Seborrheic Dermatitis

Seborrheic dermatitis (Fig. 1) is a common chronic, superficial inflammatory disease of the scalp, face (especially the eyebrows and nasolabial folds), ears, and central chest, affecting 2% to 5% of the population. Clinically, the disease is characterized by thin erythematous plaques, often with a fine, greasy scale. Pruritus is common and can be severe.

Figure 1 Seborrheic dermatitis along the nasolabial folds in a young man.

Recognition of seborrheic dermatitis is important for the primary care physician, because it may be associated with systemic disease, such as Parkinson’s disease and human immunodeficiency virus (HIV) infection. Patients who have had a cerebrovascular accident (CVA) can develop seborrheic dermatitis on the scalp in a unilateral distribution, corresponding to the affected hemisphere. The pathophysiology of this phenomenon is not completely understood.

Differential diagnosis includes psoriasis, atopic dermatitis, allergic or irritant contact dermatitis, and dermatophyte (tinea) infections.

Treatment includes medicated shampoos containing zinc pyrithione, selenium sulfide, salicylic acid, coal tar, or ketoconazole in combination with topical corticosteroids. Alternatively, fluconazole 400 mg (one dose) may be effective in combination with a mild topical corticosteroid.

Seborrheic Keratoses

Seborrheic keratoses (Fig. 2), the most common benign cutaneous neoplasms, are warty, age-related hyperkeratotic papules and plaques that appear anywhere on the body, most commonly the trunk. Rarely, seborrheic keratoses indicate an underlying adenocarcinoma of the gastrointestinal tract if they appear suddenly in great numbers (sign of Leser-Trélat).

Figure 2 Seborrheic keratosis on the abdomen of an elderly man.

Differential diagnosis includes verruca vulgaris (warts), epidermal nevus, melanocytic nevi, and melanoma.

No treatment is necessary. If the plaques are pruritic, they can removed by curettage or cryotherapy.

Urticaria

Urticaria (Fig. 3), or hives, is most often caused by medication (commonly penicillin or other antibiotics, sulfa drugs, aspirin) or food (shellfish, nuts, chocolate), and less often by infection. Hives are pruritic, edematous, evanescent wheals that resolve within 24 hours.

Figure 3 Urticaria on the flank.

Acute urticaria typically lasts less than 6 weeks. Wheals in a fixed location for more than 24 hours suggest the possibility of urticarial vasculitis and warrant a skin biopsy. Chronic idiopathic urticaria for which no trigger can be identified often requires further testing such as serum radioallergosorbent testing (RAST) or skin prick-patch testing.

Differential diagnosis includes erythema multiforme, systemic lupus erythematosus (SLE), bullous pemphigoid, mastocytosis.

Treatment includes elimination of known causes, antihistamines (H₁ and H₂ blockers), oral corticosteroids for acute flares, and, in refractory cases, immunosuppresants such as sulfasalazine and cyclosporine.

Erythema Multiforme

Erythema multiforme (Fig. 4), a cutaneous hypersensitivity reaction, is usually caused by infection (herpes simplex virus or Mycoplasma pneumoniae) and less commonly by drug sensitivity (sulfonamides, barbiturates, antibiotics). Division of erythema multiforme into two subsets based on clinical severity has been proposed: erythema multiforme minor and erythema multiforme major or Stevens-Johnson syndrome.¹ Macules, papules, plaques, vesicles, or bullae, often with a targetoid or iris appearance, occur on the skin, often with an acral distribution (extremities). Erythema multiforme can also occur on mucosal surfaces. Prodromal symptoms are uncommon. Erythema multiforme minor is self limited and usually resolves within 2 to 4 weeks.¹

Figure 4 Targetoid plaques on the dorsal surface of the fingers.

Differential diagnosis includes urticaria, bullous arthropod reaction, drug eruption, and bullous pemphigoid.

Treatment includes suppressive oral antiviral agents such as acyclovir or valacyclovir, for herpes infection; discontinuation of possible causative medications; and supportive care.

Vitiligo

Vitiligo (Fig. 5) is characterized by a focal or generalized distribution of depigmented macules and patches. The hairs in the vitiliginous areas are usually white. Vitiligo commonly occurs in periorificial areas (mouth, orbits, vagina, anus) or at sites of trauma (hands, elbows, knees). The disorder is often associated with autoimmune thyroid disease, insulin-dependent diabetes mellitus, pernicious anemia, or Addison’s disease.

Figure 5 Vitiligo on the hands.

Differential diagnosis includes tinea versicolor, pityriasis alba, postinflammatory hypopigmentation, and hypopigmented mycosis fungoides.

Treatment includes broad-spectrum sunscreens, potent topical corticosteroids, topical calcineurin inhibitors (tacrolimus or pimecrolimus), narrow band ultraviolet (UV) B phototherapy, psoralen with UVA (PUVA) therapy, or total depigmentation for extensive disease.

Erythema Nodosum

Erythema nodosum (Fig. 6), the most common type of panniculitis, is characterized by painful, erythematous nodules on the shins and occasionally elsewhere. Erythema nodosum occurs most commonly in young women, with a peak incidence between 20 and 40 years.¹ In addition to the cutaneous findings, patients can have fever, malaise, arthralgias, or arthritis. Typically the eruption is self limited, lasting an average of 3 to 6 weeks.¹

Figure 6 Erythema nodosum on the leg of a young woman.

The most common cause of erythema nodosum in the pediatric population is streptococcal pharyngitis. Other infectious causes include tuberculosis, gastrointestinal (GI) infections with Yersinia, Salmonella, or Shigella, and systemic fungal infections. Less common causes include drug sensitivity (sulfonamides, salicylates, iodides, oral contraceptives or hormone replacement therapy), and a variety of systemic diseases, most often inflammatory bowel disease (Crohn’s disease more than ulcerative colitis) and sarcoidosis.

Differential diagnosis includes nodular vasculitis and other types of panniculitis.

Treatment includes identifying and eliminating known causes, bed rest and elevation of the extremities, aspirin or nonsteroidal anti-inflammatory medications (NSAIDs), colchicine, and supersaturated potassium iodide.

Pemphigus Vulgaris

Pemphigus vulgaris (Fig. 7) is an uncommon chronic and debilitating blistering disease characterized by painful mucosal erosions and flaccid blisters that become erosive. Ninety percent of patients have mucosal disease, and erosions can outnumber intact bullae. Biopsy reveals characteristic suprabasilar acantholysis and intraepidermal bullae formation. Direct immunofluorescence reveals a chicken-wire pattern of deposition of immunoglobulin (Ig) G within the epidermis.

Figure 7 Eroded bullae on the back of an elderly man with pemphigus vulgaris.

Pemphigus vulgaris can develop at any age, but it most commonly occurs in the fourth to sixth decades of life, usually in people of Mediterranean or Jewish ancestry.² Morbidity and mortality are significant, even with treatment.

Differential diagnosis includes bullous pemphigoid, Stevens-Johnson syndrome, and epidermolysis bullosa acquisita.

Treatment includes good wound care for affected skin, systemic corticosteroids, various steroid-sparing immunosuppressants, rituximab, intravenous immunoglobulin (IVIg), and plasmapheresis.

Bullous Pemphigoid

Bullous pemphigoid (Fig. 8) is the most common bullous disease and is characterized by large, tense subepidermal blisters, which are often pruritic. Mucosal disease is rare. Biopsy reveals subepidermal bullae and an infiltrate of eosinophils. Direct immunofluorescence reveals a linear deposition of IgG at the dermal-epidermal junction.

Figure 8 Intact bullae lateral to the knee in a middle-aged woman with bullous pemphigoid.

Bullous pemphigoid occurs most commonly in the elderly, with an onset between 65 and 75 years of age. Prognosis is influenced by age and general condition of the patient, not by extent of disease activity.³ Treatment of older patients in poor health requires caution.

Differential diagnosis includes bullous SLE, epidermolysis bullosa acquisita, cicatricial pemphigoid, and dermatitis herpetiformis.

Treatment includes topical and systemic corticosteroids, steroid-sparing immunosuppressants, and tetracycline in combination with niacinamide.

Epidermolysis Bullosa Acquisita

Epidermolysis bullosa acquisita (Fig. 9) is an uncommon bullous disease characterized by skin fragility, milia (small cysts), scarring alopecia, and nail dystrophy. Skin disease typically follows trauma and occurs primarily on the hands, feet, elbows, and knees. Immunofluorescence is similar to bullous pemphigoid, with IgG deposition at the dermal-epidermal junction.

Figure 9 Bullae and erosions on the hands are characteristic of epidermolysis bullosa acquisita.

Differential diagnosis includes bullous pemphigoid and bullous SLE.

Treatment includes topical and systemic corticosteroids, steroid-sparing immunosuppressants, colchicine, and plasmapheresis.

Cutaneous Metastases

Cutaneous metastases (Fig. 10), are uncommon, and the reported prevalence varies from 0.7% to 10% of all patients with cancer.⁴ Any malignant neoplasm can metastasize to the skin. Cutaneous metastases from cancers of the lung, large intestine, and kidney are most commonly found in men; cancers of the breast and large intestine are the most likely primary tumors to metastasize to the skin in women.⁴ Metastases to the skin are usually flesh-colored to violaceous nodules that appear in close proximity to the primary neoplasm; most common sites are the head (scalp), neck, and trunk.

Figure 10 Cancer.

A, Carcinoma en cuirasse in a woman with metastatic breast cancer. B, Metastatic prostate cancer in an elderly man.

Differential diagnosis includes pilar or epidermal inclusion cyst, adnexal tumor, neurofibroma, and lipoma.

Treatment depends on the primary neoplasm and overall prognosis.

Paget’s Disease

Paget’s disease of the breast (Fig. 11) is an uncommon condition characterized by unilateral eczematous plaque of the nipple and areola. The disease is strongly associated with an underlying invasive carcinoma of the affected breast or ductal carcinoma in situ (DCIS).⁵

Figure 11 Paget’s disease of the nipple in a middle-aged woman.

Extramammary Paget’s disease is typically a persistent, eczematous plaque of the anogenital or axillary regions whose morphology and histology strongly resemble Paget’s disease of the breast. Extramammary Paget’s disease affects older adults and is often associated with an underlying adnexal (apocrine) carcinoma or an underlying cancer of the genitourinary tract or distal gastrointestinal tract.

Differential diagnosis includes allergic or irritant contact dermatitis (especially if bilateral), psoriasis, and dermatophyte (tinea) infection.

Treatment includes surgical excision, radiation therapy, and photodynamic therapy. Referral to oncology is recommended.

Acanthosis Nigricans

Acanthosis nigricans (Fig. 12) is characterized by smooth, velvet-like, hyperkeratotic plaques in intertriginous areas (e.g., groin, axillae, neck). Three types of acanthosis nigricans have been recognized.

Figure 12 Acanthosis nigricans in the axilla of an obese man.

Type I is associated with malignancy. Occasionally, acanthosis nigricans is a marker of an underlying adenocarcinoma, especially of the gastrointestinal tract (60% gastric). Malignant acanthosis nigricans has a sudden onset and more extensive distribution, including the face, palms, and trunk. Type II is the familial type, with autosomal dominant transmission. It is very rare and appears at birth or soon after. Type II has no malignancy association. Type III acanthosis nigricans is associated with obesity and insulin resistance. Type III is the most commonly occurring type.

Acanthosis nigricans can develop following the use of some medications, such as systemic corticosteroids, nicotinic acid, diethylstilbestrol, and isoniazid (INH).

Differential diagnosis includes confluent and reticulated papillomatosis of Gougerot and Carteaud and Dowling-Degos disease.

Treatment for type I acanthosis nigricans includes identifying and removing the malignant tumor. Treatment for types II and III includes weight loss and treatment of the underlying endocrine disorder, if applicable. Topical treatments including tretinoin, calcipotriol, urea, and salicylic acid may be helpful.

Cowden’s Syndrome

Cowden’s syndrome, an autosomal dominant cancer syndrome caused by mutations in the tumor suppressor gene PTEN, is characterized by multiple tricholemmomas (wartlike growths) around the mouth, nose, and ears; cancer of the breast, endometrium, or thyroid gland; and thyroid disease (adenomas or goiter), mental retardation, and fibrocystic disease of the breast.

Sweet’s Syndrome

Sweet’s syndrome (Fig. 13), or acute febrile neutrophilic dermatosis, has a strong association with acute myelocytic or myelomonocytic leukemia. Affected patients, usually middle-aged women, have painful erythematous to violaceous plaques on the face, extremities, and trunk. Most have fever, malaise, arthralgias, myalgias, and conjunctivitis.

Figure 13 An erythematous edematous plaque on the arm of a woman with Sweet’s syndrome.

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