A 20-year-old woman complains of skin problems and is noted to have erythematous papules on her face with blackheads (open comedones) and whiteheads (closed comedones). She has cystic lesions on her chest and back. She is prescribed topical tretinoin and topical clindamycin, but without a totally acceptable result. You are considering oral antibiotics, but the patient requests oral isotretinoin.
Which of the following statements is correct?
Comedonal acne is first managed with topical retinoids. Mild to moderate disease usually requires the use of topical antibiotics and topical retinoids. The combination of topical retinoids and topical antibiotics has been shown to be better than topical retinoids alone. Oral combination contraception decreases sebum production and is useful in moderate acne. Moderate to severe acne is managed with oral antibiotics, usually tetracycline derivatives, added to topical therapy. The more severe papulonodular forms require oral isotretinoin to inhibit sebaceous gland sebum production. Intralesional steroids for cystic lesions may be considered, but may cause thinning of the subcutaneous fat. Oral tetracycline and isotretinoin may cause pseudotumor cerebri and should never be used together. Isotretinoin has a high potential for teratogenicity and should not be used in women in their childbearing years unless two effective forms of contraception are being practiced. Isotretinoin can cause hypertriglyceridemia, hepatotoxicity, musculoskeletal pains and drying of mucous membranes. It should be reserved for severe or refractory acne.
A 22-year-old man presents with a 6-month history of a red, nonpruritic rash over the trunk, scalp, elbows, and knees. These eruptions are more likely to occur during stressful periods and have occurred at sites of skin injury. The patient has tried topical hydrocortisone without benefit. On examination, sharply demarcated plaques are seen with a thick scale. Pitting of the fingernails is present. There is no evidence of synovitis.
What is the best first step in the therapy of this patient’s skin disease?
The rash described is classic for psoriasis, a common chronic inflammatory skin disorder. Its characteristic features include sharply bordered papules or plaques with silver scale, usually located on the knees, elbows, and scalp. Stress, certain medications such as lithium, and skin injury commonly exacerbate the disease. The distribution of the described rash would make contact dermatitis unlikely. In the differential of psoriasis are lichen planus (polygonal pruritic purple papules with lacy mucous membrane lesions), pityriasis rosea (herald patch on trunk, spreading in a Christmas tree pattern), and dermatophytes (usually less well demarcated; affecting skin, hair, and nails). Topical corticosteroids of moderate or high potency are the first agents to try in psoriasis without joint involvement.
Topical vitamin D analogues such as calcipotriene or calcitriol may be combined with topical steroids in refractory cases, but they are less effective and much more expensive than topical steroids. Psoralens with UVA phototherapy (PUVA) are reserved for moderate to severe widespread cases because of an increased risk of squamous cell carcinoma of the skin. Methotrexate, cyclosporine, and immune response modifiers such as etanercept are useful in difficult cases, but carry a higher risk of side effects.
A 25-year-old complains of fever, nausea, and myalgias for 5 days, and now has developed a macular rash over his wrists, palms, ankles, and soles with some petechial lesions. The rash recently ascended to his arms and legs. The patient recently returned from a summer camping trip in Tennessee.
Which of the following is the most likely cause of the rash?
The rash described is most consistent with Rocky Mountain spotted fever, for which a tick is the intermediate vector. Secondary syphilis could present with a macular rash in the same distribution, but does not cause an acute febrile syndrome with myalgia. Always think of these two diagnoses when a rash begins on the palms and soles. Contact dermatitis does not cause petechial lesions. The skin lesions in disseminated gonococcal infection can be distal, but are usually few in number and are pustular. Giardiasis is acquired from contaminated water but does not cause fever or a rash. Trichinosis, acquired from the ingestion of contaminated pork, can cause myalgias and a maculopapular rash, but rarely shows the distal involvement seen in this patient. Trichinosis causes prominent periorbital edema and eosinophilia.
A 17-year-old adolescent girl presents with a pruritic rash localized to the wrist and chest at the sternal notch. Papules and vesicles are noted in a bandlike pattern, with oozing from some lesions.
Contact dermatitis causes pruritic plaques or vesicles localized to an area of contact. In this case, nickel in her bracelet and pendant is the inciting agent. Contact dermatitis may produce vesicles with weeping lesions. The process may be related to direct irritation of the skin from a chemical or physical irritant or may be immune mediated. Herpes simplex produces grouped vesicles, but they are painful and are unlikely to occur around the wrist. Herpes zoster is painful and occurs in a dermatomal distribution. Atopic dermatitis usually affects skin creases (especially the antecubital fossae) and the hands. It may be vesicular but is more often associated with skin thickening (lichenification) as a result of constant scratching. Seborrheic dermatitis presents as red, scaly nonpruritic lesions localized to the eyebrows, nasolabial folds, scalp, and retroauricular areas.
A 35-year-old asthmatic woman develops an itchy rash over her back, legs, and trunk a few minutes after sitting in a public hot tub. Erythematous, edematous plaques are noted. The wheals vary in size. There are no mucosal lesions and no swelling of the lips.
What is the best first step in management of her symptomatic rash?
Urticaria, or hives, is a common dermatologic problem characterized by pruritic, edematous papules and plaques that vary in size and come and go, often within minutes or hours. In cholinergic urticaria, mast cells may be stimulated by heat, cold, pressure, water, stress, or exercise. Immunologic mechanisms can also cause mast cell degranulation. Patients with atopic conditions, such as asthma or eczema, are more likely to suffer from cholinergic urticaria. Folliculitis caused by P aeruginosa can cause a rash after exposure to hot tubs, but the lesions are not as diffuse, with a line of demarcation depending on the water level, and are usually pustular. This “hot tub” dermatitis begins 8 to 48 hours after exposure to contaminated water (ie, long enough for superficial infection to develop). Systemic antibiotics are seldom necessary, and tetracyclines would be the wrong choice against pseudomonads. Cercarial dermatitis (swimmer’s itch) may occur after swimming or wading in fresh water during spring and summer. Diffuse pruritic papules may appear four to 48 hours after exposure. Treatment is symptomatic. Avoidance of the offending agent, when it is identifiable, is most important in management of urticaria. Oral nonsedating antihistamines provide symptomatic relief and are safely used prophylactically. Glucocorticoids play a minimal role in management of urticaria unless the process is severe and unremitting. Epinephrine plays no role unless there is concomitant anaphylaxis. Agents such as aspirin or alcohol, which aggravate cutaneous vasodilation, are contraindicated.
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