditions. Accurate histologic diag-
nosis, although sometimes difficult to achieve, is essential for
clinical management.
4.1 Xerosis
As the skin ages, decreased epidermal thickness is accompanied
by a decrease in water and lipid content as well as reduced sebum
production and sweating, resulting in dryer skin.[70] Normal dry-
ing of the skin is often accompanied by degeneration of the normal
process of keratinocyte maturation and adhesion, resulting in a
condition characterized by rough, dry, and scaly skin called
xerosis (asteatosis).[16] Xerotic skin may have visible fissuring (in a
cracked porcelain pattern) of the stratum corneum, particularly
on the lower legs, a condition called ‘eczema craquelé.’[70] Fissures
can penetrate sufficiently deep as to disrupt dermal capillaries and
cause bleeding.[70] Xerosis is often accompanied by intense itch-
ing,[16] and repetitive scratching can result in secondary lesions.[70]
Xerosis is the most common dermatosis of the skin, occurring
equally in men and women,[11] with a prevalence as high as 85%.[4]
By age 70 years, nearly all adults are affected.[50] The condition is
aggravated by low humidity[16] and its onset is often linked to the
initiation of home heating,[50] earning the nickname ‘winter
itch.’[71] Surface irritants such as harsh soaps and other cleansers
can further aggravate xerosis.[16]
The key to managing xerosis in the aging patient is first to
rehydrate the skin, then to seal in the hydration.[31] Because a
relative humidity level of 60% is required for atmospheric water
concentration to supplement stratum corneum hydration,[8] use
of room humidifiers, especially in the winter months, is ad-
visable.[50] Use of humectant forms of moisturizers can increase
epidermal water content.[31] Bathing, which has traditionally
been discouraged in patients with xerosis, actually rehydrates the
stratum corneum.[72] Taking tepid baths is recommended,[8] with
soaking continued for at least 10 minutes to enable the stratum
corneum to absorb water.[73] Use of soaps should be kept to a
minimum and consist of gentle, non-irritant preparations
only.[70] However, bathing must be immediately followed by
liberal application of moisturizers, which plug the spaces between
keratinocytes with lipids[31] and encourage degradation of the
ª 2009 Adis Data Information BV. All rights reserved.
Farage et al.
corneodesmosome.[74] Application of petrolatum products also
helps to prevent transepidermal water loss.[75,76] Lotions con-
taining ammonium lactate have proven effective in the treatment
of xerosis.[77] Topical corticosteroids can be prescribed for espe-
cially severe cases.[16]
4.2 Pruritus
Pruritus (itch) is a widespread dermatologic problem in the
elderly, with a reported prevalence as high as 29%.[78] It is more
common in men than in women.[79] Itching, which can be intense,
may be accompanied by sensations of tingling or even burning[80]
and typically increases in severity at night, a finding believed to be
related to a nocturnal rise in internal body temperature.[81]
The causes and mechanisms of itching are so diverse that
elucidation of an individual patient’s condition, which can be
intense to the point of suicidal thoughts, can be very challen-
ging.[82] A study by Thaipisuttikul[11] of 149 elderly patients
identified numerous causes of senile pruritus, including, in order
of prevalence, xerosis, inflammatory eczematous disorders, lichen
simplex chronicus, skin infections, psoriasis vulgaris, urticaria,
reactions to various drugs, anogenital itching, and insect bites.
Pruritus is also a common feature of neuropsychiatric disease.[78]
Effective management of pruritus begins with a systematic
approach to discovering the origin of each individual case.[82]
Pruritus often occurs without any dermatologic abnormality
(over 100 drugs can cause pruritus without any visible lesion[78]).
However, chronically scratched skin can become thickened and
hyperpigmented, a process known as lichenification.[82] Evalua-
tion often defies objective analysis, as there is no correlation with
physical findings.[78] The reality of the patient’s subjective com-
plaints, however, is confirmed in what has been termed ‘scratch
radar’– nocturnal scratching that shows a direct correlation be-
tween the severity of reported signs and measurable nocturnal
limb movement.[78] The origin of pruritus, in fact, often proves to
be multifactorial, and in as many as 30% of all patients, is idio-
pathic.[83] Idiopathic pruritus increases in both frequency and
severity with increasing age;[84] 69% of patients with idiopathic
pruritus in one study by Beare[85] were aged >60 years.
The most common cause of pruritus (associated with a
thickened and cracked stratum corneum[84]) is xerosis (see section
4.1), which was reported in one survey by Thaipisuttikul[11] to
comprise almost 40% of all patients with pruritus. Patients with
pruritus have clinically drier skin than matched control in-
dividuals, with severity being directly associated with the degree
of xerosis, skin surface conductance, and presence of intracorneal
adhesions, implying that an abnormality of keratinization may
be involved.[84]
Am J Clin Dermatol 2009; 10 (2)
Clinical Implications of Aging Skin
Table II. Pruritus screen for underlying disease[65,82,85]
Laboratory analysis Abnormal finding
Complete blood count Anemia
Eosinophilia
Lymphopenia
Polycythemia
Plasma viscosity Out of normal range
Ferritin Iron deficiency
Electrolytes Out of normal range
Liver function Out of normal range
Thyroid function Out of normal range
Autoantibodies Out of normal range
Renal function Elevated blood creatinine levels
Chest x-ray Mass
Enlarged mediastinal lymph nodes
Underlying systemic disease is a common source of pruritus
without obvious visible signs, and indeed accounts for up to half
of all cases.[78] In addition, numerous types of pharmaceuticals
produce varying degrees of pruritus; these include antibacterials,
diuretics, NSAIDs, and calcium channel antagonists.[83] With-
drawal of the drug responsible may precede resolution of
symptoms by several weeks.[86] Generalized pruritus often coin-
cides temporally with the onset of emotional or psychological
stress, with stress acting to increase the perception of itch sti-
muli.[78] The elderly often have severe and insoluble emotional
difficulties, including bereavement, financial pressures, chronic
health issues, boredom, and loneliness,[78] which should not be
discounted as possible contributors to itching.[87]
Sudden onset of generalized persistent itching should initiate
aggressive pursuit of an internal etiology. Investigations should
include, at a minimum, a complete blood count, urinalysis,
thyroid evaluation, tests of renal function, and a chest x-ray
(table II).[58,65,82]
Treatment of pruritus depends on the specific source of the
patient’s symptoms. Treatment for itching believed to be xerotic
in origin is as described for xerosis (see section 4.1). Topical
corticosteroids, cooling agents, anesthetics, and antihistamines,
as well as systemic antihistamines and corticosteroids, have also
been employed. Physical therapies have included phototherapy,
acupuncture, thermal stimulation, and transcutaneous electrical
nerve stimulation.[82] The most commonly prescribed oral ther-
apy for pruritus is an antihistamine; systemic corticosteroids are
used in approximately 30% of cases.[83] Treatment decisions in
the elderly, however, must take into account that antihistamines
can cause unacceptable sedation, and corticosteroids can ac-
ª 2009 Adis Data Information BV. All rights reserved.
81
Possible etiology of pruritus
Lymphoma/leukemia, myelodysplastic syndrome, iron deficiency
Drug reaction, infestation
Leukemia, AIDS
Polycythemia vera
Myeloma, infection, malignancy
Anemia
Renal failure
Obstructive jaundice (gallstones, tumor, primary biliary cirrhosis)
Hypothyroidism, hyperthyroidism
Thyroid disease, primary biliary cirrhosis
Diabetes mellitus
Carcinoma of the bronchus
Lymphoma
centuate atrophy in skin already compromised by sun damage.[34]
Preparations used to treat pruritus can cause contact sensitivity
that presents as weeping, vesicular, crusting dermatitis.[18]
Resolution of symptoms occasionally proves elusive, espe-
cially in the elderly. Pruritus is associated with a release of
histamine, which can induce a perpetuating cycle.[88] Senile
insomnia increases the time available for scratching.
Chronic scratching can result in a condition called lichen
simplex chronicus, characterized by persistent itching as well as
lichenified scaly plaques[50] or thick raised papules with linear
excoriation exclusively on sites accessible to scratching.[89] Lichen
simplex chronicus is more prevalent in women than in men and
generally clears quickly when scratching can be prevented.[89]
4.3 Eczema
Although atopic eczema is less common in elderly than in
younger individuals, discoid or nummular eczema is more pre-
valent.[38] Nummular eczema is associated with temperature
changes, low humidity, or asteatotic eczema, occurs most often in
elderly men and is characterized by coin-shaped macules, pa-
pules, or vesicles on the extremities that may ooze and crust over,
superimposed on scaly, inflamed, or raw skin.[90] Stress may
worsen the symptoms of nummular eczema.[91] The presentation
of nummular eczema can vary widely, ranging from a sudden
onset of florid patches of erythema with vesicles and swelling to
slow-growing dry patches of scale.[91] The lesions, which vary
greatly in number, are generally between 1 and 5 cm in diameter
and may be mistaken for ringworm or psoriasis.[91] High-potency
topical corticosteroids represent first-line therapy.[18] Topical
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82
tacrolimus is effective but does not cause the skin atrophy asso-
ciated with corticosteroid use.[86]
4.4 Contact Dermatitis
Contact dermatitis occurs in as much as 11% of the elderly
population and includes both irritant and allergy-type reactions.[31]
Reduced ability to mount a delayed-type hypersensitivity
reaction[92] in the elderly decreases individual susceptibility to
allergic contact sensitivity because of a reduction in the number of
Langerhans cells,[93] a decrease in T cells, and diminished vascular
reactivity;[92] however, decades of potential sensitization[94] and an
increased level of exposure mean the potential for allergic contact
sensitivity in the geriatric population remains.[26] Allergic contact
sensitivity is more common in elderly women than in elderly
men;[11] the most common culprit is topical medications or their
non-drug components.[95] Up to 81% of patients being treated for
chronic leg ulcers, for example, exhibit allergic reactions to topical
medications.[95] Patch testing before the use of topical medications
may be beneficial, especially in high-risk populations such as those
being treated for dermatitis or ulceration of the lower extre-
mities.[94] Testing should include medicaments and dressings, as
well as dental prostheses and medications for ocular disease.[94]
While the elderly patient remains susceptible to allergic der-
matitis, he/she is possibly less susceptible to irritant contact
dermatitis.[96] Contact dermatitis begins at the site of exposure
but may spread, presenting as erythema and edematous plaques
with the potential for development of vesicles.[50] However, in the
elderly, subtle, chronic irritant dermatitis may be more difficult
to distinguish because of a delayed and diminished inflammatory
response, and may in fact represent unrecognized thermal in-
jury.[6] Patients should be instructed to avoid use of strong soaps
and contact with household cleaners and other products that
have the potential to irritate their fragile skin.[6] Common aller-
gens include lanolin paraben esters, dyes, plants, balsams, rub-
ber, nickel, and topical medications.[50]
Treatment of contact dermatitis first demands removal of the
offending agent.[96] In severe cases, removal of all products may
be indicated until the specific agent can be identified.[31] Treat-
ment may consist of administration of topical corticoster-
oids[97,98] with addition of oral antihistamines when needed.[96-98]
4.5 Seborrheic Dermatitis
Seborrheic dermatitis is a common inflammatory disorder
thought to result from chronic infection of the lipid-rich areas of
the skin. The causative organism is believed to be Malassezia
yeasts, a component of the normal flora to which some
ª 2009 Adis Data Information BV. All rights reserved.
Farage et al.
individuals apparently have an abnormal host response.[99]
Affecting slightly more male than female patients, the disorder
most commonly involves the areas of the head and trunk where
sebaceous glands are most prominent, particularly the eyebrows,
the paranasal area, pre- and post-auricular regions, presternal
and intrascapular areas, the scalp, the axillae, and the groin
(dandruff is a form of this disorder).[100] Female patients tend to
have more severe symptoms than male patients.[101]
Seborrheic dermatitis has a prevalence as high as 31% in the
elderly.[31] It presents as inflammatory changes (erythema) as well
as chronic dermatitis, but occasionally also includes dramatic
exacerbations of greasy red-brown papules[58] covered by scaly
yellow flakes and plaques.[100] Chronic dermatitis with pruritus,
resembling psoriasis, may develop in seborrheic areas.[100] The
disorder also occurs in disproportionate numbers among patients
with neurologic disorders such as Parkinson disease, epilepsy, and
CNS disease or trauma,[102] although the reason for an association
with neurologic disorders is unclear.[100] Seborrheic dermatitis
may intensify during times of increased stress and fatigue.[30]
Although seborrheic dermatitis is not health threatening, it
may be distressing for those afflicted. Therapies include anti-
inflammatory preparations (e.g. corticosteroids or calcineurin
inhibitors), keratolytic agents (e.g. pyrithione zinc, sulfur, coal
tar, salicylic acid), and antifungal medications (e.g. ketocona-
zole), often administered in the form of medicated shampoos.
Ciclopirox, piroctone olamine, and climbazole are also used
outside the US.[100] Shampoos should be lathered abundantly,
rubbed into the scalp, and left on the scalp for about 5 minutes;
regular applications are required.[100]
5. Management of Cutaneous Disorders in the Elderly
Management of skin disease in the elderly must take into
account the sociophysiologic characteristics of that population.
Elderly patients often experience dementia or memory loss as
well as impaired vision, hearing, and/or mobility.[65,103] They may
not have caregivers or may lack adequate housing or nutrition.[65]
The patient’s physical ability to comply with therapy should be
taken into consideration (and often is not),[38] and simple topical
regimens should be used whenever possible to maximize both
efficacy and compliance.[38] For example, aged patients with
limited physical function may need provision for regular foot
care[86] or assistance with topical therapies or dressings if they live
alone.[38] Physicians need to ensure that compliance with the re-
gimen prescribed is actually feasible and they should ensure that
medications are applied correctly and regularly.[86]
When prescribing treatments, it is important to recognize the
structural fragility of aged skin.[30] Skin integrity in the elderly is
Am J Clin Dermatol 2009; 10 (2)
Clinical Implications of Aging Skin 83

Table III. Cutaneous eruptions and possible drug etiology by classification of lesions[104,105]
Type of rash or eruption Possible drug etiology
Exanthems b-Lactam antibacterials, sulfonamides, erythromycin, gentamicin, antiepileptic agents, gold salts
Eczema, lichenification Anti-arrhythmic agents, antiepileptic agents, antituberculosis agents, gold, quinidine, methyldopa
Acne-like Corticosteroids, bromides, iodides
Urticara and angioedema ACE inhibitors, NSAIDs, opioids, curare, antibacterials (especially penicillins), blood products
Bullous Penicillamine, bleomycin, iodides
Fixed drug Penicillins, phenolphthalein, tetracycline, nalidixic acid, barbiturates, sulfonamides, gold salts
Exfoliation Gold
Anticoagulant skin necrosis Warfarin, heparin
Nodular eruption Sulfathiazole, salicylates, oral contraceptives
Rash on sun-exposed areas Coal-tar derivates, psoralens, chlorpromazine, tetracycline, doxycycline, NSAIDs, phenothiazines,
chlorothiazide, dimeclocycline, griseofulvin, oral antihyperglycemics, sulfonamides
Erythema Antihistamines, penicillins, sulfonamides, barbiturates, bismuth
Erythema, multiforme target lesions, SJS, TEN Allopurinol, barbiturates, dapsone, digoxin, phenobarbital, carbamazepine, phenytoin, gold,
hydralazine, salicylates, sulfonamides, penicillin, quinolone, cephalosporins, NSAIDs, tetracycline,
cotrimoxazole (trimethoprim/sulfamethoxazole)
Urticaria Antibacterials (especially penicillins), blood products
SJS = Stevens-Johnson syndrome; TEN = toxic epidermal necrolysis.

compromised by intrinsic structural changes, cumulative skin
damage, and co-morbidities.[38] Increased skin fragility, the pre-
valence of polypharmacy, and the likelihood that treatments will
need to be taken over the long term should also heighten safety
concerns about any medication prescribed.[86,94] For all of these
reasons, therapeutic regimens that are routinely administered in
younger patients may require modification in the elderly.[30]
Stronger medications should be chosen only when the ther-
apeutic benefit justifies the risk,[79] and second-line therapies are
sometimes indicated in the earlier stages of treatment.[65]
In addition, treatment efficacy (as always) is dependent on
accurate diagnosis. Many elderly patients take many drugs,
which means drug reactions are common and elucidating the
etiology of any cutaneous eruption is therefore more difficult.[94]
Many diseases of the skin can easily be confused with drug
eruptions, and drug eruptions can simulate almost any derma-
tologic disease (table III),[86] with any particular reaction de-
pending on individual factors such as genetics, dietary habits, and
concomitant medications.[94] Patients also need to be questioned
specifically about use of over-the-counter medications, homeo-
pathic remedies, and laxatives, as these are often not viewed by
patients as drugs and thus may not be reported.[86,104] Diagnosis
of skin disorders in the elderly must be undertaken with the
awareness that polypharmacy in this age group produces a high
risk of drug eruptions, which must be distinguished from cuta-
neous eruptions of other origin.[86]
Risk of a cutaneous adverse drug reaction is higher in female
patients and those with an underlying kidney or liver disorder.[105]
As a general rule, non-eczematous dermatoses are likely to be
drug induced,[94] and may take the form of exanthems, urticaria,
vasculitis, fixed drug eruptions, erythema multiforme, contact
dermatitis, photodermatitis, or skin necrosis.
Exanthems, when drug induced, are maculopapular, morbil-
liform, or erythematous in bilateral distribution; pruritus is
commonly associated. Lesions typically appear within 1 week of
drug therapy and resolve within 2 weeks of drug discontinuation,
although they can appear as late as 2 weeks after therapy has
ended.[105] Urticaria and angioedema lesions range from small
papules to large annular plaques, typically appearing transiently,
sometimes reappearing, but disappearing rapidly when the drug
is discontinued. These eruptions can progress to anaphylactic
shock.[105]
Drug-induced cutaneous vasculitis presents as purpuric ma-
cules and papules on the lower limbs or buttocks with associated
soreness; blistering and necrosis can occur. Rash is not un-
commonly accompanied by fever, aching, and fatigue.[105] Fixed
drug eruptions are rare, and typically consist of single ery-
thematous or bullous plaques that appear at the same site within
30 minutes to 8 hours after drug administration, typically on the
hands, feet, or genitals, but sometimes around the eyes or
mouth.[106] These lesions may be painful and tend to result in
residual hyperpigmentation.[105]

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84
Erythema multiforme is a hypersensitivity reaction char-
acterized by typically target-like macules, papules, and vesicles
on the extremities and trunk accompanied by fever. Cutaneous
involvement can be minor and self-resolving or may develop into
life-threatening syndromes known as Stevens-Johnson syndrome
or toxic epidermal necrolysis. Fever usually accompanies the
reaction.[105]
Allergic contact dermatitis follows topical application of an
allergen and is characterized by erythematous, papular, urticar-
ial, or vesicular plaques with pruritus. Dermatitis typically re-
appears within 24 hours of every use of the allergenic medicament
or any structurally similar compound. Photosensitive dermatitis
appears when drug administration is followed by exposure to
UV light, typically UVA.[105] Photosensitive dermatitis can be
phototoxic, a dose-related response that resembles a sunburn, or
photoallergic, with erythematous, eczematous, or bullous lesions
that appear only on sun-exposed skin. Photoallergic reactions
may persist after the medication has been discontinued.[105]
Cutaneous eruptions of pharmaceutical origin may be very
difficult to distinguish from other disorders with similar cuta-
neous presentation.[105] However, prompt, accurate diagnosis is
critical as early withdrawal of the culprit drug is often necessary
to avoid serious complications.[107] The elderly are at increased
risk of morbidity and mortality from adverse drug reactions.[108]
If the eruptions are not drug-induced reactions, correct diagnosis
is required before appropriate treatment can be administered.[107]
Sudden onset of any dermatosis in a patient without prior skin
disease (particularly in the elderly, who often take many drugs)
should be viewed as a possible drug reaction.[109] Diagnosis of
any drug eruption should take into account the medical history
and results of the physical examination. The sequence of events is
a key part of the history when attempting to distinguish drug
eruptions from skin disorders of other origin. Drug reactions
typically occur 7–10 days after the initiation of a drug regimen[65]
but can occur as late as 8 weeks after initial exposure, sometimes
manifesting after drug exposure has ceased.[86] Urticaria and
angioedema, as noted previously, tend to be temporally asso-
ciated with drug administration, appearing shortly after drug
administration and disappearing shortly after drug dis-
continuation.[105] For most drug reactions, an improvement in
symptoms, particularly in lichenification responses, may not take
place until weeks after cessation of the drug.[86,94]
6. Conclusion
The barrier function of aging skin becomes progressively more
compromised by the additive effects of both intrinsic and
extrinsic skin aging, predictably producing an increase in the
ª 2009 Adis Data Information BV. All rights reserved.
Farage et al.
incidence of diseases and disorders over the lifespan.[14] Most
people aged >65 years have at least one skin disorder, and many
have two or more.[110] Common diseases of the elderly such as
xerosis, pruritus, eczema, psoriasis, and seborrheic dermatitis,
although relatively non-threatening, can produce chronic
discomfort or distress in the elderly population.[111] Furthermore,
vascular disorders of the skin such as pressure ulcers and stasis
dermatitis, autoimmune disorders such as bullous pemphigoid
and pemphigus vulgaris, and infections largely specific to the el-
derly, can cause substantial morbidity and mortality in this age
group.[5,15,16] Other relatively minor skin disorders, if left un-
treated in an elderly individual, can contribute to a potentially life-
threatening breach of skin integrity.[65] Effective management of
these conditions requires that primary-care physicians ‘take
ownership’ of their aging patients’ cutaneous health,[112] mon-
itoring the patient’s skin and distinguishing lesions that are a
normal part of aging from clinically significant lesions that should
be treated and may be a sign of impending cutaneous break-
down.[6] Ongoing surveillance by family practitioners of their
patients’ skin should prompt referrals to the dermatologist as
needed for appropriate treatment.[6] Therapies must be
modified to meet the needs of the elderly patient, taking into
consideration their increased skin fragility, numerous co-mor-
bidities, probable polypharmacy, and possible lack of mobility
and social support.[103] Appropriate care, continuing surveillance
by practitioners of their patients’ skin, judicious limitation of
unnecessary risk factors (particularly exposure to solar radiation),
and prompt, relevant, and thoughtful treatment of any clinically
significant cutaneous disorder can prolong life and substantially
improve the quality of life of patients during their later years.[5]
Acknowledgments
No sources of funding were used to assist in the preparation of this
review. Dr Miranda W. Farage and Kenneth W. Miller are employees of
Procter & Gamble. The other authors have no conflicts of interest that are
directly relevant to the content of this review. The authors are grateful to Drs
S. McClanahan, Randy Nunn, Keith Ertel, Don Bissett, and Joe Kacz-
vinsky for their critical review of this manuscript, and to Ms Zeinab Schwen
and Ms Wendy Wippel (Strategic Regulatory Consulting, Cincinnati, OH,
USA) for their assistance in the preparation of this manuscript.
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Correspondence: Dr Miranda A. Farage, The Procter & Gamble Company,
Winton Hill Business Center, 6110 Center Hill Road, Box 136, Cincinnati, OH
45224, USA.
E-mail: farage.m@pg.com
Am J Clin Dermatol 2009; 10 (2)