Abstract
Scale is the common characteristic of the diseases discussed in this chapter. Scaling disorders have also been called the papulosquamous (squamous means scaly) diseases. As previously emphasized, scale represents thickened stratum corneum and is to be distinguished from crust , which represents dried surface fluid, as found in the vesicular and pustular disorders. The elevation of scaling papules and plaques results from thickening of the epidermis (acanthosis) or underlying dermal inflammation. A patch is a scaling macule. It is flat because it has no epidermal thickening (the epidermis may even be atrophic) and little dermal inflammation.
Chapter Contents
- 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.
| 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
- 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 ).
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).
- ●
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.
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
- 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.
| 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
- 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 ).
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.
- ●
Nummular eczema
- ●
Pityriasis rosea
- ●
Psoriasis
- ●
Impetigo
- ●
Erythema annulare centrifugum
- ●
Granuloma annulare
Tinea Cruris
- 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.
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.
- ●
Candidiasis
- ●
Intertrigo
- ●
Psoriasis
- ●
Seborrheic dermatitis
- ●
Erythrasma
Tinea Faciale
- 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 ).
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 ).
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