Scaling Papules, Plaques, and Patches


Key Points

  • 1.

    Scaling disorders have multiple causes – immunologic, infectious, and neoplastic

  • 2.

    Borders are usually distinct, in contrast to eczema

  • 3.

    Scaling (stratum corneum) is not crusting (dried fluids and blood)

The papulosquamous disorders have diverse causes, as seen in Table 9.1 . The lesions, in addition to being scaly, are sharply demarcated. The latter feature helps to distinguish them from scaling lesions of eczematous dermatitis, in which the borders usually are indistinct. Exceptions are nummular ( coin-shaped ) eczema , which can resemble tinea corporis, and seborrheic dermatitis , which in the scalp can be confused with psoriasis and on the chest can be confused with tinea corporis. Lichen planus often is also included in the papulosquamous disorders, but usually, the scale is not readily evident, so we have designated this disease as a papular disorder (see Chapter 11 ). Tinea versicolor can appear as finely scaling patches, but patients more often present because the lesions appear as white spots; hence, this disease is discussed in Chapter 13 .

In papulosquamous lesions, the borders are sharply demarcated; in eczematous lesions, they are usually not.

Table 9.1
Scaling Papules, Plaques, and Patches a
Frequency (%) b Etiology Physical Examination Differential Diagnosis Laboratory Tests
Appearance of Lesions Characteristic Distribution
Lupus, discoid 0.2 “Autoimmune” Red to purplish papules and plaques with adherent scale and follicular plugging ; older lesions atrophic Sun-exposed areas favored Psoriasis
Lichen planus
Subacute cutaneous lupus erythematosus
Biopsy with immunofluorescence; antinuclear antibodies
Fungus 2.5 Infection (dermatophyte) Annular patches with elevated borders surmounted by scale Anywhere (See Table 9.2 ) Potassium hydroxide preparation; fungal culture
Mycosis fungoides 0.2 Neoplastic (lymphoma) Yellowish-red or violaceous , irregularly shaped patches and plaques with only slight scale Asymmetric ; girdle area is often the first area involved Psoriasis
Parapsoriasis
Eczema
Erythroderma
Biopsy
Pityriasis rosea 1.1 Human herpesvirus 6 and 7 Tannish-pink oval papules and patches with delicate collarette of scale ; rash preceded by herald patch “Christmas tree” pattern on trunk; spares face and distal extremities Secondary syphilis
Tinea corporis
Lichen planus
Pityriasis lichenoides chronica
Guttate psoriasis
Psoriasis 5.2 Unknown Erythematous plaques with silvery scales Anywhere; scalp, elbows, knees, and intergluteal cleft are favored locations; nails often involved Seborrheic dermatitis
Tinea cruris
Candidiasis
Intertrigo
Pityriasis rosea
Tinea corporis
Dermatitis
T-cell cutaneous lymphoma
Onychomycosis
Secondary syphilis < 0.1 Infection (spirochete) Red brown or copper-colored scaling papules and plaques, sometimes annular in shape Generalized; palms and soles often included; mucous membranes sometimes involved Pityriasis rosea
Viral exanthem
Drug eruption
Sarcoidosis
Serologic test for syphilis

a See also discussions of seborrheic dermatitis ( Chapter 8 ), lichen planus ( Chapter 11 ), and tinea versicolor ( Chapter 13 ).

b Percentage of new dermatology patients with this diagnosis seen in the Hershey Medical Center Dermatology Clinic, Hershey, PA.

The diagnostic approach to scaling diseases should include consideration of the distribution of the lesions, and sometimes also the presence or absence of nail and mucous membrane involvement. Of the laboratory tests that are listed, the one that should be done most frequently is a potassium hydroxide (KOH) preparation of the scale to look for fungal elements. The general rule for scaling rashes of uncertain etiology is: “If it scales, scrape it!”

For rashes of uncertain etiology, “If it scales, scrape it!”

Discoid Lupus Erythematosus

Key Points

  • 1.

    Whitish, scaling, scarring plaques in sun-exposed areas

  • 2.

    A small proportion have systemic lupus erythematosus

  • 3.

    Skin biopsy is diagnostic

Definition

Discoid lupus erythematosus (DLE) is one of several rashes that can occur in lupus. DLE is the rash that scales and scars. Immunoglobulins are found in the skin in this autoimmune disease. Clinically, the lesions appear as disk-shaped plaques surmounted by a white adherent scale that also involves the hair follicles. DLE may be limited to the skin, or it may be one of the manifestations of systemic lupus erythematosus (SLE).

Discoid lupus erythematosus (DLE) may be limited to the skin or may be a manifestation of systemic lupus erythematosus (SLE).

Incidence

The disease affects primarily young and middle-aged adults. It is uncommon, but the exact incidence in the general population is not known. Of all new patients seen in the authors’ dermatology clinic, 2 per 1000 were seen for DLE.

History

The eruption may be slightly pruritic but is more often asymptomatic. Patients may give a history of exacerbation after exposure to sunlight. In patients with DLE, a history should be taken for symptoms of possible SLE, including photosensitivity, hair loss, nasal and oral ulcerations, Raynaud’s phenomenon, arthritis, and other extracutaneous organs.

Physical Examination

The earliest lesion is a purplish-red plaque, which accumulates scale as it matures. The scale is white and usually cohesive, so it can often be removed in one piece. When this is done, the underside of the scale may show small, spiny projections. These have been called “carpet tacks,” and they represent the keratinous plugs that had been present in dilated hair follicles. The oldest lesions appear as depressed , atrophic plaques, often with pigmentary change, usually hypopigmentation in the center with a hyperpigmented rim ( Fig. 9.1 ).

Figure 9.1, Discoid lupus erythematosus. A. Erythematous, scaling, atrophic plaque with hyperpigmented border. B. Epidermis – hyperkeratosis with follicular plugging; vacuolar degeneration of basal cell layer. Dermis – perivascular and periappendageal inflammatory cell infiltration.

The distribution of the DLE lesion favors sun-exposed areas (i.e., the face, neck, upper trunk, and dorsal arms). An occasional patient has widespread cutaneous involvement. Erosions in the oral cavity, particularly of the palate, are occasionally found in patients with DLE. The scalp is frequently involved with scarring alopecia (see Chapter 20 ).

Differential Diagnosis

Psoriasis may be the most common misdiagnosis. The finding of atrophy helps to differentiate the two. Lichen planus lesions are also purplish, but they are usually small (papular), have scant scale, and do not result in depressed scars. The scaling patches and plaques that occur in subacute cutaneous lupus erythematosus (SCLE) also do not scar; frequently they are annular and are often accompanied by circulating anticytoplasmic antibodies—anti-Ro (SSA) and anti-La (SSB).

Differential Diagnosis of Discoid Lupus Erythematosus

  • Psoriasis

  • Lichen planus

  • Subacute cutaneous lupus erythematosus

Laboratory and Biopsy

Skin biopsy establishes the diagnosis ( Fig. 9.1B ). In addition to the history and physical examination, a laboratory screen for SLE should be done on all patients with DLE. This includes a complete blood cell count, a urinalysis, and an antinuclear antibody (ANA) test. If the latter is positive, an anti-DNA antibody test should be ordered. Patients with DLE who have positive ANA tests or persistent complete blood cell count abnormalities are more likely to develop SLE subsequently.

Patients with DLE should be screened for SLE with:

  • 1.

    Complete blood cell count

  • 2.

    Urinalysis

  • 3.

    Antinuclear antibody test

Therapy

Topical therapy is usually adequate. Steroids, applied topically or injected intralesionally, are used most often. Sun protection is important, and sunscreens that protect against both short UV (UVB) and long UV (UVA) light should be strongly recommended to all patients. Patients with extensive or recalcitrant disease sometimes require systemic therapy; antimalarials, such as chloroquine (Aralen) 250 mg daily or hydroxychloroquine (Plaquenil) 200 to 400 mg daily are used most often. Patients receiving these antimalarial drugs should undergo ophthalmologic examination every 12 months to monitor for the retinal toxicity that rarely is encountered with the dosages used in DLE. For patients with DLE not responding to the above measures, alternative systemic therapies, including retinoids (isotretinoin or acitretin), dapsone, thalidomide, azathioprine, mycophenolate mofetil, methotrexate, and oral gold may be used.

Therapy for Cutaneous Lupus

Initial

  • Topical steroids (e.g., clobetasol cream 0.05% b.i.d.)

  • Sunscreens (Anthelios) and sun protective clothing

Alternative

  • Antimalarials (e.g., hydroxychloroquine 200 mg b.i.d., chloroquine 250 mg daily)

  • Retinoids (e.g., isotretinoin, acitretin)

  • Thalidomide

  • Azathioprine

  • Mycophenolate mofetil

  • Methotrexate

  • Dapsone

  • Gold

Course and Complications

The course of the disease is chronic but, with therapy, usually controllable. New lesions may continue to appear over a course of years as old ones become inactive. Eventual remission occurs spontaneously in approximately 50% of patients. Scarring and postinflammatory hypopigmentation and hyperpigmentation are common and may result in disfigurement, particularly in blacks. In the scalp, the scarring leads to permanent alopecia; if extensive, this can be a cosmetic problem. In patients presenting with only DLE lesions, the risk of subsequently developing SLE is 5% to 10%.

5% to 10% of patients presenting with DLE subsequently develop SLE.

Pathogenesis

Lupus erythematosus has been classified as an autoimmune disease because of the autoantibodies found in the disease. In DLE, these are in the form of IgG and IgM deposited at the dermal–epidermal junction. The cause of this deposition and the role that these immunoglobulins play in the pathogenesis of the skin lesions are not clear. UV light has been implicated as a pathogenic factor. Circumstantial evidence for this includes the localization of lesions mainly in sun-exposed areas, the finding that many patients note that sun exposure exacerbates their skin disease, and experimental induction of skin lesions with UV light. A sequence of pathogenic events has been proposed as follows. UV light damages epidermal cells, releasing their nuclear antigens. These diffuse to the dermal–epidermal junction, where they combine with antibodies from the circulation, initiating an inflammatory reaction resulting ultimately in the clinical lesion.

T-cell dysregulation has also been implicated in the pathogenesis of cutaneous lupus. For example, increased activity of the Th2 subset of helper T cells has been found in lesional skin. The main function of these cells is to augment humoral immunity. Genetic predisposition to DLE is possible, but familial disease and association with specific HLA phenotypes have been reported more frequently with SLE than with DLE. Current evidence suggests that most patients with DLE have a genetically different disease from that in patients with SLE, a concept that accounts for the observation that most patients with DLE never develop SLE.

Fungal Infections

Key Points

  • 1.

    If it scales, consider scraping it for a KOH preparation

  • 2.

    Superficial fungi, dermatophytes, cause tinea infections

Definition

These disorders result from infection of the skin by fungal organisms collectively called dermatophytes ( phyte is the Greek word for plant). Various clinical lesions can result, but the most common are scaling, erythematous papules, plaques, and patches, which often have a serpiginous or worm-like border. The word tinea (Latin for worm) is used for these superficial fungal infections. It is followed by a qualifying term that denotes the location of the infection on the body. For example, tinea capitis is a fungal infection of the scalp, and tinea pedis is a dermatophyte infection of the feet. Tinea versicolor is the only exception; its name derives from the several shades of color that lesions may have in this disease.

Synonyms for fungal infection of the skin:

  • 1.

    Dermatophytosis

  • 2.

    Tinea

  • 3.

    “Ringworm”

  • 4.

    Incidence

Dermatophytic infections are common, in aggregate representing 2.5% of the authors’ new patients. The incidence is higher in warmer, more humid climates. Table 9.2 gives the prevalence of four of the more common skin infections in the general U.S. population.

Table 9.2
Fungal Infections
Prevalence in General Population (rate per 1000) a Location Clinical Appearance Differential Diagnosis
Tinea capitis b Scalp Round, scaling area of alopecia
Diffuse scaling
Red, boggy, swollen area with pustules (kerion)
Alopecia areata
Seborrheic dermatitis
Bacterial infection
Tinea corporis Body Annular, “ringworm” Nummular eczema
Pityriasis rosea (herald patch)
Psoriasis
Impetigo
Erythema annulare centrifugum
Granuloma annulare
Tinea cruris 7 Groin Sharply demarcated area with elevated, scaling, serpiginous borders Psoriasis
Seborrheic dermatitis
Intertrigo
Candidiasis
Erythrasma
Tinea faciale Face Slightly scaling, erythematous patches and plaques; border may not be well demarcated in all areas Photodermatitis
Lupus erythematosus
Seborrheic dermatitis
Contact dermatitis
Tinea manuum Hand Diffuse dry scaling, usually on only one palm Contact dermatitis
Xerosis
Psoriasis
Tinea pedis 39 Feet Interdigital maceration
Diffuse scaling on soles and sides of feet (“moccasin”)
Vesicles and pustules on instep
Maceration
Xerosis (dry skin)
Contact dermatitis
Dyshidrotic eczema
Pustular psoriasis
Tinea unguium (onychomycosis) c 22 Nails Subungual debris with separation from the nail bed Psoriasis
Trauma
Tinea versicolor d 8 Trunk White, tan, or pink patches with fine desquamating scale Vitiligo (white)
Seborrheic dermatitis (tan or pink)

a Data from the United States National Health Survey, 1978.

b See Chapter 20 .

c See Chapter 21 .

d See Chapter 13 .

History

In most dermatophytic infections, the patient presents with a scaling rash. Pruritus is common, and often the chief complaint. A history of exposure to infected persons or other mammals (e.g., dogs, cats, cattle) may be elicited.

Physical Examination

The physical findings and differential diagnosis vary with the different tineas. The findings in tinea capitis are discussed in Chapter 20 , and those in tinea unguium in Chapter 21 . Because tinea versicolor most often presents as white spots, it is discussed in Chapter 13 . The physical findings and differential diagnosis of the remaining dermatophyte infections are considered below.

Tinea Corporis

Key Points

  • 1.

    Annular patch with clear center and scaling, serpiginous border

  • 2.

    Scrape the border scales for the KOH preparation

Tinea corporis is the classic “ringworm.” Often, patients have a history of exposure to an infected animal such as a pet dog or cat.

Physical examination

The typical lesion is annular, with an elevated, scaling border and tendency for central clearing. One or several lesions may be present. In patients predisposed to chronic infection, the eruption may be widespread, and not all the lesions may be annular. In these instances, the finding of elevated serpiginous borders in some of the lesions is a helpful clue ( Fig. 9.2 ).

Figure 9.2, A. Tinea corporis – erythematous, scaling patches with serpiginous borders. B. Tinea. Epidermis – thickened stratum corneum infiltrated with fungal hyphae ( arrow ). Dermis – inflammation.

Differential diagnosis

The coin-shaped lesions of nummular eczema are usually multiple and are located on the extremities. They are often mistaken by the patient, and sometimes by the physician, as ringworm. In nummular eczema, one usually sees no central clearing, and the KOH preparation is negative.

Pityriasis rosea starts with a single herald patch, which is frequently mistaken for tinea. The correct diagnosis usually becomes evident when the generalized eruption develops within a few weeks. Although occasionally annular, lesions of psoriasis are usually thicker and more scaling than those of fungal infections. More typical lesions of psoriasis usually are also found, and, of course, the KOH examination is negative.

Uncommonly, impetigo presents in an annular configuration (see Fig. 3.8 ). The finding of vesicles, pustules, and crusts in annular lesions should lead one to suspect a bacterial, rather than fungal, cause.

Erythema annulare centrifugum and granuloma annulare (see Chapter 18 ) are two uncommon diseases that may be confused with ringworm. Clinically, the differences are that in erythema annulare centrifugum the scale is inside the elevated border and the KOH preparation is negative. In granuloma annulare, the border is more indurated and is not scaling. A skin biopsy is helpful in confirming the diagnosis of these two disorders. Both conditions are idiopathic and are usually localized, but occasionally generalized. The generalized form of erythema annulare centrifugum is called erythema gyratum repens , a rare condition that is almost always associated with an internal malignant disease. Generalized granuloma annulare is sometimes associated with diabetes mellitus.

Differential Diagnosis of Tinea Corporis

  • Nummular eczema

  • Pityriasis rosea

  • Psoriasis

  • Impetigo

  • Erythema annulare centrifugum

  • Granuloma annulare

Tinea Cruris

Key Points

  • 1.

    Erythematous patch with a serpiginous scaling border

  • 2.

    Scrotum and penis are not involved

A groin rash has several common causes ( Fig. 9.3 ); dermatophytic infection is one. Patients with tinea cruris (“jock itch”) frequently also have tinea pedis (“athlete’s foot”). The perspiration that occurs with exercise is probably the common predisposing denominator in these “athletic” rashes.

Figure 9.3, Tinea cruris – sharply marginated oval groin patches. Note typical sparing of penis and scrotum.

Physical examination

Dermatophytic infection in the groin may not appear as an annular lesion, but the border is elevated, serpiginous, and scaling. Often, lesions have a tendency for central clearing. The scrotum and penis are seldom involved.

Differential diagnosis

In addition to dermatophytic infection, there are two other common causes of a groin rash. Candidiasis appears as a bright, intensely erythematous (“beefy red”) eruption with poorly defined borders and satellite papules and pustules. The scrotum is often affected. Intertrigo represents simple irritant dermatitis, most often found in obese patients in whom moisture accumulates between skin folds in the inguinal area and, along with friction, causes skin irritation. The eruption is not as erythematous as that of candidiasis, and not as sharply demarcated as tinea cruris. The KOH preparation is positive in tinea cruris and candidiasis but negative in intertrigo. On occasion intertrigo can be complicated by a candidal infection.

Three major causes of a groin rash:

  • 1.

    Tinea cruris

  • 2.

    Candidiasis

  • 3.

    Intertrigo

Less often, psoriasis and seborrheic dermatitis selectively affect the groin. Erythrasma is an uncommon disease of intertriginous skin caused by Corynebacterium minutissimum . Clinically, it appears as a velvety patch with fine scale that, under Wood’s light examination, fluoresces a diagnostic coral pink.

Differential Diagnosis of Tinea Cruris

  • Candidiasis

  • Intertrigo

  • Psoriasis

  • Seborrheic dermatitis

  • Erythrasma

Tinea Faciale

Key Points

  • 1.

    Look for a sharp serpiginous border

  • 2.

    When in doubt, do a KOH preparation

This is an uncommon but often missed fungal infection of the skin ( Fig. 9.4 ).

Figure 9.4, Tinea faciale – oval, sharply demarcated, erythematous patch with slightly scaling inflammatory border and cleared center.

Physical examination

Tinea faciale appears as an erythematous, usually asymmetric, eruption on the face. An annular pattern is frequently not evident, but usually at least some of the borders are well demarcated and are often serpiginous, providing the clue to the fungal origin. Pustules may be present and may further obscure the clinical diagnosis ( Fig. 9.5 ).

Figure 9.5, Tinea barbae – erythematous plaque with alopecia and pustule.

Differential diagnosis

The lesions in seborrheic dermatitis are usually symmetric and are not well demarcated.

Rashes resulting from sunlight ( photodermatitis ) are distinguished by their distribution, which usually is symmetric, sparing areas that are relatively protected from the sun, such as the eyelids and under the chin. Contact dermatitis may also be confused with tinea faciale.

Occasionally, tinea faciale can appear as a butterfly rash, resembling that of lupus erythematosus . The finding of sharp serpiginous borders should heighten the suspicion of a fungal origin. However, for any of these conditions, if there is scale and any doubt, scrape it!

Differential Diagnosis of Tinea Faciale

  • Seborrheic dermatitis

  • Photodermatitis

  • Contact dermatitis

  • Lupus erythematosus

Laboratory tests

The single most important laboratory test for all of these fungal infections is the KOH preparation ( Fig. 9.6 ). The details of this procedure are outlined in Chapter 3 . The finding of hyphae on a KOH preparation is diagnostic of a dermatophytic infection, whereas a candidal infection will have hyphae and oval yeast on microscopic examination. Usually, the clinical presentation distinguishes between the two, with candida having satellite pustules around a beefy red patch and tinea having an annulare scaling patch with a clear center.

Figure 9.6, Tinea – positive potassium hydroxide examination showing hyphae ( arrow ).

If desired, one can also obtain scales for fungal culture. Cultures distinguish between candidal and dermatophytic infections, and are sometimes helpful in patients in whom dermatophytic infections are suspected but the KOH examination is negative.

A skin biopsy is not indicated. If a biopsy is done to rule out other disorders, the dermatopathologist may miss the fungal elements in the stratum corneum ( Fig. 9.2B ). Contrary to some misconceptions, a Wood’s light (black light) is of no help in diagnosing dermatophytic infection of the skin. A Wood’s light fluoresces infected scalp hairs in one type of tinea capitis, but infected skin does not show fluorescence.

Tinea Manuum

Key Points

  • 1.

    One hand, two feet are typically involved

  • 2.

    For the hand with the “dry” scaling unilateral palm, do a KOH preparation

Dermatophytic infection of the palm is uncommon but not rare. It virtually always occurs in a patient who has coexisting tinea pedis.

Physical examination

Typically, tinea manuum involves only one hand, resulting in the “one hand, two feet” syndrome ( Fig. 9.7 ). It appears as diffuse scaling of the palmar surface, much like the plantar scaling type of tinea pedis. The border on the wrist side is often sharply demarcated.

Figure 9.7, Tinea manuum – diffuse scaling patch of only one hand in a patient with tinea pedis – the “one hand, two feet” syndrome.

Differential diagnosis

Chronic contact dermatitis and dry skin, xerosis , can also appear as chronic scaling of the palms. However, these conditions usually involve both palms, and the border is generally not well demarcated.

Psoriasis can affect the palms with sharply demarcated scaling plaques. Usually, these plaques are bilateral, and are more elevated and erythematous than in tinea manuum; often, lesions of psoriasis elsewhere on the body support the diagnosis. KOH preparation is necessary in case of doubt.

Differential Diagnosis of Tinea Manuum

  • Contact dermatitis

  • Xerosis

  • Psoriasis

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